Press the Home key not bad iphone7 you expect it?        

  Home key

  Home key as the indispensable parts with ipone, but users often use, due to the frequent use, easy to press the Home key has been broken by the user to worry about. However, for users, this fear of the future may become redundant. why? Because Apple is likely to use in the next generation of virtual Home button iphone7, a Home button that nature iphone easily broken, it will become history!

  Press the Home key not bad iphone you expect it?

  Recently, media sources said that Apple's upcoming Home key iPhone7 to be change, does not allow the user to press down, Apple will offer several modes to complete the operation, such as clicking a return to the desktop, press and evocative Siri, call the weight the background, double-click brings up the one-handed mode, in addition, iPhone7 Force touch the Home button provides touch operation, pressing the Home key, then, will feedback on the efforts. Meanwhile, the Home key or have Touch ID function, and unlock more accelerated rate.

  If Apple really did believe iPhone7 the Home key will give users a new experience. Home key is not pressed, the biggest benefit is the Home key will not be so easily broken, the previous iPhone's Home button Press bad is often a user will encounter problems, and repair the Home key cost is not low.

  In addition to the Home key change, iPhone7 there is a change in fruit powder is very much looking forward, it is the body to store changes. Apple will cancel the fuselage on iPhone7 16GB storage, replaced by a 32GB storage started at the appearance and not much change in circumstances, body storage increases, is expected to attract more consumers.

  Although iPhone7 little change, but some of the details in place, Apple is still very hard, at the same time, iOS 10 introduction of the system as well as A10 processor is mounted, also highlights iPhone7 lies. As iPhone7 Plus, even more highlights, the biggest highlight is the dual camera, which is a number of local fruit powder whom echocardiography, dual camera brings a strong ability to take pictures.

  For such iphone7 is not very looking forward to it?


          Dr. Cohen-Maman Laureen        
Cohen Maman Laureen

Specialty

  • Pediatric cardiology and cardiac echocardiography

Clinical Experience

  • August 2014 - Actually: Cardiologist in Macabi and Private Practice-Marom medical center Kfar Saba
  • Feb 2013 - Actually Internal medicine doctor and cardiologist in Medix Medical service
  • Feb 2010 - May 2010 cardiologist in ICU Ambulance in Shahal 
  • Nov 2008 - May 2009: Weekly shifts as a cardiologist in Intensive care unit and inpatient. Clinic La Casamance - Aubagne and Clinic Clairval - Marseille

Academic Experience

  • Cardiologist in catheterization room as Echocardiographist Prof Banai
  • Cardiologist in internal medicine Unit- Pr Rogowsky
  • Cardiologist in cardio thoracic surgery in outpatient clinic
  • Tel Aviv Medical Center - Ihilov Pr Rogowsky
  • Tel Aviv Medical Center – Ihilov - Prof Oretsky
  • Tel Aviv Medical Center – Ihilov - Prof Yeshurun

Education

  • Sept 1998 - Oct 2004 Education Medical studies:University of Mediterranean Aix-Marseille II, School of medicine
  • DES (diploma of specialty) Oral exam passed in Oct 2008 on Transcatheter balloon dilation versus surgical treatment in neonates with critical aortic stenosis
  • DIU (subspecialty diploma) of pediatric cardiology
  • DU (subspecialty diploma) of cardiac echocardiography
  • Master degree in Human pathology specialty genomic and health - Prof J.L Mege
  • Certificates for completion of master
  • Secondary studies: Sept 1995 - jun1998 Lycée Yavné Marseille Scientific High School: Graduate with honors ( Baccalauréat avec mention)

Presentation in congresses

  • Jun 2009: L.Cohen, A.Dragulescu, V.Fouilloux, B.Bonello, B.Kreitmann, D.Metras, A. Fraisse, Timone Children's Hospital, Marseille, France“Transcatheter balloon dilation versus surgical commisurotomy in neonates with critical aortic stenosis”. L.Cohen, A.Fraisse, A.Dragulescu, P.Amedro, D.Metras, B.Kreitmann, S.Camilleri Timone Children's Hospital, Marseille “Outcome of pulmonary artery angioplasty in children”
  • 5th World congress of pediatric cardiology and cardiac surgery Cairns-Australia
  • Jan 2006: L.Cohen, A.Fraisse, F.Rouault, G.Habib, P.Ambrosi. Timones’s Hospital, Marseille “Patent Ductus arteriosus in the elderly” - Journées européennes de cardiologie Paris-France

Board Memberships and Affiliations

  • Israel heart association as affiliate
  • French society of cardiology as affiliate
  • European society of cardiology as affiliate
  • SAFIR Association of French medical practitioner as Treasurer

          Endo Pills - 14        
Informação cientifica de ação rápida - Ano 3 N° 14

Curso de Especialização em Endocrinologia - PUC
Instituto Estadual de Diabetes e Endocrinologia Luiz Capriglione
Prof.: Luiz César Povoa (A48)
Ricardo Martins Rocha Meirelles (A38)
Editores: Rosa Rita Santos Martins (A34), Isabela Bussade (A8) e Denise Momesso (R2)
Editores Associados: Walmir Coutinho (A22), Edna Pottes (A35) e Claudia Pieper (A22)
Composição Gráfica: Wallace Margoniner

Prezados colegas, nesta edição do Endo Pills trazemos alguns pôsteres apresentados no ICE- International Congress of Endocrinology pelo IEDE.

O ICE foi um grande orgulho, não só para o Brasil por ter sido sede de tão importante evento, mas principalmente para o Rio de Janeiro e nossa Instituição, que teve na presidência e vice presidência Dr Amélio Godoy e Dr Ricardo Meirelles, além de participação expressiva de grande numero de staffs e alunos do IEDE, tanto como congressistas, palestrantes como nas apresentações orais e pôsteres.
Nesta edição temos a possibilidade de ver, ou rever, o excelente nível do material científico que representou nossa instituição neste importante evento.
Boa leitura a todos
Isabela Bussade

HYPERPARATHYROIDISM AFTER RADIOACTIVE IODINE THERAPY

OBJECTIVE: To describe a case of parathyroid adenoma (pa) emerging 18 years after radioactive iodine therapy (rait).

MATERIAL AND METHODS: We report a case of a patient with graves` disease who developed primary hyperparathyroidism (hpt) 18 years after rait in the endocrinology service of the IEDE.

RESULTS: AASD, 63 years-old (yo), female with a previously known history of graves` disease, first diagnosed in 1973, with ocular disease associated, when she was 25 yo. Initial therapy was with methimazol for about 3 years. First remission occurred in 1976 when she stopped her medical treatment. On follow-up there was a recurrence in 1978 when she again restarted treatment, this time with propiltiouracil. In 1979 achieved remission again. For more two times on evolution remissions and fails occurred. After the last recurrence she underwent rait with 9 mci of 131i and thus hypothyroidism developed. levotiroxin (lt4) therapy was initiated and tittered until a dose of 62,5mcg per day. in 2005 she started bilateral legs and arms pain and fatigue that worsened in 2007 when laboratorial analysis was ordered as follows: total calcium (ca) 14,1mg/dl [normal range(nr): 8,5-10,2]; phosphorus (p) 1,8mg/dl (nr: 2,8-4,1); pth: 496pg/ml (nr: 16,6-65). Medical therapy for hypercalcemia was started with saline infusion, furosemide and pamidronete but was no effective. The new dosages of ca, p and pth were respectively 14; 2, 3 and 666. An ultrasound was obtained and a nodule in the posterior aspect of the left lobe was found. A fine needle aspiration (fna) with subsequent imunohistochemical analysis showed parathyroid cells. An inferior left parathyroid was performed and demonstrated a parathyroid adenoma.

CONCLUSION: according to some authors, the rait could be a risk factor for hpt, including pa. observations indicate that not only external radiation, but also radiation from 131i is a risk factor for development of hpt and it is emphasized that age at the time of radiation treatment may be of decisive importance in this context. In a recent review of cases the average latency time to the development of hpt after rait was 13,5 ± 9,1 years. Serum calcium surveillance has been suggested for patients who have undergone rait treatment.
Warszawski L; Canton APM; Puppin BA; Novaes FS; Frota RSC; Zagury RL; Campos SC

EXHAUSTED ACROMEGALY: CASE REPORT

INTRODUCTION: Pituitary apoplexy is a rare event, particularly in functioning pituitary adenomas. Tumor size reduction may follow, but endocrine remission has been rarely described.

CASE REPORT: A case of pituitary apoplexy resulting in acromegaly endocrine remission is reported. a 37-year-old male patient was referred to the diabetes and endocrinology state institute (IEDE), presenting acromegalic phenotype, with a 15- year evolution prior to diagnosis, along with recent complaints of headache, asteny and mucous-cutaneous paleness. A computed tomography (ct) scan was performed and revealed an intrasellar hipodense mass suggestive of pituitary adenoma. One year later, the patient had clinical and laboratorial findings of panhypopituitarism and was admitted for diagnostic procedures. A magnetic resonance imaging (mri) demonstrated disappearance of the mass and empty turcic sella.

DISCUSSION: acute pituitary apoplexy is the sudden neurological breakdown that follows a fulminant expansion of the gland, caused by isquemic or haemorrhagic events. The typical clinical presentation, with marked neurological signs and symptoms, is observed in only 6 to 10% of the cases, and can be the first pituitary adenoma manifestation. In the rest of the patients, the pytuitary function is rather preserved, with moderate symptoms, such as headache. In those cases, subclinical pituitary apoplexies frequently go underdiagnosed. Depending on the amount of destruction, permanent or transient, posterior or anterior pituitary disfunction might occur. gonadotrophins deficiency is more frequent, followed by acth and tsh deficiency, and less usually, abnomal prolactin secretion. Empty sella may appear as an outcome of massive pituitary tumor infarction. a few cases of growth hormone-secreting pituitary adenoma necrosis resulting in spontaneous remission and panhypopituitarism have been described in the literature. However, the term cure is not applicable, once the definitive evolution of those cases is still unknown.

CONCLUSION: this case report is ment to raise awareness of this rarely described syndrome, which is also known as exhausted acromegaly. Furthermore, the apoplexy is generally subclinical; wich imposes an even greater diagnostic challenge. Therefore, pituitary adenoma spontaneous resolution may be more prevalent than estimated.
Warzawsky L, Costa DFP, Bragança JB, Lemos H, Sterza L, Farage M

CASE HISTORY OF COEXISTENT THYROTOXICOSIS AND JAUNDICE

OBJECTIVE: to describe the association of the rare complication of jaundice with thyrotoxicosis.

MATERIALS AND METHODS: we report the clinical and laboratory findings of a case of severe jaundice (total bilirubin levels: 52, 30 mg/dl) associated with hiperthyroidism and heart failure. We made an overview of previously published cases of c oexistent thyrotoxicosis and jaundice, methimazole- and carbimazole-induced hepatotoxicity and approach to treatment found in a medline search.

RESULTS: in a 54 year-old white woman with hyperthyroidism, treatment with methimazole 40 mg /day was initiated. One month later, scleral icterus, dark urine, fatigue and abdominal discomfort prompted discontinuation of the therapy. Laboratory findings were: alanine and aspartate aminotransferase 46 u/i (n: <31) and 87 u/i (n: <31) respectively, alkaline phosphatase 226 u/i (n: 35-104), gamma-glutamyl transpeptidase 138 iu/i (n: 7-32) and bilirubin 44 mg/di (n: <1). Abdominal ultrasonography showed normal bile ducts; echocardiography showed heart failure. Lithium therapy was applied before radioiodine therapy. She was treated with 17 mci of 131i and, persisting in hyperthyroidism, five months later received a new treatment with 25 mci of 131i. The highest values of bilirubin were found in moments of heart failure exacerbation, reaching the upper value of 52, 30 mg/dl. Resolution of the jaundice occurred after 28 weeks without methimazole.

CONCLUSION: the data strongly suggest that in this patient, the hepatic dysfunction was primarily due to hyperthyroidism observing the long time to resolution of her jaundice. It is a rare complication and h ypotheses regarding the cause of cholestasis in hyperthyroidism per se suggest that the hypermetabolic state increases the hepatic oxygen consumption without simultaneous increasing in the hepatic blood flow thus lowering the oxygen tension and interfering with bile transport. Besides, increased liver metabolism in response to thyroid hormone increases the rate of bile flow to the point of saturation. Also, there is the possibility of direct toxic effect of t4, but studies have not confirmed this. Considering her cardiovascular disorder, therapy with lithium carbonate was a useful adjunct to rai therapy to prevent exacerbation of thyrotoxicosis. Coexistent heart failure is a predisponent factor to severe jaundice in association with hyperthyroidism.
Novaes, FS; Souza, MVL; Canton, APM; Puppin, BA

REVERSIBLE PULMONARY HYPERTENSION AND RIGHT HEART FAILURE ASSOCIATED WITH HYPERTHYROIDISM.

INTRODUCTION: Hyperthyrodism may present with a variety of cardiovascular symptoms. Recent reports suggest an association between hyperthyroidism with pulmonary hypertension (ph) and isolated right heart failure. We described a case report of a ph secondary to hyperthyroidism which improved after restoration of euthyroid state.

CASE REPORT: 72 years old women presented with exertion dyspnea, fatigue, palpitation, bilateral leg edema, ascites and weight lost. Physical examination showed irregular heart beat, signs of right heart failure and no evidence of pulmonary congestion or disease. atrial fibrillation was confirmed by electrocardiogram. Echocardiogram revealed isolated right heart failure, severe tricuspid regurgitation and ph, with pulmonary artery pressure (pap) of 65 mmhg. work up for the common secondary causes of ph was negative, including, congenital intra-cardiac shunts, left-side atrial or ventricular heart disease, disorders of the respiratory system including hypoxemia and pulmonary tromboembolism, collagen vascular disease, primary portal hypertension, hiv infection, schistossoma mansoni infection, as well as ph secondary to drugs or toxins. The only concurrent illness identified was graves disease, by laboratory findings of thyrotoxicosis and positive thyroid peroxidase (tpo) autoantibody. Treatment was initiated with propylthiouracil, oral anticoagulation (because of atrial fibrillation) and diuretics. One month later, euthyroid state was achieved and there was clinical resolution of right heart failure. After one year of outpatient follow-up, an echocardiogram was performed and revealed improvement of ph, with pap of 35 mmhg, mild tricuspid regurgitation and normal right heart function.

CONCLUSION: elevated pulmonary pressure may be a frequent finding in thyrotoxicosis, but often unrecognized. It may be asymptomatic or associated with right heart failure. The exact reasons for the development of ph in thyroid disease are not clear. Most importantly, hyperthyroidism is a potential reversible cause of ph and it should be included in the etiology of secondary pulmonary hypertension.
Momesso DP; Puppin BA; Tavares P; Mattos PE; Souza MVL.

MAURIAC SYNDROME: STILL A CONCERN?

INTRODUCTION:Mauriac’s Syndrome (MS) is a rare complication of diabetes mellitus type 1 (dm1), characterized by hepatomegaly, growth failure and poor glycemic control, described mainly in children and teenagers. We present an adult female with ms.

CASE REPORT: 22 years old female with dm1 since age of 6, presenting hepatomegaly, high hba1c and variability on smbg , great elevation of liver enzymes, triglicerides (>1000 mg/dl), total cholesterol (543 mg/dl), ldlc (245 mg/dl) and hba1c (13%), modest elevation of alkaline phosphatase and normal billirubin. weight 44 kg, height 1,51m, bmi of 18,8kg/m2. ultrasound detected hepatomegaly and fatty infiltration aspect. hepatitis panel showed only hepatitis b past immunization. ceruloplasmin, ferritin, transferring saturation were normal. autoimmune hepatitis was excluded. liver biopsy showed glycogen deposits in the hepatocytes and evidence of steatohepatitis. she was treated with pioglitazone, ursodiol, genfibrozil, atorvastatin , glargine and lispro insulins. liver enzymes trended downwards as her glucose management improved, but it took 4 years to normalize.

DISCUSSION: The differential diagnosis of her liver disease included autoimmune hepatitis, acute hepatitis, wilson`s disease and hemochromatosis, which were excluded. Her signs and symptoms could be explained by ms: hepatomegaly, glycogen infiltration of the liver and short stature in people with poorly controlled diabetes. hypertriglyceridemia is due to poor glycemic control and ms. steatosis and glycogenosis should be distinguished by histology. Whereas steatosis may progress to fibrosis and cirrhosis, glycogenosis does not. Liver biopsy, on this case, showed both glycogenosis and steatohepatitis. The better glycemic control reverted liver enzymes alterations and hepatomegaly, suggesting that the major component of hepatic disease was glycogenosis. Other medications, such as pioglitazone, might have collaborated to improvement.

CONCLUSION: even though ms has become rare, it should be considered not only in children, but also in adults with dm1, acute hepatomegaly and abnormal liver function. The diagnosis is important because prolonged improvement of hba1c can normalize liver function, hypertriglyceridemia and also prevent dm1 acute and chronic complications.

Kupfer R, Farage M, Costa DFP, Bragança JB, Sterza L, Lemos H - IEDE

ATIPICAL PROGRESSION OF GRAVES´ ORBITOPATHY AFTER THYROID RESSECTION.

INTRODUCTION: Thyroid eye disease (ted), the most frequent extrathyroidal manifestation of graves` disease, is an auto-immune disorder. It can occur before, concomitantly or after hyperthyroidism. Different forms of treatments for thyrotoxicosis can influence the ted course. thyroidectomy should be theoretically more beneficial to graves` orbitopathy outcome because of the removal of the source of both thyroid- orbit cross reaction auto antigens and auto reactive t lymphocytes.

CASE REPORT: A 58 years old women presented with graves disease and was initially treated with thionamides for two years. At the diagnosis she had only mild left exophthalmos and no eye complaint. Subsequently, thyroid resection was indicated as a result of goiter enlargement, development of nodules and compressive symptoms. euthyroid state was achieved. Four months after surgery, progression of orbitopathy was observed. She developed ocular manifestations like pain on eye movement, eyelid edema, conjunctival injection, double vision and bilateral exophthalmos. Orbital radiotherapy and intravenous glucocorticoids used in combination improved her eye disease.

DISCUSSION: According to literature, thionamides are associated with improve or does no affect the course of ted. The relationship between radioiodine therapy and ted is a matter of controversy. The few randomized and controlled studies available, suggest a small but definitive risk of causing ted progression, but can be prevented by concomitant glucocorticoids. The effect of thyroid surgery on ted has been extensively reported in the literature, and the reports usually advocate thyroid resection as an important treatment to improve eye disease. We described a case in which ted occurred after surgery, despite the removal of the source of autoantigens and the control of thyroid function. This observation suggests that the choice of treatment for thyrotoxicosis may not influence ted outcome.

CONCLUSION: Graves´ orbitopathy pathogenesis and natural history may involve several different mechanisms which have still to be more deeply studied. Most importantly, ted might have a clinical course independent of thyroid disease and type of treatment.
Puppin, BA; Momesso, DP; Satake, F; Canton, AP; Souza, MVL.

TYPE 1 DIABETES MELLITUS AND MYASTHENIA GRAVIS: ASSOCIATION OR COINCIDENCE?

INTRODUCTION: Autoimmune diseases often coexist in clinical practice and may be associated with autoimmune polyendocrine syndrome (aps). the diagnosis of aps should be suspected in the natural history of any autoimmune disease.

CASE REPORT: 25 year-old woman, presented with muscle weakness and dysarthria that increased during periods of activity. Myasthenia gravis was diagnosed and treatment with pyridostigmine and prednisone was started. After 2 weeks, she developed blurred vision, polydipsia, polyuria, vaginal pruritus and was admitted in our hospital with non-ketotic hyperglycemia. Laboratory evaluation: glycemia=1374mg/dl, c peptide=5.1ng/ml (1.1–5.0), anti-insulin antibody (ab) =3.0u/ml (<1.0), anti-gad ab=1.0u/ml (<1.0), anti-islets ab=1.1u/ml (<1.0), anti-acetylcholine receptor ab=9.02nmol/l (<0.15), anti-peroxidase<20 ui/ml (<40). Subcutaneous rapid insulin, then nph, was started. She was discharged in use of nph 28 + 12 ui, rapid insulin before meals according to scale and pyridostigmine. At the outpatient clinic, adequate metabolic control was achieved (hba1c=5%) with low doses of insulin (0.2u/kg/day) and the posterior laboratory evaluation showed positive anti-gad ab=9.6u/ml and normal c peptide level=1.7ng/ml. After 2 years, she developed polydipsia, polyuria, nausea, vomiting and hyperglycemia, hba1c was 10.7% and it was necessary to increase insulin doses. A morning plasma cortisol of 22mcg/dl excluded adrenal insufficiency.

DISCUSSION: Screening of serological organ-specific autoantibodies identifies patients who may develop autoimmune polyendocrinopathies. aps type ii involves the coexistance of addison´s disease with type 1 diabetes mellitus (dm) and/or autoimmune thyroid disease. Some patients also present with, or later develop other organ-specific autoimmune disorders, including myasthenia gravis. This patient presented with myasthenia gravis and type 1 dm. at the moment, there is no evidence of adrenal insufficiency in order to diagnose aps ii, but in up to 30% of patients dm1 is diagnosed before adrenal insufficiency.

CONCLUSION: Patients with endocrine autoimmune diseases should be screened for the presence of APS.
Lima GAB, Mattos PE, Tavares P, Momesso DP, Henriques RP, Kupfer R.

GLYBURIDE INDUCED CUTANEOUS VASCULITIS

OBJECTIVE: To describe a case of cutaneous vasculitis glyburide induced and to discuss its frequency, clinical, pathophisiological and histological issues.

materials and methods- 51 year’s old male with long standing type 2 diabetes mellitus admitted as an inpatient to our hospital with an itching cutaneous rash, fever, polyartalgia, malaise and edema of the upper and lower limbs. He related a recent onset of glyburide use two weeks before presentation. He denied use of other medications. On physical examination there was a generalized cutaneous discamation with exulcerations and fissure associated. Superior and inferior limbs edema, bilateral cervical, mandibular and inguinal adenopathy was also seen.he had right superior quadrant tenderness and hepatomegaly on abdominal palpation. glyburide was then discontinued and intensive insulin therapy was started. Laboratory analysis was ordered to check wbc, rbc, platelet count, erythrocyte sedimentation rate (esr), alt, ast, sodium, potassium, urea, creatinin, glucose and a skin biopsy.

RESULTS: The exams revealed an normocitic and normochromic anemia, esr elevation with normal liver tests. The skin biopsy showed a difuse mononuclear inflammatory infiltration with eosinophils within it. thickness of capilar walls and extravasation of hematias suggestive of drug induced vasculitis. eight days after drug withdrawal, anti-hystaminic oral therapy and topical corticosteroids the patient underwent a complete resolution of the lesions and was discharged to our outpatient clinic.

CONCLUSION: After extensive medical literature research on the major journals of the area we have found only a few case reports similar to this one. Over a clinical point of view we can classificate this picture as a pharmacodermia probably glyburide induced. The physiopathology is centered on the immune complex deposition due to chronic exposition to the drug itself or its radicals so eventually cross reaction is seen with sulfonamides antibiotics. The hystopathologic analysis confirms the clinical hypothesis as drug induced cutaneous vasculitis. The clinical manifestations can be restricted to the skin but in some cases as it was in the case described above systemic involvement is seen denoting a more severe form. cutaneous parefects of glyburide are rarely seen although once its wast use its real incidence maybe higher than described on literature.

Rosane Kupfer, Maria Teresa Menegat, Rosana Leal Santos, Roberto Zagury, Roberta Frota, Ronei Gustavo Paim de Vargas.
          What Echocardiographic Measure Should Be Used to Assess Right VentricularFunction in Tetralogy of Fallot        
Jill J Savla, Valerie De Matteo, Yan Wang, Laura MercerRosa
          Heart Care at Jackson-Madison County General Hospital Receives New Accreditation, Approval by Women        

West Tennessee Heart & Vascular Center at Jackson-Madison County General Hospital has received an Adult Transthoracic Echocardiography Accreditation by the Intersocietal Accreditation Commission and has been named one of America’s Best Hospitals for Patient Experience in Heart Care by WomenCertified, Inc.

(PRWeb March 03, 2014)

Read the full story at http://www.prweb.com/releases/2014/03/prweb11633427.htm


          Medical Wearable Devices to Register Record Sales – To Drive Wearable Medical Devices Market         
The advent of medical wearable devices has propelled the growth of the global medical devices market. Leading players in the global medical devices market are engaged in manufacturing advanced yet affordable wearable devices. Technology has helped leading players to introduce innovations in the medical devices. Currently, the global wearable medical devices market is the most opportunistic market in the global medical devices industry.  The benefits of wearable medical devices were clear, soon after this technology was first introduced. Since then, wearable medical devices have revolutionized patients, doctors, manufacturers of medical devices, and the health care centers.  The advent of wearable medical devices was credited to a larger social disposition towards IoT. Even though the Internet of Things has been around in the global market since many years, it has recently picked up grip. A trending ecosystem of smart phones and mobile operating systems including iOS and Android coupled with a consistently improving cloud computing system has boosted the success of the global medical technology segment.  The advent of technology has given manufacturers a chance to design and develop cheap wearable medical devices, thus boosting their sales. The demand for wearable heart rate monitors, activity monitors, electrocardiographs, and wearable sleep monitors has increased from hospitals, healthcare centers, and private clinics. Wearable medical devices are being increasing used by home healthcare centers, sports and fitness institutes, and for remote patient monitoring.  Changing lifestyles demand better wearable medical devices to diagnose and treat various health issues. Technology is constructing a better future for the wearable medical devices by introducing devices that assure people to live a healthier life. Many startups are entering the global wearable medical devices market to contribute their range of products. The introduction of new devices by leading players will further boost the growth of the global market.

Original Post Medical Wearable Devices to Register Record Sales – To Drive Wearable Medical Devices Market source Twease
          Advances and Future of Medical Imaging        
Medical imaging refers to the process of producing visual representations of the internal aspects of the body for analysis, diagnosis and treatment. Noninvasive medical imaging devices enable to create a database of the physiology for future reference and to identify any defects. Medical imaging tools include radiography, Magnetic Resonance Imaging (MRI), ultrasound, tomography, tactile imaging, elastography, angiography, mammography, fluoroscopy, etc. Digital imaging modalities have a wide scope for use in various branches and sub-disciplines of medicine: preventive or curative, and the global medical imaging market [http://www.marketresearchreports.biz/analysis/187912] for existing devices, as well as new time-saving and life-enhancing devices is ever growing. The field of neuroimaging – one of the non-diagnostic imaging sectors, photoacoustics, and use of imaging devices in pharmaceutical clinical trials is relatively new and unexplored and is one if the driving forces in the market today. Traditionally, MRI and CT scans generated 2D images, but recent techniques have been developed which enable 3D images that are invaluable in the course of surgical treatment. The use of imaging devices requires trained technical, medical and engineering personnel to ensure safe and effective procedures. Moreover, the spaces using imaging modalities must adhere to radiation protection regulations.  Diagnostic imaging devices and their functions  X-ray machines: X-ray imaging creates visuals of the internal anatomy of the body. X-rays are used mostly for checking broken bones. But they can also be used to detect pneumonia via chest x-rays, or breast cancer using mammograms. CT scans: A Computed Tomography (CT) uses x-ray equipment to create cross-sectional images of the body. CT scans are used to detect cancers, blood clots, internal bleeding, signs of heart diseases, etc. A CAT scan, or Computed Axial Tomography, is used in case of brain injuries or even eye-related disorders.  MRI: Magnetic Resonance Imaging (MRI) uses a large magnet and radio waves to view internal organs and structure of the body. MRIs are most useful in brain and spinal cord examinations. Patients with cochlear implants, pacemakers, metallic foreign bodies and ferromagnetic implants are contraindications to using MRI. Ultrasound: An ultrasound is a diagnostic tool that uses high-frequency sound waves to examine internal organs such as kidneys, liver, blood vessels and heart. An ultrasound (ultrasonography) is also used to view the fetus during pregnancy. An echocardiography uses ultrasound to view detailed structures of the heart. Advantages of medical imaging devices Medical imaging technology has revolutionized medicine, and allows doctors to detect abnormalities earlier and results in better patient outcome. Being noninvasive, the devices can be used for patients of all age groups and across any medical field. While there are risks of medical radiation, scientists have developed innovations that have reduced dose of radiation by nearly 75%. Furthermore, medical imaging allows a microscopic view of the anatomy that is highly personalized, effective and accurate. Medical modalities also generate large-scale employment to technical and non-technical workers.  Advances in diagnostic imaging and its future Diagnostic imaging is an ever-evolving field and many remarkable changes have been tracked since its introduction to everyday medicine: shift of x-rays files from film to digital, unclear MRIs to high-quality images, and compact and portable ultrasound equipment. Medical imaging has a wide scope for innovation. A wide variety of noninvasive diagnostic innovations offer options to patients who either have fear of physicians, or are unable to visit a doctor. Researchers suggest, and are working on, a scanner-embedded bathroom mirror that detects retinopathy, or a toilet that identifies kidney infections or diabetes through urine analysis.  Overview of the global medical imaging market Reports by a leading market research firm suggests that the market for diagnostic imaging devices will continue to boom at an increasing pace over the next few years. The market value for these devices stood at approximately USD 20.7 billion in 2010, and revenues are estimated to reach USD 25.3 billion by 2015, and USD 26 billion by 2016-end. Technical development and advancement in medicine will positively affect the growth of medical imaging. North America is currently dominating the market with over 35% of the global industry share, followed by Europe and Asia. Among all imaging devices, x-ray machines dominate the market share with revenues to reach USD 9.1 billion, and annual growth rate to reach 3.5% by 2017. Some of the key players in the global medical imaging devices market include Philips Healthcare, Siemens Healthcare, GE Healthcare, Toshiba Medical System Corp and Hitachi Medical Corp.  About Us Marketresearchreports.biz is the most comprehensive collection of market research reports. Marketresearchreports.biz services are especially designed to save time and money of our clients. We are a one stop solution for all your research needs, our main offerings are syndicated research reports, custom research, subscription access and consulting services. We serve all sizes and types of companies spanning across various industries. For more information: http://www.marketresearchreports.biz/

Original Post Advances and Future of Medical Imaging source Twease
           Pulmonary valve papillary fibroelastoma diagnosed by echocardiography: a case report         
Biočić, Stanko and Pukšić, Silva and Vincelj, Josip and Đurašević, Željko and Sutlić, Željko and Manojlović, Spomenka (2009) Pulmonary valve papillary fibroelastoma diagnosed by echocardiography: a case report. European Journal of Echocardiography, 10 (5). pp. 726-8. ISSN 1525-2167
          The Atlas of Emergency Medicine, Third Edition        
http://hotfile.%20com/dl/23839331/%20a03b8d6/Emergenc%20y_Medicine.%20pdf.html


The most complete and trusted visual compendium of emergency medicine—extensively updated with 1500 full-color illustrations

Ideally suited to the bedside practice of emergency medicine, The Atlas of Emergency Medicine is the ultimate visual guide to the diagnosis and treatment of common and uncommon conditions encountered in the Emergency Department. Filled with 1500 crisp, clear full-color images, this essential clinical companion is logically organized by organ system and then by problem, making it a practical quick reference for medical students, residents in training, new graduates preparing for their certification exam, the practicing physician, and instructors. The third edition of The Atlas of Emergency Medicine features an even more streamlined presentation with clear, concise text and an unmatched collection of diagnoses-speeding images. Forming the core of the book, these images show you what to look for and are accompanied by brief, high-yield descriptions of clinical problems. The new edition also features an enhanced template, and new coverage of airway emergencies, tropical conditions, toxicologic emergencies, and electrocardiographs .

NEW TO THIS EDITION

* 1,500 full-color clinical photographs (more than twice the amount found in the previous edition)

New chapter template:“Clinical Summary”: clinically relevant observations on differential diagnosis

“Emergency Department Treatment and Disposition”: a brief overview of need-to-know diagnostic guidelines and recommendations

“Clinical Pearls”: instructive tips and insights on specific aspects of conditions which are difficult to find in other texts
*Four new chapters that enhance the book’s hands-on value:
Tropical Medicine: reflects an increased emphasis on global access to healthcare and easier patient travel
Toxicology: features an up-to-date, authoritative review of how to diagnose and treat selected toxicological emergencies
ECG Abnormalities: presents turnkey insights into the rapid recognition of pathological ECG’s, highlighting the electrocardiographi c characteristics of each featured clinical problem
Airway Procedures: includes essential information that guides, improves, and expedites the management of airway emergencies
          M-N        

1.    McARDLE (MALADIE DE).
Maladie métabolique héréditaire transmise sur le mode autosomique récessif liée au déficit en une ou plusieurs enzymes impliquées dans la synthèse ou la dégradation du glycogène (glycogénose >), ce qui entraîne son dépôt en quantité et en qualité anormale dans les tissus. Elle se traduit cliniquement par des signes musculaires (d'où son classement dans le groupe des myopathies métaboliques), principalement des crampes survenant à l'effort. La vie quotidienne est subnormale. Cependant, la moitié des patients feront une myolyse (destruction des fibres musculaires favorisée par un effort violent ou le froid) qui peut conduire à une insuffisance rénale aiguë dans un quart des cas.


2.    McCUNE-ALBRIGHT-STERNBERG (SYNDROME DE) ou SYNDROME D'ALLBRIGHT.
Syndrome associant des anomalies osseuses unilatérales (dysplasie fibreuse), des taches café au lait du même côté et une puberté précoce chez la fille.


3.    McDUFFIE (SYNDROME DE).
Affection s'observant plus souvent chez la femme, due à une inflammation des petits vaisseaux (angéite) d'origine allergique. Elle se manifeste par de la fièvre, une atteinte cutanée (papules à centre clair, macules brunâtres, purpura), des douleurs articulaires migratrices et fugaces, et des douleurs abdominales. L'évolution se fait vers la guérison après plusieurs poussées.


4.    McLEOD (SYNDROME DE)
ou SYNDROME DE SAWYER-JAMES (ou SWYER-JAMES) .
Emphysème pulmonaire unilatéral souvent découvert lors d'un examen systématique. Les voies aériennes sont normales mais le nombre d'alvéoles est réduit. La cause semble être une infection survenue avant l'âge de 8 ans où le nombre d'alvéoles augmente encore. Le plus souvent, l'artère pulmonaire du côté atteint est anormale. La principale complication est la survenue d'infections à répétition, imposant parfois un geste chirurgical.








5.    MACHADO-JOSEPH (MALADIE DE).
Définition et causes.
Maladie héréditaire transmise sur le mode autosomique dominant caractérisée par une dégénérescence nerveuse localisée au niveau du cervelet et du tronc cérébral.

Epidémiologie.
Elle s'observe dans les familles portugaises originaires des Açores.

Signes et symptômes.
La maladie débute à l'âge adulte et a une expression très variable avec l'association d'une ataxie progressive (troubles de la coordination des mouvements) et une paralysie oculaire. En général, les fonctions intellectuelles sont préservées.

Investigations.
L'IRM retrouve l'atrophie du cervelet et du tronc cérébral.

Evolution, complications et pronostic.
 L'évolution est progressive avec un décès en dix à trente ans.

Traitement.
Il est uniquement symptomatique.

Prévention et éducation.
Le conseil génétique est utile.


6.    MACROSOMIE FŒTALE.
Enfant de poids supérieur à 4000, voire 4 500 g. Les facteurs prédisposants sont une obésité maternelle, un facteur ethnique, la multiparité, les antécédents de macrosomie, un hydramnios
(liquide amniotique anormalement abondant), une prise de poids importante et la survenue d'un diabète. La mère est exposée à un risque accru de traumatisme (déchirures périnéales, rupture utérine), d'hémorragies de la délivrance et de complications infectieuses. Le risque pour le fœtus est dominé par les traumatismes (fracture de la clavicule ou de l'humérus, paralysie du plexus brachial, souffrance lors de l'accouchement) et les complications métaboliques. L'accouchement est à risque et l'obstétricien doit être disponible pour effectuer des manœuvres appropriées ou une césarienne.













7.    MADELUNG (MALADIE DE).
Malformation héréditaire, de transmission autosomique dominante, caractérisée par une déformation, généralement bilatérale, du poignet. Elle est due à une anomalie de croissance de l'extrémité inférieure du radius, dont la partie postérieure se développe plus vite que l'antérieure. Cliniquement, il existe une flexion du poignet qui semble luxé.


8.    MADUROMYCOSE
ou PIED DE MADURA ou MYCÉTOME.
Maladie infectieuse du pied (et, parfois, du membre supérieur), se rencontrant sous les tropiques, due à Nocardia ou à différents champignons, caractérisée par une tuméfaction évoluant sur des années avec des atteintes profondes et des fistulisations. Le traitement médicamenteux est indiqué si le germe est sensible à un agent anti-microbien ; sinon, la chirurgie, avec parfois une amputation, est nécessaire pour éviter une surinfection avec une septicémie et un décès.


9.    MAFFUCI (SYNDROME DE) .
Phacomatose (>) caractérisée par des angiomes cutanés diffus (malformations vasculaires tubéreuses ou plan), des télangiectasies (dilatations vasculaires), des lymphangiomes (malformations des vaisseaux lymphatiques) et une dyschondroplasie (malformation des cartilages) prédominante initialement aux extrémités. Ce syndrome est très évolutif jusqu'à la puberté et, dans 20 % des cas, des tumeurs de type sarcome se développent. Les manifestations neurologiques sont liées soit aux localisations cérébromédullaires des angiomes, soit à des tumeurs (gliomes), soit à la dyschondroplasie de la base du crâne.


10.    MAL DE POTT
Il s'agit d'une spondylodiscite (>) tuberculeuse.




















11.    MAL AIGU DES MONTAGNES
Définition et causes.
Ensemble de signes dus à une mauvaise adaptation de l'organisme à l'altitude. Ils sont liés à une diminution de l'oxygène dans l'air inspiré (à 5 000 m, la pression partielle en oxygène diminue de moitié). Leur cause semble être un œdème cérébral débutant, associé à une rétention d'eau. Il existe une grande susceptibilité individuelle.

Epidémiologie.
Il se manifeste chez environ la moitié des sujets se rendant à plus de 3 000 m et y séjournant plus de 6 heures (voyages dans les Andes, au Tibet...). Il peut apparaître dès 2 000 m.

Signes et symptômes.
Les principaux signes sont des céphalées, une insomnie, une perte d'appétit, des nausées, des vertiges, une toux sèche, une dyspnée et des œdèmes localisés (yeux, face, mains, cheville).

Investigations.
Le diagnostic est clinique.

Evolution, complications et pronostic.
Les deux principales complications sont l'œdème cérébral de haute altitude (>) et l'œdème pulmonaire de haute altitude (>) dont le pronostic peut être très mauvais.

Traitement.
La conduite à tenir dépend de la gravité des signes. Dans les formes simples, l'arrêt de la montée en altitude et des antalgiques (aspirine) peuvent suffire. En cas de forme sévère, la redescente est impérative.

Prévention et éducation.
Un dénivelé de 300 m par 24 heures au-dessus de 3000 m permet en général de s'acclimater sans problème. L'acétazolamide peut également être utilisée à titre préventif chez certains sujets très sensibles. Des consultations spécialisées permettent d'effectuer des tests de tolérance avant de partir en voyage.


















12.    MAL CHRONIQUE DES MONTAGNES ou (-*) MALADIE DE MONGE.


13.    MAL DES TRANSPORTS .
Définition et causes.
Ensemble de manifestations déclenchées par les accélérations et les décélérations répétitives lors de l'utilisation d'un moyen de transport (voiture, bateau, avion...). La cause est une susceptibilité individuelle à la stimulation de l'appareil vestibulaire au niveau de l'oreille interne qui joue un rôle essentiel dans les sensations de position et d'équilibre.

Epidémiologie.
Très fréquent, en particulier chez les enfants.

Signes et symptômes.
Le tableau comprend une sensation de malaise avec pâleur, sueurs, hypersalivation, hyperventilation, rapidement suivie de nausées et de vomissements.

Evolution, complications et pronostic.
Le soulagement apporté par les vomissements est souvent fugace. Chez les personnes fragiles, les troubles digestifs peuvent entraîner des pertes de liquides importantes dont les conséquences peuvent être sévères en l'absence de traitement.

Traitement, prévention et éducation.
Le traitement est essentiellement préventif. Les conseils d'usage sont d'éviter d'avoir trop ou pas mangé, d'éviter les boissons gazeuses et l'alcool, d'éviter de regarder les vagues ou d'autres objets mouvants, de se mettre en position de repos le plus près du centre de gravité du bateau ou de l'avion, d'éviter les accélérations et les coups de freins vifs en voiture... Les médicaments disponibles sont des anticholinergiques   ou des antihistaminiques Hl.




















14.    MAL PERFORANT PLANTAIRE.
Définition et causes.
Principale altération cutanée observée au cours des troubles neurologiques des membres inférieurs, dont l'origine peut être familiale, toxique, métabolique (diabète), infectieuse ou traumatique. L'atteinte neurologique entraîne une anesthésie avec des troubles de la microcirculation qui sont à l'origine de lésions cutanées et ostéoarticulaires en regard des points d'appui ou de microtraumatismes répétitifs du pied.

Epidémiologie.
Très fréquent, notamment chez le diabétique.

Signe et symptômes.
Ulcération chronique, indolore, non inflammatoire qui s'installe insidieusement sur ou sous une callosité. Elle est de forme ovalaire, d'une taille de quelques millimètres à plus d'l cm, avec des bords saillants et un bourrelet périphérique.

Investigations.
Elles ont pour objectif de rechercher l'étiologie lorsque celle-ci n'est pas connue, d'évaluer l'étendue de l'atteinte neurologique et de rechercher une éventuelle atteinte ostéoarticulaire sous-jacente.

Evolution, complications et pronostic.
L'évolution est chronique, avec une cicatrisation lente et difficile.

Traitement.
Il associe des soins locaux minutieux, une décharge des zones d'appui, la correction des troubles nutritionnels, métaboliques ou neurologiques et, parfois, la chirurgie.

Prévention et éducation.
La prévention est essentielle (orthèse plantaire) chez tous les patients à risque, notamment les diabétiques. L'éducation du patient est indispensable.



















15.    MALACOPLAKIE.
Définition et causes
Maladie inflammatoire diffuse ou localisée dont la cause reste obscure. Les principaux organes touchés sont le tractus urinaire et le tube digestif. Les lésions muqueuses sont caractéristiques : plaques brun jaunâtre ayant tendance à s'ulcérer en leur centre.

Epidémiologie
Rare. Elle survient après 50 ans et touche principalement la femme.

Signes et symptômes
Au niveau rénal, les principaux signes sont une difficulté pour uriner (dysurie), une hématurie, des infections urinaires résistantes et une insuffisance rénale avec hypertrophie rénale. La forme digestive se manifeste par une fièvre, des rectorragies, une diarrhée, des douleurs abdominales, mais dans 80 % des cas elle est associée à une autre affection (dont 40% de cas) dont les signes prédominent.

Investigations
Les biopsies par voie endoscopique montrent des lésions caractéristiques : granulomes avec des macrophages contenant des inclusions cytoplasmiques (corps de Michaelis et Gutman).

Evolution, complications et-pronostic.
Le pronostic est mauvais (extension de l'atteinte rénale, évolution de l'affection digestive associée).

Traitement
Une antibiothérapie prolongée est parfois efficace. La chirurgie est utile dans les formes digestives chaque fois qu'une résection est possible.


















16.    MALADIE CŒLIAQUE
ou INTOLÉRANCE AU GLUTEN.
Définition et causes
Malabsorption intestinale chronique provoquée par une intolérance au gluten (protéine des céréales). Une liaison avec un type HLA particulier est présente dans 99 % des cas et les formes familiales représentent 10 % des cas.

Epidémiologie
L'incidence est de 1/2 500 en France. Elle peut se révéler à n'importe quel âge, mais prédomine chez le nourrisson et l'enfant.

Signes et symptômes
Chez le nourrisson et le jeune enfant, les manifestations sont une dénutrition, une apathie, des vomissements fréquents, une diarrhée chronique avec des selles grasses ainsi qu'un abdomen météorisé et flasque. Dans la seconde enfance existent un retard statural, une insuffisance pondérale modérée et peu de signes digestifs. Chez l'adulte, les signes sont une diarrhée chronique, un syndrome carentiel avec des troubles osseux, cutanés et une anémie.

Investigations
L'endoscopie avec biopsie du grêle montre une atrophie villositaire. L'examen des selles montre une stéatorrhée (trop de graisses dans les selles). Le test au D-Xylose et la recherche d'anticorps anti-endomysium aident au diagnostic.

Evolution, complications et pronostic.
Chez l'enfant, la réponse est constante au régime sans gluten, avec une possibilité de rechute lors de sa réintroduction après l'âge de 4 ans. Chez l'adulte, le régime doit être poursuivi indéfiniment et il existe un risque important de lymphome intestinal.

Traitement
Il associe une alimentation sans gluten et une supplémentation des carences (vitamines, sels minéraux...). La nutrition parentérale et les corticoïdes seront utilisés dans les formes graves.

Prévention et éducation
Les associations de patients apportent des informations sur la teneur en gluten des aliments et sur les produits diététiques de remplacement. Le risque de cancérisation fait discuter la nécessité d'un régime sans gluten à vie.



17.    MALADIE EXOSTOSANTE
ou (>) EXOSTOSES MULTIPLES.







18.    MALADIE GÉLATINEUSE DU PÉRITOINE
ou (>) PSEUDOMYXOME PÉRITONÉAL.



19.    MALADIE HÉMOLYTIQUE NÉONATALE
ou (>) IMMUNISATION SANGUINE FOETO-MATERNELLE.



20.    MALADIE DES MEMBRANES HYALINES.
Définition et causes.
Détresse respiratoire du nouveau-né survenant chez le prématuré du fait d'un défaut de synthèse du surfactant, produit permettant de maintenir les alvéoles ouvertes même en expiration.

Epidémiologie.
Survient chez les prématurés de moins de 35 semaines. Plus l'enfant est prématuré, plus le risque est grand.

Signes et symptômes.
Le nouveau-né présente une détresse respiratoire avec tirage, battement des ailes du nez et geignement expiratoire dès la naissance ou dans les heures qui suivent.

Investigations.
Le diagnostic est essentiellement clinique. Les gaz du sang et la radiographie de thorax permettent d'évaluer la gravité de l'atteinte.

Evolution, complications et pronostic.
En l'absence de traitement, le déficit en oxygène (hypoxémie) entraîne la défaillance de nombreux organes et la mort. Chez les survivants, des séquelles neurologiques sont possibles.

Traitement.
Le traitement utilise l'installation endotrachéale de surfactant de synthèse ou semi-naturel, associé à l'oxygénothérapie. La ventilation artificielle est parfois nécessaire.

Prévention.
L'injection de corticoïdes à la mère (accélération de la maturation pulmonaire du fœtus) est une mesure de prévention efficace mise en œuvre en cas d'accouchement prématuré prévisible.









21.    MALADIES MITOCHONDRIALES
Terme utilisé pour désigner différentes maladies affectant la structure des mitochondries (organites cellulaires jouant un rôle essentiel dans l'utilisation de l'énergie dans l'organisme). Les principales sont les suivantes : maladie de Leber, syndrome de Kearns et Sayre, MERRF syndrome, MELAS syndrome, MIDD, NARP syndrome, syndrome de Wolfram.


22.    MALADIE MITRALE.
Définition et causes.
Insuffisance et rétrécissement mitral associés à des degrés divers. Elle est presque toujours une séquelle d'un rhumatisme articulaire aigu (RAA).

Epidémiologie.
La quasi-disparition du RAA depuis la diffusion des antibiotiques va faire diminuer progressivement la fréquence de cette maladie.

Signes et symptômes.
Le principal symptôme est une dyspnée d'effort progressivement croissante. L'auscultation est typique: souffle systolique irradiant dans l'aisselle, daquement d'ouverture mitrale, roulement diastolique.

Investigations.
L'échodoppler cardiaque permet le diagnostic.

Evolution, complications et pronostic.
 La complication la plus fréquente est la survenue de troubles du rythme auriculaires (fibrillation auriculaire) exposant à des embolies artérielles. Plus rarement, un oedème pulmonaire ou des hémoptysies peuvent survenir. Comme dans toutes les valvulopathies, il existe un risque d'endocardite.

Traitement.
Le traitement médical comporte un régime pauvre en sel, l'abstention des efforts physiques importants, des diurétiques, des tonicardiaques, des vasodilatateurs associés à des antiarythmiques et à des anticoagulants en cas de troubles du rythme. Dès qu'apparaissent des signes de mauvaise tolérance, une intervention chirurgicale (plastie ou remplacement valvulaire) doit être envisagée.



23.    MALADIE DE L'OREILLETTE
(>) OREILLETTE (MALADIE DE L')








24.    MALADIE PÉRIODIQUE ou FIÈVRE FAMILIALE MÉDITERRANÉENNE.
Définition et causes.
Maladie familiale, de transmission autosomique récessive à pénétrance variable, qui fait partie des syndromes auto-inflammatoires (>). Elle est caractérisée par des crises douloureuses fébriles apparaissant dès l'enfance et dues à une inflammation des séreuses (péritoine, plèvre...).

Epidémiologie.
Elle touche principalement les sujets du pourtour méditerranéen, particulièrement les juifs séfarades (1/2 000), avec une prédominance masculine.

Signes et symptômes.
Association d'une fièvre, de crises douloureuses abdominales pouvant mimer une péritonite, thoraciques avec dyspnée, douleur basithoracique et frottement pleural, et articulaires avec un gonflement important. Des plaques cutanées érythémateuses (rouges) sont également possibles.

Investigations.
Il existe un syndrome inflammatoire important (VS augmentée) et une hyperleucocytose.

Evolution, complications et pronostic.
Les crises durent quelques jours et se reproduisent régulièrement, avec des périodes de latence et des intensités variables. La régression des signes est spontanée. La principale complication est la survenue d'une amylose (>) rénale et/ou cardiaque qui transforme une maladie invalidante mais bénigne en une maladie mortelle.

Traitement.
La colchicine prévient ou diminue les accès chez plus de 90 % des patients. En cas de crise, le traitement est symptomatique. Lors du premier accès, une urgence chirurgicale abdominale vraie (appendicite, cholécystite...) doit être éliminée.



25.    MALADIE RYTHMIQUE AURICULAIRE ou (>) OREILLETTE (MALADIE DE L').


26.    MALADIE SÉRIQUE.
Réaction allergique qui apparaît généralement 7 à 12 jours après l'injection de certains médicaments (pénicilline, par exemple) ou, plus rarement, d'un sérum hétérologue (sérum de cheval). Les principales manifestations sont une urticaire, des douleurs articulaires (polyarthrite) et des adénopathies. La régression se fait habituellement en quelques jours.






27.    MALAISE GRAVE DU NOURRISSON.
Définition et causes ;
Survenue inopinée d'un accident qui laisse à l'entourage la crainte d'une mort imminente et justifie de sa part des manœuvres de « réanimation ». Les principales causes identifiées sont le reflux gastro-œsophagien, l'hyperréflextivité vagale et les apnées isolées récidivantes.

Epidémiologie ;
C'est un problème fréquent à l'origine de multiples hospitalisations des enfants entre 1 et 6 mois.

Signes et symptômes ;
Le malaise survient souvent pendant l'éveil. La forme hypertonique comprend un blocage respiratoire avec une cyanose, une révulsion oculaire, une perte de connaissance avec un accès de pâleur intense durant quelques dizaines de secondes, suivi du réveil de l'enfant. La forme syncopale se caractérise par une hypotonie brutale, avec une pâleur, une apnée et, parfois, des convulsions.
           
Investigations ;
Le bilan à la recherche de la cause comprend notamment : pHmétrie, fibroscopie œsophagienne, recherche du réflexe oculocardiaque avec un enregistrement électrocardiographique, enregistrement du sommeil.

Evolution, complications et pronostic ;
Le risque de récidive est estimé entre 10 à 20 % La grande complication est la survenue d'une mort subite.

Traitement ;
Le traitement est avant tout celui de la cause, si elle est identifiée. Dans l'hyperréflectivité vagale, on utilise un dérivé atropinique, le diphémanil. En cas d'apnées récidivantes ou en l'absence de cause retrouvée, un monitorage à domicile est utile (poursuivi jusque vers la fin de la première année).



















28.    MALLORY-WEISS (SYNDROME DE).
Définition et causes.
Dilacération de l'oesophage distal et de l'estomac proximal au cours d'efforts de vomissements ou de hoquet.

Epidémiologie.
Il est responsable de 5 % des hémorragies digestives hautes. L'association avec une hernie hiatale ou un alcoolisme est fréquente.

Signes et symptômes.
La séquence classique comprend des vomissements alimentaires suivis de vomissements de sang rouge.

Investigations.
La fibroscopie permet le diagnostic.

Evolution, complications et pronostic..
La guérison est spontanée dans 90 % des cas sous traitement médical. Le risque principal est le retentissement hémodynamique de l'hémorragie.

Traitement
Le traitement médical se limite à une surveillance hémodynamique et à d'éventuelles transfusions. La sonde à ballonnet, l'électrocoagulation endoscopique ou la chirurgie sont indiquées en cas d'hémorragie active abondante.


29.    MALTE (FIÈVRE DE)
ou (>) BRUCELLOSE.


30.    MANNOSIDOSE.
Maladie métabolique héréditaire, de transmission autosomique récessive, due à un déficit enzymatique qui entraîne l'accumulation cellulaire de substances qui sont à l'origine des symptômes. Elle débute entre 6 et 18 mois. Il existe un retard mental, un faciès grossier avec une hypertrophie de la langue (macroglossie), un gros foie et/ou une grosse rate (hépato- et/ou splénomégalie), des anomalies osseuses et des atteintes oculaires.


31.    MARASME
Tableau de malnutrition du nourrisson qui est l'aboutissement d'une carence énergétique globale prolongée, le plus souvent en raison d'un allaitement insuffisant ou de l'utilisation de laits dilués. L'amaigrissement est progressif, avec un déficit pondéral sévère, une disparition de la graisse sous-cutanée et une fonte musculaire. Les enfants ont un aspect de « petit vieux». La renutrition doit être très progressive, avec la correction des carences éventuelles associées (vitamines, fer...).




32.    MARBURG (FIÈVRE DE)
(>) FIÈVRE DE MARBURG.


33.    MARCHIAFAVA-BIGNAMI (MALADIE DE).
Démence rare, d'apparition progressive, avec un syndrome frontal (excitation, jovialité, désinhibition des instincts) survenant chez les alcooliques chroniques; elle est due à une démyélinisation du corps calleux. La régression est possible en quelques mois, mais une évolution vers la mort avec des convulsions et un coma est parfois possible.


34.   
1.    McARDLE (MALADIE DE).
Maladie métabolique héréditaire transmise sur le mode autosomique récessif liée au déficit en une ou plusieurs enzymes impliquées dans la synthèse ou la dégradation du glycogène (glycogénose >), ce qui entraîne son dépôt en quantité et en qualité anormale dans les tissus. Elle se traduit cliniquement par des signes musculaires (d'où son classement dans le groupe des myopathies métaboliques), principalement des crampes survenant à l'effort. La vie quotidienne est subnormale. Cependant, la moitié des patients feront une myolyse (destruction des fibres musculaires favorisée par un effort violent ou le froid) qui peut conduire à une insuffisance rénale aiguë dans un quart des cas.


2.    McCUNE-ALBRIGHT-STERNBERG (SYNDROME DE) ou SYNDROME D'ALLBRIGHT.
Syndrome associant des anomalies osseuses unilatérales (dysplasie fibreuse), des taches café au lait du même côté et une puberté précoce chez la fille.


3.    McDUFFIE (SYNDROME DE).
Affection s'observant plus souvent chez la femme, due à une inflammation des petits vaisseaux (angéite) d'origine allergique. Elle se manifeste par de la fièvre, une atteinte cutanée (papules à centre clair, macules brunâtres, purpura), des douleurs articulaires migratrices et fugaces, et des douleurs abdominales. L'évolution se fait vers la guérison après plusieurs poussées.


4.    McLEOD (SYNDROME DE)
ou SYNDROME DE SAWYER-JAMES (ou SWYER-JAMES) .
Emphysème pulmonaire unilatéral souvent découvert lors d'un examen systématique. Les voies aériennes sont normales mais le nombre d'alvéoles est réduit. La cause semble être une infection survenue avant l'âge de 8 ans où le nombre d'alvéoles augmente encore. Le plus souvent, l'artère pulmonaire du côté atteint est anormale. La principale complication est la survenue d'infections à répétition, imposant parfois un geste chirurgical.








5.    MACHADO-JOSEPH (MALADIE DE).
Définition et causes.
Maladie héréditaire transmise sur le mode autosomique dominant caractérisée par une dégénérescence nerveuse localisée au niveau du cervelet et du tronc cérébral.

Epidémiologie.
Elle s'observe dans les familles portugaises originaires des Açores.

Signes et symptômes.
La maladie débute à l'âge adulte et a une expression très variable avec l'association d'une ataxie progressive (troubles de la coordination des mouvements) et une paralysie oculaire. En général, les fonctions intellectuelles sont préservées.

Investigations.
L'IRM retrouve l'atrophie du cervelet et du tronc cérébral.

Evolution, complications et pronostic.
 L'évolution est progressive avec un décès en dix à trente ans.

Traitement.
Il est uniquement symptomatique.

Prévention et éducation.
Le conseil génétique est utile.


6.    MACROSOMIE FŒTALE.
Enfant de poids supérieur à 4000, voire 4 500 g. Les facteurs prédisposants sont une obésité maternelle, un facteur ethnique, la multiparité, les antécédents de macrosomie, un hydramnios
(liquide amniotique anormalement abondant), une prise de poids importante et la survenue d'un diabète. La mère est exposée à un risque accru de traumatisme (déchirures périnéales, rupture utérine), d'hémorragies de la délivrance et de complications infectieuses. Le risque pour le fœtus est dominé par les traumatismes (fracture de la clavicule ou de l'humérus, paralysie du plexus brachial, souffrance lors de l'accouchement) et les complications métaboliques. L'accouchement est à risque et l'obstétricien doit être disponible pour effectuer des manœuvres appropriées ou une césarienne.













7.    MADELUNG (MALADIE DE).
Malformation héréditaire, de transmission autosomique dominante, caractérisée par une déformation, généralement bilatérale, du poignet. Elle est due à une anomalie de croissance de l'extrémité inférieure du radius, dont la partie postérieure se développe plus vite que l'antérieure. Cliniquement, il existe une flexion du poignet qui semble luxé.


8.    MADUROMYCOSE
ou PIED DE MADURA ou MYCÉTOME.
Maladie infectieuse du pied (et, parfois, du membre supérieur), se rencontrant sous les tropiques, due à Nocardia ou à différents champignons, caractérisée par une tuméfaction évoluant sur des années avec des atteintes profondes et des fistulisations. Le traitement médicamenteux est indiqué si le germe est sensible à un agent anti-microbien ; sinon, la chirurgie, avec parfois une amputation, est nécessaire pour éviter une surinfection avec une septicémie et un décès.


9.    MAFFUCI (SYNDROME DE) .
Phacomatose (>) caractérisée par des angiomes cutanés diffus (malformations vasculaires tubéreuses ou plan), des télangiectasies (dilatations vasculaires), des lymphangiomes (malformations des vaisseaux lymphatiques) et une dyschondroplasie (malformation des cartilages) prédominante initialement aux extrémités. Ce syndrome est très évolutif jusqu'à la puberté et, dans 20 % des cas, des tumeurs de type sarcome se développent. Les manifestations neurologiques sont liées soit aux localisations cérébromédullaires des angiomes, soit à des tumeurs (gliomes), soit à la dyschondroplasie de la base du crâne.


10.    MAL DE POTT
Il s'agit d'une spondylodiscite (>) tuberculeuse.




















11.    MAL AIGU DES MONTAGNES
Définition et causes.
Ensemble de signes dus à une mauvaise adaptation de l'organisme à l'altitude. Ils sont liés à une diminution de l'oxygène dans l'air inspiré (à 5 000 m, la pression partielle en oxygène diminue de moitié). Leur cause semble être un œdème cérébral débutant, associé à une rétention d'eau. Il existe une grande susceptibilité individuelle.

Epidémiologie.
Il se manifeste chez environ la moitié des sujets se rendant à plus de 3 000 m et y séjournant plus de 6 heures (voyages dans les Andes, au Tibet...). Il peut apparaître dès 2 000 m.

Signes et symptômes.
Les principaux signes sont des céphalées, une insomnie, une perte d'appétit, des nausées, des vertiges, une toux sèche, une dyspnée et des œdèmes localisés (yeux, face, mains, cheville).

Investigations.
Le diagnostic est clinique.

Evolution, complications et pronostic.
Les deux principales complications sont l'œdème cérébral de haute altitude (>) et l'œdème pulmonaire de haute altitude (>) dont le pronostic peut être très mauvais.

Traitement.
La conduite à tenir dépend de la gravité des signes. Dans les formes simples, l'arrêt de la montée en altitude et des antalgiques (aspirine) peuvent suffire. En cas de forme sévère, la redescente est impérative.

Prévention et éducation.
Un dénivelé de 300 m par 24 heures au-dessus de 3000 m permet en général de s'acclimater sans problème. L'acétazolamide peut également être utilisée à titre préventif chez certains sujets très sensibles. Des consultations spécialisées permettent d'effectuer des tests de tolérance avant de partir en voyage.


















12.    MAL CHRONIQUE DES MONTAGNES ou (-*) MALADIE DE MONGE.


13.    MAL DES TRANSPORTS .
Définition et causes.
Ensemble de manifestations déclenchées par les accélérations et les décélérations répétitives lors de l'utilisation d'un moyen de transport (voiture, bateau, avion...). La cause est une susceptibilité individuelle à la stimulation de l'appareil vestibulaire au niveau de l'oreille interne qui joue un rôle essentiel dans les sensations de position et d'équilibre.

Epidémiologie.
Très fréquent, en particulier chez les enfants.

Signes et symptômes.
Le tableau comprend une sensation de malaise avec pâleur, sueurs, hypersalivation, hyperventilation, rapidement suivie de nausées et de vomissements.

Evolution, complications et pronostic.
Le soulagement apporté par les vomissements est souvent fugace. Chez les personnes fragiles, les troubles digestifs peuvent entraîner des pertes de liquides importantes dont les conséquences peuvent être sévères en l'absence de traitement.

Traitement, prévention et éducation.
Le traitement est essentiellement préventif. Les conseils d'usage sont d'éviter d'avoir trop ou pas mangé, d'éviter les boissons gazeuses et l'alcool, d'éviter de regarder les vagues ou d'autres objets mouvants, de se mettre en position de repos le plus près du centre de gravité du bateau ou de l'avion, d'éviter les accélérations et les coups de freins vifs en voiture... Les médicaments disponibles sont des anticholinergiques   ou des antihistaminiques Hl.




















14.    MAL PERFORANT PLANTAIRE.
Définition et causes.
Principale altération cutanée observée au cours des troubles neurologiques des membres inférieurs, dont l'origine peut être familiale, toxique, métabolique (diabète), infectieuse ou traumatique. L'atteinte neurologique entraîne une anesthésie avec des troubles de la microcirculation qui sont à l'origine de lésions cutanées et ostéoarticulaires en regard des points d'appui ou de microtraumatismes répétitifs du pied.

Epidémiologie.
Très fréquent, notamment chez le diabétique.

Signe et symptômes.
Ulcération chronique, indolore, non inflammatoire qui s'installe insidieusement sur ou sous une callosité. Elle est de forme ovalaire, d'une taille de quelques millimètres à plus d'l cm, avec des bords saillants et un bourrelet périphérique.

Investigations.
Elles ont pour objectif de rechercher l'étiologie lorsque celle-ci n'est pas connue, d'évaluer l'étendue de l'atteinte neurologique et de rechercher une éventuelle atteinte ostéoarticulaire sous-jacente.

Evolution, complications et pronostic.
L'évolution est chronique, avec une cicatrisation lente et difficile.

Traitement.
Il associe des soins locaux minutieux, une décharge des zones d'appui, la correction des troubles nutritionnels, métaboliques ou neurologiques et, parfois, la chirurgie.

Prévention et éducation.
La prévention est essentielle (orthèse plantaire) chez tous les patients à risque, notamment les diabétiques. L'éducation du patient est indispensable.



















15.    MALACOPLAKIE.
Définition et causes
Maladie inflammatoire diffuse ou localisée dont la cause reste obscure. Les principaux organes touchés sont le tractus urinaire et le tube digestif. Les lésions muqueuses sont caractéristiques : plaques brun jaunâtre ayant tendance à s'ulcérer en leur centre.

Epidémiologie
Rare. Elle survient après 50 ans et touche principalement la femme.

Signes et symptômes
Au niveau rénal, les principaux signes sont une difficulté pour uriner (dysurie), une hématurie, des infections urinaires résistantes et une insuffisance rénale avec hypertrophie rénale. La forme digestive se manifeste par une fièvre, des rectorragies, une diarrhée, des douleurs abdominales, mais dans 80 % des cas elle est associée à une autre affection (dont 40% de cas) dont les signes prédominent.

Investigations
Les biopsies par voie endoscopique montrent des lésions caractéristiques : granulomes avec des macrophages contenant des inclusions cytoplasmiques (corps de Michaelis et Gutman).

Evolution, complications et-pronostic.
Le pronostic est mauvais (extension de l'atteinte rénale, évolution de l'affection digestive associée).

Traitement
Une antibiothérapie prolongée est parfois efficace. La chirurgie est utile dans les formes digestives chaque fois qu'une résection est possible.


















16.    MALADIE CŒLIAQUE
ou INTOLÉRANCE AU GLUTEN.
Définition et causes
Malabsorption intestinale chronique provoquée par une intolérance au gluten (protéine des céréales). Une liaison avec un type HLA particulier est présente dans 99 % des cas et les formes familiales représentent 10 % des cas.

Epidémiologie
L'incidence est de 1/2 500 en France. Elle peut se révéler à n'importe quel âge, mais prédomine chez le nourrisson et l'enfant.

Signes et symptômes
Chez le nourrisson et le jeune enfant, les manifestations sont une dénutrition, une apathie, des vomissements fréquents, une diarrhée chronique avec des selles grasses ainsi qu'un abdomen météorisé et flasque. Dans la seconde enfance existent un retard statural, une insuffisance pondérale modérée et peu de signes digestifs. Chez l'adulte, les signes sont une diarrhée chronique, un syndrome carentiel avec des troubles osseux, cutanés et une anémie.

Investigations
L'endoscopie avec biopsie du grêle montre une atrophie villositaire. L'examen des selles montre une stéatorrhée (trop de graisses dans les selles). Le test au D-Xylose et la recherche d'anticorps anti-endomysium aident au diagnostic.

Evolution, complications et pronostic.
Chez l'enfant, la réponse est constante au régime sans gluten, avec une possibilité de rechute lors de sa réintroduction après l'âge de 4 ans. Chez l'adulte, le régime doit être poursuivi indéfiniment et il existe un risque important de lymphome intestinal.

Traitement
Il associe une alimentation sans gluten et une supplémentation des carences (vitamines, sels minéraux...). La nutrition parentérale et les corticoïdes seront utilisés dans les formes graves.

Prévention et éducation
Les associations de patients apportent des informations sur la teneur en gluten des aliments et sur les produits diététiques de remplacement. Le risque de cancérisation fait discuter la nécessité d'un régime sans gluten à vie.



17.    MALADIE EXOSTOSANTE
ou (>) EXOSTOSES MULTIPLES.







18.    MALADIE GÉLATINEUSE DU PÉRITOINE
ou (>) PSEUDOMYXOME PÉRITONÉAL.



19.    MALADIE HÉMOLYTIQUE NÉONATALE
ou (>) IMMUNISATION SANGUINE FOETO-MATERNELLE.



20.    MALADIE DES MEMBRANES HYALINES.
Définition et causes.
Détresse respiratoire du nouveau-né survenant chez le prématuré du fait d'un défaut de synthèse du surfactant, produit permettant de maintenir les alvéoles ouvertes même en expiration.

Epidémiologie.
Survient chez les prématurés de moins de 35 semaines. Plus l'enfant est prématuré, plus le risque est grand.

Signes et symptômes.
Le nouveau-né présente une détresse respiratoire avec tirage, battement des ailes du nez et geignement expiratoire dès la naissance ou dans les heures qui suivent.

Investigations.
Le diagnostic est essentiellement clinique. Les gaz du sang et la radiographie de thorax permettent d'évaluer la gravité de l'atteinte.

Evolution, complications et pronostic.
En l'absence de traitement, le déficit en oxygène (hypoxémie) entraîne la défaillance de nombreux organes et la mort. Chez les survivants, des séquelles neurologiques sont possibles.

Traitement.
Le traitement utilise l'installation endotrachéale de surfactant de synthèse ou semi-naturel, associé à l'oxygénothérapie. La ventilation artificielle est parfois nécessaire.

Prévention.
L'injection de corticoïdes à la mère (accélération de la maturation pulmonaire du fœtus) est une mesure de prévention efficace mise en œuvre en cas d'accouchement prématuré prévisible.









21.    MALADIES MITOCHONDRIALES
Terme utilisé pour désigner différentes maladies affectant la structure des mitochondries (organites cellulaires jouant un rôle essentiel dans l'utilisation de l'énergie dans l'organisme). Les principales sont les suivantes : maladie de Leber, syndrome de Kearns et Sayre, MERRF syndrome, MELAS syndrome, MIDD, NARP syndrome, syndrome de Wolfram.


22.    MALADIE MITRALE.
Définition et causes.
Insuffisance et rétrécissement mitral associés à des degrés divers. Elle est presque toujours une séquelle d'un rhumatisme articulaire aigu (RAA).

Epidémiologie.
La quasi-disparition du RAA depuis la diffusion des antibiotiques va faire diminuer progressivement la fréquence de cette maladie.

Signes et symptômes.
Le principal symptôme est une dyspnée d'effort progressivement croissante. L'auscultation est typique: souffle systolique irradiant dans l'aisselle, daquement d'ouverture mitrale, roulement diastolique.

Investigations.
L'échodoppler cardiaque permet le diagnostic.

Evolution, complications et pronostic.
 La complication la plus fréquente est la survenue de troubles du rythme auriculaires (fibrillation auriculaire) exposant à des embolies artérielles. Plus rarement, un oedème pulmonaire ou des hémoptysies peuvent survenir. Comme dans toutes les valvulopathies, il existe un risque d'endocardite.

Traitement.
Le traitement médical comporte un régime pauvre en sel, l'abstention des efforts physiques importants, des diurétiques, des tonicardiaques, des vasodilatateurs associés à des antiarythmiques et à des anticoagulants en cas de troubles du rythme. Dès qu'apparaissent des signes de mauvaise tolérance, une intervention chirurgicale (plastie ou remplacement valvulaire) doit être envisagée.



23.    MALADIE DE L'OREILLETTE
(>) OREILLETTE (MALADIE DE L')








24.    MALADIE PÉRIODIQUE ou FIÈVRE FAMILIALE MÉDITERRANÉENNE.
Définition et causes.
Maladie familiale, de transmission autosomique récessive à pénétrance variable, qui fait partie des syndromes auto-inflammatoires (>). Elle est caractérisée par des crises douloureuses fébriles apparaissant dès l'enfance et dues à une inflammation des séreuses (péritoine, plèvre...).

Epidémiologie.
Elle touche principalement les sujets du pourtour méditerranéen, particulièrement les juifs séfarades (1/2 000), avec une prédominance masculine.

Signes et symptômes.
Association d'une fièvre, de crises douloureuses abdominales pouvant mimer une péritonite, thoraciques avec dyspnée, douleur basithoracique et frottement pleural, et articulaires avec un gonflement important. Des plaques cutanées érythémateuses (rouges) sont également possibles.

Investigations.
Il existe un syndrome inflammatoire important (VS augmentée) et une hyperleucocytose.

Evolution, complications et pronostic.
Les crises durent quelques jours et se reproduisent régulièrement, avec des périodes de latence et des intensités variables. La régression des signes est spontanée. La principale complication est la survenue d'une amylose (>) rénale et/ou cardiaque qui transforme une maladie invalidante mais bénigne en une maladie mortelle.

Traitement.
La colchicine prévient ou diminue les accès chez plus de 90 % des patients. En cas de crise, le traitement est symptomatique. Lors du premier accès, une urgence chirurgicale abdominale vraie (appendicite, cholécystite...) doit être éliminée.



25.    MALADIE RYTHMIQUE AURICULAIRE ou (>) OREILLETTE (MALADIE DE L').


26.    MALADIE SÉRIQUE.
Réaction allergique qui apparaît généralement 7 à 12 jours après l'injection de certains médicaments (pénicilline, par exemple) ou, plus rarement, d'un sérum hétérologue (sérum de cheval). Les principales manifestations sont une urticaire, des douleurs articulaires (polyarthrite) et des adénopathies. La régression se fait habituellement en quelques jours.






27.    MALAISE GRAVE DU NOURRISSON.
Définition et causes ;
Survenue inopinée d'un accident qui laisse à l'entourage la crainte d'une mort imminente et justifie de sa part des manœuvres de « réanimation ». Les principales causes identifiées sont le reflux gastro-œsophagien, l'hyperréflextivité vagale et les apnées isolées récidivantes.

Epidémiologie ;
C'est un problème fréquent à l'origine de multiples hospitalisations des enfants entre 1 et 6 mois.

Signes et symptômes ;
Le malaise survient souvent pendant l'éveil. La forme hypertonique comprend un blocage respiratoire avec une cyanose, une révulsion oculaire, une perte de connaissance avec un accès de pâleur intense durant quelques dizaines de secondes, suivi du réveil de l'enfant. La forme syncopale se caractérise par une hypotonie brutale, avec une pâleur, une apnée et, parfois, des convulsions.
           
Investigations ;
Le bilan à la recherche de la cause comprend notamment : pHmétrie, fibroscopie œsophagienne, recherche du réflexe oculocardiaque avec un enregistrement électrocardiographique, enregistrement du sommeil.

Evolution, complications et pronostic ;
Le risque de récidive est estimé entre 10 à 20 % La grande complication est la survenue d'une mort subite.

Traitement ;
Le traitement est avant tout celui de la cause, si elle est identifiée. Dans l'hyperréflectivité vagale, on utilise un dérivé atropinique, le diphémanil. En cas d'apnées récidivantes ou en l'absence de cause retrouvée, un monitorage à domicile est utile (poursuivi jusque vers la fin de la première année).



















28.    MALLORY-WEISS (SYNDROME DE).
Définition et causes.
Dilacération de l'oesophage distal et de l'estomac proximal au cours d'efforts de vomissements ou de hoquet.

Epidémiologie.
Il est responsable de 5 % des hémorragies digestives hautes. L'association avec une hernie hiatale ou un alcoolisme est fréquente.

Signes et symptômes.
La séquence classique comprend des vomissements alimentaires suivis de vomissements de sang rouge.

Investigations.
La fibroscopie permet le diagnostic.

Evolution, complications et pronostic..
La guérison est spontanée dans 90 % des cas sous traitement médical. Le risque principal est le retentissement hémodynamique de l'hémorragie.

Traitement
Le traitement médical se limite à une surveillance hémodynamique et à d'éventuelles transfusions. La sonde à ballonnet, l'électrocoagulation endoscopique ou la chirurgie sont indiquées en cas d'hémorragie active abondante.


29.    MALTE (FIÈVRE DE)
ou (>) BRUCELLOSE.


30.    MANNOSIDOSE.
Maladie métabolique héréditaire, de transmission autosomique récessive, due à un déficit enzymatique qui entraîne l'accumulation cellulaire de substances qui sont à l'origine des symptômes. Elle débute entre 6 et 18 mois. Il existe un retard mental, un faciès grossier avec une hypertrophie de la langue (macroglossie), un gros foie et/ou une grosse rate (hépato- et/ou splénomégalie), des anomalies osseuses et des atteintes oculaires.


31.    MARASME
Tableau de malnutrition du nourrisson qui est l'aboutissement d'une carence énergétique globale prolongée, le plus souvent en raison d'un allaitement insuffisant ou de l'utilisation de laits dilués. L'amaigrissement est progressif, avec un déficit pondéral sévère, une disparition de la graisse sous-cutanée et une fonte musculaire. Les enfants ont un aspect de « petit vieux». La renutrition doit être très progressive, avec la correction des carences éventuelles associées (vitamines, fer...).




32.    MARBURG (FIÈVRE DE)
(>) FIÈVRE DE MARBURG.


33.    MARCHIAFAVA-BIGNAMI (MALADIE DE).
Démence rare, d'apparition progressive, avec un syndrome frontal (excitation, jovialité, désinhibition des instincts) survenant chez les alcooliques chroniques; elle est due à une démyélinisation du corps calleux. La régression est possible en quelques mois, mais une évolution vers la mort avec des convulsions et un coma est parfois possible.


34.   
1.    LABYRINTHITE .
Inflammation du labyrinthe au niveau de l'oreille interne. Elle peut être d'origine virale ou bactérienne. La labyrinthite suppurée, souvent secondaire à une otite moyenne aiguë ou à une méningite purulente, est caractérisée par de violents vertiges, avec une surdité complète et, parfois, une paralysie faciale. Dans ce cas, le traitement associe chirurgie (drainage du labyrinthe) et antibiotiques. La surdité est définitive.


2.    LADD (SYNDROME DE).
Malformation due une rotation incomplète du mésentère qui entraîne une compression du duodénum. Elle se manifeste, chez le nouveau-né, par des vomissements et une altération de l'état général.


3.    LAFORA (MALADIE DE)
ou ÉPILEPSIE MYOCLONIQUE PROGRESSIVE DE TYPE 2.
Maladie héréditaire, de transmission autosomique récessive, qui fait partie du groupe des épilepsies myocloniques progressives. Les premiers signes surviennent lors de la seconde enfance et sont caractérisés par des crises d'épilepsie et des secousses myocloniques. Puis apparaît une détérioration des fonctions cérébrales aboutissant à un état de dépendance complète du patient.


4.    LAMB SYNDROME.
Syndrome associant des lentigines (grains de beauté), un myxome de l'oreillette (auricular myxoma) et des nævus bleus (taches cutanées surélevées colorées en bleu). Cette ancienne appellation est aujourd'hui intégrée dans la maladie appelée syndrome de Carney (>).


5.    LAMBERT-EATON (SYNDROME DE).
Syndrome paranéoplasique (associé à un cancer) rare, ressemblant à la myasthénie. Il est caractérisé par une faiblesse musculaire des membres, due à un trouble au niveau de la jonction musculaire. Il peut précéder, survenir avec, ou apparaître après le diagnostic de cancer. Le traitement repose sur celui du cancer; la guanidine améliore souvent les symptômes.







6.    LAMBLIASE ou (—>) GIARDIASE.


7.    LANDAU-KLEFFNER (SYNDROME DE).
Forme rare d'épilepsie de l'enfant caractérisée par des troubles du langage, des convulsions et un tracé électroencéphalographique caractéristique. L'âge de début se situe entre 3 et 8 ans, avec une prédominance masculine. Les médicaments antiépileptiques ont une efficacité variable. Dans la moitié des cas, l'évolution est favorable; dans l'autre moitié, des troubles plus ou moins sévères du langage persistent.


8.    LANDOUZY-DÉJERINE (MALADIE DE) ou DYSTROPHIE MUSCULAIRE FACIO-SCAPULO –HUMÉRALE.
Maladie génétique de transmission autosomique dominante, de la famille des myopathies, caractérisée par un déficit des muscles faciaux et de la ceinture scapulaire. Son incidence est de 1/20000. Elle débute entre 7 et 20 ans et l'espérance de vie est normale.


9.    LANGER-GIEDON (SYNDROME DE).
Affection génétique, de transmission autosomique dominante, caractérisée par un nez bulbeux, des oreilles décollées, des cheveux clairsemés, des malformations squelettiques (phalanges, excroissances cartilagineuses multiples) et un retard mental léger à modéré.


10.    LANGUE NOIRE VILLEUSE.
Inflammation de la langue (> Glossite) caractérisée par un allongement et une coloration noire de papilles. Les facteurs favorisants sont l'utilisation prolongée d'antiseptiques locaux, une antibiothérapie récente, une irritation chronique (tabac...). La suppression de la cause et l'application locale de trétinoïne, complétées par des brossages quotidiens du dos de la langue, permettent, en général, la régression des signes.

















11.    LAPAROSCHISIS.
Définition et causes.
Hernie des viscères abdominaux à travers un défaut de la paroi abdominale, généralement à droite de l'insertion du cordon ombilical. La cause est un défaut de croissance fœtale et de fermeture de la paroi abdominale.

Epidémiologie.
Beaucoup plus rare que l'omphalocèle (>). Il est rarement associé à d'autres anomalies.

Signes et symptômes.
À la naissance, les anses intestinales sont libres, sans sac et fortement oedématiées par le fait d'avoir baigné dans le liquide amniotique contenant de l'urine fœtale.

Investigations.
Le diagnostic prénatal (échographie) permet de faire accoucher la mère dans un centre adapté.

Evolution, complications et pronostic.
La souffrance intestinale existant à la naissance impose une alimentation parentérale initiale. Le pronostic est bon, avec 90 % de survie sans séquelles.

Traitement.
Le traitement chirurgical doit intervenir dans les plus brefs délais après la naissance. Il doit parfois se faire en plusieurs temps, en utilisant des plaques de silicone permettant une fermeture progressive.



12.    LA PEYRONIE (MALADIE DE).
Plaque de fibrose au niveau du corps caverneux du pénis qui se rencontre de manière non exceptionnelle chez l'homme adulte. Cette plaque entraîne souvent des douleurs et une courbure de la verge en érection, qui peut parfois empêcher la pénétration vaginale. Le traitement utilise les corticoïdes locaux ou la chirurgie.


13.    LARMES DE CROCODILE (SYNDROME DES)
ou SYNDROME DE BOGORAD.
Sécrétion de larmes survenant par crises au moment de la mastication. Elle peut être secondaire à une paralysie faciale. Elle est due à une anomalie de la régénération des fibres qui innervent la glande lacrymale.


14.    LARON (SYNDROME DE) .
Syndrome rare, de transmission autosomique récessive, qui se traduit par un nanisme. La cause est une résistance à l'hormone de croissance (trouble de l'utilisation de l'hormone de croissance, sécrétée en abondance, liée à l'absence d'un médiateur d'origine hépatique: la somatomédine).


15.    LARSEN (SYNDROME DE).
Maladie génétique caractérisée par un nanisme associé à une hyperlaxité articulaire et à des luxations multiples.



16.    LARVA MIGRANS CUTANÉE ou LARBISH.
Définition et causes.
Éruption cutanée due à des larves d'ankylostomes de chien et de chat (Ancylostoma caninum et Ancylostoma brasiliense), qui pénètrent par la peau à partir de la terre souillée (marche pieds nus sur les plages).

Epidémiologie.
La diffusion est large en zone tropicale, avec une recrudescence pendant la période des pluies.

Signes et symptômes.
L'infestation se manifeste par un prurit, un érythème et une éruption papulovésiculeuse (vésicules surélevées). 2 à 4 jours plus tard apparaît un sillon sinueux, très prurigineux, progressant de quelques centimètres par jour, de façon irrégulière. Les lésions sont uniques ou multiples, siégeant au point de contact avec le sol.

Investigations.
Elles sont inutiles.

Evolution, complications et pronostic.
L'évolution se fait vers la mort spontanée de la larve en 2 à 8 semaines. La principale complication est la surinfection des lésions de grattage.

Traitement.
Il repose sur le thiabendazole (Mintézol®), par voie générale ou locale, ou sur l'ivermectine, associé à des antiprurigineux locaux.

Prévention et éducation.
Il faut éviter de marcher pieds nus, notamment sur les plages infestées.



17.    LARVA MIGRANS VISCÉRALE.
Syndrome dû à des larves d'helminthes (vers) qui ne peuvent effectuer leur cycle complet chez l'homme (impasse parasitaire) et qui migrent dans les différents organes. Il en existe trois types: la toxocarose (>), l'angiostrongylose (>) et l'anisakiase (>).








18.    LARYNGITE AIGUË DE L'ENFANT.
Définition et causes.
Inflammation aiguë de la muqueuse laryngée, due le plus souvent à une infection virale. On distingue : la forme sous-glottique (en dessous des cordes vocales) ou laryngite œdémateuse, la plus fréquente; la forme sus-glottique ou épiglottite; et la forme striduleuse.

Epidémiologie.
La laryngite œdémateuse est très fréquente chez l'enfant de 1 à 6 ans et se manifeste le plus souvent dans le cadre d'épidémies hivernales.

Signes et symptômes.
Au décours d'une rhinopharyngite apparaît, souvent la nuit, une gêne respiratoire à l'inspiration avec un tirage (dépression de la paroi thoracique) et un cornage (sifflement à l'inspiration) que l'on appelle une dyspnée laryngée. Le cri et la toux sont rauques, l'expiration est libre.

Investigations.
Le diagnostic est clinique.

Evolution, complications et pronostic.
L'évolution vers une forme grave est toujours possible, avec une détresse respiratoire nécessitant une intubation, voire une trachéotomie d'urgence.

Traitement.
Il associe les corticoïdes (per os ou par voie injectable) et l'humidification de l'air (initialement, faire couler de l'eau chaude dans la salle de bain pour dégager de la vapeur, puis aérosols). En l'absence d'amélioration, l'hospitalisation s'impose.























19.    LARYNGITE CHRONIQUE.
Définition et causes.
Inflammation chronique affectant le larynx, notamment les cordes vocales. Les facteurs favorisants sont le tabac, le climat (métiers au grand air...) ou le surmenage vocal (enseignants...).

Epidémiologie.
Très fréquente.

Signes et symptômes.
L'altération chronique de la voix (enrouement) est le signe capital. Elle peut être accompagnée de toux et de sensations de gêne au niveau de la gorge.

Investigations.
La laryngoscopie avec d'éventuelles biopsies pour éliminer des lésions cancéreuses permet le diagnostic.

Evolution, complications et pronostic.
Au-delà de la chronicité qui peut entraîner des répercussions socioprofessionnelles, la principale complication est l'évolution cancéreuse.

Traitement.
L'arrêt du tabac et le repos vocal sont les premières mesures. Dans certains cas, le laser et la microchirurgie sur les cordes vocales sont utiles.


20.    LARYNGITE STRIDULEUSE.
Forme particulière de laryngite où l'œdème est localisé au niveau de la partie basse du pharynx. Le début est brutal, nocturne, associant des quintes de toux suivies d'accès de suffocation et une grande dyspnée inspiratoire avec cornage (sifflement). Ces épisodes surviennent souvent dans le cadre d'une rhinopharyngite et sont généralement de courte durée. Le traitement repose sur l'humidification de l'atmosphère, les corticoïdes et la désinfection rhinopharyngée.


21.    LARYNGOCÈLE.
Hernie de la muqueuse laryngée. Elle peut être congénitale, apparaissant chez le sujet jeune et favorisée par une toux chronique ou l'utilisation d'instruments à vent (trompette), ou acquise dans le cadre d'un cancer du larynx. Les signes de découverte sont une modification de la voix ou l'apparition d'une masse au niveau du cou. Le traitement est l'exérèse chirurgicale.


22.    LASSA (FIÈVRE DE)
(>) FIÈVRE DE LASSA.





23.    LASTHÉNIE DE FERJOL (SYNDROME DE).
Affection psychiatrique caractérisée par une pathomimie, ou maladie auto-induite, au cours de laquelle la vie du sujet s'organise autour de l'entretien des troubles.


24.    LATHYRISME.
Intoxication par une variété de fèves, consommée dans certaines régions d'Asie en période de disette, contenant une neurotoxine. Elle se manifeste par une paraplégie spastique.


25.    LAUBRY PEZZI (SYNDROME DE).
Cardiopathie congénitale caractérisée par une communication interventriculaire haute qui entraîne secondairement un dysfonctionnement d'une valvule sigmoïde, attirée dans le ventricule, à l'origine d'une insuffisance aortique.


26.    LAUNOIS-BENSAUDE (MALADIE DE) ou (>) LIPOMATOSE
DE LAUNOIS-BENSAUDE.


27.    LAURENCE-MOON-BIEDL-BARDET (SYNDROME DE).
Maladie héréditaire, de transmission autosomique dominante, se manifestant chez l'adulte jeune. Elle associe des manifestations neurologiques (retard mental, ataxie = troubles de la coordination, paraplégie spastique progressive), ophtalmologiques (rétinite pigmentaire) et endocriniennes (hypogonadisme).





















28.    LAXATIFS (MALADIES DES).
Définition et causes.
Affection digestive due à l'usage prolongé et intensif des laxatifs, survenant en général dans un contexte de phobie de la constipation ou dans le but de maigrir.

Epidémiologie.
Maladie rare, survenant 9 fois sur 10 chez des femmes présentant des troubles graves de la personnalité.

Signes et symptômes.
Les principaux signes sont une diarrhée, des douleurs abdominales diffuses, une asthénie, des nausées et des vomissements. La patiente est généralement maigre et la prise de laxatifs est, le plus souvent, niée.

Investigations.
Le bilan biologique montre en général une hypokaliémie et une hypoprotidémie. La coloscopie retrouve parfois des anomalies évocatrices, comme une coloration sombre de la muqueuse (mélanose colique).

Traitement.
Au-delà des mesures symptomatiques concernant les troubles hydroélectrolytiques et digestifs, la base du traitement est une prise en charge psychologique.


29.    LEBER (>) ATROPHIE OPTIQUE DE LEBER
ET (>)       AMAUROSE CONGÉNITALE DE LEBER .


30.    LEDDERHOSE (MALADIE DE).
Fibrose de l'aponévrose plantaire, unilatérale ou bilatérale, formant des nodules à la partie moyenne de la voûte plantaire. Elle s'observe chez l'adulte de sexe masculin et est parfois associée à une maladie de Dupuytren. Elle peut entraîner une gêne et des douleurs qui justifient un geste chirurgical.


31.    LEGG-PERTHES-CALVÉ (MALADIE DE) ou (-->) COXA PLANA.











32.    LÉGIONELLOSE. 
Définition et causes.
Infection pulmonaire due à Legionella pneumophila, bactérie qui se développe dans les milieux humides, notamment les circuits de climatisation et les canalisations d'eau chaude. La contamination humaine se fait par voie aérienne (gouttelettes d'eau dans l'air inspiré).

Epidémiologie.
Les légionelloses représentent environ 5 % des pneumopathies hospitalisées. Environ 10 % semblent acquises à l'hôpital ou des épidémies sont possibles.

Signes et symptômes.
Les principaux signes sont une fièvre avec des frissons, une toux sèche puis productive, une bradycardie, des troubles digestifs (nausées, diarrhée, vomissements) et des signes neurologiques (céphalées, confusion).

Investigations.
L'identification du germe se fait à partir de prélèvements bronchiques par des techniques immunologiques ou par culture. Un sérodiagnostic est disponible. La radiographie pulmonaire montre des opacités alvéolaires, mais n'a rien de spécifique.

Evolution, complications et pronostic.
Le taux de mortalité est de 15 % environ et est directement lié aux lésions pulmonaires.

Traitement.
L'antibiotique de choix est l'érythromycine. Les quinolones et la clarithromycine peuvent également être utilisées.

Prévention.
En cas d'épidémie, les sources de contamination (pommes de douche, circuits d'air conditionné...) doivent être identifiées et stérilisés.


33.    LEIGH (MALADIE DE)
ou ENCÉPHALOMYOPATHIE NÉCROSANTE SUBAIGUË.
Maladie du groupe des myopathies mitochondriales (anomalie des mitochondries dans les fibres musculaires). Elle débute dans l'enfance avec des crises d'épilepsie, une ataxie cérébelleuse (mouvements maladroits et désorganisés) et une atteinte relativement modérée des fonctions intellectuelles.











34.    LEINER-MOUSSOUS (MALADIE DE) ou ÉRYTHRODERMIE DESQUAMATIVE GÉNÉRALISÉE DU NOURRISSON.
Définition et causes.
Dermatose généralisée. L'origine est inconnue.

Épidémiologie.
C'est une affection rare qui touche l'enfant avant trois mois.

Signes et symptômes.
Il existe des plaques de couleur rouge foncée avec des squames grasses sur l'ensemble du corps.

Investigations.
Aucun examen complémentaire n'est nécessaire.

Evolution, complications et pronostic.
Les principales complications sont les troubles caloriques, les pertes protéiques et hydroélectrolytiques qui peuvent entraîner un retentissement hémodynamique. Les surinfections sont possibles et peuvent déboucher sur une septicémie. Dans la plupart des cas, l'évolution est favorable en quelques semaines.

Traitement.
Un savonnage, un shampooing quotidien ainsi que l'application d'antiseptiques locaux sont nécessaires jusqu'à disparition des squames. Les corticoïdes locaux peuvent être utilisés pendant quelques jours.


35.    LÉIOMYOSARCOME.
Tumeur maligne développée aux dépens des fibres musculaires lisses. Elle est très rare. Les principales localisations sont l'estomac, la veine cave supérieure et inférieure. Au niveau gastrique, le traitement est chirurgical alors qu'au niveau de la veine cave ce geste n'est pas toujours possible et qu'il faut recourir à la chimiothérapie et/ou à la radiothérapie.


36.    LEISHMANIOSE CUTANÉE ou (-) BOUTON D'ORIENT.











37.    LEISHMANIOSE VISCÉRALE ou KALA-AZAR.
Définition et causes.
Parasitose due à un protozoaire (animal unicellulaire), Leishmania donovani, qui est transmis par des insectes (phlébotomes) et qui envahit le sang ainsi que le système réticulo-endothélial. L'incubation est de 3 mois.

Epidémiologie.
Elle est présente en Inde, en Chine, en Asie centrale, en Afrique, dans le bassin méditerranéen et en Amérique du Sud. L'OMS estime entre 1 et 1,5 million le nombre de nouveaux cas annuels. L'enfant et l'adulte immunodéprimé sont particulièrement vulnérables.

Signes et symptômes.
Association d'une fièvre oscillante avec altération de l'état général et pâleur, d'une hépatosplénomégalie et de micro-adénopathies généralisées.

Investigations.
Il existe une pancytopénie (diminution de toutes les lignées cellulaires sanguines) associée à un syndrome inflammatoire. Le myélogramme met en évidence le parasite. La sérologie assure le diagnostic.

Evolution, complications et pronostic.
En cas d'immunodépression, l'évolution est souvent fatale dans un tableau de diarrhées fébriles et de lésions cutanées (tâches de couleur foncée fourmillant de leishmanies, d'où le nom de kala-azar, « mort noire » en sanscrit). Une guérison sans séquelles est obtenue avec un traitement précoce.

Traitement.
On utilise l'antimoniate de méglumine , le stibogluconate de sodium , la pentamidine   ou l'amphotéricine B  , selon les cas.

Prévention.
La prévention consiste à utiliser des répulsifs antimoustiques et des moustiquaires imprégnées.


38.    LEMIÈRE (SYNDROME DE)
Syndrome caractérisé par la survenue, après une angine, d'une thrombophlébite jugulaire avec septicémie et abcès métastatiques, principalement pulmonaires. Le germe en cause est Fusobacterium necrophorum. Une antibiothérapie adaptée et prolongée permet la guérison.











39.    LENÈGRE (MALADIE DE)
Maladie dégénérative primitive touchant le tissu conjonctif du coeur, sans atteinte du myocarde ou du squelette fibreux du coeur. Elle est à l'origine de troubles de la conduction cardiaque (bloc auriculoventriculaire avec des blocs de branche) dont le traitement repose sur la pose de stimulateurs cardiaques.


40.    LENNOX-GASTAUT (SYNDROME DE). 
Une des formes les plus sévères d'épilepsie de l'enfant, débutant en général entre 3 et 5 ans. De prédominance masculine, elle peut se développer chez des enfants sains ou dans le cadre d'une affection ayant pu entraîner, en particulier, un syndrome de West (4). Les états de mal sont fréquents, les traitements décevants et le pronostic très mauvais. Un nouvel antiépileptique, le rifunamide (Inovelon) semble apporter une amélioration.


41.    LENTIGO.
Tache lenticulaire (en forme de lentille) arrondie, de quelques millimètres de diamètre, bien limitée, plane, lisse, de coloration brune ou noire uniforme. L'enfant est atteint sur les zones exposées au soleil (lentigo solaire juvénile) ; chez l'adulte, les tâches peuvent être très nombreuses, avec une tendance à la disparition chez le vieillard.


42.    LEOPARD (SYNDROME).
Ensemble de malformations héréditaires dont les initiales, en anglais, forment le nom: lentigines (petites taches pigmentées de la peau), electrocardiographic conductive defects (troubles de la conduction cardiaque), ocular hypertelorism (écartement excessif des yeux), pulmonary stenosis (sténose pulmonaire), abnormalities ofgenitalia (malformations génitales), retardation of growth (retard de croissance), deafneass (surdité). Un retard mental est associé.





















43.    LÈPRE ou MALADIE DE HANSEN.
Définition et causes.
Maladie infectieuse chronique, à transmission interhumaine directe par voie respiratoire ou cutanée, due à un bacille acido-alcoolo-résistant, Mycobacterium leprae, ayant un tropisme cutané et nerveux. L'incubation est de 3 à 20 ans.

Epidémiologie.
Le nombre de cas mondiaux est passé de 5 millions en 1985 à 600 000 environ en 2000. Elle reste endémique dans les pays en voie de développement de la zone tropicale, avec environ 100 cas par an actuellement dans les DOM-TOM.

Signes et symptômes.
On distingue trois formes :
  • La forme tuberculoïde, la plus fréquente, qui se caractérise par des taches cutanées hypo-chromiques (peu pigmentées) avec une perte de la sensibilité;
  • La forme lépromateuse, avec des papules fermes et brillantes, les lépromes;
  • La forme borderline, intermédiaire entre les deux formes précédentes.
  •  
Investigations.
La bascilloscopie retrouve le bacille sur des prélèvements de lésions dans la forme lépromateuse. La biopsie cutanée permet le diagnostic dans la forme tuberculoïde.

Evolution, complications et pronostic.
L'évolution se fait, en général, sur un mode chronique avec la survenue de déficits sensitifs ou moteurs, se traduisant par des troubles trophiques, des paralysies et des déformations progressives des pieds et des mains. Des épisodes aigus sont possibles.
Traitement.
Les protocoles OMS utilisent l'association DDS , rifampicine et clofazimine  pendant 6 à 24 mois.

Prévention.
La lèpre tuberculoïde est considérée comme non contagieuse. Pour les autres, la contagion est rapidement réduite parla chimiothérapie. L'éradication de la lèpre est un objectif possible, car le seul réservoir connu est l'être humain.


EMCrit by Rory Spiegel.


          Paroxysmal Supraventricular Tachycardia (PSVT)        
PSVT is a common arrhythmia that occurs among all age groups in both ambulatory and inpatient settings. Although most patients with PSVT are symptomatic in some way from this arrhythmia (with lightheadedness, awareness of rapid heart beat or palpitations), hemodynamic compromise is usually not seen if the patient is otherwise healthy and does not have underlying heart disease. In contrast, sudden development of this arrhythmia is much more likely to be consequential when it occurs in older patients, in very young children, or adults with significant underlying cardiac disease. Hemodynamic decompensation is especially likely to develop in such individuals when the rate of PSVT is very rapid and/or the rhythm persists for long periods of time. 

Electrocardiographically, the diagnosis of PSVT is suggested by the finding of a regular supraventricular (narrow complex) tachycardia in which normal atrial activity is lacking on the surface ECG. Terminology of the various forms of PSVT may be confusing, because there are a number of different mechanisms that may produce a similar electrocardiographic picture. Most commonly the phenomenon of "reentry" exists, in which the electrical impulse continually circulates over a well defined reentrant pathway. In a primary care setting, the overwhelming majority of adults who present with the ECG picture of PSVT (regular narrow complex tachycardia at a rate of between 140-240 beats per minute without evidence of normal atrial activity) will have a reentrant tachycardia in which at least a portion of the reentry circuit involves the AV node. Surprisingly, up to one-third of these patients have an accessory pathway involved in reentry circuit that is "concealed" (not manifested by delta waves on the surface ECG), reflecting the fact that conduction only occurs over the accessory pathway in retrograde fashion. This reentrant form of PSVT is said to manifest orthodromic conduction, because the electrical impulse travels first down the normal AV nodal pathway and then back up the accessory pathway. As a result of this sequence of activation, the usual ECG hallmarks of an accessory pathway (short PR interval, delta wave, QRS widening) are not seen. 

Clinically, initial management of patients with PSVT from a concealed accessory pathway (i.e., with orthodromic conduction first through the AV node, and then back up the accessory pathway in retrograde fashion) is similar to management of the more common form of PSVT in which the entire reentry circuit is contained within the AV node (atrioventricular nodal reentrant tachycardia, or AVNRT). In both cases, the arrhythmia behaves as an "AV nodal dependent" tachycardia, in that interventions aimed at altering AV nodal conduction properties may interrupt the reentry circuit just long enough to block propagation of the circulating impulse, and therefore convert the arrhythmia to sinus rhythm. 

Acute treatment of patients with AV nodal dependent forms of PSVT may include use of a vagal maneuver, and/or administration of IV verapamil, diltiazem, or adenosine (Adenocard). Although each of these drugs is effective in converting PSVT more than 90 percent of the time, adenosine is often preferred in an emergency setting because of its rapid onset. Unfortunately, recurrence may be seen with this agent because of its short dura-tion of action. If this occurs, either adenosine may be repeated, or use of a longer acting agent (verapamil or diltiazem) may be tried. Alternatively, use of digoxin or a beta-blocker could be considered. The addition of an anxiolytic agent may be a helpful adjunct for treatment of PSVT because it reduces the anxiety that often accompanies this arrhythmia, as well as the physiologic effect it may have in attenuating sympathetic tone and therefore altering conduction properties in one or both arms of the reentrant pathway.

Long-term management of the patient with PSVT includes elimination of all stimulants (including caffeine), alcohol, tobacco, and other substances of possible abuse, sympathomimetic agents, and diet pills. Selected patients can be taught the Valsalva maneuver, to be performed when necessary. 

Consideration may sometimes be given to administration of drugs on an episodic basis for patients with infrequent attacks, or daily for more frequent occurrence. Intermittent therapy may be appropriate for selected individuals whose PSVT only occurs at infrequent intervals, in which the treating physician prescribes the use of verapamil, diltiazem, or a beta-blocker that may be taken by the patient at home at the time of the episode. Such therapy should not be used unless the mechanism of the arrhythmia has been clearly defined. However, when appropriate, use of intermittent therapy for treatment of PSVT is well received by patients because it restores a measure of control over their condition and avoids the need to take a medication daily when their arrhythmia only occurs at infrequent intervals. The addition of a benzodiazepine to the rateslowing regimen may be beneficial because it reduces the anxiety that accompanies PSVT during the time that it takes the oral regimen to work (usually 30 to 90 minutes). 

Several points should be emphasized regarding the management of PSVT. First, patients with frequent episodes of PSVT that do not readily respond to medical therapy should be referred for electrophysiologic study. Doing so allows identification of a group of patients who may be suitable candidates for catheter ablation therapy, a procedure that may be curative in more than 90 percent of cases with only minimal risk of complications. This evaluation and treatment course should be especially considered for patients with PSVT that is known to be associated with conduction over an accessory pathway-since such individuals may retain the potential to suddenly develop antegrade (forward) conduction down the accessory pathway in association with tachycardia. In particular, development of atrial fibrillation in such a patient with antidromic conduction over an accessory pathway may lead to excessively rapid ventricular rates (of 250 beats per minute, or more) with associated life-threatening hemodynamic compromise. Electrophysiologic study of these patients allows identification of the culprit accessory pathway in most cases, which may then be ablated with cure of the arrhythmia. 

Finally, it should be appreciated that a small percentage of patients who present with the ECG picture of PSVT in reality have an "AV nodal independent" mechanism responsible for their arrhythmia. This group of tachyarrhythmias include entities such as sinus node reentry, intra-atrial reentry, and ectopic (automatic) atrial tachycardia, as may occur with digitalis toxicity. The importance of being aware of these much less commonly occurring arrhythmias is that the usual measures used for treatment of AV nodal dependent PSVT rhythms may not be effective if the AV node is not involved in the genesis and/or maintenance of the arrhythmia. For example, withholding digoxin may be all that is needed for resolution of atrial tachycardia with block that arises as a manifestation of digoxin toxicity. Clinically, sinus node reentrant tachycardia and intra-atrial reentrant tachycardia are both often resistant to treatment with standard antiarrhythmic agents. Early referral for electrophysiologic study should be strongly considered for such patients.

          Ventricular Arrhythmias        
 Ventricular arrhythmias are a broad category of conditions that include premature ventricular contractions (PVCs), ventricular tachycardia, accelerated idioventricular rhythm, torsades de pointes, ventricular flutter and
fibrillation.

Premature Ventricular Contractions. Prudent medical practice dictates that therapy for PVCs be based on "the company they keep". They are common in the general population, and if no heart disease is present, they are generally benign. Accompanying conditions that increase catecholamine levels, as well as hypoxia, electrolyte abnormalities, and drug toxicity, should be treated.

If, however, the PVCs occur with acute ischemic heart disease or any other organic heart disease, they may be of greater signifi-cance. PVCs themselves are not a cause of mortality, unless they lead to sustained VT or VF. Clinically, one should look first for disorders associated with increased catecholamine levels, hypoxia, electrolyte abnormalities, drug toxicity, HF, and ischemia. These conditions should be corrected if they exist. If PVCs persist, Holter monitoring could be considered in an attempt to determine if more malignant forms are present. In the absence of underlying heart  disease, PVCs, even if frequent, are generally benign and need not be treated. If the patient is symptomatic from such PVCs, a beta-blocker is the antiarrhythmic agent of choice.

In contrast, if PVCs occur in a patient who does not have underlying heart disease, cardiovascular risk is increased. The problem is that with rare exceptions, antiarrhythmic therapy has not been shown to increase survival in such patients. If treatment is deemed necessary, a beta-blocker is again the agent of choice. It should be kept in mind that antiarrhythmic drugs are not benign and, in 5 to 10 percent of cases, may be associated with a proarrhythmic effect, in which they paradoxically exacerbate the arrhythmia. This is a major reason for the reluctance to treat PVCs in recent years.

Ventricular tachycardia. When short episodes of VT occur in a normal heart, they are usually benign. However, once VT is found, intensive cardiac evaluation is usually indicated to assess the patient for underlying heart disease. If heart disease is not present, no therapy may be needed.

On the other hand, when VT occurs with organic heart disease, the risk of VF is higher and, therefore, the risk of sudden cardiac death increases. Full evaluation with echocardiography, cardiac catheterization, and/or electrophysiologic studies should be strongly considered. Treatment options include amiodarone or other antiarrhythmic therapy or an implantable defibrillator, depending upon the LVEF and how inducible the VT is with electrophysiologic studies. For example, VT is much more likely to be inducible in a patient with ischemic cardiomyopathy compared to one with a nonischemic cardiomyopathy. In appropriately selected patients, use of an implantable cardioverterdefibrillator (ICD) may result in a greater than 90-percent survival rate at five years in those patients who otherwise would be at very high risk for sudden cardiac death.

Recently, the Multicenter Automatic Defibrillator Implantation Trial (MADIT) was completed, in which prophylactic implantation of an ICD appeared to benefit a select group of patients with nonsustained VT and impaired left ventricular function following myocardial infarction. Although additional data are needed to confirm these results, it would seem that  patients with sustained VT and underlying heart disease should be referred for extensive cardiac evaluation including electrophysiologic study. Management decisions are less clear at this time for patients with asymptomatic episodes of nonsustained ventricular tachycardia (NSVT) who have underlying heart disease. At the least, control of potentially exacerbating causes of ventricular arrhythmias (whenever possible) is essential in such patients, including correction of electrolyte abnormalities and treatment of ischemia, heart failure and/or hypoxia. Preference should be given to use of ACE inhibitors and beta-blockers when appropriate for treatment of these underlying conditions. Whether or not patients with asymptomatic NSVT and underlying heart disease hould be routinely referred for electrophysiologic study remains controversial at this time, and is a decision that should be individualized for each patient depending on specific circumstances of the particular case at hand.

Finally, for patients who develop either cardiac arrest from ventricular fibrillation and/or sustained ventricular tachycardia associated with hemodynamic compromise that is not the result of acute myocardial infarction, recent data suggest the superiority of treatment with an ICD over treatment with antiarrhythmic drugs. Patients with these presentations should be referred for electrophysiologic evaluation unless extenuating circumstances exist.

          Valvular Heart Disease        
About valvular heart disease
Valvular heart disease is the name given to any dysfunction or abnormality of one or more of the heart’s four valves, including the mitral valve and aortic valve on the left side, and the tricuspid valve and pulmonic valve on the right side. In a normally functioning heart, the four valves (flaps made of tissue) keep blood flowing in one direction and only at the right time. They act as gates that swing open to allow blood to flow through and then tightly shut until the next cycle begins.

According to the American Heart Association’s 2006 Heart and Stroke Statistical Update, valvular heart disease is responsible for nearly 20,000 deaths each year in the United States and is a contributing factor in about 42,000 deaths. The majority of these cases involve disorders of the aortic valve (63 percent) and the mitral valve (14 percent). Deaths due to pulmonic and tricuspid valve disorders are rarer (0.06 percent and 0.01 percent, respectively).

Valvular heart disease in women may pose a greater risk of complications in pregnancy – to the mother and to the fetus. This is largely due to the normal increase in the amount of blood flow to the body from the heart (cardiac output) during pregnancy. Some heart valve conditions, like mitral valve prolapse, are not typically associated with pregnancy complications. Severe aortic stenosis, though, should be corrected before a woman becomes pregnant. Depending on the type of valve disorder, women will be advised to have regular visits to a cardiologist during the course of their pregnancy.

There are a number of types of valvular heart disease, including:

• Valvular stenosis. A condition in which there is a narrowing, stiffening, thickening, fusion or blockage of one or more valves of the heart. As a result, the defective valve can interfere with the smooth passage of blood through it. Depending on which valve is affected, the diagnosis may be aortic stenosis, mitral stenosis, pulmonic stenosis or tricuspid stenosis.

• Valvular regurgitation. A condition in which blood leaks back in the wrong direction because one or more of the heart’s valves is closing improperly. The nature and severity of the leakage, in turn, may keep the heart from circulating an adequate amount of blood through the defective valve. Depending on which valve is affected, the diagnosis may be aortic regurgitation, mitral regurgitation, pulmonary regurgitation or
tricuspid regurgitation.

• Atresia of one of the valves. A serious condition in which one of the valves has failed to develop properly and is completely closed at birth. Depending on which valve is affected, the diagnosis may be aortic atresia, mitral atresia, pulmonary atresia or tricuspid atresia.

• Mitral valve prolapse. A common and rarely serious condition in which the two flaps of the mitral valve (located between the left atrium and the left ventricle cannot close properly, and may result in blood leaking back into the left atrium (mitral valve regurgitation). It is due to either one (or both) of the flaps being too large, or because the muscle “hinges” of the flaps are too long.
valvular regurgitation 
People who slowly develop valvular heart disease may not notice any symptoms because the heart is given time to adjust. However, valve disease that develops suddenly can cause a variety of symptoms including palpitations, chest pain and edema (swelling) in the ankles, feet or abdomen. Weakness, dizziness and rapid weight gain may also occur. The severity of a patient’s symptoms does not always reflect the severity of their condition. Patients with severe valvular heart disease may have no symptoms and those with severe symptoms only have a minor valve problem that does not require treatment. As a general rule, patients experiencing any new symptoms, or symptoms that are more frequent or severe, should contact a physician.
The diagnosis of valvular heart disease is usually performed by one of the following tests:
• Physical examination may reveal a murmur, evidence of heart enlargement and fluids within the lungs.
• An electrocardiogram (EKG) may reveal arrhythmias and chamber enlargement.
• Echocardiography and a Doppler ultrasound are the most widely used methods, and are very useful in assessment of presence and severity of valve disease.
• MRI can provide clear three-dimensional images of the heart and its valves.
Treatment for valvular heart disease depends on the type and severity of the diagnosis. People with minor valve problems may not require treatment. Those with more serious disorders can often be treated successfully with medications such as the following:
• ACE inhibitors. Widen blood vessels, lower blood pressure and decrease the workload of the heart (in the case of valvular regurgitation).
• Antiarrhythmics. Maintain a regular heartbeat and slow rapid heart rhythms. Therefore, the heart beats less frequently but more effectively, pumping more blood through the body.
• Antibiotics. Help prevent or treat infection.
• Anticoagulants. Help prevent the formation of blood clots.
• Diuretics. Lower excess fluid levels in the body.
• Inotropes. Increase the force of the heart’s contractions.
If medications are not successful or a valve condition worsens interventional procedures and/or surgery may be necessary. These may include heart valve repair or replacement. A heart valve repair may be done by one of the following procedures:
• Percutaneous balloon valvuloplasty. A nonsurgical, catheter-based procedure to treat valvular stenosis.
• Valvulotomy. A type of open-heart surgery in which the surgeon cuts into a valve to repair valvular damage. One such type is a commissurotomy, a procedure in which narrowed valve leaflets are widened by carefully opening the fused leaflets or commissures with a scalpel. This procedure is mostly used to correct mitral stenosis.
• Minimally invasive heart valve surgery. A surgical repair of a defective heart valve performed through a small incision (3.5 inches) and partial removal of the upper breastbone (sternum) that involves less risk, fewer complications, less pain, less bleeding and faster recovery by the patient.
If heart valve repair is not an option, a heart valve replacement could be performed. This is an open–heart surgery in which a biological or mechanical valve is used to replace a defective heart valve.
Ongoing research on valvular heart disease
Biological heart valves last about 10 years before they start to fail due to tissue disintegration. Mechanical valves, which are made from metal or other man-made (synthetic) materials, are designed to last a lifetime. They are often used if all other factors are equal. However, mechanical valves carry a higher risk of blood clots, so patients with mechanical valves must take anticoagulants for life.
Researchers are continually exploring possible causes and treatments for heart valve diseases as well as the long-term effects of those treatments. Recent findings include:
• Stem cell research is being applied to congenital heart disease. Found in bone marrow, lymphatic tissue and embryos, immature stem cells can differentiate into specific, specialized body cells, including cardiac muscle cells. In animal studies, for example, bone marrow stem cells have evolved into cardiac cells after they were injected into damaged heart muscle. These results, however, have yet to be duplicated in human beings, and any benefits from stem cell therapy may be years away.
• Robotically-assisted surgery is showing benefit for both simple and complex mitral valve repairs. Robotic surgery involves voice-activated robotic “hands” at the operating table, with the cardiac surgeon manipulating the hand controls. The surgeon views the procedure through an endoscope, a slim optical tube with an attached camera positioned inside the chest. Advantages of this and similar procedures are small incisions, less surgical trauma and a shorter operative and recovery period.
• Cells from a patient’s own blood vessels can be “grown” over biological valves taken from pigs or human cadavers. Scientists remove the cells from the biological valve, leaving only elastic tissue that retains the valve’s shape. The patient’s cultured cells are then grown over the elastic tissue. After about one year, the new valve is implanted into the patient. It has been shown that this procedure resulted in fewer post-operative complications (e.g., fever, hospital stay) compared to conventional valve replacement.
• Surgeons are exploring heart valve replacement without the need for open-heart surgery. Typically, diseased or defective valves are replaced with an artificial valve or a tissue valve (from a pig or cow). A new, less invasive procedure, known as percutaneous transcatheter heart valve implantation, involves the use of balloon catheters and large stents introduced through a puncture in the skin (in the groin area, near the femoral vein). The new heart valve is transported via the stent to the site,
where the stent is then expanded to implant the valve. For patients not able to undergo open-heart surgery, due to age and/or physical condition, percutaneous heart valve implantation may impact significantly on survival and quality of life.
• Studies are evaluating whether medical (drug) therapy can offer improvement in aortic stenosis. Stenosis can develop due to a buildup of calcium, causing decreased mobility in the aortic valve. This calcium buildup is a form of atherosclerosis. Statins, a type of cholesterol-reducing drug, have shown to be effective in reducing calcium deposits in and around the heart. Therefore, there is interest in this class of drugs for
the treatment of aortic stenosis. In early studies, researchers found that, while lower cholesterol levels did not impact on aortic stenosis, statins slowed its progression. This could be due to its effect and reducing C-reactive protein and overall inflammation around the heart – another cause of atherosclerosis.
• Treating calcification of the aortic valve with ACE inhibitors is also being explored. These are medications that block the effects of angiotensin-converting enzymes, which normally have a role in blood pressure. It is believed that angiotensin-converting enzyme (ACE) is transported by low-density lipoproteins (LDLs, so–called “bad” cholesterol) into areas damaged by plaque, contributing to calcification.
Questions for your doctor
Preparing questions in advance can help patients to have more meaningful discussions with their physicians regarding their conditions. Patients may wish to ask their doctor the following questions related to valvular heart disease:
1. Do I have any type of Valvular Heart Disease?
2. Which of my valves is affected? What does this mean?
3. Am I taking any medications that may be causing this condition? Could an underlying medical problem be responsible?
4. Do you recommend any surgeries or medications to correct my problem? Why do you feel this is the best course of action?
5. How invasive would corrective surgery be? Why is/isn't this a good option for me?
6. Are there any recent treatment breakthroughs in this area that I may benefit from?
7. Are there any lifestyle changes I can make that could improve my condition?
8. Are there any activities I should not engage in?
9. Does Valvular Heart Disease prevent me from becoming pregnant? Could it cause complications if I am already pregnant?

          Basic Echocardiography Hands on Training Course - Nahdat Al Tamayuz , Abu Dhabi         

In recent years, fetal echocardiography has been used for the screening and diagnosis of anatomical heart defects and for the detailed study of fetal cardiac function. This method is characterized by its easy implementation and good reproducibility, allowing the diagnosis of myocardial dysfunction even in its subclinical phase. The functional assessment of the fetal heart should be routinely performed in fetuses with congenital heart disease and those without anatomical malformation. Several extra-cardiac conditions may alter fetal cardiac function, by increased placental resistance, volume overload or hyperdynamic circulation, compression, or maternal systemic disease with involvement of the fetal myocardium.

This workshop addresses the main ultrasound techniques and various Doppler echocardiographic parameters available for the analysis of fetal heart function, and correlates them with clinical applicability. Various parameters available for the assessment of fetal myocardium, including those that evaluate atrial dynamics, can be used in this analysis and should be selected considering specific conditions. 

Learning Objectives

  • Identify when functional assessment should be used.
  • Analyze the fetal heart function.
  • Discuss the factors which may alter fetal cardiac functions.
  • Discuss detailed knowledge of fetal cardiac function.
  • Analyze fetal echocardiography method.
  • Discuss and gain more knowledge with the main ultrasound techniques and Doppler echocardiographic parameters.
Course/Workshop will cover
  • Lectures will include discussion of the Anatomy and Physiology of the Heart during the First week of Life and what is Echography
  • How to access Echography, views, different uses
  • Identify each of the Conotruncal Anomalies, signs, symptoms, and the diagnostic characteristics 
  • Workshop will include 45 minutes' hand-on training
Who Should Attend
  • Cardiovascular Technologist
  • Diagnostic Radiology
  • Intensive Care / Critical care Medicine
  • Medical Diagnostic Imaging
  • Pathology

Cost: Upto 600 AED

Certified


          Heart Failure        
Epidemiology
Heart failure, defined as an impairment that prevents the heart from adequately perfusing body tissues to meet metabolic demands, is a major health problem that affects between 2 and 3 million Americans. With 400,000 new cases of HF diagnosed annually, the cost to the U.S. health care system is considerable, since HF is the primary reason for an estimated 1 million hospitalizations per year. In 1990, HF was responsible for approximately $10 billion in direct (e.g., hospitalization) and indirect (e.g., prolonged nursing home stays) costs.
HF has a poor prognosis. After the onset of symptoms, the five-year mortality rate in patients with HF-based on data from the Framingham Heart Study-is 62 percent in men and 42 percent in women, with 200,000 deaths attributable to HF each year in the United States alone.

Pathophysiology
Traditionally, HF has been thought to be a result of an impairment of systolic (inotropic) function, which is a reflection of decreased contractility of myocardial cells, most common in the left ventricle. More recently, impaired left ventricular (LV) filling, or diastolic dysfunction, has also been recognized as a significant contributor to the development of HF and is a reflection of reduced ventricular compliance related to scar tissue, ischemia, or hypertrophy of normal myocardial cells. Many cases of HF have components of both systolic and diastolic dysfunction.
hypertrophic responseshypertrophic responseshypertrophic responses 
Figure 1 Schematic illustration of selected types of hypertrophic responses. In A, the left ventricular dimensions are normal. With end-stage systolic dysfunction (B), cardiac chamber wall thickness remains the same or decreases in association with generalized dilatation of several cardiac chambers. Contractile activity is globally reduced. In lesser degrees of  systolic dysfunction, contractility is reduced, but cardiac chambers do not necessarily demonstrate marked dilatation. In pure diastolic dysfunction (C), symmetric thickening of the IVS and LVFW occurs at the expense of left ventricular  cavitary volume. Cardiac contractility is typically preserved, if not increased, resulting in corresponding preservation (or increase) in ejection fraction. However, overall cardiac output is reduced because the ventricle never completely  fills.
IVS = interventricular septum;
LA = left atrium; LV = left ventricle;
LVFW = left ventricular free wall;
RA = right atrium; RV = right ventricle.

In HF due to systolic dysfunction, the left ventricle is enlarged and overstretched (i.e., thinned) (Figure 1B; Figure 1A corresponds to a normal heart). Systolic dysfunction is the result of decreased cardiac contractility, which causes low cardiac output. Common causes of systolic dysfunction include scarring due to mycardial infarction and viral cardiomyopathy. The heart in end-stage HF due to systolic dysfunction is easily recognized on echocardiography as a Òbig, baggy heart.
In HF due to diastolic dysfunction, cardiac contractility is preserved or even increased (Figure 1C). The thickened and stiffened ventricle limits the amount of blood that can enter the heart, resulting in decreased ventricular filling during diastole. Ventricular dysfunction is often mixed, however, and has elements of both systolic and diastolic dysfunction.
Unfortunately, the physical examination will usually not allow the physician to reliably distinguish between systolic and diastolic dysfunction. Sometimes, a laterally displaced, dilated point of maximum impulse (PMI) may suggest that HF has a component of systolic dysfunction. On the other hand, in pure diastolic dysfunction, the PMI is not typically displaced or dilated, albeit the impulse may be abnormally sustained in duration.
It is important to recognize that diastolic and systolic dysfunction often overlap and may occur in the same patient. As an example, hypertensive patients commonly develop concentric hypertrophy with diastolic dysfunction as a result of the increase in afterload associated with persistent hypertension. If the hypertension is not controlled, LV function eventually deteriorates, and systolic dysfunction becomes superimposed on the initially hypertrophied left ventricle. Eventually, the left ventricle dilates and the diastolic dysfunction present in the early HF of hypertension evolves to dilated cardiomyopathy, so that the component of diastolic dysfunction may no longer be recognized.
Myocardial function is controlled by preload, afterload, ventricular contractility, heart rate, and heart rhythm. In HF, impaired heart function results in hemodynamic stress in the form of falling cardiac output. This stress unleashes a series of interdependent acute and chronic compensatory events, all of which are intended to maintain perfusion to vital organs.
Myocardial cell hypertrophy and increased LV wall thickness resulting from HF are accompanied by decreased ventricular compliance (increased ventricular stiffness), and, in the elderly, increased vascular resistance. The ensuing structural deterioration transforms the left ventricle from its normal elliptical shape to a rounded shape-a process known as remodeling. The rounded, or globoid, heart of late-stage HF may be accompanied by functional mitral regurgitation, ventricular dilatation, and thinning of the ventricular wall.
Neurohormonal Activation
The functional decrease in cardiac output and atrial hypertension results in arterial hypovolemia that characterizes HF. HF activates the adrenergic (sympathetic) nervous system and the renin-angiotensin-aldosterone (RAA) system, increases release of atrial natriuretic peptide (ANP), may increase the secretion of antidiuretic hormone (ADH) and renal
prostaglandins, and has long-term pathologic consequences.
Early in the course of HF, neurohormonal responses to hypovolemia lead to plasma expansion and selective vasoconstriction. The cardiovascular system compensates for the functional decrease in circulatory volume by shunting blood away from nonvital organ systems (e.g., kidneys, gastrointestinal tract), and by increasing cardiac contractility. Long-term neurohormonal adaptation to decreased perfusion results in desensitization of the heart to sympathetic stimulation, increased impedence to LV outflow, dysfunctional vascular endothelium, impaired glycolysis in fasttwitch muscles, physical deconditioning, and muscle deterioration.
In HF, norepinephrine is chronically elevated due to an increase in release and spillover from the adrenal gland, decreased plasma clearance, and decreased neuronal and non-neuronal reuptake. Norepinephrine increases afterload, causes cardiac arrhythmias, and has a direct toxic effect on the myocardium. There is a direct correlation between norepinephrine levels and both the hemodynamic severity and the poor prognosis of HF.
Decreased cardiac output, characteristic of HF, results in constriction of the kidney's efferent arterioles, which maintain the glomerular filtration rate (GFR). As HF progresses, a point is reached at which further constriction is impossible, and the GFR becomes flowdependent and decreases in tandem with additional decreases in cardiac output.
When the GFR falls, sodium is reabsorbed by the renal tubules, which activates the RAA system. The RAA system plays a key role in regulating blood pressure and vascular tone, and maintaining salt and water homeostasis. Renin, a proteolytic enzyme stored in the juxtaglomerular complex, cleaves angiotensinogen (a glycoprotein formed in the liver) to form angiotensin I. Angiotensin I is split by angiotensin-converting enzyme into angiotensin II, a potent vasoconstrictor that also stimulates the synthesis and secretion of aldosterone, which leads to sodium retention. Activation of the RAA system in HF is thought to occur in steps, as it normalizes in early-stage, compensated HF. As HF worsens, the RAA system is reactivated, and is a major contributor to the relatively intense edema and vasoconstriction typical of decompensated HF.
ADH is produced in the posterior pituitary and promotes renal tubular reabsorption of water by the kidneys in response to decreased plasma volume, as occurs in HF. Although ADH is often increased in HF, its contribution to the vascular dynamics of HF is unclear.
ANP is produced in atrial tissue of the heart in response to atrial stretch from increased blood volume. This causes natriuresis and vasodilation, and counteracts the waterretaining effect of the adrenergic and RAA systems. In early-stage HF, the vasodilatory response of peripheral arteries to ANP is preserved, but it becomes blunted as the HF enters a decompensation phase, an effect attributed to the down-regulation of ANP receptors.
One of the compensatory responses to the chronic overstimulation of the sympathetic nervous system (SNS) and the RAA system is an increased release of prostaglandins, resulting in peripheral vasodilation.

Clinical Findings
It is essential to keep in mind that mild HF is not necessarily the same as early-stage HF. Mild HF suggests that the patient's ability to function is only "mildly" affected. Earlystage HF, on the other hand, refers to the duration of pathogenic events that occur in the compensated phase of HF.
It is also important to emphasize that LV dysfunction does not always progress in a predictable fashion, nor is the degree of LV dysfunction necessarily paralleled by the clinical severity of symptoms. Some patients may present with significant symptoms of HF, yet only have minimal alteration of LV function. Other patients with only mild symptoms may come to medical attention in later stages of HF, which reflects the efficacy of the body's compensatory mechanisms.
For practical purposes, HF may be divided into high-output failure, which is usually secondary to other, noncardiac conditions, and low-output failure, which is primarily due to cardiac pump failure. High-output HF is very unusual in clinical practice and may be due to a marked hyperdynamic circulation with minimal functional myocardial abnormalities, in which the demand outstrips the capacity, resulting in a hyperkinetic state.
In low-output HF, the cardiac output falls below the tissue requirements for oxygen. It is associated with increased vascular resistance and oxygen consumption, decreased cardiac index and oxygen saturation, and lactic acidosis. Low-output HF may be "forward,"  in which oxygenated blood does not reach peripheral tissues, or "backward," in which blood backs up in the lungs.
The symptoms of low-output forward HF include weakness, fatigue, lethargy, lightheadedness, and confusion. In decompensated HF, cardiac cachexia, which is characterized by generalized exhaustion and loss of lean muscle mass, ensues. The symptoms of lowoutput backward, or congestive, HF reflect pulmonary edema, in which fluids accumulate in the lungs and result in dyspnea, initially only on exertion. Decompensated low-output backward failure is characterized by orthopnea and paroxysmal nocturnal dyspnea.
The clinical findings in HF include peripheral edema, rales, S3 gallop, sinus tachycardia, hypotension, increased jugular venous pressure, and hepatojugular reflux. Despite the presence of one or more of these signs, HF may be misdiagnosed in up to 40 percent of patients. The severity of HF can also be evaluated with chest radiography. Chest films may demonstrate cardiac enlargement, interstitial and alveolar edema, and pulmonary vascular redistribution in HF. However, HF may also be misdiagnosed using x-ray studies. Therefore, all patients suspected of having HF should be evaluated by two-dimensional echocardiography and Doppler studies to determine LV contractility, ventricular compliance, hypertrophy, and the presence or absence of other underlying conditions, such as valve pathology.

Management Strategies
HF is a syndrome that consists of a constellation of symptoms evoked by a wide range of conditions and precipitating factors (Table 1). Its management hinges on correction (when possible) of precipitating factors, treatment of acute symptoms, and compliance with long-term strategies that are intended to prolong survival.
The surface electrocardiography (ECG) in both acute and chronic phase of ischaemic heart disease (IHD) may give crucial information about the coronary artery involved and which is the area of myocardium that is at risk or already infarcted. This information jointly with the ECG–clinical correlation is very important for prognosis and risk stratification, as will be demonstrated in this book. Therefore, we will give in the following pages an overview of the anatomy of the heart, especially the heart walls and coronary tree, and emphasise the best techniques currently used for its study.
For centuries, since the pioneering works of Vesalio, Leonardo da Vinci, Lower and Bourgery- Jacob, pathology has been a unique method to study the anatomy of the heart. Since the end of the nineteenth century, the visualisation of the heart in vivo has been possible by X-ray examination. The last 40–50 years started the era of invasive imaging techniques with cardiac catheterisation (angiography and coronary angiography) and modern noninvasive imaging techniques, first with echocardiography and later with isotopic studies, scanner and cardiovascular magnetic resonance (CMR). These techniques open a new avenue to study not only the anatomy of the heart, coronary arteries and great vessels but also the myocardial function and perfusion, and the characterisation of the valves, pericardium, etc.
The coronary angiography (Figure 1.1) is especially important in the acute phase for diagnosing the disease and correlating the place of occlusion with the ST-segment deviations. It is also useful in the chronic phase of the disease. However, in the chronic phase of Q-wave myocardial infarction (MI) the ECG does not usually predict the state of the coronary tree, because the revascularisation treatment has modified, sometimes very much, the characteristics of the occlusion responsible for the MI. Furthermore, the catheterisation technique may give important information for identifying hypokinetic or akinetic areas. The latter may be considered comparable to infarcted areas. Currently, in some cases, the noninvasive coronary multidetector computer tomography (CMDCT) may be used (Figure 1.1).coronary angiography
coronary angiographycoronary angiographycoronary angiographycoronary angiographycoronary angiographycoronary angiography
Figure 1.1 (A) Normal case: coronary angiography (left) and three-dimensional volume rendering of CMDCT (right) showing normal LAD and LCX artery. The latter is partially covered by left appendix in CMDCT. The arrow points out LAD. (B) Normal case: coronary arteriography (left) and three-dimensional volume rendering of CMDCT (right) showing normal dominant RCA. (C) 85-year-old man with atypical anginal pain: (a) Maximal intensity projection (MIP) of CMDCT with clear tight mid-LAD stenosis that correlates perfectly with the result of coronary angiography performed before PCI (b). (D) Similar case as (C) but with the stenosis in the first third of RCA ((a–d) CMDCT and (e) coronary arteriography). (E) Similar case as (C) and (D) but with the tight stenosis in the LCX before the bifurcation ((a) and (b) CMDCT and (c) coronary angiography). (F) These images show that CMDCT may also demonstrate the presence of stenosis in distal vessels, in this case posterior descending RCA ((a–b) CMDCT and (c)) coronary angiography). (G) These images show that CMDCT (a, b) may delimitate the length of total occlusion and visualise the distal vessels (see arrows in (b), the yellow ones correspond to distal RCA retrograde flow from LAD) that is not possible to visualise with coronary angiography (c). (H) A 42-year-old man sports coach with a stent implanted in LAD by anginal pain 6 months before. The patient complains of atypical pain and present state of anxiety that advises to perform a CMDCT to assure the good result and permeability of the stent. In the MIP of CMDCT (a–c) was well seen the permeability of the stent but also a narrow, long and soft plaque in left main trunk with a limited lumen of the vessel (see (d) rounded circle) that was not well seen in the coronary angiography (e) but was confirmed by IVUS (f). The ECG presents not very deep negative T wave in V1–V3 along all the follow-up.
End-diastolicend-systolicsuperimposed end-diastolic and end-systolic contours 
Figure 1.2 Echocardiography: see example of volumes, wall thickening and myocardium mass in a normal case and in a patient with post-MI. Above: (A) End-diastolic and (B) end-systolic apical long-axis views of a normal left ventricle. The endocardial and epicardial contours are traced and the built-in computer software of the ultrasound system allows calculation of volumes, wall thickening and myocardial mass. Below: Segmental wall function analysis: post-infarct lateral wall hypokinesis shown in the four view. The left ventricle is dilated. Superposition of the traced endocardial contours at end diastole (A) and end systole (B) shows the hypokinesis and compensatory hyperkinesis of the interventricular septum. (C) It shows the superimposed end-diastolic and end-systolic contours.

The era of modern non-invasive imaging techniques started with echocardiography, which is very easy to perform and has a good cost-effective relation. This technique plays an important role, especially in the acute phase, in the detection of leftventricular function and mechanical complications of acute MI (Figures 1.2). Also, it is verymuch used in chronic ischaemic-heart-disease patients for the study of left-ventricular function and also detection of hypokinetic and akinetic areas. However, echocardiography tends to overestimate the area that is at risk or necrosed, and thus its reliability is good but not excellent. The techniques of echo stress and especially isotopic studies (single-photon emission computed tomography, SPECT) have proved to be very reliable for detecting perfusion defects and necrotic areas. They are very useful in cases where there is dubious precordial pain with positive exercise testing without symptoms.  It has been demonstrated, however, that in some cases (non-Q-wave infarction) the extension of the infarction may be underestimated and that in presence of the left bundle branch block (LBBB) the estimation of some perfusion defects is doubtful.
Examples of correlation exercise test – isotopic images (SPECT)Examples of correlation exercise test – isotopic images (SPECT)Figure 1.3 Examples of correlation exercise test – isotopic images (SPECT). (A) Above: Observe the three heart planes (see Figure 1.4B) used by nuclear medicine experts (and other imaging techniques) to transect the heart: (1) short-axis (transverse) view (SA), (2) vertical long-axis view (VLA) (oblique sagittal-like) and (3) horizontal long-axis (HLA) view. Below: Normal case of perfusion of left ventricle. On the middle is (B) the bull’s-eye image of this case. The segmentation of the heart used in this book is shown (Cerqueira, Weissman and Disizian, 2002). On (A) transections of the three axes are shown. The short-axis transections is at the mid-apical level (see Figure 1.8 for segmentation). (B) Above: In the three planes (SA, VLA and HLA) see (A) normal uptake at rest (Re) and during exercise (Ex) can be observed. Middle: Abnormal uptake only during exercise of segments 7, 13 and 17 (see Figure 1.8) in a patient with angina produced by distal involvement of not long LAD. The basal part of the anterior wall of left ventricle is not involved. Below: Abnormal uptake during rest and exercise in a patient in chronic phase of MI produced by distal occlusion of very long LAD that wraps the apex involving part of inferior wall (segments 7, 13 and 17 and also 15) (see Figure 1.8), without residual ischaemia on exercise. In this case the image of abnormal uptake is persistent during rest. See in all cases the ECG patterns that may be found. This figure can be seen in colour, Plate 2.
Cardiac magnetic resonance imaging (CMR).Cardiac magnetic resonance imaging (CMR). 
Figure 1.4 Cardiac magnetic resonance imaging (CMR). (A) Transections of the heart following the classical human body planes: (1) frontal plane, (2) horizontal plane and (3) sagittal plane. (B) Transections of the heart following the heart planes that cut the body obliquely. These are the planes used by the cardiac imaging experts: (1) short-axis (transverse) view, in this case at mid-level (see B(1)); (2) horizontal long-axis view; (3) vertical long-axis view (oblique sagittal-like). Check the great difference between the sagittal plane according to human body planes (A(3)) and the heart planes (B(3). (B) It shows the four walls of the heart with the classical names: septal (S), anterior (A), lateral (L) and inferoposterior. Currently, the inferoposterior wall is named for consistency just inferior (I) (see p. 16 and Figure 1.8).
Hyperenhancement patterns found in clinical practice 
Figure 1.5 Hyperenhancement patterns found in clinical practice. If hyperenhancement is present, the subendocardium should be involved in patients with ischaemic disease. Isolated mid-wall or subepicardial hyperenhancement strongly suggests a ‘non-ischaemic’ etiology.

The most recent imaging techniques are CMR (Figure 1.4) and CMDCT (Figure 1.1). The latter is used for non-invasive study of coronary tree. CMR, which may also be used for perfusion and function studies of themyocardium, gives us the best ‘in vivo’ anatomic information about the heart. Thus, this technique, in conjunction with gadolinium injection and contrast-enhanced CMR (CE-CMR), is very useful for identifying and locating MI, as well as for determining its transmurality with extraordinary reliability, comparable to pathological studies. This is why CE-CMR has become the gold-standard technique for studying correlations between ECG findings and infarctedmyocardial areas in the chronic phase of IHD. Also, CE-CMR may distinguish according to location the hyperenhancement areas between ischaemic and non-ischaemic patients (Figure 1.5) and may show in vivo the sequence of the evolving transmural MI. The reproducibility of CE-CMR along time, especially after the acute phase, is very good. It also has the advantage of not producing radiation. The current limitation of CMR, which will probably be solved in the next few years, is the study of coronary tree. Currently, this may be performed non-invasively by CMDCT (see above Fig 1.1).
The heart walls and their segmentation: cardiac magnetic resonance (Figures 1.4–1.14)
The heart is located in the central-left part of the thorax (lying on the diaphragm) and is oriented anteriorly, with the apex directed forwards, and from right to left (Figure 1.4).
The concept of anterior and posterior infarction 
Figure 1.6 The concept of anterior and posterior infarction
left ventricle 
Figure 1.7 (A) The left ventricle may be divided into four walls that till very recently were usually named anterior (A), inferoposterior (IP) or diaphragmatic, septal (S) and lateral (L). However, according to the arguments given in this book, we consider that the ‘inferoposterior’ wall has to be named just ‘inferior’ (see p. 16). (B–D) Different drawings of the inferoposterior wall (inferior + posterior walls).

The left ventricle (LV) is cone shaped. Although its borders are imprecise, classically, it has been divided, except in its inferomost part the apex, into four walls, till very recently named septal, anterior, lateral and inferoposterior. In the 1940s–1950s the inferoposterior wall was named just posterior (Figure 1.6A), probably because it was considered opposed to the anterior wall. Later on, only the basal part of this wall, which was thought to bend upwards, was considered really a posterior wall (Figure 1.6B). Therefore, it was named ‘true posterior’ and the rest of the wall just ‘inferior wall’ (Figure 1.6). According to that, for more than 40 years the terms ‘true’ or ‘strict posterior infarction’, ‘injury’ and ‘ischaemia’ have been applied, when it was considered that the basal part of the inferoposterior wall was affected. The committee of the experts of the International Society of Computerised ECG, in accordance with the publications of Selvester andWagner, has named these walls anterosuperior, anterolateral, posterolateral and inferior, respectively. However, this nomenclature has not been popularised, and the classical names (Figure 1.7A) are still mostly used in the majority of papers, ECG books (Figure 1.7B to D), task force and statements.
short-axis view 
Figure 1.8 (A) Segments into which the heart is divided, according to the transverse (short-axis view) transections performed at the basal, mid and apical levels.
transverse transections 
Figure 1.9 Images of the segments into which the left ventricle (LV) is divided according to the transverse transections (short-axis view) performed at the basal, mid and apical levels, considering that the heart is located in the thorax just in a posteroanterior and right-to-left position.

Later on, in the era of imaging techniques, the heart was transected into different planes (Figure 1.7) and different names were given to the heart walls by echocardiographists and experts in nuclear medicine. However, recently, the consensus of the North American Societies for Imaging divided the LV in 17 segments and 4 walls: septal, anterior, lateral and inferior (Figures 1.8 and 1.9). This consensus states that the classical inferoposterior wall should be called inferior ‘for consistency’, and segment 4 should be called inferobasal instead of posterior wall. Therefore the word ‘posterior’ has to be suppressed. Figures 1.8 and 1.9 show the 17 segments intowhich the four left-ventricular walls are divided (6 basal, 6 medial, 4 inferior and the apex), and the right side of Figure 1.9 shows the heart walls with their corresponding segments on a polar ‘bull’s-eye’ map, as used by specialists innuclear medicine.Now we will explain, thanks to correlations with CMR, why we consider that this terminology is the best and it will be used further in this book. Page 16 shows the evolution of the terminology given to the wall that lies on the diaphragm.
shown out of the thorax by anatomists and pathologists 
Figure 1.10 (A) The heart, shown out of the thorax by anatomists and pathologists; (B) bull’s-eye image as it is shown by nuclear medicine and (C) transverse transection as it is shown by CMR. In both cases the position of the heart is presented as if the heart was located in the thorax in a strictly posteroanterior position. (D) The injury and infarction vectors (Inj. V and Inf. V) with the same direction but different sense may be seen.
Magnetic resonance imaging. 
Figure 1.11 Magnetic resonance imaging. (A) Thoracic horizontal axial plane at the level of the ‘xy’ line of the drawing on the right side of the figure. The four walls can be adequately observed: anterior (A), septal (S), lateral (L) and inferior (I), represented by the inferobasal portion of the wall (segment 4 of Cerqueira statement) that bends upwards in this case (B).
Infarction vector 
Figure 1.12 (A) The posterior (inferobasal) wall as it was wrongly considered to be placed. With this location an infarction vector of inferior infarction (segments 4 and 10 in case of very lean individuals) faces V1–V2 and explains the RS pattern in these leads. (B, C) The real anatomic position of inferior wall (inferobasal) and lateral wall infarctions. The infarction vector of inferobasal and mid-segment in lean individuals faces V3–V4 and not V1, and may contribute to the normal RS pattern seen in these leads. On the contrary, the vector of infarction of the lateral wall faces V1 and may explain RS pattern in this lead.
Sagittal-oblique view 
Figure 1.13 Sagittal-oblique view in case of normal-body-build subject (A) (G shape), in a man with horizontal heart (B) (C shape) and in a very lean subject (C) (U shape). We have found that the inferior wall does not bend upward in C shape (two-third of the cases), and only in very lean individuals with U shape, the largest part of the wall is posterior (5% of the cases) (C).

If we consider that the heart is located in the thorax in a strictly posteroanterior position, as is presented by anatomists and by experts in nuclear medicine, and in the transverse section of CMR images (Figure 1.10A–C), we may understand that in case of involvement (injury or infarction) of basal part of inferior wall (classically called posterior wall) especially when in lean individuals the majority of inferior wall is placed in a posterior position (Figure 1.13C), an RS (R) and/or ST-segment depression in V1 will be recorded (Figure 1.10D). However, now, thanks to magnetic resonance correlations
(Figure 1.11), we have evidence that the sagittal view of the heart is, in respect to the thorax, locatedwith an oblique right-to-left inclination and not in a strictly posteroanterior position, as was usually presented by anatomists, nuclear medicine and the transverse section of CMR (Figure 1.10). This helps us to understand how the RS (R) or predominant ST-segment depression patterns in V1 is the consequence of the infarction of or injury to the lateral, not the inferobasal, segment (classical posterior wall) (Figure 1.12).However,we have to remind that in the majority of cases except for very lean individuals (see Figure 1.13C), the part of the inferior wall that is really posterior just involves the area of late depolarisation (segment 4, or inferobasal). Therefore, in case of MI of this area, there would not be changes in the first part of QRS, because this MI does not originate a Q wave or an equivalent wave.
The CMR technique gives us real information about the in vivo heart’s anatomy (Figure 1.4). In this regard, the following
are important:
(a) CMR patterns of the frontal, horizontal and sagittal planes of the heart following the human body planes are shown in Figure 1.4A. This allows us to knowwith precision the heart’s locationwithin the thorax. In this figure we can observe these transections, performed at the mid-level of the heart.
(b) Nevertheless, bearing in mind the threedimensional location of the heart within the thorax, in order to correlate the left ventricular walls amongst themselves and, above all, to locate the different segments into which they can be divided,
it is best to perform transections following the heart planes that are perpendicular to each other (see Figure 1.4B), as has been already done in nuclear medicine (Figure 1.3; see Plate 2). These planes transect the heart following the heart planes
(Figure 1.4B)andare the following: horizontal longaxis view, short-axis view (transverse) and vertical long-axis view (oblique sagittal-like). In reality the oblique sagittal-like view (Figure 1.11B) presents, as we have said, an oblique right to left and not a strict posteroanterior direction (compare Figure 1.4A(3) with Figures 1.4B(3) and 1.11B). Therefore in the presence of infarction of the inferobasal partof inferior wall (classically calledposterior wall) and especially when the infarction involves the midinferior wall if it is located posteriorly, as happens in very lean individuals (Figure 1.13C), the vector of infarction generated in this area is directed forwards and from right to left and is recorded as RS morphology in V2–V3, but not in V1 where it presents a normal rS morphology (Figure 1.12B). On the contrary, the vector of infarction, in the case of infarction involving the lateral wall, may generate an RS pattern in V1 (Figure 1.12C).
(c) The longitudinal vertical plane (Figures 1.3(2), 1.8C and 1.11B; see Plate 2) is not fully sagittal with respect to the anteroposterior position of the thorax, but rather oblique sagittal, as it is directed from right to left. (The sagittal-like axis follows the CD line in Figure 1.11A.) Compare Figures 1.4B(3) and 1.11B with the true sagittal view – Figure 1.4A(3). The view of this plane, as seen from the left side (oblique sagittal), allows us to correctly visualise the anterior and the inferior heart walls (Figure 1.11B). We can clearly see that the inferior wall has a portion that lies on the diaphragm until, at a certain point, sometimes it changes its direction and becomes posterior (classic posterior wall), now called inferobasal segment. This posterior part is more or less important, depending on, among other factors, the body-build.We have found (Figure 1.13) that in most cases the inferior wall remains flat (C shape) (Figure 1.13B). However, sometimes a clear basal part bending upwards (G shape) (Figure 1.13A) is seen. Only rarely, usually in very lean individuals, does the great part of the inferior wall present a clear posterior position (U shape) (Figure 1.13C).
Therefore, often, the posterior wall does not exist and for this reason, the name ‘inferior wall’ seems clearly better than the name ‘inferoposterior’. On the other hand, the anterior wall is, in fact, superoanterior, as is clearly appreciated in Figure 1.11B. However, in order to harmonise the terminology with imaging experts and to avoid more confusion, we consider that the names ‘anterior wall’ and ‘inferior wall’ are the most adequate for its simplification and also, because when an infarct exists in the anterior wall, the ECG repercussion is in the horizontal plane (HP; V1–V6) and when it is in the inferior wall – even in the inferobasal segment – it is in the frontal plane (FP).
(d) The longitudinal HP (Figures 1.3(3) and 1.8B; see Plate 2) is directed from backwards to forwards from rightwards to leftwards, and slightly cephalocaudally. In Figure 1.8A (arrows), one can appreciate how, following the line AB, the heart can be opened like a book (Figure 1.8B).
(e) The transverse plane (Figures 1.4B(1), 1.3A(1) and 1.8A),with respect tothe thorax, is directedpredominantly cephalocaudally and from right to left, and it crosses the heart, depending on the transectionperformed, at the basal level, mid-levelor apical level (Figure 1.8A). Thanks to these transverse transections performed at different levels, we are able to view the right ventricle (RV) and the left-ventricular septal, anterior, lateral and inferior walls (Figures 1.3(1) and 1.8A; see Plate 2). Thus, the LV is divided into the basal area, the mid-area, the apical (inferior) area and the strict apex area (Figures 1.8A and 1.9).
In order to clarify the terminology of the heart walls, a committee appointed by ISHNE (International Society Holter Non-invasive Electrocardiography) has made the following recommendations :
1. Historically, the terms‘true’ or ‘strictly posterior’ MI have been applied when the basal part of the LV wall that lies on the diaphragm was involved. However, although in echocardiography the term posterior is still used in reference to other segments of LV, it is the consensus of this report to abandon the term ‘posterior’ and to recommend that the term ‘inferior’ be applied to the entire LV wall that lies on the diaphragm.
2. Therefore, the four walls of the heart arenamed anterior,septal,inferior and lateral. This decision regarding change in terminology achieves agreement with the consensus of experts in cardiac imaging appointed by American Heart Association (AHA) (Cerqueira, Weissman and Disizian, 2002) and thereby provides great advantages for clinical practice. However, a global agreement, especially with an echocardiographic statement, is necessary.

The coronary tree: coronary angiography and coronary multidetector computed tomography
In the past, only pathologists have studied coronary arteries. In clinical practice, coronary arteriography, first performed by Sones in 1959, has been the ‘gold standard’ for identifying the presence or absence of coronary stenosis due to IHD, and it provides the most reliable anatomic information for determining the most adequate treatment. Furthermore, it is crucial not only for diagnosis but also forperformingpercutaneous coronary intervention (PCI).Very recently, new imaging techniques, especially CMDCT, are being used more and more with a great reproducibility compared with coronary angiography (Figure 1.1). CMDCT is very useful for demonstrating bypass permeability and for screening patients with risk factors. Recently, it has even suggested its utility in the triage of patients at emergency departments with dubious precordial In chronic-heart-disease patients, there are some limitations due to frequent presence of calcium in the vessel walls that may interfere with the study of the lumen of the vessel. However the calcium score alone without the visualisation of coronary arteries is important in patients with intermediate risk, in some series even better than exercise testing, to predict the risk of IHD.CMDCT has some advantages in case of complete occlusion (Figure 1.1G) and in detecting soft plaques. It is also useful for the exact quantification of the lumen of occluded vessel that is comparablewith intravascular ultrasound (see Figure 1.1H). However, it is necessary to realise the need to avoid repetitive explorations form an economical point of view and also to avoid possible side-effects due to radiation. A clear advantage of invasive coronary angiography is that it is possible, and this is very important especially in the acute phase, to perform immediately a PCI.

The perfusion of the heart walls and specific conduction system
The myocardium and specific conduction system (SCS) are perfused by the right coronary artery (RCA), the left anterior descending coronary artery (LAD) and the circumflex coronary artery (LCX). Figure 1.1 shows the great correlation of coronary angiography and CMDCT in normal coronary tree and some pathologic cases. Figures 1.14B–D show the perfusion that the different walls with their corresponding segments receive from the three coronary arteries. The areas with common perfusion are coloured in grey in Figure 1.14A. Figure 1.14E shows the correlation of ECGleadswith the bull’s-eye image. Themyocardial areas perfused by three coronary arteries are as follows :
• Left anteriordescendingcoronaryartery(LAD) (Figure 1.14B). It perfuses the anterior wall, especially via the diagonal branches (segments 1, 7 and 13), the anterior part of the septum, a portion of inferior part of the septum and usually the small part of the anterior wall, via the septal branches (segments 2, 8andpartof 14, 3and9). Segment14 isperfused by LAD, sometimes shared with the RCA, and also parts of segments 3 and 9 are shared with the RCA. Segments 12 and 16 are sometimes perfused by the second and third diagonals and sometimes by the second obtuse branch of LCX. Frequently, the LAD perfuses the apex and part of the inferior wall, as the LAD wraps around the apex in over 80% of cases (segment 17 and part of segment 15).
the anatomical variants of coronary circulation 
Figure 1.14 According to the anatomical variants of coronary circulation, there are areas of shared variable perfusion (A). The perfusion of these segments by the corresponding coronary arteries (B–D) can be seen in the ‘bull’s-eye’ images. For example, the apex is usually perfused by the LAD but sometimes by the RCA or even the LCX. Segments 3 and 9 are shared by LAD and RCA, and also small part of mid-low lateral wall is shared by LAD and LCX. Segments 4, 10 and 15 depend on the RCA or the LCX, depending on which of them is dominant (the RCA in >80% of the cases). Segment 15 often receives blood from LAD. (E) Correspondence of ECG leads with the bull’s-eye image. Abbreviations: LAD, left anterior descending coronary artery; S1, first septal branch; D1, first diagonal branch; RCA, right coronary artery; PD, posterior descending coronary artery; PL, posterolateral branch; LCX, left circumflex coronary artery; OM, obtuse marginal branch; PB, posterobasal branch.

• Right coronary artery (RCA) (Figure 1.14C). This artery perfuses, in addition to the RV, the inferior portion of the septum (part of segments 3 and 9). Usually, the higher part of the septum receives double perfusion (LAD + RCA conal branch). Segment 14 corresponds more to the LAD, but it is sometimes shared by both arteries (see before). The RCA perfuses a large part of the inferior wall (segment 10 and parts of 4 and 15). Segments 4 and 10 can be perfused by the LCX if this artery is of the dominant type (observed in 10–20% of all cases), and at least part of segment 15 is perfused by LAD if this artery is long. Parts of the lateral wall (segments 5, 11 and 16) may, on certain occasions, pertain to RCA perfusion if it is very dominant. Sometimes segment 4 receives double perfusion (RCA + LCX). Lastly, the RCA perfuses segment 17 if the LAD is very short.
• Circumflex coronary artery (LCX) (Figure 1.14D). The LCX perfuses most of the lateral wall – the anterior basal part (segment 6) and the mid and low parts of lateral wall shared with the LAD (segments 12 and 16) and the inferior part of the lateral wall (segments 5 and 11) sometimes shared with RCA. It also perfuses, especially if it is the dominant artery, a large part of the inferior wall, especially segment 4, on rare occasions segment 10, and part of segment 15 and the apex (segment 17).
The double perfusion of some parts of the heart explains that this area may be at least partially preserved in case of occlusion of one artery and that in case of necrosis the involvement is not complete (no transmural necrosis).
Both acute coronary syndromes (ACSs) and infarcts in chronic phase affect, as a result of the occlusion of the corresponding coronary artery, one part of the two zones into which the heart can be divided (Figure 1.14A): (1) the inferolateral zone, which encompasses all the inferior wall, a portion of the inferior part of the septum and most of the lateral wall (occlusion of the RCA or the LCX); (2) the anteroseptal zone, which comprises the anterior wall, the anterior part of the septum and often a great part of inferior septum and part of the midlower anterior portion of lateral wall (occlusion of the LAD). In general, the LAD, if it is large, as is seen in over 80% of cases, tends to perfuse not only the apex but also part of the inferior wall (Figures 1.1 and 1.14).
The occlusion of a coronary artery may affect only one wall (anterior, septal, lateral or inferior) or, more often, more than one wall. ACSs and infarcts in their chronic phase, which affect only one wall, areuncommon.Even the occlusionof the distal part of the coronary arteries usually involves several walls. For example, the distal LAD affects the apical part of anterior wall but also the apical part, even though small, of the septal, lateral and inferior wall, and the distal LCX generally affects part of the inferior and lateral walls. In addition, an occlusion of the diagonal artery, although fundamentally affecting the anterior wall, often also involves the middle anterior part of the lateral wall and even the occlusion of the first septal branch artery, or a subocclusion of the LAD encompassing the septal branches involves part of the septum and often a small part of the anterior wall. Probably, the occlusion of oblique marginal (OM) (part of the lateral wall) or distal branches of a non-dominant RCA and LCX (part of the inferior wall) involves only a part of a single wall.
In fact, whetherACSs or established infarctions involve one or more walls has a relative importance. What is most important is their extension, related mainly to the site of the occlusion and to the characteristics of the coronary artery (dominance, etc.). Naturally, on the basis of all that was previously discussed, large infarcts involve a myocardial mass that usually corresponds to several walls, but the involvement of several walls is not always equivalent to a large infarct, as we have already commented. For instance, the apex, although a part of various walls, is equivalent toonly a fewsegments. Therefore knowing what segments are affected allows us to better approximate the true extension of the ventricular involvement. Lastly, although in many cases multivessel coronary disease exists, this does not signify that a patient has suffered more than one infarct.
Consequently, in order to better assess the prognosis and the extent of the ACSs, and infarcts in the chronic phase, it is very important in the acute phase to establish the correlation between the ST-segment deviations/T changes and the site of occlusion and the area at risk (p. 66), and in the chronic phase between leads with Q wave and number and location of left-ventricular segments infarcted (p. 139) (Figures 1.8 and 1.9).
The perfusion of SCS structures is as follows:
(a) The sinus node and the sinoatrial zone by the RCA or the LCX (approximately 50% in each case)
(b) The AV node perfused by the RCA in 90% of cases and by the LCX in 10% of cases
(c) The rightbundle branchand the anterior subdivision of the left bundle branch by the LAD
(d) The inferoposterior division of the left bundle branch by septal branches from the LAD and the RCA, or sometimes the LCX
(e) The left bundle branch trunk receiving double perfusion (RCA + LAD)
This information will be useful in understanding when and why bradyarrhythmias and/or intraventricular conduction abnormalities may occur during an evolving ACS.

          Echocardiography        
Introduction
Echocardiography in its current form, has becomean invaluable tool in a modern cardiac intensive care unit environment. Coupled with a clinical examination and monitoring techniques, echocardiography can provide real-time rapid and reliable diagnostic answers that are invaluable to patient care. This noninvasive test can be used to reliably evaluate cardiac anatomy of both normal hearts and those with congenital heart disease and has replaced cardiac angiography for the preoperative diagnosis of the majority of congenital heart lesions. In congenital or acquired cardiac disease, echocardiography may be further used to estimate intracardiac pressures and gradients across stenotic valves and vessels, determine the directionality of blood flow and pressure gradient across a defect, and examine the coronary arteries. Within the realm of critical care, echocardiography is useful to quantitative cardiac systolic and diastolic function, detect the presence of vegetations from endocarditis, and examine the cardiac structure for the presence of pericardial fluid and chamber thrombi. As with all tools, however, a thorough understanding of its uses and limitations are necessary before relying upon the information it provides.

Principles of Echocardiography
Echocardiography uses ultrasound technology to image the heart and associated vascular structures. Ultrasound is defined as sound frequencies above the audible range of 20,000 cycles per second. The primary components of an ultrasound machine include a transducer and a central processor. The transducer converts electrical to mechanical (sound) energy and vice versa. Electrical energy is applied to piezoelectric crystals within the transducer resulting in the generation of mechanical energy in the form of a series of sinusoidal cycles of alternating compression and rarefaction. The energy produced travels as a directable beam which may be aimed at the heart. The sound beam travels in a straight line until it encounters a boundary between structures with different acoustical impedance, such as between blood and tissue. At such surfaces, a portion of the energy is reflected back to the same crystals within the transducer, and the remaining attenuated signal is transmitted distally. Within the ultrasound, machine is circuitry capable of measuring the transit time for the beam to travel from the transducer to a given structure and back again then calculate the distance traveled. A cardiac image is constructed from the reflected energy, or so called ultrasound echoes.
Differing properties of tissues affect the portion of acoustic energy transmitted versus reflected. For example, air reflects the majority of the signal it receives and, therefore, prevents images from being obtained through windows where it is present. Anything hindering or augmenting the reflection of this acoustic signal, such as air, bone, dressings, an open chest, or lines, tubes, or other foreign bodies, will diminish the overall quality of the examination. Therefore, in the intensive care unit, an ultrasound study may be limited by difficulty in finding a good acoustic window to allow for accurate analysis.

The Anatomical Echocardiographic Examination
In order to obtain the best imaging windows, whenever possible, patients are placed in a left lateral decubitus position during a transthoracic echocardiogram. During two-dimensional (2D) echocardiography, all planes are described in reference to the heart and not the heart’s position within the body. For a complete pediatric study, standard views (see Fig.1–5) are obtained from the high left chest just lateral to the sternum (parasternal window), the left lateral chest just inferior and lateral to the nipple (apical window), sub-xyphoid area (subcostal window), and the suprasternal notch (suprasternal window). In patients with more complex anatomy, additional windows, such as the high right parasternal border, may be used to obtain additional information.
parasternal window 
Fig.1 Standard echocardiographic image planes from the high left chest just lateral to the sternum (parasternal window (a) and (b)), the left lateral chest just inferior to the nipple (apical window (c)), sub-xyphoid area (subcostal window (d)), and the suprasternal notch (suprasternal window (e) and (f)). RA right atrium; RV right ventricle; LA left atrium; LV left ventricle; Ao aortic valve; CS coronary sinus; RVOT right ventricular outflow tract; SVC superior vena cava (drawing from Steven P. Goldberg, MD) 

1.  Parasternal Window
In the anatomically normal heart, the parasternal window allows visualization of the heart aligned along its long axis and short axis. In the long axis (Fig.1a), the left ventricular inflow and outflow tracts can be seen well. As a result, comments can be made from this view regarding the aorta, including its annulus, the sinuses of Valsalva, and the proximal portion of the ascending aorta, as well as its relationship to the mitral valve. Additionally, the ballet-slipper appearance of the left ventricle is featured as the inferoposterior wall and interventricular septum are visualized. The anterior and posterior leaflets of the mitral valve can be visualized. By angulating the transducer and performing a sweep, the right ventricle is brought into focus and an examination of both its inflow including the right atrium and tricuspid valve and its outflow tract, including the pulmonary valve can be performed.
The transducer may be rotated 90° providing a series of short-axis views (Fig.1b) that assist in the evaluation of the chambers of the heart, the semilunar and atrioventricular valves, and the coronary arteries. Sweeping from the apex of the heart toward the base will allow a close cross-sectional examination of the ventricular chambers. The normal left ventricle has circular geometry with symmetric contraction, whether it is visualized at the level of the mitral valve, papillary muscles, or apex. In contrast, the normal right ventricle appears as a more trabeculated crescent-shaped structure when visualized at or below the level of the mitral valve. Sweeping farther toward the base of the heart, the mitral valve’s papillary muscles and the valve itself are viewed. Progressing to the base of the normal heart, the tri-leaflet aortic valve takes the center stage with the right ventricular outflow tract and pulmonary wrapping in an inverted “U” anteriorly and leftward. Additionally a portion of the atrial septum and the tricuspid valve may be profiled. Finally, continuing the sweep allows for the examination of the atrial appendages, ascending aorta in cross-section and branch pulmonary arteries.
parasternal window 
Fig.1b (continued)

2.  Apical Window
For those not trained in echocardiography, the images obtained with the transducer in the apical position (Fig.1c) are perhaps the most intuitive as it allows for visualization of all four chambers and valves in the heart with a simple left-to-right orientation. Imaging is begun in the four-chamber view, in which the anatomic right and left ventricles may be identified. Sweeps of the transducer from this position identify the posterior coronary sinus and may indicate abnormalities such as a left superior vena cava or unroofed coronary sinus. Proceeding more anteriorly to a five-chambered view, the atrial and ventricular septa may be visualized looking for defects and the left ventricular outflow tract and ascending aorta may be examined. The four chamber view allows for the examination of the anterior and posterior mitral valve leaflets and pulmonary veins as they enter the left atrium. By rotating the transducer to 90° from the four-chamber view, a two-chamber view of the left ventricle and left atrium can be obtained to evaluate the anterior and posterior left ventricular wall function.
the left lateral chest just inferior to the nipple (apical window) 
Fig.1c (continued)

3.  Subcostal Window
For pediatric patients with complex cardiac anatomy, the subcostal position (Fig.1d and Fig.1.e) provides the most detailed information and is often thebest starting place. In order to obtain images in this position, patients are placed supine with the transducer in the subxiphoid position. In larger cooperative patients beyond the infancy period, image quality may be improved by having the patient participate in the examination with held inspiration that allows the heart to move downward toward the transducer. Initial views in this position should determine visceral situs as well as the relationship of the inferior vena cava and aorta. Subsequent views and sweeps will provide detailed analysis of the atrial septum as well as the images related to the ventricular septum, the atrioventricular valves, atrial and ventricular chambers, and drainage of systemic veins. With the rotation of the transducer both ventricular outflow tracts may be visualized. Additionally in some patients the branch pulmonary arteries and the entire aorta may be examined from this position.
sub-xyphoid area (subcostal window) 
Fig.1d  (continued)
the suprasternal notch (suprasternal window) 
Fig.1e (continued)

4. Suprasternal Window
The views are obtained in this position by placing the transducer in the suprasternal notch (Fig.1.f) with the neck extended. The suprasternal longand short-axis views provide detailed information regarding arch sidedness, anomalies in the ascending and descending aorta and head and neck vessels, the size and branching of the pulmonary arteries, as well as anomalies of systemic and pulmonary venous systems.
the suprasternal notch (suprasternal window) 
Fig.1f (continued)

M-Mode Imaging
One of the earliest applications of ultrasound technology that remains an important tool in the evaluation of cardiac function, dimension, and timing, the M-mode echo provides an “ice-pick” view of the heart. An M-mode echo is obtained with the ultrasonic transducer placed along the left sternal border and directed toward the part of the heart to be examined. A single line of interrogation is repeatedly produced and the resultant image is displayed with time along the x-axis and distance from the transducer along the y-axis (see Fig. 2). M-mode obtains an estimate of ventricular function by measuring the short axis shortening fraction and wall thickness.
M-mode echocardiography obtained in the parasternal short axis through the right and left ventricular chambers at the level of the papillary muscles. LVEDD left ventricular end-diastolic dimension; LVESD left ventricular end-systolic dimension
Fig.2 M-mode echocardiography obtained in the parasternal short axis through the right and left ventricular chambers at the level of the papillary muscles. LVEDD left ventricular end-diastolic dimension; LVESD left ventricular end-systolic dimension

Doppler Evaluation
Frequently in an intensive care setting the clinician is concerned with new or residual flow disturbances from shunt lesions, an abnormal cardiac valve, or narrowing of a blood vessel. While 2D echocardiography determines anatomical relationships, additional information regarding movement of the blood or myocardium is provided by looking for Doppler shifts in the reflected ultrasound waves. The Doppler principle, first described by Johann Christian Doppler, states that for a stationary object, the frequency of ultrasound reflected is identical to the transmitted frequency. Inherently the heart and the blood it pumps do not fit this basic definition. Therefore, when performing a cardiac ultrasound, the moving objects alter the frequency of the reflected signal (the Doppler shift) according to the direction and velocity with which they are moving in relation to the fixed transducer. Additional insights to intracardiac and vascular hemodynamics may be obtained when velocity data is collected. Doppler data are typically displayed as velocity rather than the actual frequency shift. The velocities can then be translated into pressure data using the modified Bernoulli equation: P1 – P2= 4[(V2)2 – (V1)2]. If one assumes that the level of obstruction and therefore the velocity of V1 is negligible compared with the obstruction at V2 the formula becomes even simpler: DP = 4(Vmax)2. Although the modified Bernoulli equation can only be applied in appropriate situations, it does help predict the pressure drop across an abnormal valve or septal defect to give a general estimate of the severity of the lesion which can prove to be valuable information to help manage patients in the intensive care setting.
Of note, during Doppler imaging it is clinically important to recognize the angle of interrogation of blood flow and its impact on the accuracy of our velocity measures. It is important when performing Doppler studies that the line of beam interrogation should be directly in the line of flow, resulting in as little distortion of data as possible. The more off-angle the approach is, the increasingly more severe the underestimation of the true velocity will be. For practical purposes, an angle of interrogation less than 20° is essential to ensure clinically accurate information.
Two commonly used techniques are pulsed and continuous wave Doppler. Pulse wave Doppler allows determination of direction and velocity at a precise point within the imaged cardiac field. However, it is limited in its maximum detectable velocity by the Nyquist limit making it unusable for quantification of high-velocity flow (e.g., as seen with severe obstruction). In contrast, continuous wave Doppler interrogates all points along a given beam. Continuous wave Doppler imaging is not constrained by velocity limits and can hence record velocities exceeding those of pulsed Doppler imaging. The drawback is that while the line of interrogation is identifiable, knowledge of anatomy must already be obtained to identify the precise location of the maximum velocity. Clinically these two techniques are commonly used sequentially to identify the area of interest and then to obtain the maximum velocity.

1. Color Flow Doppler
Color flow Doppler is powerful technique for obtaining additional hemodynamic and anatomic data for patients undergoing echocardiography in the intensive care unit. Color flow Doppler allows velocity information to be overlaid on a 2D anatomic image therefore providing data regarding intracardiac and extracardiac shunts, valvar insufficiency or stenosis, and vessel obstruction. By convention, shades of red are used in identifying blood flowing toward the transducer and blue to indicate blood flowing away from the transducer. Therefore, color flow Doppler defines the presence and direction of shunts and is used to grade the severity of valvar insufficiency.

Current Clinical Applications
Clinical applications of echocardiography within the intensive care unit may be divided into the following major areas:
1. The diagnosis and post-intervention evaluation of anatomic lesions.
2. Evaluation of cardiac function.
3. Diagnosis of intracardiac masses and extracardiac effusions.
4. Guidance of intervention within the intensive care unit

Anatomic Lesions Pre and Post Intervention
Advances in technology have enabled most congenital heart defects to be diagnosed by echocardiography avoiding the risks, time, and cost of invasive cardiac catheterization. In addition, for infants and pediatric patients admitted to an intensive care unit due to being succumbed to shock, echocardiography may be useful for differentiating anatomic causes of shock from functional causes. Patients with obstruction to outflow on the left side of the heart who go undiagnosed at birth frequently present with signs of diminished cardiac output (CO) or frank shock. These lesions including aortic valve stenosis, coarctation of the aorta, and variations of hypoplastic left heart syndrome may be identified and defined by echocardiogram alone.
Following surgical or catheter-based intervention patients convalesce in the intensive care unit. Most patients undergo a postprocedural echo before getting discharged home to document adequacy of the repair and lack of significant complications. In postoperative patients this assessment may prove more complicated as access to the patient and the correct windows may be severely compromised by dressings, intracardiac lines, and chest tubes. Occasionally postoperative patients in the intensive care unit may be found to have unexpected residual lesions (see Fig.3). For example, following repair of septal defects, echocardiography may be useful to screen for the presence of residual shunts which may be less well tolerated secondary to myocardial changes following cardiopulmonary bypass. Often, the presence of a residual lesion is known in the operating room through transesophageal echocardiography or direct discussion with the surgeon. An important role of echocardiography is to distinguish those lesions with hemodynamic consequences from those whose presence has no impact on postoperative care. Transthoracic echocardiography may be used to diagnose and assess the hemodynamic sequelae of shunt lesions, residual stenosis, and function. More complicated is the assessment of coronary flow, right ventricular dynamics, and distal obstruction following intervention. In patients who are experiencing arrhythmias postoperatively, special attention should be paid to the flow within the coronary arteries to ensure that it has not been compromised or that a line or mass in the heart is not causing ectopy.
Parasternal short axis image in a patient with pulmonary atresia/VSD who acutely decompensated. White arrows demonstrate the large residual VSD than resulted when a patch dehisced. RA right atrium; RV right ventricle; AV aortic valve 
Fig.3 Parasternal short axis image in a patient with pulmonary atresia/VSD who acutely decompensated. White arrows demonstrate the large residual VSD than resulted when a patch dehisced. RA right atrium; RV right ventricle; AV aortic valve
Four chambered view demonstrating color Doppler of tricuspid regurgitation and the corresponding spectral Doppler pattern. 
Fig.4 (a) and (b): Four chambered view demonstrating color Doppler of tricuspid regurgitation and the corresponding spectral Doppler pattern. The velocity obtained by spectral Doppler may be utilized to estimate pulmonary artery pressures in the absence of downstream obstruction. A complete envelope by pulse wave or continuous wave Doppler provides the velocity of the regurgitant jet which may be translated into pressure data using the equation: DP = 4(Vmax)2. RA right atrium; RV right ventricle; LA left atrium; LV left ventricle.

Unanticipated pulmonary arterial hypertension may slow the progress of a patient in the intensive care unit. In the absence of a Swan Ganz catheter or a direct pulmonary arterial monitoring, echocardiography may be used to estimate the pulmonary artery pressures. There are several methods that may be used to determine the pulmonary artery pressures. In a patient with
tricuspid regurgitation, the velocity of the jet estimates the difference in pressure in the right atrium and the right ventricle (see Fig.4). If there is no stenosis of the pulmonary arteries, pulmonary valve, or right ventricular outflow tract, the difference in pressure between the right atrium and right ventricle plus the right atrial pressure (CVP) provides an estimate of the pulmonary arterial pressures. In the absence of tricuspid valve insufficiency, interventricular septal geometry may be used to help quantify the degree of pulmonary hypertension.

Analysis of Ventricular Function
One of the most frequent uses of echocardiography in the ICU is related to the evaluation of ventricular performance. Improvements in technology allow assessment of both systolic and diastolic function with increasing accuracy.
1. Systolic Function
Accurate and timely assessment of systolic function should be an integral part of the medical management of the hemodynamically unstable critically ill patient. Global assessment of LV contractility includes the determination of ejection fraction (EF), circumferential fiber shortening, and cardiac output (CO). There are several methods that may be used to garner this information. Each has its limitations and assumptions which are paramount to understand prior to clinically applying the information gathered. For assessment of left ventricular function, perhaps the simplest quantitative approach is to use M-mode echocardiography (see Fig.3) in either the parasternal short axis at the level of the papillary muscles or in the parasternal long axis at the tips of the mitral valve leaflets to measure the left ventricular end-diastolic dimension (LVEDD) and left ventricular end-systolic dimension (LVESD) for the determination of the fractional shortening (FS) percentage.
Fractional shortening is derived by the following:
Normal values for fractional shortening in children and infants vary slightly with age, falling typically between 28 and 44%.
Fractional shortening, therefore, provides a method of assessing circumferential change but has several obvious drawbacks. This method assumes that the ventricle being examined has a circular shape in the axis in which it is examined. As a result, changes in diameter may be mathematically related to circumferential fiber-shortening providing an estimate of ventricular function. Therefore anything that alters the circular shape of the left ventricle (anatomic abnormalities intrinsic to congenital heart disease, pre and afterload changes, or ventricular–ventricular interactions) may affect the assessment of fractional shortening by altering the movement of the septum and causing an under or over estimation of the either end-systolic or diastolic dimension.
A second method of assessing ventricular function is via ejection fraction. Ejection fraction is a volumetric appraisal of ventricular fiber shortening. Echocardiographically the most common method of calculating ejection fraction is the biplane estimation of volumes from the apical four-and two-chamber views. One of the more commonly used mathematical algorithms is the Simpson method in which the left ventricle is traced manually at the end diastole and end systole along the endocardium. Using the method of disks the left ventricle is divided into a series of parallel planes and the resultant disks are individually summed to create each volume. Ejection fraction is calculated using the following equation:
Unfortunately, the determination of an accurate ejection fraction is also subject to ventricular shape with the left ventricle assumed to be its normal prolate elliptical shape. Variations from this shape, which occur frequently in pediatrics, significantly alter the relationship between fiber shortening and volume dependence upon when this equation is applied. In addition, patients in the intensive care environment frequently have suboptimal imaging windows making the endocardium difficult to distinguish and trace.
Not infrequently in active pediatric intensive care units, a patient’s heart and/or lung function must be supported for a period of time. Two such modalities of support are extracorporeal membranous oxygenation and ventricular assist devices. Often the pediatric echocardiographer is asked to assist in the management of these patients by providing insight into the recoverability of cardiac function. This request can be one of the more challenging uses of echo in an intensive care setting. As discussed above, many of the techniques commonly used to determine ventricular systolic function and CO are dependent on the loading conditions of the heart as well as contractility. As a result, both of these support systems which unload the heart in an effort to allow recovery time severely limit echo’s utility as a prognostic indicator. Several newer methods of determining myocardial function including Tissue Doppler Imaging (TDI), strain and strain rate, color m-mode, calcium gating, and three-dimensional (3D) echocardiography are entering the realm of echo in the intensive care unit. These newer modalities may prove to be more efficacious than current standard echocardiography is at present.

Diastolic Function
Accurate assessment of diastolic function by echocardiography is an evolving field that has made great strides in the past few years. Diastolic heart failure and its impact on postoperative management also deserve consideration. Spectral Doppler evaluation is a relatively easy and useful method for evaluating diastolic function noninvasively at the bedside. A prominent pulmonary vein atrial reversal wave (a wave) is a marker of diastolic dysfunction. This finding represents marked flow reversal into the pulmonary veins during atrial systole in response to a noncompliant ventricular chamber. The mitral inflow Doppler pattern can also be a useful marker for diastolic dysfunction. Mitral inflow is composed of 2 waves – an E wave representing early passive ventricular filling (preload dependent) and the A wave representing active filling as a result of atrial systole. The E:A ratio, velocity of E wave deceleration and duration of the A wave can be altered in patients with diastolic dysfunction.
Tissue Doppler imaging (TDI) is a newer technique for assessing diastolic ventricular function. TDI allows recording of the low Doppler velocities generated by the ventricular wall motion and directly measures myocardial velocities. In spectral TDI, pulsed Doppler is placed along the myocardial wall (mitral, septal, or tricuspid annulus) recording the peak myocardial velocities. Three waveforms are obtained: a peak systolic wave (Sa), an early diastolic wave (Ea), and an end-diastolic wave (Aa) produced by atrial contraction. The tissue Doppler systolic mitral annular velocity has been shown to correlate with global LV myocardial function [14]. TDI has also been used to estimate diastolic function, and is relatively independent of preload condition. The pulsed Doppler peak early mitral inflow velocity (E) divided by the TD early diastolic mitral annular velocity (Ea) results in a ratio that correlates with the pulmonary capillary wedge pressure. The E/Ea ratio is also useful in estimating mean LV filling pressure. At this time, TDI represents one of the most accurate techniques to assess diastolic function and is therefore of particular interest in the critical care population in whom abrupt changes in preload and afterload are common, making Doppler evaluation of diastolic function less reliable.

Detection of Intracardiac Masses and Extracardiac Effusions
An abnormal area of dense reflectance that is well localized within an echo may represent a mass, thrombus, or calcification. In the postoperative or critical care patient with multiple lines in place, especially in the setting of low flow, care must be taken to evaluate these areas for thrombus formation. Echo is the imaging modality of choice for elucidating and evaluating cardiac mass lesions. Differentiating an area of concern from artifact, can be challenging. Areas that move appropriately throughout the cardiac cycle and the presence of an abnormality in more than a single view, suggest a mass rather than an artifact (see Figs. 5a–d). These findings must in turn be distinguished from such anatomical variations as a prominent Eustacian valve or Chiari network.
Demonstrate a thrombus in the right ventricle seen in parasternal short axis  
Fig.5 Demonstrate a thrombus in the right ventricle seen in parasternal short axis (a) and modified four-chamber (b) views. RV right ventricle; LV left ventricle. (c) and (d): Demonstrate a thrombus in the left atrial appendage in both parasternal short axis and a modified four chamber views. RA right atrium; RV right ventricle; AV aortic valve; AO ascending aorta; LV left ventricle.

Major factors that predispose a patient to the development of intracardiac thrombi are the presence of intracardiac lines, diminished CO, and localized stasis in addition to changes within the clotting cascade from sepsis, bypass, intrinsic clotting disorders, or heparin use. Echocardiographic evaluation of patients within the intensive care setting must include an awareness of the increased incidence of thrombus formation and a careful evaluation of areas predisposed to become a nidus for thrombus.
Following cardiac surgery it is not uncommon for patients to develop small collections of fluid in the pericardial space (see Fig.6). Typically, this is of little concern to the clinician; however, in a postoperative patient experiencing tachycardia and/or hypotension, the necessity of recognizing the potential for and screening for cardiac tamponade becomes paramount. In young infants and children, it is frequently difficult to rely on physical exam findings of increased jugular venous pressure or the late finding of pulsus paradoxus. In this instance, a directed and easily performed 2D and Doppler echocardiography can confirm the presence of an effusion and provide accurate assessment of its hemodynamic significance.
Subcostal image demonstrating a large circumferential pericardial effusion (green arrows) 
Fig.6 Subcostal image demonstrating a large circumferential pericardial effusion (green arrows)

The size and extension of a pericardial effusion may be diagnosed from parasternal, apical, or subcostal windows. The apical view is the easiest for obtaining information regarding the effusions hemodynamic significance. From the apical four chamber view both the mitral and tricuspid valve flow patterns are evaluated with the respiratory monitoring in place. Examining the changes in inflow hemodynamics with respiration allows for the evaluation of tamponade physiology. Greater than 25% variability in maximal e wave velocity of the mitral valve with inspiration or 50% of the e wave velocity of the tricuspid valve (see Figs.7a, b) is indicative of significant hemodynamic compromise resulting from the effusion. Additionally, collapse (differentiated from contraction) of the free wall of the right and left atrium (see Figs.8a, b) when the pericardial pressure exceeds the atrial pressure may be seen from this view in a patient with a significant effusion.
Respiratory changes in the mitral and tricuspid valve e wave Doppler patterns consistent with tamponade physiology. 
Fig.7 (a) and (b): Respiratory changes in the mitral and tricuspid valve e wave Doppler patterns consistent with tamponade physiology. The tricuspid valve inflow demonstrates more than 50% variability between inspiration and expiration (a). During mitral valve inflow Doppler, the peak E wave velocity alters more than 30% between inspiration and expiration (b).
Four chambered views 
Fig.8 (a) and (b): Four chambered views demonstrating right atrial and right ventricular collapse (green arrows) as a finding of tamponade physiology. RA right atrium; RV right ventricle; LA left atrium; LV left ventricle.

Echocardiography GuidedProcedures
1.  Pericardiocentesis
Performing “blind” percutaneous pericardiocentesis as a treatment for significant pericardial effusion dates back to the early eighteenth century and it is historically fraught with complications. Improved techniques in the 1970s with the advent of 2D echo allowed more accurate localization of the fluid and the development of echo-guided pericardiocentesis. Echo-guided pericardiocentesis (see Fig.9) has been found to be a safe and effective procedure with insertion of a catheter for drainage used to reduce the rate of recurrence found to complicate simple needle drainage and is considered the primary and often the definitive therapy for patients with clinically significant effusions.
Echoguided pericardiocentesis. 
Fig.9 Echoguided pericardiocentesis. Green arrow is in the pericardial space demonstrating the large fluid collection. Blue arrow is pointing to the needle that has been advanced into the pericardial space to drain the fluid collection. The large effusion allows the echocardiographer to direct the individual performing the pericardiocentesis away from areas that could lead to complications such as perforation of the myocardium.

2.  Balloon Atrial Septostomy (BAS)
Part of any echocardiographic assessment of a patient with congenital heart disease should include evaluation of the atrial septum. Cardiac lesions such as transposition of the great arteries, hypoplastic left heart syndrome, and tricuspid atresia require an adequate atrial communication. In the setting of a restrictive atrial septal communication or intact septum, a BAS is required to improve mixing and CO. In the past, the procedure, originally described by William Rashkind was performed in the cardiac catheterization laboratory under fluoroscopic guidance. However, during the last decade BAS has been routinely performed at the bedside in the intensive care unit under echocardiographic guidance (see Figs.10a–d). Most commonly either a subcostal view that includes a focused look at the atrial septum, pulmonary vein, and mitral valve or an apical four-chamber view is used. For the echocardiographer, the primary role is to provide continued visualization of the catheters and communicate well with the interventionalist. Advantages of this technique are multifactorial; echocardiography is superior to fluoroscopy during BAS due to a lack of radiation, the ability to perform the procedure at bedside rather than transporting to a catheterization laboratory, and direct, continuous visualization of the atrial septum, pulmonary veins, and mitral valve. The disadvantages of this technique include the potential for interference with maneuverability for both echocardiographer and catheter operator around a small neonate and therefore the risk of contamination of the sterile field. Additionally there is the possibility of poor acoustic windows in an ill neonate who may be mechanically ventilated. However, with proper planning and communication, the limitations of transthoracic echocardiographic guidance of BAS may be minimized.
Subcostal images demonstrating echo-guided balloon atrial septostomy (BAS) 
Fig.10 Subcostal images demonstrating echo-guided balloon atrial septostomy (BAS). (a): shows the initial small atrial communication in both 2 dimensional (2D) and color Doppler imaging. (b): reveals the deflated balloon that has been advanced across the atrial communication. It is important during this portion of the procedure for the echocardiographer to ensure that the balloon has not been advanced across the left atrioventricular valve. (c): demonstrates the inflated balloon within the left atrium. It is important to note the balloon’s position away from the mitral valve and pulmonary veins. (d): demonstrates the atrial communication following septostomy using both 2D and color Doppler imaging. RA right atrium; RV right ventricle; LA left atrium; LV left ventricle; Green arrows atrial communication.

Future Directions
There are several areas of advanced imaging that are becoming more commonplace in the practice of pediatric echocardiography. Primary assessment of cardiac mechanics by evaluating myocardial motion, strain, and strain rate has been validated in healthy children and provides additional information regarding myocardial performance. Three-dimensional real-time echocardiography has a growing role in evaluating anatomic defects, valves, and right and left ventricular function independently of geometric assumptions that constrained the previous methods.

1. Myocardial Mechanics
In the past several years, myocardial strain and strain rate have emerged as promising quantitative measures of myocardial function and contractility. Strain (e) is a dimensionless parameter defined as the deformation (L) of an object relative to its original length (Lo), and is expressed as a percentage. Strain rate (SR) is defined as the local rate of deformation or strain (e) per unit of time, and is expressed in 1/s. Strain and strain rate measurements can be obtained from data acquired by Doppler Tissue Imaging or 2D tissue tracking. Strain and strain rate should be of great help in the future in the evaluation of ventricular function, since conventional M-mode and 2D echocardiography have limitations due to complex morphology of the right ventricle and altered left ventricle morphology that occurs in complex congenital heart defects. Left and right ventricular values of strain and strain rate are available for healthy children.

2.  3D Echocardiography
Off-line 3D reconstruction consists of acquisition of sequential 2D slices which are converted to a rectangular coordinate system for 3D reconstruction and provides accurate anatomic information suitable for quantitative analysis. Left ventricular volume, mass, and function can be accurately assessed using RT3D independently of geometric assumption, and ejection fraction can be calculated. The wideangle mode is often used to acquire the entire LV volume, from which further analysis allows determination of global and regional wall motion. Wall motion is evaluated from base to apex with multiple slices from different orientations. The advantage of 3D over 2D is the ability to manipulate the plane to align the true long axis and minor axis of the LV, thus avoiding foreshortening and oblique image planes. LV volume assessment by RT3D is rapid, accurate, reproducible and superior to conventional 2D methods and is comparable to MRI, which represents the gold standard. Three dimensional reconstruction of the tricuspid valve has been shown to be helpful for anatomical assessment of Ebstein’s malformation or after atrioventricular septal defect repair. 3D Echocardiography is a useful adjunct to standard 2D imaging and should be increasingly used in the future.

          Endocarditis        
This patient was a 60 year old man with a history of cigarette smoking and alcohol use, who visited his internist with complaints of shortness of breath, intermittent fever, fatigue and weight loss. The physical exam revealed splenomegaly (4 cm below the left costal margin), a holosystolic murmur, and bilateral pulmonary rales. His laboratory tests were significant only for “mild pancytopenia” and hematuria. His liver chemistry was within normal limits. A bone marrow exam was done and reported as reactive. An abdominal CT scan was considered unremarkable except for splenomegaly. The echocardiogram showed mild to moderate mitral valve regurgitation. He was given antibiotics and was referred to a pulmonary specialist and an oncologist with the diagnoses of chronic obstructive pulmonary disease and probable lymphoma.
A few months later, the patient called the paramedics with complaints of severe dyspnea. He was found agitated and in respiratory distress. During transportation to the hospital, the patient became apneic and was intubated. He arrived to the emergency room without vital signs. Defibrillation was attempted several times without success and the patient was pronounced dead.

Gross Description
The body measured 195 cm and weighed 85 kg. The thoracic cavity was unremarkable except for bilateral pleural adhesions. No fluid accumulation was present in the pleural cavities. The heart weighed 610 g. The left atrium was dilated, but free of thrombus. The right and left ventricles measured 0.6 and 1.8 cm in thickness, respectively. The valve leaflets were translucent except those of the mitral valve, which were thick and contained large vegetations. The largest vegetation, located on the anterior leaflet, showed evidence of re-endothelialization on the closing edge along with ulceration and hemorrhage (Figures 1 and 2). The chordae tendineae were short and focally fused. The myocardium was brown-red and of average consistency. The epicardium had multiple small abscesses, but the pericardium was smooth and shiny. The coronary arteries showed up to 70% stenosis by atheromatous plaques. There were no complete occlusions. The aorta and its branches were also affected by severe atherosclerosis with plaque ulceration and hemorrhage. The lungs were edematous and had a combined weight of 1700 g. Bilateral apical bullous emphysema was evident, and the rest of the parenchyma failed to show areas of consolidation. The liver showed signs of passive congestion with a weight of 2400 g. The spleen weighed 750 g and was significantly enlarged (20 cm in length). A 3.5 x 3 cm defect and a subcapsular hematoma were located on the posterior surface compatible with acute splenic rupture (Figure 3). In addition, there were multiple acute and subacute splenic infarcts, the largest of which measured 4.0 cm in its greatest dimension. There was evidence of retroperitoneal hemorrhage with approximately 500 g of clotted blood and 2 L of ascites. The kidneys weighed 460 g combined, and were grossly unremarkable except for a healed infarct in the cortex of the right kidney and a left cyst at the corticomedullary junction measuring 0.8 cm in diameter. The cervical, mediastinal and abdominal lymph nodes were not enlarged. The brain did not show any pathologic changes.
ulceration and hemorrhage
Figure 1 Infective endocarditis, mitral valve. A large vegetation is present to the atrial surface of the leaflet (arrow). there is associated hemorrhage and ulceration
ulceration and hemorrhage
Figure 2 Infective endocarditis. The anterior leaflet of the mitral  valve has a vegetation with evidence
of re-endothelialization (arrow).
subcapsular hematoma
Figure 3 Section of the spleen showing a subcapsular hematoma (arrow). There is also softening of the parenchyma due to septic splenitis

Microscopic Description
Sections of the heart, stained with H&E, showed active infective endocarditis of the mitral valve with septic vasculitis and acute epicarditis with microabscess formation. The lungs and liver had changes of chronic passive congestion. The lungs were also affected by centrilobular emphysema. Sections from the spleen revealed multiple infarcts with cavitation, as well as hemorrhage in the area of rupture and acute inflammation. The kidneys showed interstitial chronic nephritis, but no recent infarcts. The bone marrow and lymph nodes were reactive with no evidence of malignancy.

Case Analysis
This case represents another example of cardiovascular sudden death. However, in contrast to the common fatal ventricular arrhythmia discussed previously; the cause of death in this case was directly related to a sudden but unexpected, non-arrhythmic complication of infectious endocarditis (IE). It is reasonable to say that IE virtually never causes sudden death, with the rare exception of septic embolization of a coronary or cerebral artery, arising from an infected vegetation. This case represents a rare event, but one that is instructive regarding the often subtle and difficult diagnosis of IE.
The clinical and pathological features are a classic example of what previously was called subacute bacterial endocarditis, or SBE. Today, for reasons outlined below, the generally accepted designation is infectious endocarditis. This is an unusual patient because it illustrates so clearly how elusive the diagnosis of IE can be since it may mimic an indolent systemic disease of many different etiologies. The ‘take home message’ from this case is that if the possibility of IE is not considered, reaching the correct diagnosis will be very unlikely. The consequences of such an oversight, as exemplified here, can be devastating.
What is the difference between subacute bacterial endocarditis (SBE) and acute bacterial endocarditis (ABE), and why has there been a trend away from these designations? Historically, both SBE and ABE were described in the pre-antibiotic and pre-cardiac surgery era, at a time when there was no treatment for the valvular infection(s). Thus, the natural history was
dependent on the virulence of the infective organism, and the underlying valvular pathology. SBE was usually a slow, progressive, indolent infection of a valve. Most often it involved the mitral and/or aortic valves. The rightsided disease was uncommon. The mitral valve was the most frequently affected, since pre-existing chronic rheumatic mitral valvulitis with scarring and calcification was highly prevalent. The valvular damage allowed for infection by organisms that ordinarily could not colonize ‘healthy’ valvular tissues. These organisms include Streptococcus viridans (normal mouth flora), and Staphylococcus epidermidis (normal skin colonizer). Healthy valve tissue covered by endothelium (endocardium), does not routinely permit adherence of non-pathogenic organisms. In contrast, scarred and distorted valves with turbulent blood flow over the valve surface, serve as anchor areas for the development of pathological infectious vegetations. Even nonpathogenic organisms can adhere to sub-endocardial connective tissue; and colonize small platelet and fibrin vegetations that may develop on denuded valve linings. The bacteria, particularly S. viridans,  circulate in the bloodstream following oral manipulation as common as brushing teeth. With more vigorous dental work there may be a more significant bacteremia, which explains why patients with known valvular disease, must have antibiotic prophylaxis before and after dental procedures.
Infection of valvular tissue with a non-virulent organism leads to a smoldering infection, and a prolonged clinical course. Patients with such infections could often live for many months even before antibiotics were available. The causes of death were usually valve destruction, non-cardiac tissue damage, or systemic complications of sepsis. This was the classic SBE: infection of an (almost always) abnormal heart valve persisting for more than 6-8 weeks. With the persistent, often  low-grade infection, patients have indolent symptoms of chronic disease. These may include variable weight loss, anorexia, fatigue, intermittent fever, chills, and night sweats. These are symptoms remarkably similar to those seen with occult cancers, collagenvascular disease, and tuberculosis (today, we should also consider HIV/AIDS). The weight loss, anorexia, and fatigue could also be ascribed among others, to depression, diabetes mellitus, and adrenal cortical insufficiency. The clinical presentation might suggest SBE if there were typical findings of a heart murmur that was changing in intensity at different times. Additionally, patients with SBE may have small mucocutaneous hemorrhages peripherally, particularly in their nail beds or the so-called ‘splinter hemorrhages’, and cutaneous petechiae. These lesions are generally thought to be secondary to small non-infected emboli from the valve vegetation, although infected material or immune mediation may play a role. Since the spleen is frequently enlarged, patients may present with left upper quadrant pain and tenderness. Splenic involvement includes changes associated with sepsis (‘acute splenitis’), infarction and/or abscess formation (septic emboli). Moreover, when the infection has persisted for some time, the valves leaflets or cusps are destroyed, which results in valvular insufficiency, and ultimately in ventricular failure. Often, patients succumb secondary to systemic embolization, particularly to the brain, where they might develop cerebral infarctions, abscesses, and meningitis. Patients may also develop systemic disease related to the prolonged indolent course of their infection. Specifically, the subacute infection may lead to the development of antigen-antibody complexes, with the antigen being bacterial membrane protein. These complexes can circulate in the bloodstream, and ultimately deposit in small skeletal muscle and skin vessels, and in glomerular capillaries of the kidney. In the former sites, they may lead to a necrotizing vasculitis, with tissue inflammation and necrosis. When present in the palms, finger pulp, or soles of the feet, they are known as Osler’s nodes. In the kidney, a focal, necrotizing glomerulonephritis may develop, which is not secondary to embolism of vegetations (even though classically it has been called focal embolic glomerulonephritis). Other manifestations of immune complex disease include arthralgias and arthritis.
Despite the relative ease with which the diagnosis of SBE should be made in patients who present with these clinical signs and symptoms; the fact remains that, even in this modern era of echocardiography, it is still a disease associated with a high number of mis-diagnoses. The primary reason, other than physicians not considering it, is that many patients do not present with all of these classic features. Since the infection is often a subtle one, and given the intermittent nature of active bacterial release into the blood stream, negative blood cultures may be common, unless taken frequently. Furthermore, once the bacteria extend into the valve tissue, or into the perivalvular annulus, they are not released into the bloodstream. Clinically, there may be no changing murmur; petechiae may not be present, or in darkskinned patients, may be difficult to appreciate; and complications associated with immune complexes may not develop. However, non-specific clinical symptoms may suggest cancer, or systemic diseases like lupus erythematosus. Laboratory signs such as low-grade leukocytosis (with white blood cell counts between 10,000-15,000), and elevated erythrocyte sedimentation rate (ESR) are relatively non-specific, and may not be present. So again, as stated previously, if you don’t think of the diagnosis, you won't make it!
In contrast to SBE, acute bacterial endocarditis (ABE) has different features and pathogenesis. It is generally associated with infection by virulent organisms, particularly Staphylococcus aureus, Streptococcus pneumoniae (pneumococcus), enterococci, and a number of Gram-negative bacilli. As a result of the virulence of these or other pathogens, pre-existing valve damage may or may not be present. With aggressive, rapidly growing, and destructive organisms, there is an acute and progressive tissue disruption associated with collagenolysis of valvular and annular connective tissue. Intra-valvular and annular abscesses may occur. Large platelet and fibrin vegetations develop, which are very susceptible to fragmentation and embolization. The time course of the disease is rapid, often measured in days or few weeks. Moreover, signs and symptoms of valvular insufficiency are frequent and occur early. Systemic embolization to other organs, with tissue infarction and abscess formation, is common. Because of the acuteness of the disease, there is generally not sufficient time for the immune complexes to develop. Thus, the immune complications characteristic of SBE are usually absent. Historically, death ensues in a relatively short time, usually secondary to cardiac failure with valve destruction, or septicemia. With these features, ABE has been defined as: infection of a normal or abnormal heart valve by a virulent organism, with disease generally less than 4 weeks in duration.
With such a clear distinction between SBE and ABE, why are these designations inappropriate today? Why is the preferred terminology: active infectious endocarditis? The simple answer is because antibiotics, and earlier diagnoses with the advent of echocardiography, have modified the natural history of the disease. In addition, surgical intervention has had a
major impact in the course of this disease. Prolonged survival is now possible with non-virulent and virulent organisms, allowing for the possibility of immune-mediated complications to develop. Finally, as a result of intravenous drug use and the HIV/AIDS epidemic, infections with fungi (aspergillus and Candida species, in particular), rather than bacteria, have gained tremendous attention. Although it is still true, that infection with Staphylococcus aureus and pneumococcus is more severe and more destructive than infection with S. viridans, medical intervention has changed the classic features of SBE and ABE.
This patient presented in a terminal state, and had a cardio-pulmonary arrest during transportation to the hospital. Death was a result of septicemia, cardiac failure, and acute splenic rupture. It is unlikely that he had hypovolemia, as only 500 cc of blood were found in the retroperitoneal space. The presence of 2 liters of ascites in the peritoneum was most probably from congestive heart failure (there was no evidence of cirrhosis). His heart was almost twice normal size (610 g), with a dilated and hypertrophied left ventricle, as a result of prolonged mitral valve regurgitation. The regurgitation was secondary to active and healed vegetations of his mitral valve, with ulceration, and actual partial destruction of the anterior leaflet. Vegetations, infected and bland, embolized to distant organs like the spleen, where they produced septic infarctions, and infected vasculitis. The latter, is referred to as a mycotic aneurysm. They are called mycotic even though they are usually not the result of a fungal infection. They represent an infection of the vessel wall, with eventual arterial destruction, and the development of a pseudo-aneurysm, which has the potential to rupture. This patient’s partial valvular healing was most certainly due to the antibiotics he was given for intermittent fever during his lengthy clinical course (in retrospect, at least 3-4 months in duration). Unfortunately, though gram-positive cocci were found in the valve tissues, no culture was performed. It is most likely that the organism was one of the saprophytic ones, such as S. viridans. Even though the valve was significantly distorted by the infection, it appeared to have nonspecific leaflet thickening, and focal fusion of several chordae tendineae. The latter finding may result from chronic alcohol abuse. Prior valve damage may have predisposed this man to infection with S. viridans.
As a final point, it would be instructive to consider why he was followed for months with a diagnosis of probable lymphoma, or some other type of hematologic malignancy. A local physician, based on symptoms of fatigue, weight loss, and intermittent fever made this diagnosis. He was referred to an oncologist at the same hospital where his wife was employed. In contrast to the leukocytosis one would expect from a persistent infection, this patient was pancytopenic. However, chronic or overwhelming infection may, on occasions, have bone marrow suppression. The symptoms, the peripheral blood findings, and the splenomegaly are all consistent with a diagnosis of leukemia/lymphoma. Unfortunately, the presence of a holosystolic murmur, and the confirmation of mitral valve regurgitation, was disregarded. Since the vegetations on the mitral valve were not large, they were not identified on the echocardiogram. His bone marrow showed reactive changes, which are benign findings and not confirmatory of lymphoma or leukemia. He was short of breath, and this was thought to be due to COPD, rather than CHF. Thus, he was referred to a pulmonologist  for consultation, rather than a cardiologist. The diagnosis of active infectious Endocarditis was never entertained prior to his death several months later. Again, the lesson from this case is: if you do not think of the diagnosis, you will not make it.

          Myocardial Infarction        
Clinical Presentation
The classic initial manifestations of an acute MI include prolonged substernal chest pain with dyspnea, diaphoresis, and nausea. The pain may be described as a crushing, pressing, constricting, vise-like, or heavy sensation. There may be radiation of the pain to one or both shoulders and arms or to the neck, jaw, or interscapular area. Only a few patients have this classic overall picture. Although 80% of patients with an acute MI have chest pain at the time of initial examination, only 20% describe it as crushing, constricting, or vise-like. The pain may also be described atypically, such as sharp or stabbing, or it can involve atypical areas such as the epigastrium or the back of the neck. “Atypical” presentations are common in the elderly.
The initial manifestations of an acute MI were more likely to include symptoms such as sudden dyspnea, acute confusion,
cerebrovascular events (e.g., stroke or syncope), acute CHF, vomiting, and palpitations. There is strong evidence that a substantial proportion of MIs are asymptomatic. That 28% of infarcts were discovered only through the appearance of new ECG changes (Q waves or loss of R waves) observed on a routine biennial study. These infarctions had been previously unrecognized by both patient and physician.

Physical Examination
For the patient with an “uncomplicated MI” there are few physical examination findings. The main purpose of the examination is to assess the patient for evidence of complications from the MI and to establish a baseline for future comparisons. Signs of severe left ventricular dysfunction include hypotension, peripheral vasoconstriction, tachycardia, pulmonary rales, an S3, and elevated jugular venous pressure.  Preexisting murmurs should be verified. A new systolic murmur can result from a number of causes: papillary muscle dysfunction, mitral regurgitation as a result of ventricular dilatation, ventricular septal rupture, and acute severe mitral regurgitation due to papillary muscle rupture.

Electrocardiography
The classic ECG changes of acute ischemia are peaked, hyperacute T waves, T wave flattening or inversion with or without ST segment depression, horizontal ST segment depression, and ST segment elevation. Changes associated with an infarction are (1) the fresh appearance of Q waves or the increased prominence of preexisting ones; (2) ST segment elevations; and (3) T wave inversions. It is important to recognize that with acute MI the ECG may be entirely normal or contain only “soft” ECG evidence of infarction.
In the past infarcts were classified as transmural or subendocardial, depending of the presence of Q waves. This terminology has now been replaced by the terms Q-wave and non–Q-wave MI. This distinction has more clinical relevance, as several studies have indicated differences in etiology and outcome. The key differences between these two groups are as follows: (1) Q-wave infarctions account for 60% to 70% of all infarcts and non–Q-wave infarctions for 30% to 40%. (2) ST segment elevation is present in 80% of Q-wave infarctions and 40% of non–Q-wave infarctions. (3) The peak creatine kinase tends to be higher in Q-wave infarctions. (4) Postinfarction ischemia and early reinfarction are more common with non–Qwave infarctions. (5) In-hospital mortality is greater with Q-wave infarctions (20% versus 8% for non–Q-wave infarctions). In general, it is thought that the non–Q-wave infarction is a more unstable condition because of the higher risk of reinfarction and ischemia.

Laboratory Findings
Elevation of the creatine kinase muscle and brain subunits (CK-MB) isoenzyme is essential for the diagnosis of acute MI. In general, acute elevations of this enzyme are accounted for by myocardial necrosis. Detectable CK-MB from noncardiac causes is rare except during trauma or surgery. The peak level appearance of CK-MB is expected within 12 to 24 hours after the onset of symptoms; normalization is expected in 2 to 3 days. Therefore patients should have a CK-MB level determined on admission and every 8 to 12 hours thereafter (repeated twice). Reliance on a single CK assay in an emergency room setting to rule out MI is not sensitive and should be discouraged. Cardiac troponins (T and I) are newer markers for cardiac injury. The troponins first become detectable after the first few hours following the onset of myocardial necrosis, and they peak after 12 to 24 hours. Normalization of troponin T levels requires 5 to 14 days; troponin I levels requires 5 to 10 days.

Management Guidelines
The main priority for patients with an acute MI is relief of pain. The frequent clinical observation of rapid, complete relief of pain after early reperfusion with thrombolytic therapy has made it clear that the pain of an acute MI is due to continuing ischemia of living jeopardized myocardium rather than to the effects of completed myocardial necrosis.
Effective analgesia should be administered at the time of diagnosis. Analgesia can be achieved by the use of sublingual nitroglycerin or intravenous morphine (or both). Sublingual nitroglycerin is given immediately unless the systolic blood pressure is less than 90 mm Hg. If the systolic blood pressure is under 90 mm Hg, nitroglycerin may be used after intravenous access has been obtained. Longacting oral nitrate preparations are avoided for management of early acute MI. Sublingual or transdermal nitroglycerin can be used, but intravenous infusion of nitroglycerin allows more precise control. The intravenous dose can be titrated by frequently measuring blood pressure and heart rate. Morphine sulfate is also highly effective for the relief of pain associated with an acute MI. In addition to its analgesic properties, morphine exerts favorable hemodynamic effects by increasing venous capacitance and reducing systemic vascular resistance. The result is to decrease myocardial oxygen demand. As with nitroglycerin, hypotension may occur. The hypotension may be treated with intravenous fluids or leg elevation.

Oxygen
Supplemental oxygen is given to all patients with an acute MI. Hypoxemia in a patient with an uncomplicated infarction is usually caused by ventilation-perfusion abnormalities. When oxygen is used it is administered by nasal cannula or mask at a rate of 4 to 10 L/min. In patients with chronic obstructive pulmonary disease it may be wise to use lower flow rates.

Thrombolytic Therapy
In addition to relieving pain and managing ischemia, thrombolytic therapy must be considered. Thrombosis has a major role in the development of an acute MI. Approximately 66% of patients with MIs have ST segment elevation, making it likely that the process is caused by an occlusive clot. The goal of thrombolytic therapy is reperfusion with a minimum of side effects. The most commonly used thrombolytic agents are streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), recombinant tissue-type plasminogen activator (rt-PA), urokinase, and pro-urokinase.
Early administration of thrombolytic therapy, within 6 to 12 hours from the onset of symptoms, has been associated with a reduction in mortality. Indications for thrombolytic therapy include typical chest pain >30 minutes but <12 hours that is unrelieved by nitroglycerin, and ST segment elevation in more than two contiguous leads (>1 mm in limb leads or >2 mm in chest leads) or ST segment depression in only V1 and V2 or a new left bundle branch block. Relative contraindications for thrombolytic therapy include history of stroke, active bleeding, blood pressure >180 mm Hg systolic, major surgery/ trauma in the last 3 to 6 months, recent noncompressible vascular puncture, and possible intracranial event/unclear mental status. Wright and colleagues56 present a summary of the major thrombolytic trials. Advances in this therapeutic modality during the past 5 years include new third-generation fibrinolytic agents and various strategies to enhance administration and efficacy of these agents. A number of ongoing trials are attempting to determine whether the combination of fibrinolytic therapy with low molecular weight heparin enhances coronary reperfusion and reduces mortality and late reocclusion. Also presented is a dose and cost summary of the available fibrinolytic agents.

Complications (Mechanical)
The most common complications of an acute MI are mechanical and electrical. Mechanical complications include those that are quickly reversible and those that are clearly life-threatening. Reversible causes of hypotension include hypovolemia, vasovagal reaction, overzealous therapy with antianginal or antiarrhythmic drugs, and brady- and tachyarrhythmias. Other, more serious etiologies include primary left ventricular failure, cardiac tamponade, rupture of the ventricular septum, acute papillary muscle dysfunction, and mitral regurgitation.
Classification of patients with acute MI.
Class 1: Patients with uncomplicated infarction without evidence of heart failure as judged by the absence of rales and an S3.
Class 2: Patients with mild to moderate heart failure as evidenced by pulmonary rales in the lower half of the lung fields and an S3.
Class 3: Patients with severe left ventricular failure and pulmonary edema.
Class 4: Patients with cardiogenic shock, defined as systolic blood pressure less than 90 mm Hg with oliguria and other evidence of poor peripheral perfusion.
Cardiogenic shock has emerged as the most common cause of inhospital mortality of patients with an acute MI. Despite advances in medical therapy, cardiogenic shock has a dismal prognosis (80–90% mortality). The management of patients with cardiogenic shock includes adequate oxygenation, reduction in myocardial oxygen demands, protection ofischemic myocardium, and circulatory support. The potential for myocardial salvage with emergency reperfusion should be considered in all cases.

Complications (Electrical)
The past 30 years has seen major developments in the recognition and treatment of arrhythmias. The most common include the brady- and tachyarrhythmias, AV conduction disturbances, and ventricular arrhythmias. Organized treatment protocols have been developed for each of these dysrhythmias.

Post-MI Evaluation
Recommendations for pre- and postdischarge evaluations of patients with an acute MI recommendations for testing exercise tolerance and strategies to determine those who would benefit from medical or surgical intervention. These recommendations include a submaximal ETT at 6 to 10 days and at 3 weeks to determine functional capacity.

Rehabilitation
The goal of cardiac rehabilitation includes maintenance of a desirable level of physical, social, and psychological functioning after the onset of cardiovascular illness. Specific goals of rehabilitation include risk stratification, limitation of adverse psychological and emotional consequences of cardiovascular disease, modification of risk factors, alleviation of symptoms, and improved function. Risk stratification is accomplished by exercise tolerance testing. Additionally, high-risk patients include those with CHF, silent ischemia, and ventricular dysrhythmias. All patients should undergo an evaluation to reduce risk factors (smoking, hyperlipidemia, and hypertension). Risk modification of these factors has been associated with significant reduction in subsequent cardiac events. Enrollment in a cardiac rehabilitation program with particular emphasis on exercise has been shown to reduce cardiovascular mortality.

          Cardiac Tumors        
The patient was a 34 year old African American woman, HIV negative, smoker (one pack per day for 20 years), asthmatic, with a history of positive PPD and tuberculous infection, treated with 4 antituberculous medications. As part of the work-up a CT scan of the chest was done, which revealed a large mass involving the middle and lower lobes of the right lung. In addition, a bronchial washing was reported positive for adenocarcinoma, and subsequently she underwent right pneumonectomy. The right lung as well as the mediastinal lymph nodes were involved by a moderately to poorly differentiated adenocarcinoma. Moreover, the lung showed focal emphysematous changes and several 0.5 cm arteriovenous malformations. After the operation she returned to work, but came back to the ER twice complaining of dyspnea and productive cough with yellow sputum. Jugular venous distension was absent and left breath sounds were clear. She was treated with albuterol and discharged on prednisone (20mg qd x 5 days). She then experienced increasing shortness of breath and the emergency medical service was called. The paramedics found her able to talk, but soon thereafter, she lost consciousness, suffered a cardiac arrest and died on her way to the hospital.

Gross Description
The body was that of a thin, well-developed woman measuring 168 cm and weighing 62 kg. The skin was unremarkable except for a right thoracotomy scar. Upon opening the chest, the mediastinum was noted shifted to the right side. The right border of the heart was 10 cm from the right lateral chest wall. The posterior aspect of the right thoracic cavity was occupied by scar tissue, and the anterior portion was filled with clotted blood and fibrin. The left lung was expanded. Multiple lymph nodes were present in the mediastinum, the largest being 3 cm in maximal dimension. The left lung weighed 500 g. The pleural surfaces were smooth and shiny. On section, the parenchyma revealed an area of increased firmness and hemorrhage in the lower lobe, measuring 5 cm in greatest dimension, extending to the visceral pleura. In addition, there was a moderate loss of parenchyma with formation of smooth-lined cysts of up to 0.5 cm in diameter. These cysts were present in both lobes throughout. The larynx, trachea, major and segmental bronchi were of average caliber. Organizing emboli measuring up to 3 mm occluded small branches of the pulmonary artery.
The heart was 240 g and of the expected shape. The parietal pericardium was smooth and glistening. The sac contained approximately 500 cc of serosanguineous fluid. The epicardium was thickened, dull, firm and white in a few areas with multiple hemorrhagic foci of up to 0.2 cm (Figure 1). The atria were normal and free of thrombi. The foramen ovale was closed. The right and left ventricular walls measured 0.4 cm and 1.2 cm in thickness, respectively. The valve rings measured as follows: tricuspid valve 12 cm, pulmonic valve 7 cm, mitral valve 8.5 cm, and aortic valve 6 cm. The valve leaflets were pliable and the chordae tendineae were thin and slender. The myocardium and endocardium were  unremarkable. The coronary arteries were of normal caliber and distribution. The aorta showed mild atherosclerosis in the abdominal portion.
epicardium multiple hemorrhagic 
Figure 1 Cross section of the heart showing metastatic carcinoma involving the epicardium with focal invasion of the myocardium (arrow)

The liver weighed 1400 g and was of normal size and shape. The cut surface showed marked acute centrilobular congestion and multiple tan, firm nodules measuring 0.2 to 0.4 cm. The lobular pattern was preserved otherwise. The remaining organs had no significant pathologic changes.

Microscopic Description
Sections from the epicardium showed many single and small clusters of poorly differentiated carcinoma cells, near the epicardial surface. Some of these cells contained vacuoles consistent with mucin droplets of adenocarcinoma. The malignant cells were large with pleomorphic nuclei and prominent nucleoli. Some were present within lymphatics. Metastatic carcinoma was present bilaterally in hilar lymph nodes. The firm, hemorrhagic areas in both lobes of the left lung corresponded to foci of hemorrhagic infarcts. Surrounding arteries contained numerous acute, organizing and recanalized thrombi. The tan nodules present in the liver did not represent metastatic adenocarcinoma but rather foci of adenomatosis. They were composed of thickened cords of hepatocytes separated by sinusoids and devoid of portal tracts, bile ductules or scars.

Case Analysis
The heart can be involved by primary as well as metastatic tumors. Primary tumors of the heart are rare (< 0.3 % in postmortem series), with myxoma the most frequent. Metastases from neoplasms arising in other organs are far more common and include carcinomas, sarcomas, hematologic malignancies and melanoma. Nonetheless, cardiac metastases are infrequent. Why is the heart relatively protected from metastasis? Possible explanations include the continuous forceful stroke of the heart, rapid blood flow and afferent lymphatic circulation. If these hypotheses were true, cardiac tumors would be present almost invariably in patients with previous cardiac damage with reduced pump action and blood flow, but there is no such confirmatory data in the literature. Regarding afferent lymphatics, metastatic dissemination in the heart occurs most commonly through lymphatic invasion. Overall, the heart is probably protected as a result of the combination of all these and other unknown factors. Moreover, tumor type, metabolic properties of the heart, and adhesion molecules among others, are under consideration and require further investigation.
Secondary tumors may involve the heart by direct extension, hematogenous spread or lymphatic dissemination. Direct extension occurs from tumors arising in the lungs or mediastinum (i.e. bronchogenic and esophageal carcinoma, malignant thymoma, thymic carcinoma). Hematogenous spread is often seen with sarcomas (e.g. uterine. leiomyosarcomas can reach the heart through the inferior vena cava), leukemia, multiple myeloma, and with certain types of carcinoma (e.g. hepatocellular carcinoma). However, the lymphatic pathway appears to be the most significant. This is demonstrated by the frequent metastatic involvement of the pericardium, richly supplied by lymphatic channels that drain in the anterior and posterior mediastinum. In the present case, the patient had a history of adenocarcinoma of the lung involving mediastinal lymph nodes; therefore, it is not surprising that she presented with a pericardial effusion and associated cardiac tamponade. Pericardial involvement in a patient with a known primary malignancy, should be suspected in the setting of pericardial effusion, intractable heart failure or hepatomegaly in the absence of metastatic lesions. The differential diagnosis includes congestive heart failure in a patient with a cardiomyopathy, and nonmalignant pericardial effusions (infectious and non-infectious). This patient was young, with no history of heart disease. Although she had asthma in the past and evidence of chronic obstructive pulmonary disease as per the autopsy exam, she did not have pulmonary hypertension or cor-pulmonale.
Tuberculous (TB) pericarditis is a consideration based on her prior history of PPD positivity and antituberculous treatment. TB pericarditis may develop insidiously, or acutely with a large effusion and cardiac tamponade, particularly in immunosuppressed patients. She was HIV negative and had not been treated with chemotherapeutic agents. If she had lived, the diagnosis of malignant pericardial effusion could have been made with a pericardiocentesis and cytologic examination of the fluid. Adenocarcinoma cells are readily identified in pericardial fluid by their tri-dimensional arrangement, distinct cell borders, high nuclear-cytoplasmic ratio and prominent nucleoli (Figure 2). They must be differentiated from reactive mesothelial cells, which is not often easy. Reactive mesothelial cells, especially in long-standing effusions can also exhibit a glandular arrangement, prominent nucleoli, mitotic figures and even vacuolization that mimic adenocarcinoma. Immunohistochemistry is useful in distinguishing the two. Both cell types are immunoreactive to cytokeratin, but only adenocarcinoma stains with the adenocarcinoma marker B72.3 and carcinoembryonic antigen (CEA).
prominent nucleoli 
Figurea 2 Pericardial fluid containing adenocarcinoma cells. The malignant cells have a finely vacuolated cytoplasm, irregular nuclear contours and prominens nucleoli (Papanicolaou, 60x).

Pulmonary adenocarcinoma arises preferentially in the periphery of the lung parenchyma. Central lesions may occur, but are less frequent. This type of tumor can develop in smokers as well as in non-smokers, de novo or in areas of pre-existing scarring. Our patient was a smoker for 20 years. Although she had a risk factor for lung cancer, the aggressive behavior of this tumor (stage T2, N2 at initial diagnosis) suggests a genetic predisposition.
The advent of cardiovascular imaging studies has improved the diagnosis of cardiac involvement by metastatic disease, but the prognosis remains poor. In a recent study done at the Tottori University School of Medicine in Japan, 46 of 161 patients had secondary cardiac tumors diagnosed by echocardiography. The most common primary site was the lung followed by mediastinum, liver, uterus and testis. Forty seven percent of the cases had pericardial involvement, 32% involved the right side of the heart and 14 % involved the left. Metastases on both sides of the heart were noted in 7% of cases. It is unknown why intracavitary lesions are less common, but there is evidence that certain tumors have predilection for this pattern of growth (Figures 3 and 4). In our experience, squamous carcinoma arising in different sites has the tendency to invade and seed cardiac valves, endocardium and myocardium. Prior valve damage or endothelial damage appears to be a sine qua non in such cases. As a result, death can occur due to arrhythmia with or without conduction system involvement and embolization. Changes in the electrocardiogram such as prolonged elevation of the ST segment are indicative of myocardial invasion.
Echocardiogram 
Figure 3 Echocardiogram showing an intracavitary right ventricular mass in a patient with lymphoma (circle and arrow)

hemorrhagic tumors 
Figure 4 Transverse section of the heart showing an intracavitary right-sided mass (arrow) and patchy involvement of the myocardium by a fleshy, hemorrhagic tumor. the patient had been diagnosed with Non-Hodgkin's lymphoma.

In the present case, the patient died of Cardiac tamponade due to a malignant pericardial effusion. In addition, she was in a hypercoagulable state with numerous acute and organizing pulmonary emboli leading to areas of hemorrhagic infarction. Her symptoms of dyspnea and shortness of breath were related to both the pulmonary embolism and evolving cardiac tamponade. Of note, dyspnea is the most common manifestation of Cardiac Tumors in general, and is suggestive of cardiac decompensation. Treatment is palliative, aimed at controlling effusions, arrhythmia and heart failure. Radiotherapy is the treatment of choice to manage malignant effusions. In some instances, a pericardial window is required to treat tamponade. Chemotherapy has been used to prevent further cardiac involvement, but its use is limited by its cardiotoxicity. In rare instances, surgical debulking is indicated to alleviate obstructive cardiac masses.

          Diagnosing Heart Disease        
Diagnosing Heart Disease
If your doctor suspects that you have heart disease, there are a number of tests that she can perform to find out for sure. You may get just one test or more than one. It’s normal to feel worried or anxious before having tests. Tell your doctor if your fears are keeping you from getting the tests you need.
ecocardiogrphy
Treating Heart Disease
If you have heart disease, it is extremely important to control it. You can help to do this by:
• Eating a heart healthy diet
• Quitting smoking if you smokel getting regular physical activity
• Losing weight if you are overweight or obese
• Reducing stress
• Taking medicines as directed by your doctor
1. Medicines
Along with making lifestyle changes, you may need medicines to help control your heart disease. These medicines can include:
• Cholesterol lowering medicines
• Beta blockers, calcium channel blockers, or ACE inhibitors to lower blood pressure and lighten the workload for the heart
At times, other medicines may be needed:
• Antiplatelet medicines stop blood cellscalled platelets from clumping together and forming clots.
• Anticoagulants stop clots from formingin your arteries and blocking blood flow.
• Nitrates,  such as nitroglycerin, widen the coronary arteries, which helps lessen chest pain.
• Thrombolytic agents break up blood clots that form during a heart attack. The sooner thesedrugs are given to someone having a heart attack, the better they are at pre-venting heart damage.
 
2. Special Procedures or Surgery
If lifestyle changes and medicines do not improve your heart disease symptoms, your doctor may suggest special procedures or surgery. These include:
• Angioplasty . This procedure is usually done right away if coronary angiography shows problems in blood flow in a coronary artery. A thin tube with a balloon at one end is threaded into a coronary artery that has narrowed because of plaque buildup. Once in place, the balloon is inflated to push the plaque against the artery wall. This opens the artery more so that blood can flow freely.
• Stent. A stent is a mesh tube used to hold open a narrowed or weakened artery. It is put in place during an angioplasty. Some stents are coated with a medicine to keep arteries from narrowing or becoming blocked again. Not all people who have angioplasty need a stent.
• Coronary artery bypass surgery. In this procedure, a short piece of vein or artery from another part of your body is used to reroute blood around a blockage in a coronary artery. This restores blood flow to the heart.

Other Types of Heart Disease
Other types of heart disease that affect many women include heart failure and arrhythmias. These can result from coronary artery disease or other problems.
1. Heart Failure
Heart failure happens when the heart can’t pump enough blood throughout the body. Heart failure doesn’t mean that your heart has stopped or is about to stop working. It means that your heart can’t fill with enough blood or pump with enough force, or both. Heart dfailure evelops over time as the pumping action of the heart grows weaker. It’s more common in people older than 65 years. Coronary artery disease, high blood pressure, and diabetes are leading causes. Heart failure can affect the left side, the right side, or both sides of the heart. Most cases involve the left side, in which the heart can’t pump enough blood to the rest of the body. As a result, blood and fluid back up in the lungs and you feel short of breath. When the right side of the heart is affected, blood backs up in the body, causing swelling, mainly in the lower legs and ankles. If both sides of the heart are failing, which is often the case, you also feel tired and weak because not enough blood is flowing to your muscles. Heart failure usually can’t be cured. Treatment often involves making lifestyle changes and taking medicines. If you have severe heart failure, you may need a mechanical heart pump or a heart transplant.
 
2. Arrhythmia
An arrhythmia is a problem with the speed or rhythm of the heartbeat caused by a disorder in the heart’s electrical system. There are many types of arrhythmias. Most are harmless, but some can be serious or even life threatening. The most common type of serious arrhythmia is atrial fibrillation, or AF. With AF, the walls of the atria quiver very fast (called fibrillation) instead of beating normally. As a result, blood isn’t pumped into the ventricles as it should, and it pools in the atria. This can cause blood clots to form in the atria. If a clot breaks off, it might get stuck in a blood vessel and cut off blood supply to the brain. This is a type of stroke. People with AF sometimes take blood thinners to prevent clots and medicines to slow the heart rate. Arrhythmias that start in the ventricles can be very dangerous. With ventricular fibrillations (v-fib), blood is not pumped out to the body. If the heart stops pumping entirely, the condition is known as sudden cardiac arrest. In a sudden cardiac arrest, a person will faint within seconds and die within minutes if not treated quickly.
 
Living with Heart Disease
If you are taking medicines or have undergone special procedures or surgery to treat coronary artery disease, you still need to stick with those healthy lifestyle changes to keep plaque from clogging up your arteries again. Follow your doctor’s advice on what foods to eat, how to ease back into a physical activity routine if you have had surgery, and how to reduce stress. And if you smoke, it is vital that you quit.Taking care of your emotional health is also important. People with heart disease are often depressed, especially those who have had a heart attack. If you have heart disease and find yourself  feeling depressed or “blue,” talk with your doctor about ways to get help. Treating depression may do more than just help you feel better emotionally. If you have had a heart attack, antidepressants may lower your chances of having a second heart attack or dying of heart disease. So don’t wait to seek help if you are feeling down.
Good News about Heart Health
More women are becoming aware that they are at risk of heart disease, which is the crucial first step. Even better, more women are also taking heart-healthy action.If you haven’t already joined this grow-ing trend of heart-savvy women, now is the time to start. Urge your children and other family members to join you in your efforts to lower heart disease risk. Living heart healthy takes effort. But the rewards can mean a healthier, longer life for you and your loved ones.

           Dobutamine echocardiography and thallium-201 imaging predict functional improvement after revascularisation in severe ischaemic left ventricular dysfunction.         
Senior, R; Glenville, B; Basu, S; Sridhara, BS; Anagnostou, E; Stanbridge, R; Edmondson, SJ; ... Lahiri, A; + view all <#> Senior, R; Glenville, B; Basu, S; Sridhara, BS; Anagnostou, E; Stanbridge, R; Edmondson, SJ; Handler, CE; Raftery, EB; Lahiri, A; - view fewer <#> (1995) Dobutamine echocardiography and thallium-201 imaging predict functional improvement after revascularisation in severe ischaemic left ventricular dysfunction. Br Heart J , 74 (4) pp. 358-364.
          Measure Heart Rate With iPhone, iPod, iPad and Android devices.        
Ever wanted to know how fast your heart was beating ? Believe it or not, you can actually use your iPod Touch, iPad or Phone (Android and iPhone) to measure your Heart Rate With an accuracy as good as a pulse check. With Cardiography you can accurately measure your beats per minute (BPM).  Cardiograph by MacroPinch is an impressively accurate personal heart rate meter app with a bunch of features built in.

This app is currently free on the Google Play and iOS app store so I gave it a go. All I had to do was place my finger on my iPad's front camera and with decent amount of light (Sunlight in my case) it measured my resting heart rate as 68 BPM. A normal resting heart rate is around 60-80 BPM. To test this app further I did some light exercise and remeasured my heart rate, the app showed a significant increase to 108 BPM.
Measure Heart Rate with Phone iPod Tablet Cardiograph app
68 BPM Measure with Cardiography for the Apple iPad.
Cardiograph features multiple user profiles and boasts features such tracking the location of your measurements, iCloud sync and as well as providing you with an option to add notes to each of your heart rate measurements

Note: Do note however even though the app is accurate, it is not actually a medical equipment.



          Transesophageal Echocardiography (TEE)        

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          Focused echocardiographic evaluation in resuscitation management        

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          Echocardiography        

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          Clinical Respiratory Medicine, 4th Edition        
Clinical Respiratory Medicine provides practical guidance to help you more effectively diagnose and manage the full range of pulmonary disorders, including those seen in today's most challenging patient populations. Now with over 400 brand-new review questions and 25 videos available online, this medical reference book delivers all of the answers you need to ensure the best outcomes.

  • Better manage and treat patients with pulmonary disease with complete clinical coverage of the critical information relevant to your everyday practice, presented in a templated, user-friendly format.
  • Find critical information quickly with the help of diagnostic algorithms.
  • Test your knowledge of respiratory medicine with the help of 400 brand-new review questions.
  • Watch and learn. Over 25 videos of practical procedures are available online at www.expertconsult.com.
  • Thoroughly understand the needs and recognize co-morbidities of particular patient populations through entirely new chapters on lung structure, echocardiography, and obesity and its effects.
  • Access the latest research and advancements in lung cancer, benign tumors, and the importance of pulmonary physiology in understanding lung function and the disease processes that occur.


Take a practical approach to the diagnosis and management of patients with respiratory disorders using this ideal source for reference in clinical practice.

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Clinical Respiratory Medicine: Expert Consult - Online and Print, 4e



          ECHOCARDIOGRAPHY TECHNOLOGIST - ETOBICOKE CARDIOLOGY CLINIC - Etobicoke, ON        
ADULT &amp; STRESS ECHO:. MUST HAVE 1 YEAR EXPERIENCE IN ADULT &amp; STRESS ECHO. WE ARE LOOKING FOR ECHOCARDIOGRAPHY TECHNOLOGIST TO WORK IN BRAMPTON AND ETOBICOKE...
From Indeed - Fri, 09 Jun 2017 15:36:41 GMT - View all Etobicoke, ON jobs
          Echocardiography Technologist - HART MEDICAL SERVICES INC - Greater Toronto Area, ON        
Hart Medical Services (HMS) is looking to hire *Stress* and *Stress- Echo* technicians for full time and part time employment spanning Monday to Saturday. The...
From Indeed - Thu, 27 Jul 2017 18:24:42 GMT - View all Greater Toronto Area, ON jobs
          ECHOCARDIOGRAPHY TECHNOLOGIST - TORONTO CARDIOLOGY & RADIOLOGY CLINIC - Toronto, ON        
MUST BE ABLE TO DO STRESS ECHO. WE ARE LOOKING FOR ECHOCARDIOGRAPHY TECHNOLOGIST FOR OUR WEST LOCATION....
From Indeed - Thu, 27 Jul 2017 14:23:35 GMT - View all Toronto, ON jobs
          Echocardiography Technologist - Cardiology Lab (153.17) - Women's College Hospital - Toronto, ON        
Performs Doppler Echocardiography, Stress Echo (exercise and dobutamine), Echo Contrast testing in a busy ambulatory setting....
From Indeed - Tue, 25 Jul 2017 21:00:44 GMT - View all Toronto, ON jobs
          RN - (Long Beach, California, United States)        
At MemorialCare Health System, we believe in providing extraordinary healthcare to our communities and an exceptional working environment for our employees. MemorialCare stands for excellence in Healthcare. Across our family of medical centers and physician groups, we support each one of our bright, talented employees in reaching the highest levels of professional development, contribution, collaboration and accountability. Whatever your role and whatever expertise you bring, we are dedicated to helping you achieve your full potential in an environment of respect, innovation and teamwork. Specific Job Responsibilities: It is the duty of all employees to understand and perform their job tasks to the highest level at all times. Room patients, take and document vital signs, and assist provider with medical exam. Evaluate patients for immediate medical need and report to provider. Perform accurate charting, assessments, and intervention and follow-up per scope of practice. Assist with scheduling of appointments as required for inside or outside health care providers, including hospital/out-patient surgeries. Collaborates with the Medical Provider and TAN regarding phone messages, pharmacy refills and ancillary test results in a timely manner. Maintains the capability of performing Paramed procedures; i.e., phlebotomy, spirometry, audiometry, electrocardiography, etc. Responsible for weekly facility orders per facility training and scheduling. Respond to and participate in all clinical emergencies and maintenance of emergency equipment. Performs procedures and administers medications and narcotics per scope of licensure/certification. Assist nursing department in procedures, tasks and duties specific to the job role of the licensed nurse scope of practice. Adhere to infection control, universal precautions, and use of personal protective equipment as needed for all patient care procedures, maintenance of equipment, and disposal of waste. Access and interpret needed information from facility MSDS book or MSDS on-line in a prompt manner. Attends and participates in all mandatory nursing/administrative department meetings/inservices. Perform any additional/miscellaneous duties (not inclusive of job description) as requested by the management team within the scope of licensure. Qualifications/Skills: Qualified candidate must excel in interpersonal communication and customer service and be able to work both independently and as part of a team. Candidate must also excel in organization and attention to details and follow through. Additionally, they must have the ability to problem solve to logical conclusion and demonstrate initiative and responsibility. Must be able to effectively and clearly communicate (written and verbal.) Experience: Prior experience in an ambulatory care environment. Education: High school graduate or equivalent. Current California RN license. CPR for Healthcare Provider Card. MemorialCare Medical Group is a physician-based organization established to provide advanced comprehensive, effective and efficient health care. With over 30 locations from Long Beach to Dana Point, MemorialCare Medical Group includes more than 250 physicians in the areas of internal medicine, family medicine, pediatrics, geriatric medicine, cardiology, cardio thoracic surgery, gastroenterology, neurology, pulmonology, psychiatry, psychology, rheumatology, sleep medicine and therapeutic acupuncture. In addition to multiple locations throughout Orange County, MemorialCare Medical Group offers Urgent Care Centers that are open 365 days-a-year, Telephone Advice Nurses available 24 hours-a-day, 7 days-a-week; and lab and digital X-ray services available on-site at most locations.
          RN - (Fountain Valley, California, United States)        
At MemorialCare Health System, we believe in providing extraordinary healthcare to our communities and an exceptional working environment for our employees. MemorialCare stands for excellence in Healthcare. Across our family of medical centers and physician groups, we support each one of our bright, talented employees in reaching the highest levels of professional development, contribution, collaboration and accountability. Whatever your role and whatever expertise you bring, we are dedicated to helping you achieve your full potential in an environment of respect, innovation and teamwork. Specific Job Responsibilities: It is the duty of all employees to understand and perform their job tasks to the highest level at all times. Room patients, take and document vital signs, and assist provider with medical exam. Evaluate patients for immediate medical need and report to provider. Perform accurate charting, assessments, and intervention and follow-up per scope of practice. Assist with scheduling of appointments as required for inside or outside health care providers, including hospital/out-patient surgeries. Collaborates with the Medical Provider and TAN regarding phone messages, pharmacy refills and ancillary test results in a timely manner. Maintains the capability of performing Paramed procedures; i.e., phlebotomy, spirometry, audiometry, electrocardiography, etc. Responsible for weekly facility orders per facility training and scheduling. Respond to and participate in all clinical emergencies and maintenance of emergency equipment. Performs procedures and administers medications and narcotics per scope of licensure/certification. Assist nursing department in procedures, tasks and duties specific to the job role of the licensed nurse scope of practice. Adhere to infection control, universal precautions, and use of personal protective equipment as needed for all patient care procedures, maintenance of equipment, and disposal of waste. Access and interpret needed information from facility MSDS book or MSDS on-line in a prompt manner. Attends and participates in all mandatory nursing/administrative department meetings/inservices. Perform any additional/miscellaneous duties (not inclusive of job description) as requested by the management team within the scope of licensure. Qualifications/Skills: Qualified candidate must excel in interpersonal communication and customer service and be able to work both independently and as part of a team. Candidate must also excel in organization and attention to details and follow through. Additionally, they must have the ability to problem solve to logical conclusion and demonstrate initiative and responsibility. Must be able to effectively and clearly communicate (written and verbal.) Experience: Prior experience in an ambulatory care environment. Education: High school graduate or equivalent. Current California RN license. CPR for Healthcare Provider Card. MemorialCare Medical Group is a physician-based organization established to provide advanced comprehensive, effective and efficient health care. With over 30 locations from Long Beach to Dana Point, MemorialCare Medical Group includes more than 250 physicians in the areas of internal medicine, family medicine, pediatrics, geriatric medicine, cardiology, cardio thoracic surgery, gastroenterology, neurology, pulmonology, psychiatry, psychology, rheumatology, sleep medicine and therapeutic acupuncture. In addition to multiple locations throughout Orange County, MemorialCare Medical Group offers Urgent Care Centers that are open 365 days-a-year, Telephone Advice Nurses available 24 hours-a-day, 7 days-a-week; and lab and digital X-ray services available on-site at most locations.
          Per Diem RN - (San Juan Capistrano, California, United States)        
At MemorialCare Health System, we believe in providing extraordinary healthcare to our communities and an exceptional working environment for our employees. MemorialCare stands for excellence in Healthcare. Across our family of medical centers and physician groups, we support each one of our bright, talented employees in reaching the highest levels of professional development, contribution, collaboration and accountability. Whatever your role and whatever expertise you bring, we are dedicated to helping you achieve your full potential in an environment of respect, innovation and teamwork. Specific Job Responsibilities: It is the duty of all employees to understand and perform their job tasks to the highest level at all times. Room patients, take and document vital signs, and assist provider with medical exam. Evaluate patients for immediate medical need and report to provider. Perform accurate charting, assessments, and intervention and follow-up per scope of practice. Assist with scheduling of appointments as required for inside or outside health care providers, including hospital/out-patient surgeries. Collaborates with the Medical Provider and TAN regarding phone messages, pharmacy refills and ancillary test results in a timely manner. Maintains the capability of performing Paramed procedures; i.e., phlebotomy, spirometry, audiometry, electrocardiography, etc. Responsible for weekly facility orders per facility training and scheduling. Respond to and participate in all clinical emergencies and maintenance of emergency equipment. Performs procedures and administers medications and narcotics per scope of licensure/certification. Assist nursing department in procedures, tasks and duties specific to the job role of the licensed nurse scope of practice. Adhere to infection control, universal precautions, and use of personal protective equipment as needed for all patient care procedures, maintenance of equipment, and disposal of waste. Access and interpret needed information from facility MSDS book or MSDS on-line in a prompt manner. Attends and participates in all mandatory nursing/administrative department meetings/inservices. Perform any additional/miscellaneous duties (not inclusive of job description) as requested by the management team within the scope of licensure. Qualifications/Skills: Qualified candidate must excel in interpersonal communication and customer service and be able to work both independently and as part of a team. Candidate must also excel in organization and attention to details and follow through. Additionally, they must have the ability to problem solve to logical conclusion and demonstrate initiative and responsibility. Must be able to effectively and clearly communicate (written and verbal.) Experience: Prior experience in an ambulatory care environment. Education: High school graduate or equivalent. Current California RN license. CPR for Healthcare Provider Card. MemorialCare Medical Group is a physician-based organization established to provide advanced comprehensive, effective and efficient health care. With over 30 locations from Long Beach to Dana Point, MemorialCare Medical Group includes more than 250 physicians in the areas of internal medicine, family medicine, pediatrics, geriatric medicine, cardiology, cardio thoracic surgery, gastroenterology, neurology, pulmonology, psychiatry, psychology, rheumatology, sleep medicine and therapeutic acupuncture. In addition to multiple locations throughout Orange County, MemorialCare Medical Group offers Urgent Care Centers that are open 365 days-a-year, Telephone Advice Nurses available 24 hours-a-day, 7 days-a-week; and lab and digital X-ray services available on-site at most locations.
          Adult Cardiac Sonographer - Non-Invasive Cardiology (PD Days) - (Long Beach, California, United States)        
At MemorialCare Health System, we believe in providing extraordinary health care to our communities and an exceptional working environment for our employees. MemorialCare stands for excellence in Health Care. Across our family of medical centers, we support each one of our bright, talented employees in reaching the highest levels of professional development, contribution, collaboration and accountability. Whatever your role and whatever expertise you bring, we are dedicated to helping you achieve your full potential in an environment of respect, innovation and teamwork. Long Beach Memorial Medical Center is a major regional provider of medical and surgical services. A Magnet®-designated teaching hospital, Long Beach Memorial Medical Center has 420 beds. We consistently achieve national accolades for our quality care, including ranking as one of “America’s Best Hospitals” for Orthopedics by U.S. News & World Report magazine. Our unique environment allows for a range of medical services, from childhood to adulthood, to be structured under one roof. With our technology, our vision, and especially our talented professionals, we ensure our patients receive the best possible care. Currently seeking a Per Diem/Adult Cardiac Sonographer The Adult Cardiac sonographer independently performs common and complex cardiac sonography of adult patients. This individual has an excellent understanding of adult physiology and anatomy with knowledge of the related cardiac pathophysiology. This individual independently performs and provides timely input of findings on patients including young adult, adult and geriatric patients with known or suspected cardiac related diagnosis. He/she, under the direction of the Medical Director of Echocardiography and the Memorial Heart Institute Director, maintains a high standard of quality for all procedures performed. Qualifications/Work Experience 3+ years of experience as a cardiac sonographer in an acute care facility. Advanced knowledge of cardiac anatomy and physiology. Problem solving,Advanced knowledge of and ability to learn and apply complex cardiac s onography principles, instrumentation and techniques and new techniques for the capture, display and analysis of echocardiograph data. time management, and organizational skills required. Excellent interpersonal and patient service skills. Education/Licensure/Certification Graduate ASE (American Society of Echocardiography) recognized program for echocardiography. ASE RDCS (Registered Diagnostic Cardiac Sonographer) certification for adults or CCI ( Cardiac Crendtialing International) certification. Current BLS required.
          Comment on Accredited Ultrasound Technician Schools 2017 by Lisa Parmley        
Thank you for your inquiry. We are pleased to read you have chosen a career in sonography. There is a Diagnostic Medical Sonography program at Ohio State University. It offers a baccalaureate program, and you can choose between one of two concentrations – general or vascular. The next nearest program is at Central Ohio Technical College in Newark, Ohio which is only 40 miles from Columbus. Central Ohio Technical College offers an associate degree program with a choice of three concentrations – cardiac, general, and vascular. You can also consider the Diagnostic Medical Sonography program at Marion Technical College program in Marion, Ohio. The school is approximately 51 miles from Columbus. If you own a car or can arrange transportation, both Ohio State University and Central Ohio Technical College are an easy driving distance from Columbus. One option with Ohio State University is to live in one the dorms which financial aid could help pay for, along with tuition and fees. The Ultrasound Technician Center has explored the nearest cities to Columbus offering a CAAHEP accredited sonography program. We encourage you to visit here for more information. There are sonography program in Kettering, Cincinnati, Canton, and Rio Grande, but these programs are more than 75 miles from Columbus. There are <a href="http://www.ultrasoundtechniciancenter.org/state/11-accredited-ultrasound-technician-schools-in-ohio.html" target="_blank" rel="nofollow">12 CAAHEP accredited sonography programs in the state of Ohio</a>. You should only attend one of the CAAHEP accredited sonography programs because they will fully prepare you for taking the ARDMS exams without the need for additional clinical training. They are also the programs assessed for quality. There are <a href="http://www.ultrasoundtechniciancenter.org/online-sonography-programs/online-sonography-schools.html" target="_blank" rel="nofollow">online CAAHEP-accredited sonography programs</a> that are described on the Ultrasound Technician Center site. Jackson College in Jackson, Michigan is one option that may meet your needs. All the coursework is online, but you will need to complete clinical training at a medical facility approved by the program. You should talk to the program faculty to discuss whether it would be possible to do your clinical training at a Columbus, Ohio medical facility. Program completion leads to an Associate in Applied Science. The University of Wisconsin-Milwaukee also has online sonography programs leading to a bachelor’s degree or baccalaureate. In these programs, the echocardiography students can complete all coursework online, while the general and vascular programs require some on-campus work. The University decides on the clinical placement. Good luck in future endeavors. If we can answer any further questions, please do not hesitate to ask. We encourage you to browse our website and use the search box to find additional relevant information.
          Comment on Accredited Ultrasound Technician Schools 2017 by Lisa Parmley        
Thank you for your question. You are interested in a sonography specialty offering excellent career opportunities. As far as CAAHEP accredited programs offering a pediatric cardiac concentration in California, there is one. The <a href="http://www.ultrasoundtechniciancenter.org/state/accredited-ultrasound-technician-schools-in-california.html" target="_blank" rel="nofollow">Community Regional Medical Center</a> is Fresno, CA offers a Certificate in Pediatric Cardiac Sonography. However, this is a very limited program in which instructors choose students from among those who have completed the Adult Cardiac Track to participate in the Pediatric Cardiac Track Description (<a href="http://www.communitymedical.org/sites/default/files/library/corporate/files/sonographyprogramdetails.pdf" target="_blank" rel="nofollow">more information</a>). One option is to complete an adult cardiac or vascular sonography program. You can earn a Registered Diagnostic Cardiac Sonographer credential with pediatric sonography specialty (see <a href="http://www.ardms.org/get-certified/RDCS/Pages/pediatric-echocardiography.aspx" target="_blank" rel="nofollow">here</a>) by taking the SPI and PS exams. Another option is to earn ARDMS registration for general sonography, and then study appropriate material to pass the PS credential exam at a future date. If you can get on-the-job experience at the same time, that is even better. Another option is to specialize in OB/GYN sonography and leverage that into Pediatric Cardiac Sonography. Yet another option is to focus on general sonography, take the SPI exam, take continuing education course in Pediatric Cardiac Sonography, and eventually take the PS credential exam. The important point is to make a career plan. Make education and career decisions based on the ultimate goal. An associate degree in echocardiography or vascular ultrasound will not restrict you from pediatric cardiac. Careers are based on a mixture of education and experience. We wish you a great career as a Diagnostic Medical Sonographer. If you have any more questions, please be sure to contact us.
          Comment on Accredited Ultrasound Technician Schools 2017 by Michelle        
I reside in Orange County, California. I am hoping to pursue a career in pediatric cardiac sonography from a CAAHEP accredited institution. What schools should I be considering? I have researched a few schools, but it seems that there aren't any in California that specialize in pediatric cardiac. Orange Coast College provides an associates degree in echocardiography and vascular ultrasound, but would that restrict me from pediatric cardiac? Please help!
          Comment on 4 Factors Affecting Ultrasound Tech Salary by Lisa Parmley        
Thank you for your question. The ARDMS recognizes three credentials, and each one has a corresponding specialty. The RDMS credential specialties include abdomen, breast, fetal echocardiography, obstetrics and gynecology, and pediatric sonography. The RDCS credential specialties are adult echocardiography, fetal echocardiography and pediatric echocardiography. The RVT credential specialty Is vascular technology. To earn an ARDMS credential with a specialty requires taking the appropriate exams. All credentials require passing the SPI exam, but you then choose the corresponding specialty exams you wish to take. However, to be eligible for the exams, you must meet certain requirements that include coursework and clinical training. You cannot earn a specialty on the job. For this reason, it is important to <a href="http://www.ultrasoundtechniciancenter.org/education/schools-directory.html" target="_blank" rel="nofollow">attend a CAAHEP accredited sonography program because they ensure students are prepared to sit for the exams after graduation</a>. There are several factors to take into consideration when choosing the credential and corresponding specialty or specialties. First, you need to consider the specialties that hold the most interest for you personally. Second, the field of sonography is rapidly expanding as new technology expands the type of procedures that benefit from ultrasound. The fastest growing specialty areas are in the cardiac and vascular areas. Note that you can even choose to specialize in fetal, adult and/or pediatric echocardiography. Another factor to consider is salary. The vascular sonographers earn more than the pediatric cardiac sonographer or the cardiac sonographer, but each of these specialties are in the top paying specialties for sonographers. Good luck in your future endeavors. We wish you a great career as a Diagnostic Medical Sonographer. If we can be of further assistance, do not hesitate to ask.
          Comment on 2017 Best Ultrasound Certificate Programs by Ada Jarvis        
Dear Sirs, I am very interested to study Medical Sonography. The problem I am facing now is that I live in Las Vegas, NV and I do not see any CAAHP accredited program Institution that I can attend. We have an institute named American Institute of Medical Sonography that seems to be a good institute to study this career (web site "www.aimsed.edu). They offer two specialties: Diagnostic Medical Sonography and Echocardiography. The American Institute of Medical Sonography is accredited by the accrediting Commission of Career Schools and Colleges (ACCSC), but not for CAAHEP. I talked to its director and he told me that the AIMS prepares the students to take the test at ARMDS to get the certification. I was going to start soon at AIMS, but I have doubts if, or how I could be affected since they are not register at CAAHEP at the moment I apply to get my certification with ARDMS. The school have been 11 year around, but unfortunately I do not know anybody who have graduated from there. I would appreciate all your advice and recommendation and /or if you know about students graduated from AIMS. Thank you so much for your prompt answer. Ada Jarvis
          Intro        
DISCLAIMER: I am not a doctor, and this is blog is not intended to diagnose, treat, or cure any condition. My intention here is simple: after going through hell for 2 years with mitral valve prolapse syndrome (MVPS), as opposed to merely mitral valve prolapse (MVP), largely left to discover the causes and effects empirically, I want to benefit other suffers by sharing what I've learned. Use it as a launchpad for your own research, and to suggest questions for your cardiologist, neurologist, or other medical expert. Above all, I would like to share some practical suggests for symptom management, if not improvement in the underlying pathology.

Bear in mind that MVPS is still a hotly debated syndrome, with some doctors questioning its mere existence. Herein, from firsthand experience, I will present my own definition. Eventually, I suspect that the medical community will define which symptoms are and are not associated with this condition.

By the way, some research has indicated that MVP may be inherited or spontaneous. However, according to Scordo (see book references below), it does not appear in babies at all, and thus develops as one's genome interacts with the environment over time. Perhaps this implies that MVPS follows the same pattern, although this is uncertain due to ambiguity in its definition.

So call me Mitral Mike. In 2006, I was diagnosed with mitral valve prolapse using an echocardiography, which essentially means that I have leaky heart valve.

The events leading up to this diagnosis, and following it for about a year, constituted the hardest and most terrifying part of my life. Perhaps I'll tell you my story later, but right now, I'd rather focus on helping you get well.

Let me begin by telling you the bottom line: In April, 2007, I ended up on the floor of my apartment, hyperventilating intensely for probably half an hour, with my vision gradually going blurry at the periphery, and tightness in my chest. I could hardly breathe. I could hardly move. Waves of terror radiated through my brain, each one passing like a suffocating wave. I clawed my way across the floor to my cell phone, and struggled to dial my friend's number.

Now, in January 2009, I live profoundly free of fear, in a way which I never imagined humanly possible even before my diagnosis; and the symptoms of my MVPS are rare and fleeting, and though they may startle me, do not result in persistent panic. I can tell you how I accomplished the first part, but you probably won't believe me, so let's just focus on the clinical stuff that we can address empirically, which I hope will help you manage your symptoms.

Consider the following books as essential supplemental reading. I'd suggest reading the Scordo book before the Hendricks book. Jointly, they started me on the path to wellness, which I have gradually augmented with my own symptom management techniques, often based on tips from discussion sites on the internet. (Not everything on the Web is junk, you know. You have to experiment and research carefully for yourself.)

Suggested Reading


1. Taking Control: Living with the Mitral Valve Prolapse Syndrome by Dr. Kristine A. Scordo

2. Conscious Breathing: Breathwork for Health, Stress Release, and Personal Mastery by Gay Hendricks, PhD


Because MVP is comparatively well-defined and understood, this blog is mostly about MVPS. In my view, MVP is one of many symptoms of MVPS. However, because heart valves are easy to analyze scientifically, compared to "panic attacks" or the other subjective symptoms of the latter, the former was deemed the disease, and the latter, one of its side effects . In reality, I think that a small set of genes is the cause, and the heart valve anomaly just happens to be the most obvious effect. Frankly, I would not be surprised if it turned out that decades of heart-pounding adrenaline attacks characteristic of MVPS contributed to the heart valve pathology that is MVP. (However, MVPS cannot be the entire cause of MVP, as we do know that MVP is also associated with a connective tissue disorder, which would at least partly explain the infirmity of the valve leaflets, and thus perhaps their susceptibility to damage by adrenaline-induced heartrate acceleration.)

As this article from Emedicine puts it:

"Besides the symptoms attributable to the MR, various neuroendocrine and autonomic disturbances occur in some patients with mitral valve prolapse. In these patients, prolapse may be an epiphenomenon of the underlying autonomic or neurohumoral illness. The term mitral valve prolapse syndrome is often used to refer to the collection of these manifestations. However, in a significant proportion of patients, the mitral valve prolapse is trivial, and no such associated manifestations are present. In these patients, mitral valve prolapse constitutes an essentially benign condition."

Common MVPS Symptoms


1. MVP.

You can have all the other symptoms of MVPS, and not have MVP. Or occasionally, the reverse may be true. This is further evidence that there is a common genetic cause to most aspects of MVPS, including MVP; MVP does not cause MVPS and visa-versa, perhaps with exception of adrenaline-induced valve pathology, about which I conjectured above.

2. "Head spins" and "mental resets".

Sudden disorientation, lasting about a second, and directly pursuant to
premature ventricular contractions
(PVCs).

I am not talking about syncope (fainting), although this does occur in a minority of patients. When these events occur, I get the sensation that time has skipped a fraction of a second, and perhaps the room is spinning for this brief moment. The spinning is not persistent, as would be the case with vertigo. Most likely, the "time skippage" is due to the brain reacting to a very unexpected sudden alteration in the heart rhythm, which has the side effect of temporarily suppressing conscious thought. (After all, it's well known that our thought processes largely switch off in emergencies; to the uneducated brain stem, a change in heart rhythm is definitely an emergency.) The more severe PVCs, when I used to get them (I get only little ones now), could jolt my brain so hard that I'd forget the last few seconds of thoughts.

I'm not kidding about this. One night, when I was having massive and frequent PVCs, I did a little experiment: I would think of several words, and imagine corresponding images in my mind. For example, I would think "apple" and simultaneously see an apple in my mind's eye. Then, as soon as I realized that I had suffered a PVC, I would go back and try to remember the last 5 words. Again and again, I would remember only the first 3 or 4; it was always the last word(s) that were missing -- those which I was thinking about at the time of the PVC. It would appear that these head spins have the effect of hitting the reset button on shortterm memory, which would certainly explain the perception of "time skippage".

If you're wondering whether these events are due to something else, I've had 3 full brain MRIs. Except for a spot which was tracked by 3 neurologists and found to be benign (perhaps the result of a bicycle accident when I was younger), no pathology is evident, such as an arteriorvascular malformation, which might otherwise explain the above. And these events are 100% correlated to a time period of about 5 seconds after the sensation of a PVC in my chest. Case closed.

I've also considered that, because PVCs are preceded by "weak beats", i.e. the heart beats once very hard in order to compensate for the previous beat being too weak, it's possible that the head spins are actually due to temporary brain hypoxia. While you can hold your breath for much longer, and still think clearly, it's possible that the temporarily reduced blood pressure associated with a PVC causes brain hypoxia much more rapidly, resulting in the perceptions described above. But as I mentioned above, I think there is a second mechanism at work, which is the brain stem's obsession with perfect heartbeat: the strange sensations are partly due to the brain stem briefly switching into panic mode, then (usually) back out of it, in response to an unexpected irregular heart beat. Occasionally, particularly with larger PVCs, the brain stem fails to exit panic mode, in which case cognitive thought processes remain suppressed, and a full-fledged panic attack (discussed below) may ensue. In any event, PVCs are merely one of many causes of MVPS panic attacks, the latter being discussed more below.

3. Orthostatic hypotension (or more generally, low blood volume).

If you feel light-headed when you stand up quickly, you may simply have too little blood in your system to keep your brain fully oxygenated during this exercise. Your heart may beat more rapidly (tachycardia) in order to compensate, but it may be unable to do so quickly enough due to the leaky valve. In some sense, this is a desirable condition, since it may imply that you have low blood pressure (which I think is a better problem than high blood pressure).

There are a few easy measures you can take to mitigate this problem:

(1) As you rise from your chair or bed, inhale over the course of the rise. This creates increased pressure in your chest, which tends to sustain higher blood pressure. Actually, fighter pilots use a similar technique to maintain consciousness during high-G-force manoeuvers: they wear "G pants", which squeeze their legs at the proper time in order to prevent their blood from draining from their heads to their feet. Thus, by inhaling over the course of a few seconds as you stand up, the increased blood pressure will help keep blood in your brain.

(2) Stand more slowly. If 2 seconds is too fast, take 3. Or 5.

(3) Keep hydrated. For one thing, this means that you always have sufficient liquid in your body for optimal performance. As a result, your blood volume is larger, which means that the pressure will be slightly higher, allowing you to more easily maintain brain oxygenation as you stand. But make no mistake: hydration isn't just about water! You need salt (and, in my opinion, a proper balance of all required trace minerals). You also need sugar. (For all the bad press that it has received since Dr. Atkin's diet, sugar not only keeps you alive, it induces insulin to open your cell membranes, allowing nutrients to go where they are needed. For this reason, I think it's better to eat superfruits like berries, followed by your morning workout; than complex carbs like beans, followed by you sitting at a desk, or worse, going to bed. I also think caloric restriction is superior to a calorically unrestricted low-carb diet. Anyway, remind me if I forget to post my Atkins rant!) For now, just remember: hydration is critical to the management of orthostatic hypotenion and MVP itself, but hydration does not mean binging on distilled water!

4. Intermittant and migratory chest pain.

If you have any sort of chest pain, you need to identify the cause immediately in order to rule out life-threatening conditions. Just because your chest pain is characteristic of MVPS does not mean that it's due to MVPS.

Anyway, MVPS chest pain seems to focus on certain areas -- in my case, the upper right pectoral muscle, and occasionally the right side of the sternum -- but grow, shrink, and move from time to time.

Most doctors seem to be convinced that MVPS chest pain does not come from MVP. Indeed, there is a small (but in my opinion, still meaningful) statistical significance to the number of MVP sufferers reporting chest pain, compared to non-MVP-sufferers. (See Scordo's book, and of course Google, for the numbers.)

I would say, incontrovertably from my own experience, that chest pain can indeed result from MVPS. I say "incontrovertably" due to the evidence of precise time correlation: my chest pain would be worst immediately following an adrenaline burst. Think about it: an MVPS-induced adrenaline burst is associated with an increase in sympathetic nervous system activity, which results in an increase in pain sensitivity (i.e. never take caffeine before a visit to your dentist); second, adrenaline bursts pound on the cardiac and respiratory system, rather like flooring the accelerator of one's car, inevitably resulting in aches in the chest.

Most doctors say that MVP does not cause chest pain. There is some evidence that MVP does cause chest pain under certain pathological conditions, potentially due to mechanical stress on the valve or the heart's attempt to compensate for lower efficiency. Nonetheless, I think that most MVP sufferers who experience chest pain do so due to MVPS-related hyperadrenalization, and not MVP.

In my case, the evidence could hardly be more compelling: when the adrenaline burst occurs, the pain flares up; both usually subside within a minute. This is a clear correlation between the MVPS-induced adrenaline bursts and chest pain. But the relationship goes deeper than that:

Sometimes, however, post-burst pain would remain for hours, occasionally giving rise to the sensation of a heart attack. Why? In my case, which is no doubt not unique in this regard, it would persist because I had consumed large doses of inflammatory foods the same day: sugar, simple carbs, or (especially) cheeses (including cottage cheese).

Cheeses, in particular, seem not only to cause more lasting chest pain, but also an increased incidence of PVCs. The lasting pain may result from the high omega-6 content in cheese, which is proinflammatory. Cottage cheese contains more protein and less omega-6, but it causes increased PVCs as well, if not extended chest pain. I could be wrong about the omega-6 theory. But test it yourself: cheese of any type will result in increased PVCs within 6 to 12 hours (or if you already eat it, cut it out for a few days and monitor the effect). There's something in these dairy products which causes this. To a lesser degree, the same happens with milk. Omega-9-rich olive oil, and omega-3-rich fish and flaxseed oil, do not have this effect. Coconut milk, which is rich in saturated fat but is not a dairy product, seems to produce little or no increase in PVCs. Thus, perhaps, it's something else. Lactose? I don't know, but the effect is unmistakable.

Frankly, it might not be a chemical issue so much as a blood thickness issue: eating dairy products may increase blood viscosity, in particular by raising plasma triglycerides. Thicker blood puts more hydrodynamic drag on the valve leaflets. This is the main reason why boats move more slowly than airplanes: water is much more viscous than air. So axe the cheese from your diet, and closely monitor the effect on PVC number and severity. Cutting out cottage cheese, milk, and coconut milk may also help to some extent, but potentially to the detriment of your calcium and protein intake. (I take "Tums" as a supplement after breakfast, but no dairy products or coconut milk, and hardly ever have PVCs anymore.)

Interestingly, when I eat organic peanut butter, I do not experience an increase in PVCs, despite the obvious high viscosity and high omega-6 content of this food. This may be due to: (1) the fact that I pour off all the peanut oil into the trash before eating the "dry" butter, (2) the fact that it's rich in niacin, which is good for the heart, and (3) its high vitamin E content, which is antiinflammatory. By the way, organic peanut butter contains large amounts of the antioxidant, p-coumaric acid, which is actually increased by the otherwise oxidative roasting process used to produced roasted peanut butter.

Superdark (85%+) chocolate bars also do not cause me increased PVCs, despite having a high saturated and omega-6 fat content. This is consistent with the generally accepted principle that the moderate consumption of dark chocolate (particularly the nonalkalized variety) is conducive to cardiac health. But this would appear to contradict my theory that PVC intensity and frequency relate primarily to blood viscosity. However, superdark chocolate probably does not significantly increase plasma tryglycerides. Hmm... maybe my "Triglyceride-Induced PVC" theory is true.

My worst bout of chest pains ever, followed by a horrendous hyperventilating panic attack, was preceded by a night of gorging on pizza cheese without the crust. (What do you do when you're on a low-carb diet, and you're out with the guys, who have nothing to offer you but pizza? Smart answer: starve. Dumb answer: gorge on mozerrella, and flirt with disaster.)

5. Panic attacks.

These events are characteristically preceded by the sensation of a wave or cloth washing through the entire head for about a second, most perceptible on the face, and may or may not have an obvious environmental cause.

Many doctors (who no doubt do not have MVPS themselves) think that the panic attacks associated with MVPS are somehow indirectly due to the patient becoming anxious about his/her newly identified "heart problem". While such a discovery, however benign, might make anyone anxious, I can tell you from deeply personal, visceral experience that the "bad" news is not the cause of the panic attacks. Having analyzed myself under conditions of sudden extreme terror (which I assure you, is possible, albeit difficult), they result largely from one of the following causes:

(1) a PVC which temporarily interrupts normal blood rhythm to the brain, triggering some sort of massive sympathetic nervous system response in the brain stem, as suggested by the recent discovery that the brain monitors the heart rhythm with a level of diligence hidden to our conscious mind, to which I alluded in the above discussion of head spins;

(2) a sudden change in electrolyte balance, as by ingesting a large dose of potassium (e.g. low-sodium vegetable juice or several bananas) or highly bioavailable iron (e.g. eating a vitamin pill on an empty stomach, or eating more than 100g of dark chocolate in a day);

(3) a sudden change in body fluid volume (and probably therefore blood pressure and electrolyte concentration), as by urinating or donating blood;

(4) a very light wind which cools and tingles the skin, and thus mimics, to the unconscious mind, certain perceptions of electrolyte imbalance;

(5) the memory of any of the foregoing;

(6) the consumption of large amounts of chocolate (especially dark or organic) or walnuts, both of which produce migraine with aura in sensitive individuals, triggering fear and panic, and entirely separate from the bioavailable iron panic pathway related to the former.

6. Unusually flexible joints.

This is most obvious in the fingers. This is the connective tissue anomaly so often mentioned in MVPS literature. In the presence of chronic stress, it probably aids the gradual deformation of the valve, which ultimately manifests as MVP. According to Scordo's book, essentially no one is born with MVP; it develops as one ages. My theory is that when one combines the frequent adrenaline bursts of MVPS with overly stretchable connective tissue, then the result is eventually a floppy valve that doesn't quite snap shut. It's kind of like stretching a rubber band too many times; eventually, it becomes less inclined to snap back into its original shape.

It would be interesting to study whether teaching children with MVPS to suppress excessive adrenaline releases would manifest in a lower rate of MVP later in life. I guess the medical community must first decide on a clinical definition of MVPS!

More on adrenaline bursts below.

7. A depressed or indented sternum -- a "breast bone valley".

8. Scoliosis.

9. A straight spine, which I take from the literature to mean a spine without concavity at the base.

10. Electrolyte hypersensitivity.

Sensitivities to sudden changes in electrolytes, particularly involving potassium or iron, as discussed above. Critically, if you have MVPS, do not donate blood before speaking to your doctor. If you have the low blood volume typical of many MVPS sufferers, it could cause you to faint in response to blood donation. (It happened to me in 2004, at a blood drive at work. I wondered, at the time, why I couldn't tolerate the process as well as much much less fit colleauges!)

My first bout with electrolyte sensitivity was in around 1998. I had just had a visit to the dentist. During this particular visit, the dentist removed a number of mercury-silver fillings. Even today, dentists continue to use mercury-silver amalgum in fillings because they assert that they leach only trivial amounts of mercury. I might agree, but when they're heated and aerosolized during removal, I think it's possible that a dangerous amount of mercury is released.

Now, I knew about this threat, and knew that it might be preempted by injesting a vitamin pill (to thwart further mineral absorption) and vitamin C (which chealates heavy metals). However, I forgot to take either before the appointment. So immediately afterward, I headed to the nearest drug store and bought a bottle of vitamin pills, as I was on the way to work, and had no time to return home.

When I arrived at work, I ingested 3 vitamin pills in rapid succession. (DO NOT do this.) Worse, on account of the dental appointment, my stomach was empty. So an hour or so later later, I had something like 300% RDA of iron (beyond the tolerable upper intake level) flowing around in my blood.

Rapidly, my skin became numb at the surface, causing a "pins-and-needles" sensation. Though I may have made some slight progress in inhibiting the blood plasma uptake of mercury from the intestines, I had given myself some level of iron poisoning. I spent the next hour or so slowly and carefully sipping water, and urinating myself back to homeostasis.

Nowdays, I keep a 7-day pill organizer full with all my supplements, including multivitamins, to ensure that I get sufficient but not excessive nutrition. I even break my vitamins into a couple pieces for ingestion at different times of day, in order to maintain more stable plasma electrolyte levels and systemic hydration.

11. Chest tightness.

Diffuse but possibly intense, often mistaken for anxiety-related chest tightness, but persistent for days at a time, and only marginally relieved by sleep.

This tightness is constricting, rather like wearing a sweater that is much too small. However, it is distinct from the migratory chest pain described above.

This was one of the worst symptoms of my MVPS. I think, in my case, it related to the onset of sleep apnea which went undiagnosed for years, for which I have since received corrective surgery. It would not surprise me if there were a correlation between MVP, MVPS, and sleep apnea, as the latter increases adrenaline stress on the heart, and contributes to panic disorder, on account of terrifying hypoxic episodes.

Here's how I fixed my chest tightness, which at times was so intense that I could hardly get enough air to walk (this, after being a near-Olympian just days prior to the hyperventilation attack in April, 2007 that started the tightness): I tried all manner of foods -- eating more or eating less -- trying to discover a cause or find relief. Finally, after months of work, I discovered that salmon, milk, and shiitake mushrooms -- and nothing else in my diet -- relieved the condition to some extent; milk was the fastest. Truly perplexed by how these radically different foods were acting in a common way, I did some homework.

But first, I sought professional help. I had several doctors tell me that it was all just stress-related. In a sense, they were correct: MVPS was stressing out my autonomic nervous system, resulting in this problem. But in the sense of anxiety, they were wrong. I felt happy most of the time. In fact, I could generally breathe better when I was angry, perhaps due to improved respiratory function under the influence of adrenaline. On the other hand, I could be perfectly content with life, and the tightness would be there. The severity was mostly dependent on whether or not I was asleep, and on how recently I had had one of these "magic foods". It was also somewhat better in the morning than the evening. The worst tightness was immediately after exercise, suggesting that it had something to do with hydration, blood pressure, and electrolyte balance.

It turns out that the magic foods are all excellent sources of vitamin D (as D2 or D3), which is otherwise very hard to obtain (except from solar exposure). Somehow, vitamin D was allowing me to get some degree of chest tightness relief. Not surprisingly, I was subsequently diagnosed with a vitamin D defficiency (18, where optimal is something like 40-60, depending which study you read). (Just in case you think the docs always have the answers, I was the one who suggested the test, based on my empirical analysis. Sure enough, I was short on vitamin D.)

Using 800IU daily supplements, I cured the defficiency over a period of months. However, the tightness persisted to some extent. That's when my friend introduced me to Hendrick's book about breathing, noted above. Combined with yoga, it completely fixed the problem. My chest is so relaxed now that I no longer practice yoga, but I probably should. In fact, for a while, I was so relaxed that I had to encourage myself to adrenalize a bit on the highway, for safety reasons. As far as I can tell, these focussed exercises allowed me to reprogram my breathing rhythm, reducing the tightness.

The final piece of the solution was getting surgery to alleviate sleep apnea. With a wider airway, I was no longer struggling to breathe during the daytime, and my chest tightness has never returned since.

12. Adrenaline bursts.

These events occur seemingly without cause, manifesting in a pounding heart, as though you is about to crash your car, when in fact you may be relaxing on the beach. If you have these, check with your endocrinologist for other rare conditions such as adrenal tumors. But likely as not, this is just MVPS. I used to have these, until intensive self-monitoring allowed me to intervene and arrest them before they could occur.

Everyone gets adrenaline bursts when they're nervous. They are an important part of our fight-or-flight mechanism: if a tiger is about to eat you, it's time to run! Psychologists have long known that this ancient wiring causes stress reactions in our bodies today, despite the fact that we don't need to run from a dentist, or use super strength to invest in a crazy stock market. In short, our wiring has not kept pace with the shift in the nature of our threats, from physical to psychological.

The adrenaline bursts characteristic of MVPS are similar to anxiety-related adrenaline releases, but they are overexpressed. And typically, many more occur per day than one's stress load would otherwise suggest. For example, I would get terrifying heart poundings every time the phone rang. I would, of course, calm down, but not before slamming my heart valve and respiratory system for this completely unjustifiable reason. At my worst, I had probably a thousand perceptible spikes per day, which on average is one every several seconds for many hours.

Low-carb diets are often touted as a solution to such hyperadrenalization. In my case, it only made things worse. The reason, I think, is that hydration is difficult with these diets because the high fat content inhibits the absorption of water-soluble nutrients, particularly in the absence of sugar. At the time, I didn't realize this. As a result, no doubt, my electrolyte concentrations varied much more throughout the day than they should have, which no doubt contributed to the problem.

Positive imaging is commonly suggested as a solution: psychologists often tell us to imagine a beautiful beach scene when we're under immense stress. I think this only causes more stress, as it reminds us that we might not survive long enough to get there! In my case, it offered no help at all.

One of the most significant improvements came with medical hypnosis. I went to a medical hypnotist who, believe it or not, was recommended by my endocrinologist who did the vitamin D test. After a single session, I experienced approximately a 75% reduction in daily adrenaline spike count. It cost $300, but in my case, was highly effective. Part of the reason for my success is that I knew that the spikes were almost never justifiable, and thus had an irrational basis of activation, likely related to subconscious activity in the brain stem. Because I knew that the response was irrational, it was easier to combat with the help of a hypnotist; otherwise, I am virtually immune to hypnosis. After yoga and certain mental focus exercises, my adrenalization dropped so low that, as I mentioned above with regards to chest tightness, I had to struggle to adrenalize enough to avoid traffic accidents!

One other technique for minimizing adrenaline bursts may be to eat garlic or garlic gelcaps. There is ample evidence that they lower blood pressure, and seem to promote mood stability, perhaps via seretonin regulation. I haven't done much research on this, but I've read enough on reputable websites to recommend that you research it. At the very least, it might make your dinner taste better.

13. Plasma magnesium defficiency

According to this 1997 study, some cases of MVP are caused by plasma magnesium defficiency. Though magnesium defficiency as examined in the study is strictly a cause of MVP and not MVPS, I suspect that it also relates to the latter, as magnesium is critical for neurological function, implying that defficiency may contribute to the hyperadrenergic symptoms observed in MVPS sufferers. Note that the study does not say "insufficient dietary intake of magnesium", but rather refers to plasma (blood) levels of the element. So while you may get sufficient magnesium in your diet, it may or may not end up in your blood, depending on how well it is absorbed with the rest of the food that you eat.

My magnesium level is normal. However, I didn't test it until long after I had started occasional supplementation. So I don't know whether it was one of the causes of my MVPS.

Back in 2007 or so, I found a nurse on an MVPS discussion board who recommended magnesium glycinate as an MVPS treatment. Intrigued, I tried some.

For me, this stuff kills palpitations within an hour. It's incredible. In particular, I took a 200mg dose, which is 1 tablet. (The bottle says "400", but the serving size is 2 tables. Is this dangerous, or what?)

However, before you try this yourself, I would suggest that you try my other suggestions for eliminating palpitations, including cardiovascular exercise as recommended by your cardiologist. The reason is that we were not evolved to ingest pure concentrated minerals. Therefore, these tablets are hard on the kidneys, which are responsible for electrolyte balance. Also, like other magnesium supplements, they tend to cause mental confusion if used in sufficiently high doses for sufficiently many days in a row. The effect seems stronger than with magnesium oxide, which is likely due to the glycinate component: I believe that the glycinate allows the magnesium to penetrate neurons, including those in the brain, much more easily. For this reason, it may be equivalent, in a neurological sense, to a much higher dose of magnesium oxide.

Here's what the National Institutes of Health has to say about magnesium. In particular, see their comments on excess intake. Again, I think magnesium glycinate may be neurologically equivalent to several times as much magnesium oxide.

From my perspective, it beats the side effects of beta blockers. Therefore, on the rare occasion that I have palpitations, I take one of these.


           CARDIOLOGIC ABNORMALITIES IN NOONAN SYNDROME - PHENOTYPIC DIAGNOSIS AND ECHOCARDIOGRAPHIC ASSESSMENT OF 118 PATIENTS         
BURCH, M; SHARLAND, M; SHINEBOURNE, E; SMITH, G; PATTON, M; MCKENNA, W; (1993) CARDIOLOGIC ABNORMALITIES IN NOONAN SYNDROME - PHENOTYPIC DIAGNOSIS AND ECHOCARDIOGRAPHIC ASSESSMENT OF 118 PATIENTS. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY , 22 (4) pp. 1189-1192.
           Investigation of vascular compression of the trachea: the complementary roles of barium swallow and echocardiography.         
Burch, M; Balaji, S; Deanfield, JE; Sullivan, ID; (1993) Investigation of vascular compression of the trachea: the complementary roles of barium swallow and echocardiography. Arch Dis Child , 68 (2) pp. 171-176.
          Fetal Echocardiography Accreditation        

Perinatal Assoicates of New Mexico was awarded the Fetal Echocardiography Accreditation by the AIUM.

The post Fetal Echocardiography Accreditation appeared first on PANM.


          Cardiac Screening in High School and College Aged Athletes        
Beth Druvenga, M.S. Ed, LAT, ATC

Posted March 3, 2017

By Beth Druvenga, M.S. Ed, LAT, ATC

The inherent risk of injury when participating in some form of competitive athletics is widely accepted. Athletes suffer sprains, strains, concussions, fractures, contusions and lacerations to name a few injuries. A risk not so widely accepted is the risk of sudden cardiac arrest (SCA) or sudden cardiac death (SCD).

We have all seen the stories on the news or read the articles: A young athlete gone too soon. Athletes are in shape and generally in good health; they are not supposed to be participating one minute and unresponsive the next. As an empathetic, reasoning and rational culture, we cannot accept young lives being taken unexpectedly during athletic participation. But, it does happen. As an Athletic Trainer (AT) there is a list of potentially fatal events which may occur every day. I have to take a time out before games to internally review my emergency action plan (EAP), to prepare myself for the worst.

According to a 2011 study by Harmon et al., “SCD is the leading medical cause of death in NCAA athletes, is the leading cause of death during sport and exercise, and occurs at a much higher rate than previously accepted.”1 Hypertrophic cardiomyopathy and coronary artery anomalies account for 53 percent of all sudden cardiac deaths.2 Universally, professionals in the cardiac and sports medicine world alike have a common goal of preventing sudden cardiac death in athletes.4

To help prevent SCD, scientists and researchers have encouraged cardiac screening as a tool to detect underlying cardiac disorders and take the necessary steps for prevention. In fact, the Fédération Internationale de Football Association or International Federation of Association Football (FIFA) and the Union of European Football Associations (UEFA) have made cardiac screening mandatory before competition, and the International Olympic Committee encourages it as best practice.3 However, in the United States, only the National Basketball Association (NBA) mandates electrocardiograms (ECGs) or echocardiography annually.2

In Italy and Israel, it is required as part of a pre-participation examination (PPE) to have a cardiac screening.4 While in the United States a PPE involves a medical questionnaire and physical examination by a healthcare professional.2 And although the American Heart Association (AHA) supports pre-participation cardiovascular screening, it also acknowledges that it is not practical in mass context or nationwide mandate, due to the cost being an estimated 2 billion dollars per annum. Thus, the question remains. How do we move forward?

Until a nationwide, homogenous standard for cardiovascular screening is established for all high school and college aged athletes, take a look at some ways to combat SCA and SCD.

- Review your PPE questionnaire to confirm it includes questions the AHA supports for detection of potential cardiovascular disorders. Verify that these exams are being performed by a physician, nurse practitioner or physician assistant; someone who is trained and comfortable with detection of cardiovascular problems. According to the AHA, there is an increasing trend of states allowing chiropractors and naturopaths to perform PPE screenings, though they lack the cardiovascular screening training.2

- Review your facility’s EAP with not only your sports medicine staff but with people in the building who will be present when the EAP is put in to action. I am certain there are coaches and administrators who receive their EAPs but fail to read them and are not familiar enough to confidently put them into action.

- Get an automated external defibrillator (AED). I repeat, get an AED! Early defibrillation is essential during SDA to increase the chances of survival. If your school doesn’t have an AED, there are many grants and resources available to assist you in acquiring one.

- Consider providing cardiac screening for your school. There are many companies that perform cardiac screening, so reach out to your community and see what is out there. The most basic cardiac screening consists of a 12-electrode ECG which analyzes resting heart rhythm. This can help detect cardiac anomalies which may require further testing.

You, as an AT, are the best resource. Advocate for your athletes. I know ATs who have lost a student athlete to SCD. My hometown lost a student athlete to SCD during a wrestling tournament a little over a year ago. It all begins with YOU. Do your research to help prevent SCD and protect your athletes. Below are resources for cardiac screening and resources for AED grants, and I urge you to utilize them.

Cardiac Screening Resources

Parent Heart Watch: https://parentheartwatch.org/events/

AED Resources

Sudden Cardiac Arrest Foundation: www.sca-aware.org/school/funding-sources

References

1. Harmon, K., Asif, I., Klossner, D., & Drezner, J. (2011). Incidence of Sudden Cardiac Death in National Collegiate Athletic Association Athletes. Circulation, 1594-1600.

2. Maron, B., Thompson, P., Ackerman, M., Balady, G., Berger, S., Cohen, D., et al. (2007). Recommendations and Considerations Related to Preparticipation Screening for Cardiovascular Abnormalities in Competitive Athletes: 2007 Update. Circulation, 1643-1655.

3. Schmied, C., & Borjesson, M. (2013). Sudden cardiac death in athletes. Journal of Internal Medicine, 93-103.

4. Steinvil, A., Chundadze, T., Zeltser, D., Rogowski, O., Halkin, A., Galily, Y., et al. (2011). Mandatory Electrocardiographic Screening of Athletes to Reduce Their Risk for Sudden Death: Proven Fact or Wishful Thinking? Journal of the American College of Cardiology, 1291-1296.


          Would ECHO testing during the PPE prevent sudden cardiac death?        
Mike McKenney, MS, ATC

Posted November 2, 2016

By Mike McKenney, MS, ATC

During the pre-participation examination (PPE), many healthcare practitioners employ a traditional cardiac questionnaire and physical examination to detect potential abnormalities and other serious medical conditions that may impact safe participation in sport. However, a physical examination and history are not always sufficient to detect abnormalities of the heart that can result in sudden cardiac death (SCD). More recently, there has been increasing support for broader implementation of electrocardiograph (ECG) testing at all levels of sport. This includes attempts to mandate ECG testing for all high school athletes. Barriers to mandatory ECG testing typically revolve around cost, but there are other factors to consider before requiring this form of screening in an athletic population.

The intended purpose of an ECG is to assess electrical activity of the heart and assist clinicians in determining if a cardiac abnormality is present, whether it be genetic, structural or conductive in nature. However, only 3 percent of cases that result in SCD are of conduction-related causes.1, 2 In young, competitive athletes, structural abnormalities represent the largest percentage of SCD, 84 percent of reported cases,1 which includes conditions such as hypertrophic cardiomyopathy (HCM). Simply put, mandating ECG testing in sport may not be the best step forward due to the test’s limitations in screening for the primary causes of SCD.

The difficulty in utilizing ECG to detect structural abnormalities is reflected in a high false-positive rate due to detection of cardiac adaptations regularly found in trained athletes,1, 3 and other variations that are common with normal cardiac rhythm.3Furthermore, ECG lacks the specificity to reliably detect HCM,3 which is a condition that is largely asymptomatic until an SCD event occurs.2 Additionally, results can be interpreted differently between physicians if consistent standards are not being applied.4 Due to the aforementioned factors, athletes are often subject to unnecessary referrals for further screening that often turn out to be of no concern,4 and add further cost to the evaluation process.2

Echocardiograms (ECHO) are the gold standard for visualizing the heart and are what athletes typically receive when referred to a cardiologist for advanced evaluation. Traditionally, the ECHO is performed in a cardiologist’s office. However, with advances in portable ultrasound technology, there is an emerging application for ECHO testing to be conducted by a front-line physician at a school’s sports medicine facility.2 At Northeastern University, a study5 was conducted utilizing this procedure and found that referral to a cardiologist was reduced by 33 percent. There were no differences between measurements obtained by the school’s physician and an outside cardiologist. In addition, research currently in review found the portable ECHO procedure to be significantly quicker than a traditional history and physical or ECG.2 This finding could potentially lead the way to a more thorough and efficient PPE process.

The costs associated with cardiac screening will always be a point of contention, but results of the previously discussed research are going to shift the discussion in a new way. It is not yet known if on-site portable ECHO testing will be a cost saving measure.  However, in theory, a reduction in unnecessary referrals should reduce the overall cost of screening. Moreover, clinicians will have the added benefit of being able to visualize conditions that can result in SCD, instead of trying to infer their presence from electrical activity alone. If we are to continue advocating for access to advanced cardiac screening, future efforts should be focused on methods and services that provide a more efficient and accurate assessment.

Resources

1. Maron BJ, Thompson PD, Ackerman MJ, et al. Recommendations and considerations related to preparticipation screening for cardiovascular abnormalities in competitive athletes: 2007 update: a scientific statement from the American Heart Association Council on Nutrition, Physical Activity, and Metabolism: endorsed by the American College of Cardiology Foundation. Circulation. 2007;115(12):1643-1455.

2. Kerkhof D, Gleason C, Basilico F, Corrado G. Is there a role for limited echocardiography during the preparticipation physical examination?. PM & R: The Journal of Injury, Function, And Rehabilitation. March 2016;8(3 Suppl):S36-S44.

3. Maron B, Friedman R, Thompson P, et al. Assessment of the 12-lead ECG as a screening test for detection of cardiovascular disease in healthy general populations of young people (12-25 Years of Age): a scientific statement from the American Heart Association and the American College of Cardiology. Circulation.2014;130(15):1303-1334.

4. Hainline B, Drezner J, Thompson P, et al. Interassociation consensus statement on cardiovascular care of college student-athletes. Journal Of The American College Of Cardiology. 2016;67(25):2981-2995.

5. Yim E, Basilico F, Corrado G. Early screening for cardiovascular abnormalities with preparticipation echocardiography: utility of focused physician-operated echocardiography in preparticipation screening of athletes. Journal Of Ultrasound In Medicine: Official Journal Of The American Institute Of Ultrasound In Medicine.2014;33(2):307-313.

About the Author

Mike McKenney is an Athletic Trainer (AT) at Northeastern University in Boston, Massachusetts, where he is the Medical Coordinator for their Division I men’s ice hockey program.  Prior to Northeastern University, he served as an AT in multiple settings including secondary schools, Division I athletics and professional cycling; additionally, he worked as an AT who extends the services of a physician for a large orthopedic group.  He has also provided services for many organizations to include the Boston Marathon, USA Cycling and USA Volleyball.

McKenney is a hydration and electrolyte replacement consultant for the Atlanta Hawks of the NBA.  His professional interests include hydration, electrolyte replacement, thermoregulation in sport and postural restoration.  McKenney completed his athletic training education at Gustavus Adolphus College in Saint Peter, Minnesota and master’s degree at North Dakota State University in Fargo, North Dakota.  His graduate research was published in the February 2015 edition of the Journal of Athletic Training.

 


          Echocardiography Technician - Cardiology - PRN - Days - WellSpan Health Services - Gettysburg, PA        
Contacts Biomed Department for major malfunctions. Under the general supervision of the Medical Director &amp; the Manager-Noninvasive Cardiology, and the...
From WellSpan Health Services - Sat, 15 Jul 2017 05:34:45 GMT - View all Gettysburg, PA jobs
          New perioperative medicine pre-assessment clinic at London Bridge Hospital        
Dr O’Brien and Professor Schilling have worked together on these procedures for many years. They have all three areas continuously audited by auditors independent of the London AF Centre. The team reviews these results regularly and informed how they have evolved their practice to now offer excellent clinical outcomes, an excellent safety record and an excellent patient experience. For every procedure undertaken at the London AF Centre, Dr Ben O’Brien can offer a pre-assessment clinic to discuss all aspects of your peri-procedure care and answer any questions you may have. It is not uncommon to feel apprehensive ahead of a procedure and for those that prefer not to wait until the day of the intervention to speak with your anaesthetist- this may be the best option for you. Dr O’Brien will take you through the process step-by-step, explaining everything from admission to discharge. From the extensive feedback we receive, we have learnt that understanding all the facts before a procedure is reassuring to the patient and this service has been set up as a direct response to such feedback. Clinical outcomes, safety & optimal patient experience The consultation is based around your preferences, whether you come in to the hospital, or would choose to have the consultation via Skype (video link). The fee for such a separate consultation will be billed to your insurer. Should your insurance not cover it, please discuss the options with Dr O’Brien’s secretary, Mrs Melanie Todd (020 7234 2288 / melanie.todd@medicaladminservices.co.uk). Dr O’Brien is very keen to provide you with the best possible experience and will be happy to offer this service for a nominal self-pay fee, if there were any problems with insurance cover. If you do not wish to see Dr O’Brien ahead of your admission, he will of course come to see you on the day of the procedure and will explain all aspects of your perioperative medicine care then. No matter how you wish to proceed, Dr O’Brien and the rest of the team here at London Bridge Hospital have every confidence that together we can cover everything you need to know in order to help you feel as safe and comfortable as possible before your intervention. Dr O’Brien will discuss the options and agree a personalised perioperative care plan with you. The scope of Dr O’Brien’s Perioperative Medicine Practice includes: Transoesophageal Echocardiography (fully accredited by the European Society of Cardiology). Anaesthesia for cath lab interventional procedures and cardiac and thoracic surgical procedures. This covers the whole spectrum from sedation to General Anaesthesia. Pre-procedure optimisation and post-intervention care, including critical care and preventing or treating pain or nausea. Your care will be planned around your individual circumstances, such as allergies, previous problems with nausea, preferences between GA and sedation et cetera. Based on recent feedback we learnt that 97% said they were ‘very satisfied’ with the service (‘Satisfied’: 2%, ‘Neutral’: 1%, none were ‘Dissatisfied’/‘Very Dissatisfied’/‘Don’t know’: 0% !). 90% of patients did not experience any kind of pain or discomfort at all after the operation and only 4% said they experienced nausea, which in all cases could be swiftly treated. Below are some comments from patients who have undergone a procedure involving the general anaesthetic experience: “Very caring and compassionate to my condition. Provided me with confidence that I was in the right place with the right anaesthetist. Extremely professional and just glad that Dr O’Brien was in charge.” “Highly satisfied with no unpleasant side effects. A very comfortable experience.” “Excellent – I was very nervous but everything was clearly explained and the experience was extremely positive.” “Excellent pre-op briefing, including details about how nausea potential would be controlled. The actual experience matched the briefing perfectly.” “The team made me feel relaxed and confident in their care. Having met them I had total confidence in their ability of ensuring I had an excellent, comfortable experience.” We also ask patients to compare the different options of sedation and GA, for those who have also experienced both alternative options: “It was superb; I would choose general anaesthetic over sedation every time.” “Absolutely perfect. Zero hangover, about to leave and I feel fine.” “Excellent and professional. NO after effects – felt fine within 2 hours of the procedure.” “General anaesthetic was 100% improvement from the last two times when I was given local anaesthetic." For more information visit our AF Centre website on londonadcantre.london.
          Tricuspid Annular Plane Systolic Excursion (TAPSE)        

Due to the right ventricle’s (RV) unique geometry and cylindrical contraction pattern, assessing its function on echocardiography can be difficult. One of the more simple and reproducible techniques used to determine RV function is the tricuspid annular plane systolic excursion (TAPSE).  This is easy to do at the bedside using transthoracic echocardiography (TTE). After obtaining […]

The post Tricuspid Annular Plane Systolic Excursion (TAPSE) appeared first on RK.md.


          Penyembelihan Syari'at Islam vs Cara Barat        

Di bawah ini ada tulisan yang disadur dan diringkas oleh Usman Effendi AS., dari makalah tulisan Nanung Danar Dono, S.Pt., M.P., Sekretaris Eksekutif LP.POM-MUI Propinsi DIY dan Dosen Fakultas Peternakan UGM Yogyakarta.

Melalui penelitian ilmiah yang dilakukan oleh dua staf ahli peternakan dari Hannover University, sebuah universitas terkemuka di Jerman. Yaitu: Prof.Dr. Schultz dan koleganya, Dr. Hazim. Keduanya memimpin satu tim penelitian terstruktur untuk menjawab pertanyaan: manakah yang lebih baik dan paling tidak sakit, penyembelihan secara Syari'at Islam yang murni (tanpa proses
pemingsanan) ataukah penyembelihan dengan cara Barat (dengan pemingsanan)?

Keduanya merancang penelitian sangat canggih, mempergunakan sekelompok sapi yang telah cukup umur (dewasa). Pada permukaan otak kecil sapi-sapi itu dipasang elektroda (microchip) yang disebut Electro-Encephalograph (EEG).
Microchip EEG dipasang di permukaan otak yang menyentuh titik (panel) rasa sakit di permukaan otak, untuk merekam dan mencatat derajat rasa sakit sapi ketika disembelih. Di jantung sapi-sapi itu juga dipasang Electro Cardiograph (ECG) untuk merekam aktivitas jantung saat darah keluar karena disembelih. Untuk menekan kesalahan, sapi dibiarkan beradaptasi dengan EEG maupun ECG yang telah terpasang di tubuhnya selama beberapa minggu. Setelah masa adaptasi dianggap cukup, maka separuh sapi disembelih sesuai dengan Syariat Islam yang murni, dan separuh sisanya disembelih dengan menggunakan metode pemingsanan yang diadopsi Barat.

Dalam Syariat Islam, penyembelihan dilakukan dengan menggunakan pisau yang tajam, dengan memotong tiga saluran pada leher bagian depan, yakni: saluran makanan, saluran nafas serta dua saluran pembuluh darah, yaitu: arteri karotis dan vena jugularis.

Patut pula diketahui, syariat Islam tidak merekomendasikan metoda atau teknik pemingsanan. Sebaliknya, Metode Barat justru mengajarkan atau bahkan mengharuskan agar ternak dipingsankan terlebih dahulu sebelum disembelih.

Selama penelitian, EEG dan ECG pada seluruh ternak sapi itu dicatat untuk merekam dan mengetahui keadaan otak dan jantung sejak sebelum pemingsanan (atau penyembelihan) hingga ternak itu benar-benar mati. Nah, hasil penelitian inilah yang sangat ditunggu-tunggu!

Dari hasil penelitian yang dilakukan dan dilaporkan oleh Prof. Schultz dan Dr. Hazim di Hannover University Jerman itu dapat diperoleh beberapa hal sbb.:

Penyembelihan Menurut Syariat Islam

Hasil penelitian dengan menerapkan praktek penyembelihan menurut Syariat Islam menunjukkan:

Pertama, pada 3 detik pertama setelah ternak disembelih (dan ketiga saluran pada leher sapi bagian depan terputus), tercatat tidak ada perubahan pada grafik EEG. Hal ini berarti bahwa pada 3 detik pertama setelah disembelih itu, tidak ada indikasi rasa sakit.

Kedua, pada 3 detik berikutnya, EEG pada otak kecil merekam adanya penurunan grafik secara bertahap yang sangat mirip dengan kejadian deep sleep (tidur nyenyak) hingga sapi-sapi itu benar-benar kehilangan kesadaran. Pada saat tersebut, tercatat pula oleh ECG bahwa jantung mulai meningkat aktivitasnya.

Ketiga
setelah 6 detik pertama itu, ECG pada jantung merekam adanya aktivitas luar biasa dari jantung untuk menarik sebanyak mungkin darah dari seluruh anggota tubuh dan memompanya keluar. Hal ini merupakan refleksi gerakan koordinasi antara jantung dan sumsum tulang belakang (spinal cord). Pada saat darah keluar melalui ketiga saluran yang terputus di bagian leher tersebut, grafik EEG tidak naik, tapi justru drop (turun) sampai ke zero level (angka nol).

Hal ini diterjemahkan oleh kedua peneliti ahli itu bahwa: "No feeling of pain at all!" (tidak ada rasa sakit sama sekali!).

Keempat, karena darah tertarik dan terpompa oleh jantung keluar tubuh secara maksimal, maka dihasilkan healthy meat (daging yang sehat) yang layak dikonsumsi bagi manusia. Jenis daging dari hasil sembelihan semacam ini sangat sesuai dengan prinsip Good Manufacturing Practise (GMP) yang menghasilkan Makanan Sehat (Healthy Food).

Penyembelihan Cara Barat

Pertama, segera setelah dilakukan proses stunning (pemingsanan), sapi terhuyung jatuh dan collaps (roboh). Setelah itu, sapi tidak bergerak-gerak lagi, sehingga mudah dikendalikan. Oleh karena itu, sapi dapat pula dengan mudah disembelih tanpa meronta-ronta, dan (tampaknya) tanpa (mengalami) rasa sakit. Pada saat disembelih, darah yang keluar hanya sedikit, tidak sebanyak bila disembelih tanpa proses stunning (pemingsanan).

Kedua, segera setelah proses pemingsanan, tercatat adanya kenaikan yang sangat nyata pada grafik EEG. Hal itu mengindikasikan adanya tekanan rasa sakit yang diderita oleh ternak (karena kepalanya dipukul, sampai jatuh pingsan).

Ketiga, grafik EEG meningkat sangat tajam dengan kombinasi grafik ECG yang drop ke batas paling bawah. Hal ini mengindikasikan adanya peningkatan rasa sakit yang luar biasa, sehingga jantung berhenti berdetak lebih awal. Akibatnya, jantung kehilangan kemampuannya untuk menarik dari dari seluruh organ tubuh, serta tidak lagi mampu memompanya keluar dari tubuh.

Keempat, karena darah tidak tertarik dan tidak terpompa keluar tubuh secara maksimal, maka darah itu pun membeku di dalam urat-urat darah dan daging, sehingga dihasilkan unhealthy meat (daging yang tidak sehat), yang dengan demikian menjadi tidak layak untuk dikonsumsi oleh manusia. Disebutkan dalam khazanah ilmu dan teknologi daging, bahwa timbunan darah beku (yang tidak keluar saat ternak mati/disembelih) merupakan tempat atau media yang sangat baik bagi tumbuh-kembangnya bakteri pembusuk, yang merupakan agen utama merusak kualitas daging.

Bukan Ekspresi Rasa Sakit!

Meronta-ronta dan meregangkan otot pada saat ternak disembelih ternyata bukanlah ekspresi rasa sakit! Sangat jauh berbeda dengan dugaan kita sebelumnya! Bahkan mungkin sudah lazim menjadi keyakinan kita bersama, bahwa setiap darah yang keluar dari anggota tubuh yang terluka, pastilah disertai rasa sakit dan nyeri. Terlebih lagi yang terluka adalah leher dengan luka terbuka yang menganga lebar.!

Hasil penelitian Prof. Schultz dan Dr. Hazim justru membuktikan yang sebaliknya. Yakni bahwa pisau tajam yang mengiris leher (sebagai syariat Islam dalam penyembelihan ternak) ternyata tidaklah 'menyentuh' saraf rasa sakit. Oleh karenanya kedua peneliti ahli itu menyimpulkan bahwa sapi meronta-ronta dan meregangkan otot bukanlah sebagai ekspresi rasa sakit, melainkan sebagai ekspresi 'keterkejutan otot dan saraf' saja (yaitu pada saat darah mengalir keluar dengan deras). Mengapa demikian? Hal ini tentu
tidak terlalu sulit untuk dijelaskan, karena grafik EEG tidak membuktikan juga tidak menunjukkan adanya rasa sakit itu.

http://forum.detik.com/showpost.php?p=13323692&postcount=58
http://www.seputar-indonesia.com/edisicetak/content/view/405403/
          Stress-echocardiography is underused in clinical practice: a nationwide survey in Austria        
Background: The wide area of application, including coronary artery disease, valvular heart disease, or pulmonary hypertension makes stress echocardiography (SE) a powerful, cost-effective imaging modality in cardiology. The role of this technique in...
          Pemeriksaan Jantung Koroner Menggunakan BPJS        

 
                Oktober 2016 lalu, saya menjalani beberapa prosedur pemeriksaan penyakit jantung. Mulai dari masuk UGD, sampai proses kateterisasi jantung (angiografi koroner). Pengalaman saya bisa dibaca di sini dan di sini. Saya terdaftar sebagai peserta BPJS Non PBI, ikut suami saya yang PNS. Kelas rawat kelas I. Sebagian besar prosedur tersebut di-cover oleh BPJS.

Memancing Rujukan

Mengapa hanya sebagian? Karena pada awal sakit, permintaan rujukan saya sempat ditolak dokter keluarga. Alasannya, dokkel melihat kondisi umum saya baik, tak masuk kriteria sakit serius atau gawat. Padahal saat itu, saya merasa sesak di dada dan kesemutan di semua bagian kepala. Sambil minta maaf, dokkel menyarankan saya untuk periksa mandiri dulu. Jika nanti hasilnya menjurus ke sesuatu, baru dia bisa memberikan rujukan ke RS. 

Akhirnya, saya periksa mandiri ke dokter spesialis penyakit dalam di RSUD. Dokter tersebut, alhamdulillah, merespon serius keluhan saya. Saya diminta cek darah (gula darah sewaktu, asam urat, dan profil lipid - kolesterol total, trigliserida), foto rontgen dada/thorax (untuk mendeteksi pembesaran jantung), dan EKG (elektrokardiografi/rekam jantung). Total biaya Rp216 ribu rupiah.

Dokter mencurigai hasil EKG saya, didiagnosa iskemik (kekuarangan oksigen) pada jantung. Hasil lab, kolesterol total 20 poin di atas normal. Rontgen didapati gambaran bronchitis pada paru-paru. Lainnya bagus. Beliau menyarankan saya ke klinik jantung RSUP di Semarang. 

Nah, semua itu saya bawa ke dokkel. Barulah dokkel setuju bahwa saya sakit dan perlu pemeriksaan lanjutan. Saya diberi rujukan ke RSUD, menemui dokter sp penyakit dalam lagi, untuk kemudian dibuatkan rujukan ke klinik jantung RSUP dr. Kariadi Semarang. 

Jadi, bila Anda yakin Anda sakit, ada sesuatu yang salah dengan jantung Anda, namun tak cukup sakit sesuai kriteria rujukan BPJS, bisa coba tip ini: memancing rujukan. :(

Echocardiography/ECG, Treadmill Test dengan BPJS

          Di RSUP dr Kariadi Semarang, pasien jantung dilayani di 2 tempat. Untuk pasien bayar mandiri, di Gedung Elang (klinik eksekutif khusus jantung dan pembuluh darah/UPJ). Sedangkan pasien BPJS, dilayani di klinik jantung Gedung Merpati. Jangan khawatir, yang memeriksa langsung dokter spesialisnya, kok. Bukan residen. ;)

      Saya diberi obat-obatan plus dirujuk untuk echocardiography(USG jantung) dan treadmill test. Sebab, terlihat indikasi penyakit jantung koroner pada EKG saya. 

-                -ECG untuk melihat struktur dalam jantung (jika bayar mandiri, sekitar Rp600-700 ribu)
-          -Treadmill test, pasien diminta berjalan di atas treadmill (alat olahraga yang kecepatannya bisa distel), sambil dihubungkan dengan mesin EKG. 

Semua di-cover BPJS. Hanya, biasanya waktunya harus antre. Saya bisa ECG sekitar 10 hari kemudian, sedang treadmill sebulan ke depan. Namun saya belum jadi treadmill, karena sewaktu ECG dokter langsung menyarankan kateterisasi. Semua prosedur ini dilakukan di Gedung Elang.

Syarat ke klinik jantung RSUP dr Kariadi Semarang, siapkan:
1-   Surat rujukan asli dan fotokopinya
2-      SEP (surat penjaminan/ACC dari BPJS di faskes tk. II/RSUD)
3-      Kartu BPJS asli dan fotokopi
4-      KTP asli dan fotokopi
5-      Kartu Berobat RSUP dr Kariadi (jika sudah ada)
6-      Buku obat warna hijau (jika ada)
7-      Jangan LUPA, daftar dulu via telpon/SMS untuk mendapat nomor antrean dokter jantung yang Anda tuju (ada kuota pasien setiap harinya)
Telepon: (024) 841-7200
Via SMS: 0858-6548-3323 (formatnya: REG#nomor rekam medis Anda#kode klinik#kode dokter#tahun-bulan-tanggal)
Pendaftaran dilayani Senin – Jumat. Bisa mendaftar sebulan sebelumnya.

Kateterisasi Jantung dengan BPJS

                Setelah di-echo/ECG (20 Oktober 2016), saya disarankan untuk kateterisasi. Karena hasil ECG, ada hipokinetik di jantung saya, diduga akibat penyempitan. Kateterisasi jantung atau angiografi dilakukan untuk melihat benarkah ada penyempitan pembuluh darah jantung, di mana lokasinya, dan seberapa parah. Dari sini, dokter bisa menentukan pengobatan selanjutnya. 

                Sebagai pasien BPJS, saya diantar suster mendaftar ke bed manager Gedung Elang/UPJ, untuk pesan kamar. Sebab, pasien program kateterisasi harus bed restpascatindakan. Rawat inap selama 1 hari. Dokumen pada saat pendaftaran ini sudah lengkap/lanjutan dari saat echo. Setelah beres, saya diberi rujukan oleh mbakbed manager untuk cek darah ke lab, sebagai persiapan kateterisasi.

                Oya, ada disclaimer berikut dari pihak BPJS: jika pada hari H tak tersedia kamar sesuai hak rawat inap, maka pasien setuju untuk diturunkan kelas rawatnya.(Saya mikir, kalau turun kelas, dapet kembalian, dong? :p)

                Saya terjadwal pada 31 Oktober 2016. Pada hari H, saya harus check in maksimal pukul 9 pagi. Ini yang harus saya dan pasien program kateterisasi bawa:
1   -Hasil laboratorium, ECG, rontgen
2   - Surat rujukan kateterisasi (disebut juga program PAC, kalau pasang ring PCI)
3   - Fc Kartu Keluarga
4   - Fc kartu BPJS
5   - Fc KTP, masing-masing 2 lembar kalau tidak salah
6   - Jangan lupa PUASA (pasien harus puasa makan, sesuai instruksi. Saya puasa sejak pukul 7 pagi)
*Siapkan saja fotokopian semua dokumen sebanyak beberapa lembar. Lebih baik berlebih, daripada ada yang kurang. Bakal repot!

Nanti pasien juga diminta tanda tangan banyak dokumen, antara lain persetujuan tindakan, persetujuan rawat inap. Lalu, pasien  dibawa ke kamar rawat, ganti baju rumah sakit, dan dipasang infus. Saya langsung diinfus karena rencana tindakan pukul 1 siang.

Prosedur kateterisasi membutuhkan waktu sekitar setengah - satu jam. Sebetulnya, tindakannya sih sebentar. Tapi, persiapan dan antre ruang cath lab-nya yang tak bisa diprediksi. Saya diantar ke cath lab pukul setengan satu siang, keluar pukul setengah tiga. Padahal, lama antrenya di dalam, hehehe. RSUP dr Kariadi memiliki 3 ruang cath lab.

Untuk prosedur PAC, dokter hanya akan melihat dan menilai kondisi jantung. Jika diharuskan ada tindakan lanjutan, misal pasang ring(PCI), maka akan dibuatkan jadwal berikutnya. Jadi, kateterisasinya lebih dari sekali. :(

Sekedar info, di rekening RS, tertera biaya prosedur kateterisasi yang saya jalani total sekitar Rp11 juta. Sedangkan bila pasang ring, berkisar Rp60 juta (tergantung jumlah dan kualitas ring/stent).

Demikian sharing pengalaman saya mendeteksi dan mengobati penyakit jantung koroner. Semoga membantu, ya. Dan untuk Anda, para calon pasien, pasien, maupun keluarga pasien, tetap semangat. Lebih baik mengetahui penyakit dalam tubuh, agar bisa mulai berhati-hati. Optimis, dengan ikhtiar menuju sehat, insyaAllah, Allah Yang Maha Kuasa tak akan menutup mata. Aamiin. 

Salam sehat, sayangi jantung Anda!


          DIAGNOSIS KEHAMILAN        
A. 14 tanda kehamian tidak pasti 
   1.  aminore 
   2. mual dan muntah
   3. Mastodinia
   4. Quickening
   5. Keluhan kencing   
   6. Konstipasi
   7. Perubahan berat badan
  8. Perubahan temperature basal 
  9. Perubahan warna kulit 
 10. Perubahan payudara 
 11. Perubahan-perubahan pada pelvis 
 12.Pembesaran perut
 13. Kontraksi uterus
 14.Balotement

B. 5 tanda kehamilan pasti
 1. Denyut jantung janin (DJJ) 
 2.Palpasi 
3. Rontgenografi 
4. Ultrasonografi 
5. Fetal ECG


A.      14 Tanda kehamilan tidak pasti
1.      Aminorea
Bila seorang wanita dalam masa mampu , apalagi sudah kawin mengeluh terlambat haid, maka pikirkanlah bahwa ia hamil meskipun keadaan seperti ketidakseimbangan ovarium-hipofisis, infeksi local, stress, obat-obatan, penyakit kronis dapat pula menyebabkan terlambat haid.
2.      Mual dan muntah
Merupakan gejala umum, mulai dari rasa tidak enak sampai muntah yang berkepanjangan.dalam kedokteran lebih dikenal dengan istilah morning sickness karena munculnya sering pagi hari. Penyebab hal ini belum jelas, tetapi kemungkinan disebabkan oleh meningkatnya estrogen yang mempengaruhi metabolism hepar, serta menurunya motilitas lambung. Mual dan muntanh diperberat oleh makanan yang baunya menusuk dan juga oleh emosi penderita yang tidak stabil. Untuk mengatasinya penderita perlu diberikan makanan yang ringan, mudah dicerna dan jangan lupa beritahu bahwa keadaan ini masih dalam batas normal pada orang hamil. Bila berlebihan dapat juga diberikan anti muntah.
3.      Mastodinia
Rasa kencang dan sakit pada payudara disebabkan oleh pembesaran payudara . vaskularisasi bertambah, asinus dan duktus berproliferasi karena pengaruh estrogen dan progesterone.

4.      Quickening
Adalah persepsi gerakan janin pertama yang diteruskan melalui peritoneum parietal yang memiliki inervasi somatic. Biasanya disadari oleh wanita pada kehamilan 18-12 minggu dan lebih dini dirasakan oleh wanita multigravida. Tanda ini terlalu sering dirasakan pada wanita hysteria yang menganggap dirinya hamil (pseudocyesis).
5.      Keluhan kencing
Frekuensi kencing bertambah dan sering kencing malam, disebabkan oleh desakan uterus yang membesar dan tarikan oleh uterus ke cranial.
6.      Konstipasi
Ini terjadi karena efek relaksasi progesterone pada tonus otot usus atau dapat juga karena perubahan pola makan.
7.      Perubahan berat badan
Pada kehamilan 2-3 bulan sering terjadi penurunan berat badan karena nafsu makan berkurang dan muntah-muntah. Pada bulan selanjutnya BB akan selalu meningkat sampai stabil menjelang aterm.
8.      Perubahan temperature basal
Kenaikan temperature basal lebih dari 3 minggu biasanya merupakan tanda telah terjadi kehamilan.
9.      Perubahan warna kulit
Perubahan ini antara lain kloasma yakni warna kulit yang kehitam-hitamn pada dahi,punggung hidung, dan kulit daerah sekitar pipiterutama wanita dengan warna kulit tua. Biasanya muncul setelah minggu ke 16. Pada daerah areola dan putting payudara, warna kulit menjadi lebih hitam.
Perubahan ini disebabkan oleh stimulasi MSH ( melanocyte stimulating hormone). Pada kulit daerah abdomen dan payudara dapat mengalami perubahan yang disebut striegravidarum, yaitu suatu perubahan warna kulit seperti jaringan parut. Diduga ini terjadi karena pengaruh adrenokortikosteroid. Kadang-kadang pula taleangiektasia karena pengaruh estrogen yang tinggi.
10.  Perubahan payudara
Pada usia kehailan 6-8 minggu tuberkel Montgomery mulai menonjol akibat stimulasi prolaktin dan HPL. Kemudian, payudara mensekresi kolostrum biasanya setelah kehamilan lebih dari 16 minggu.
11.  Perubahan-perubahan pada pelvis
a.      Dinding vagina mengalami kongesti, warna kebiru-biruan (Chadwick’s sign). Cairan vagina keputihan, encer, berisikan sel-sel eksfloiasi vagina , yang terjadi karena pengaruh estrogen dan progesterone . servik berwarna kebiru-biruan (livid)
b.      Hagar’s sign
Tanda ini berupa pelunakan pada daerah istmus uteri sehingga daerah tersebut pada pemeriksaan bimanual mempunyai kesan lebih tipis dan uterus mudah difleksikan ( tanda ini mulai terlihat pada minggu ke 6 dan menjadi nyata pada minggu 7-8)
c.       Pembesaran uterus terjadi pada minggu ke-10, 2x sebelum hamil (besar normalnya adalah antara 7-8 cm x 4-5 cm). uterus membesar kesalah satu sisi hingga menonjol jelas ke sisi pembesaran tersebut ( tanda piscaseck).
12.  Pembesaran perut
Pembesaran perut menjadi nyata pada minggu ke 16 karena pada saat ini uterus telah keluar dari rongga pelvis dan menjadi organ rongga perut. Penurunan tinggi fundus uteri (TFU) pada minggu 38-40 disebut lightening.karena penurunan janin pada segmen bawah rahim dan servik sebagai persiapan persalinan. TFU bukan pedoman untuk mengatahui maturitas janin.
13.  Kontraksi uterus
Tanda ini muncul belakangan dan pasian mengeluh perutnya kenceng tapi tidak disertai rasa sakit.
14.  Balotement
Tanda ini muncul pada minggu ke 16-20, setelah rongga rahim mengalami obliterasi dan cairan amnion cukup banyak. Ballottement adalah tanda adanya benda terapung atau melayang dalam cairan

B.      Tanda kehamilan pasti
1.      Denyut jantung janin (DJJ)
DJJ dapt di dengarkan dengan stetoskop laenec pada minggu 17-18. Pada orang gemuk lebih lambat lagi. Dengan stetoskop ultrasonic (Doppler), DJJ dapat di dengar lebih awal sekitar minggu ke 12
2.      Palpasi
Yang harus di tentukan adalah outline janin. Biasanya menjadi lebih jelas pada minggu ke 22. Gerakan janin dapat jelas terasa pada minggu ke 24
3.      Rontgenografi
Gambar tulung –tulang janin tampak setelah minggu 12-14. Pemeriksaan ini hanya boleh dilakukan bila terdapat keragu-raguan dalam diagnosis kehamilan, dan atas indikasi yang mendesak sekali sebab janin sangat peka terhadap sinar X , sekarang penggunaan sinar X telah terdesak oleh ultrasonografi (USG)
4.      Ultrasonografi
Alat ini menjadi sangat penting dalam diagnosis kehamilan dan kelainan-kelainanya, karena gelombang suara sampai saat ini dinyatakan tidak berbahaya. Pada minggu ke 6, sudah terlihat adanya kantong kehamilan
Pada Minggu 6-7 : kutub jantung
Pada Minggu 7-8 : denyut jantung
Pada Minggu 8-9  : gerakan janin                        
Pada Minggu 9-10 : plasenta
Pada Minggu 12    : biparietal diameter (BPD)
Adanya 2 kantong kehamilan pada minggu ke 6 sudah dapat menyatakan adanya kehamilan ganda.
5.      Fetal ECG
Dapat direkam pada minggu ke 12 dengan alat fetalcardiography


daftar pustaka:
sastrawinata, sulaiman.1983.obsteti fisiologi.bandung:eleman-bandung
siswosudarno, risanto dkk.2008.obsteri fisiologi.yogyakarta:pustaka cendikia

          Cardiac Sonographer - Register - (Edinburg)        
The Registered Cardiac Sonographer prepares patients for and performs adult, pediatric and Stress Echocardiograms in accordance with established procedures to assist physicians in the delivery of patient care. The Registered Cardiac Sonographer is also responsible for the following:* Prepares patients for and assists physician performing transesophageal echocardiogram in accordance with established procedures* Measures and calculates results from various echocardiographic studies utilizing the appropriate equipment and calculation packages* Assists in creating a quality environment for patient care* Prepares TEE probe for re-use following proper cleaning procedures and on a consistent basis* Provides assistance in training and guidance in "hands-on" experience for Cardiology fellows, junior technicians, and others as needed* Maintains cleanliness of work area on a regular basis* Fulfills continuing education and/or certification requirements to maintain required qualificationsThe ideal Cardiac Sonographer takes responsibility to understand and complete professional and technical requirements and performs required duties in a competent, professional and courteous manner.Location/Facility The Heart Hospital Baylor PlanoFor more information on the facility, please click our Locations link.* Specialty/Department/Practice Cardiology* Shift/Schedule PRN DayShift withcall coverage weekend shift 8:00 AM - 4:30 PM* Benefits Our competitive benefits package includes*:* Immediate eligibility for health and welfare benefits* 401(k) savings plan with dollar-for-dollar match up to 5%* Tuition Reimbursement* PTO accrual beginning Day 1*Note: Benefits may vary based upon position type and/or level.Baylor Scott & White Health (BSWH) is the largest not-for-profit health care system in Texas and one of the largest in the United States. With a commitment to and a track record of innovation, collaboration, integrity and compassion for the patient, BSWH stands to be one of the nation's exemplary health care organizations.
          Most Popular Cardiac Technology Content in July 2017 on DAIC        
Left Atrial Pressure Monitor from Vectorious Medical Technologies Offers New Hope for Heart Failure Patients

On of the top stories in July was the introduction of a left atrial pressure monitor from Vectorious Medical Technologies to prevent heart failure patient hospitalizations or readmissions. Read the article"Left Atrial Pressure Monitor Offers New Hope for Heart Failure Patients."

Aug. 1, 2017 — Here is the list of the most popular articles and videos on the Diagnostic and Interventional Cardiology (DAIC) magazine website from the month of July, based on website analytics of the month’s 106,727 pageviews:  

1. First Patient in World Enrolled in Study Evaluating TAVR for Asymptomatic Severe Aortic Stenosis

2. What is New in Electrophysiology Technologies

3. Philips Acquires Spectranetics, Expanding its Image-guided Therapy Device Offerings

4. Left Atrial Pressure Monitor Offers New Hope for Heart Failure Patients

5. New Handheld Scanner to Give Instant Heart Disease Diagnosis 

6. FDA Expands CoreValve TAVR Valve Use for Intermediate Risk Patients 

7. Top Echocardiography News and Video From ASE 2017

8. CMS to Require Appropriate Use Criteria Documentation for Medical Imaging Orders

9. Pre-PCI Impella 2.5 Insertion Improves Survival in Left Main Coronary Artery Heart Attacks

10. Low Doses of Radiation Could Harm Cardiovascular Health

11. Artificial Intelligence Detects AFib Using Apple Watch Heart Rate Sensor

12. Use of Artificial Intelligence to Locate Standard Echo Heart Views

13. CT Calcium Scoring for Heart Disease May Lead to Prevention, Treatments

14. Wearable Cardiac Monitors Are Effective for Tracking Atrial Fibrillation Following Ablation

15. Medtronic Reactive ATP Therapy Slows Progression of Atrial Fibrillation in Real-World Population

16. Biotronik Launches DX Technology for U.S. Heart Failure Patients

17. Study Demonstrates Strain Imaging Utility With Contrast-Echo Studies

18. Novel Approach May Improve Valve Function in Some Patients

19. FFR-CT Gains CPT Code for Reimbursement

20. A Glimpse Into the Future of Cardiac Ultrasound

 

Top Videos from July 2017:

1. CRT Optimization Using Echo - ASE 2017 

2. Clinical Evidence Shows CT Should be the Primary Cardiac Imaging Modality 

3. New CPT Reimbursement Codes for Cardiology 

4. Editor's Choice of Most Innovative New Cardiac Ultrasound Technology at ASE 2017 

5. Role of Cardiac CT in Value-based Medicine
 


          Comparison of CMS Reimbursements in Cardiac Imaging Between 2017 and 2018        
Cardiac CT scan showing plaque and calcification in the coronary arteries, from a Toshiba CT scanner

July 19, 2017 — The Society of Cardiovascular Computed Tomography (SCCT) created a reimbursement fee chart for cardiac imaging showing various reimbursements for cardiac CT, MRI, echocardiography and SPECT perfusion. It breaks down the differences in payments between 2017 and what is being proposed by the Centers of Medicare and Medicaid Services (CMS) for 2018.

The chart can be accessed at http://scct.org/?page=2017ReimbursementCha

The chart includes the current procedural terminology (CPT) codes, and sections for the Medicare Physician Fee Schedule (MPFS) professional component (PC) and technical component (TC) payment for 2017; proposed MPFS PC and TC for 2018; OPPS TC payment in 2017 and the proposed OPPS TC payments for 2018. 

Payment Rates for Non-Excepted Off-campus Provider-Based Hospital Departments Paid Under the MPFS

Statute requires that certain items and services furnished by off-campus hospital outpatient provider-based departments be no longer paid under the Hospital Outpatient Prospective Payment System (OPPS) beginning January 1, 2017. For Calendar Year (CY) 2017, CMS finalized the MPFS as the applicable payment system for most of these items and services.

For CY 2018, CMS is proposing to reduce current MPFS payment rates for these items and services by 50 percent. CMS currently pays for these services under the MPFS based on a percentage of the OPPS payment rate. The proposal would change the MPFS payment rates for these services from 50 percent of the OPPS payment rate to 25 percent of the OPPS rate. CMS believes that this adjustment will encourage competition between hospitals and physician practices by promoting greater payment alignment.

2018 Hospital Outpatient Prospective Payment System (OPPS) Proposed Rule Overview

 

Restructuring of Imaging Ambulatory Payment Classification (APC) Groups

For 2017, CMS implemented a significant restructuring of the imaging Ambulatory Payment Classification groups, resulting in the consolidation of such groups from 17 in 2016 to seven imaging APCs for 2017.  CMS stated the purpose of this restructuring was to more adequately reflect resource costs and clinical characteristics of services assigned to the various APCs.  This restructuring translated to a negative impact on technical component (TC) reimbursement for many imaging procedures.   However, cardiac CT services saw an increase of approximately $30 under this restructuring.  For 2018, CMS proposes to add an additional imaging APC – Level 5 Imaging without contrast - for low volume, high cost services.  Preliminary review indicates the TC of CPT codes 75572, 75573 and 75574, would be cut by $30 under the proposed rule for 2018.  Please see the attached reimbursement chart for effects of the proposed rules on professional and technical component reimbursement for cardiac CT services.

Read the related article "SCAI Highlights News from Medicare Trustees Report and 2018 Medicare Physician Fee Schedule"
 

for more information: scct.org


          VIDEO: Surgical Options for RV Dysfunction and TR in LVAD Patients        

This video educational session, provided in partnership with the American Society of Echocardiography (ASE), is titled "Surgical Options for Right Ventricular (RV) Dysfunction and Tricuspid Regurgitation (TR) in Left Ventricular Assist Device (LVAD) Patients." It is presented by Nahush Mokadam, M.D., FACC, FACS, LeRoss Endowed Professor of cardiovascular surgery, director of heart transplant and mechanical circulatory support, program director cardiothoracic residency, University of Washington. This is one of the sessions presented at the ASE 2016 annual scientific sessions, one of the premier meetings for cardiac ultrasound education. For more information, visit asescientificsessions.org. 


          Comment on Vision by Is Open-Source Hardware Really “Open”? - FTI Strategic Communications        
[…] it doesn’t stop there; from open source beehives to building open source cars to open source electrocardiograph machines, open source hardware enthusiasts are enthusiastically […]
          Evaluation of left ventricular functions in patients with primary hyperparathyroidism: is there any effect of parathyroidectomy?        
Our aim was to evaluate left ventricular (LV) systolic and diastolic functions of primary hyperparathyroidism (pHPT) patients with detailed echocardiographic analysis and investigate the effect of parathyroidectomy on echocardiographic parameters....
          Sports cardiology: Can ultraendurance events damage the heart?        
Is it safe for this athlete to exercise? Are ultraendurance events and training for them leading to reversible cardiac fatigue to frank damage and fibrosis? How should one investigate the athlete who may be in the ‘grey zone’ between benign ‘athletes heart’ and potentially fatal cardiomyopathy? Dr Andre La Gerche, an internationally renowned sports cardiologist with experience in Europe and Australia took time out from his keynote role at the American Medical Society for Sports Medicine conference (2015) to answer those questions with BJSM’s Dr Michael Turner. Relevant links include: The right ventricle following prolonged endurance exercise: are we overlooking the more important side of the heart? A meta-analysis – this was discussed on the podcast. http://goo.gl/TWgpnr Ventricular arrhythmias associated with long-term endurance sports: what is the evidence? By Dr La Gerche and colleagues. http://goo.gl/TuF4mQ ECG interpretation in athletes – free (minor signing in, takes <30 seconds) – Learning Modules: More than 10,000 clincians have taken these CPD modules. http://goo.gl/lxb9oJ Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’ This paper is the classic (right now!) guide to interpreting ECGs in athletes – but this is being revised over the summer of 2015. Watch for the 2016 update! http://goo.gl/0kXd5T

Jon Drezner from the archive - Jon Drezner and the 2012 sudden cardiac death update: two new key messages http://bit.ly/1aYmnyX


          Using ultrasound in sports medicine - office, sideline - wide range of options (via @TheAMSSM)        
Drs Jon Finnoff and John DiFiori on sports ultrasound. For several years, primary care sports medicine doctors have been mastering musculoskeletal ultrasound. With new technology comes a sharp learning curve and as the field matures, we begin to realise the full utility of point of care ultrasound. As sports medicine practitioners, we are now understanding that ultrasound has applications outside of the musculoskeletal system that may be advantageous for our practices. A couple of examples of this include FAST exam to look at abdominal trauma and limited echocardiography in pre-participation examination. This podcast highlights 2 articles that will be published in the AMSSM themed edition of BJSM in February, 2015. One on a new sports ultrasound curriculum for sports medicine fellowships and the other on a position paper on US- guided interventional procedures. Dr Ken Mautner discusses these articles with the chair of the AMSSM MSK US Task force, Dr Jon Finnoff, as well as with the immediate past president of AMSSM, Dr John Difiori. They will shed much more light on the transition to this new term “Sports Ultrasound” and how it may impact your practice. They will also discuss some aspects of their interventional position paper on MSK US which is timely as there is continued downward trends in reimbursement for interventional US. See also: American Medical Society for Sports Medicine (AMSSM) position statement: interventional musculoskeletal ultrasound in sports medicine: http://bjsm.bmj.com/content/early/2014/10/19/bjsports-2014-094219.full American Medical Society for Sports Medicine recommended sports ultrasound curriculum for sports medicine fellowships:

http://bjsm.bmj.com/content/early/2014/10/31/bjsports-2014-094220.full


          David Epstein – ‘The Sports Gene’ author (Part 2) – Hearts and blood        
If you enjoyed Part 1 of David Epstein’s BJSM podcast listen to this one to hear about the genetic contribution to hypertrophic cardiomyopathy, the reason it is so hard to detect in all cases, and real life choices that some players made when offered genetic screening opportunities. We finish by discussing whether an Olympic cross-country ski champion with a hematocrit of 65 is a blood-doper or the carrier of an unusual single-gene mutation. I learned a great deal from David Epstein in both podcasts; David has put the bar very high for future podcast guests. Recorded at the Summit – Leaders in Performance – New York (June 17/18 2014); with permission from Leaders (James Worrall). David Epstein’s session at Leaders was sponsored by Aspetar Orthopedic and Sports Medicine Hospital, Doha, Qatar. For more related content: Sports Cardiology module on BMJ Learning including Seattle Criteria: bit.ly/1lI8djo J Drezner, M Ackerman, J Anderson et al, Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’ bit.ly/1ic8P6i Advances in Sports Cardiology November 12, Volume 46: bit.ly/1pitAMf J Drezner, Standardised criteria for ECG interpretation in athletes: a practical tool, bit.ly/1lYQc5f Bruce Hamilton, Ben Levine, Paul Thompson, Greg Whyte, Mathew Wilson, Debate: challenges in sports cardiology; US vs European approaches bit.ly/1lEudzX Unravelling the grey zone: cardiac MRI volume to wall mass ratio to differentiate hypertrophic cardiomyopathy and the athlete's heart: http://bit.ly/1t1LlmQ Sudden Cardiac Arrest and Cardiac Screening: A trainee perspective: http://bit.ly/1oUOWSk Peripheral vascular structure and function in hypertrophic cardiomyopathy: http://bjsm.bmj.com/content/46/Suppl_1/i98.full Unraveling the grey zone: cardiac MRI volume to wall mass ratio to differentiate hypertrophic cardiomyopathy and the athlete's heart: http://bjsm.bmj.com/content/early/2013/06/13/bjsports-2013-092360.full

Screening athletes for cardiovascular disease in Africa: a challenging experience: http://bjsm.bmj.com/content/47/9/579.full


          Assistant Professor Aaron Baggish – Sports Cardiologist / Boston Marathon        
In this concise, information-rich BJSM podcast, sports cardiologist Aaron Baggish shares his expertise on the critical issue of sudden cardiac death in sport. He explains how to determine which ECG changes in athletes are sinister and which may not be (such as right bundle branch block). He argues for a detailed screening program for elite athletes and gives advice for those whose care is not covered by a professional sporting organization. The Boston Marathon has provided valuable lessons for where to locate defibrillators in this type of event. A sports cardiology refresher in just 11 minutes! Recorded at the Summit – Leaders in Performance – New York (June 17/18 2014); with permission from Leaders (James Worrall). Aaron Baggish's session at Leaders was sponsored by Aspetar Orthopedic and Sports Medicine Hospital, Doha, Qatar. See also: J Drezner, M Ackerman, J Anderson et al. Electrocardiographic interpretation in athletes: the ‘Seattle Criteria’ bit.ly/1ic8P6i P Biddinger, A Baggish, L Harrington, P d’Hemecourt, J Hooley, The Boston Marathon and Mass-Casualty Events bit.ly/1lEtkaK BMJ Learning: ECG interpretation in athletes: bit.ly/1lI8djo Incidence of sudden cardiac death in athletes: a state-of-the-art review: http://bjsm.bmj.com/content/48/15/1185.full The FIFA medical emergency bag and FIFA 11 steps to prevent sudden cardiac death: setting a global standard and promoting consistent football field emergency care: http://bjsm.bmj.com/content/47/18/1199.full Cardiovascular screening in adolescents and young adults: a prospective study comparing the Pre-participation Physical Evaluation Monograph 4th Edition and ECG: http://bjsm.bmj.com/content/48/15/1172.full Mass ECG screening of young athletes: http://bjsm.bmj.com/content/42/9/707.full Sudden Cardiac Arrest and Cardiac Screening: A trainee perspective: http://blogs.bmj.com/bjsm/2012/10/18/sudden-cardiac-arrest-and-cardiac-screening-a-trainee-perspective/

David Epstein – ‘The Sports Gene’ author (Part 2) – Hearts and blood: https://soundcloud.com/bmjpodcasts/david-epstein-the-sports-gene-author-part-2-hearts-and-blood


          Manager, PACS and RIS - Trillium Health Partners - Mississauga, ON        
Echocardiography, Pulmonary Function, Vascular ultrasound) Management of all equipment, maintenance and service contracts related to PACS / RIS Project and...
From Trillium Health Partners - Thu, 08 Jun 2017 00:38:48 GMT - View all Mississauga, ON jobs
          Comparison of 3 Symptom Classification Methods to Standardize the History Component of the HEART Score        
imageObjectives: The History, Electrocardiography, Age, Risk factors, Troponin (HEART) score enables rapid risk stratification of emergency department patients presenting with chest pain. However, the subjectivity in scoring introduced by the history component has been criticized by some clinicians. We examined the association of 3 objective scoring models with the results of noninvasive cardiac testing. Methods: Medical records for all patients evaluated in the chest pain center of an academic medical center during a 1-year period were reviewed retrospectively. Each patient’s history component score was calculated using 3 models developed by the authors. Differences in the distribution of HEART scores for each model, as well as their degree of agreement with one another, as well as the results of cardiac testing were analyzed. Results: Seven hundred forty nine patients were studied, 58 of which had an abnormal stress test or computed tomography coronary angiography. The mean HEART scores for models 1, 2, and 3 were 2.97 (SD 1.17), 2.57 (SD 1.25), and 3.30 (SD 1.35), respectively, and were significantly different (P < 0.001). However, for each model, the likelihood of an abnormal cardiovascular test did not correlate with higher scores on the symptom component of the HEART score (P = 0.09, 0.41, and 0.86, respectively). Conclusions: While the objective scoring models produced different distributions of HEART scores, no model performed well with regards to identifying patients with abnormal advanced cardiac studies in this relatively low-risk cohort. Further studies in a broader cohort of patients, as well as comparison with the performance of subjective history scoring, is warranted before adoption of any of these objective models.
          Destaque na revista científica norte-americana Journal of American Society of Echocardiography        
Centro médico e formador de especialistas em Cardiologia, Instituto do Coração de Marília tem estudo publicado na conceituada revista científica norte-americana Journal of American Society of EchocardiographyNovidades na prevenção de doença cardíaca Prof. Dr. Fábio Villaça, chefe da Clínica Médica e disciplina de Cardiologia da FAMEMA – Divulgação Considerada como ...
          Evaluation of left atrial volume and function using single-beat real-time three-dimensional echocardiography in atrial fibrillation patients        
This study was aimed to evaluate the feasibility and accuracy of real-time three-dimensional echocardiography (RT-3DE) measurement of left atrial (LA) volume and function in comparison with two-dimensional ech...
          Manager, PACS and RIS - Trillium Health Partners - Mississauga, ON        
Echocardiography, Pulmonary Function, Vascular ultrasound) Management of all equipment, maintenance and service contracts related to PACS / RIS Project and...
From Trillium Health Partners - Thu, 08 Jun 2017 00:38:48 GMT - View all Mississauga, ON jobs
          Contoh Soal Latihan Bahasa Inggris Kelas VIII SMP Semester Ganjil        

Contoh Soal Latihan Bahasa Inggris Kelas VIII SMP Semester Ganjil


1.Aldi : “lets go to the canteen!’
 mira : “…….. I am hungry”
a. It’s a good idea
b. it’s not good idea
c. I disagree
d. I hate it

2. Andre : “……… of our new friend?
joni : “She is beautiful and friendly”
a. Who is the girl
b. what a beautiful girl
c. Would you mind
d. what do you think

3. To get high score in the final exam, we have to….. ..every day.
a. help mother
b. study hard
c. to be lazy
d. go to beach

4. Cow and buffaloes are ……. But tigers and lion are carnivorous.
a.Reptiles
b. microbes
c. herbivorous
d. viruses

5. Mr. farhan is a/an ….. He looks after some animals in his large garden behind in his house.
a. Fish monger
b. animals liver
c. fruit seller
d. game lover

6. Mytha : “ I want you to come to my party tonight.”
Aliana : “……….. I have a lot of homework to do.”
a.It’s a great
b. I agree with you
c. I am afraid I can’t
d. it is a good idea

Read the text carefully then answer the question based on the text below.

Yesterday my mother was ill. My father and I took her to the doctor. First my father talked to the lady who was in charge of registration. She typed the data about my mother on the computer. Then we waited for my mother’s turn.
When her turn comes, I accompanied her to enter the doctor’s room. The doctor listened to my mother’s complained patiently. Then the doctor examined my mother by putting the stethoscope on my mother’s chest. After that, a nurse who help the doctor, taking my mother’s temperature so she put a thermometer in my mother’s armpit. He told me that my mother had a bad influenza. He wrote a prescription and gave it to me. He advised my mother to stay in bed for three days and come back after a week.
Then my father took my mother home directly and then  I went to the nearest dispensary.

7. Who was sick yesterday?
a.My mother
b. the writer’s mother
c. my father
d. the writer’s father

8. What did the doctor do first after the patience enter his room?
a.Examined the patient first after the patients enter his room.
b.Took the patient’s blood pleasure by using spignomonometer.
c.Listened to the patient’s complain patiently.
d.Wrote a prescription and gave it to the writer.

9. What is used to take the patient’s temperature?
a.Thermometer
b.stethoscope
c.spignomonometer
d.electrocardiograph

10. “After that, he took my mother’s blood pleasure…’(second paragraph). The underline word means….
a.Examining
b. complaining
c. putting
d. using

11. Why does the writer write such kind of text?
a. To present his pointing of view
b. To retell events for the purpose of informing
c. To persuade the readers to go to the doctor
d. To explain how the doctor explain the patients

The following text is for number 12-14
Two year ago when I (11)…….in elementary school, I (12) …. Two close friends. At that time we usually (13) …..Football every afternoon.

12. a. am b. was c. will be d. have been

13. a. had b. will have c. have been d. have

14. a. played b. plays c. play d. are playing

15. Arrange the following words in to good sentences Were – stewardess – very – the – kind – helpful – and 1 2 3 4 5 6 7
a. 2-1-4-6-5-3-7
b. 4-2-1-3-5-7-6
c. 3-5-2-1-4-7-6
d. 4-2-1-6-3-7-5

16. Bambang : “ how was your flight?
Wati : Oh, It’s was ……enjoyable. I like it.’
a. Rather
b. about
c. not
d. really

17. Her school ….. an excursion a week ago.
a. Took
b. takes
c. taking
d. taken

18.Tarlia went to Borobudur temple yesterday. She used …. Own car to travel.
a. Mine
b. her
c. you
d. him

19. Wahdin wrote a letter ……
a. Tomorrow
b. yet
c. last night
d. at present

20. A big boat is a/an…..
a. Means of air transportation
b. means of sea transportation
c. Means of sky transportation
d. means of land transportation


=Good Luck=

          EchoSAP 5 - Echocardiography Self-Assessment Program 5        
EchoSAP 5 - Echocardiography Self-Assessment Program 5
WinApp | EchoSAP 5 | 79.2MB

EchoSAP is designed to help you hone your skills in echocardiography by giving you a comprehensive overview of the field, plus more than 50 brand new case studies and self-assessment questions to help you sharpen your decision-making skills and prepare for the National Board of Echocardiography (NBE) exam.

EchoSAP5 Features
Comprehensive overview of echocardiography by James D. Thomas, MD, FACC
50+ brand new case studies of varying degrees of difficulty that cover topics such as:
Cardiomyopathies and heart failure syndromes
Pericardial disease
Coronary artery disease
Congenital heart disease
Diseases of the aorta and vascular system
Valvular heart disease
New echocardiographic techniques
Hundreds of expertly processed clinical images
A panel of more than 40 expert authors, including:
Elyse Foster, MD, Editor
Gerard Aurigemma, MD
Karen Hamilton, MD
Smadar Kort, MD
Patricia Pellikka, MD
Athena Poppas, MD
Mary Roman, MD
Samuel Siu, MD
Kirk Spencer, MD
Dozens of multiple-choice self-assessment questions with detailed commentary
Up to 31 hours of AMA PRA Category 1 CreditsTM

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ECG-SAP III - Electrocardiography Self-Assessment Program
WinApp | ECG-SAP III | 75.6MB

24 single ECG tracings six pairs of serial tracings seven computer overreads 21 ECG clinical correlations five cases on stress testingup to 12 hours of AMA PRA Category 1 credit topics covered include—
Bradyarrhythmia and Conduction Myocardial Injury and Infarction STT Changes and Other Conditions Ventricular and Supraventricular Arrhythmias Chamber Hypertrophy and Enlargement

Accreditation Statement
The American College of Cardiology Foundation (ACCF) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The American College of Cardiology foundation takes responsibility for the content, quality, and scientific integrity of this CME activity.

ACCF designates this educational activity for a maximum of 12 AMA PRA Category 1 CreditsTM. Physicians should only claim credit commensurate with the extent of their participation in the activity.

ECG-SAP III does not provide extensive training or offer certification in the field of cardiology.

Learning Objectives:
Improve your interpretive skills and your understanding of electrocardiography
Help you identify the specific areas in ECG Interpretation in which you may be deficient


ECG-SAP 3's editors have recently reviewed it's content and deemed that it remains important and applicable for practicing physicians. Given this, ACC will continue to grant CME credit for the product beyond the original term of approval date.

Date of Original Release: March 2001
Original Term of Approval: March 2004
Extended Term of Approval: March 2009

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ShenProfessional 2.0.09.12.2006
TCM - Traditional Chinese Medicine - Practice Management
Win App | 184.2mb | BIN | 3% recovery

ShenProfessional is software for Acupuncture and TCM. Additionally, ShenProfessional is an amazing tool to manage the most demands in your daily practice. The software manages your patients data, appointments, letters as well as invoices. Here are the main features:

Acupuncture

* 409 acupuncture points with extra points
* Display acupuncture points on the skin, the muscles, the bones or - new in this version - on inner organs with vessels and nervs.
* Every acupuncture chart is printable.
* Detailed point information with name, location, functions, indications, qualification, explanation of the pinyin name and informatione about needling and moxibustion.
* Enlarge point information by your own notes.
* Search function
* Compiling your own acupoint combinations with the Point search
* Document your and treatments and the used points in the Patients folder.
* Display the used needling method by special symbols

Traditional Chinese Medicine

* Paper on the foundations of TCM
* Paper on Chinese gynecology
* Paper on Extraordinary vessels inclusive special palpatory diagnosis.
* Interactive hyperlink course for beginners and advanced
* TCM Information with symptoms, causes, treatment tips, root and branch and point combination to each TCM diagnosis
* Symptoms catalogue with more than 4000 symptoms, indications and Western medical diagnoses with accompanying TCM diagnostics. This is problably the world's most detailed reference book
* Save and diagnose your patients symptoms with the mouse
* Diagnosis Analysis with overview of involved organs and with special root and branch diagnosis

Praxismanagement

* Patients file
* Document your findings and treatments
* Assing Billing Codes to appointments
* Communication with Calendar and Billing in real time
* Interface to MS Word: Write personal letters with using the patients data saved in ShenProfessional
* Create and print mass mailings, labels, envelopes or lists with MS Word using data saved in ShenProfessional
* Calendar
* postpone appointments by drag and drop
* easy printing of scheduled appointments
* send scheduled appointments using your e-mail client
* change the time units to your needs
* today, 5-day-week, 7-day-week, month
* the month view displays the number of working hours according to the scheduled appointments
* Billing for any faculty
* Single invoice or collective invoice just with a click
* view due billing, due payment or paid invoices
* print invoices with Shen templates
* print invoices with MS Word
* edit existing or add new billing codes
* generate reminders

Modular structure

* ShenProfessional contains 5 modules (folders), which can be opened alone or together: Patients folder, Calendar, Billing, TCM Tutorial, TCM Theory
* All folders are resizable
* Fodlers have an overview and one or several docking folders (e.g. overview of acupuncture points with docking folders Acupuncture Charts and Point Information). Undock docking folders and study several informations simultaneously
* The use of the Navigator is the fastest way to get to the essential areas of ShenProfessional 2.0.



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          ECG-SAP II Electrocardiography Self-Assessment Program        

ECG-SAP II Electrocardiography Self-Assessment Program

Win App | 154.8 MB + 3% recover

ECGSAP I, II and III were developed by the ACC to provide physicians with a means to compare their proficiency in ECG interpretation to that of others and to improve their own proficiency. ECGSAP is also intended to help physicians prepare for the ECG exam. ECGSAP III has recently become available. A competent ECG reader should also be able to recognize potential clinical diagnoses on the basis of ECGs.

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Adult Clinical Cardiology Self-Assessment Program

American College of Cardiology

ACCSAP 2000 | Item A2000 | CD-ROM with print | Issue 6/99 | 642 mb + 3% recovery

Editor-in-Chief: C. Richard Conti, MD, MACC

Associate Editor: Richard P. Lewis, MD, MACC

ACCSAP 2000, the ACC's award-winning self-assessment program in adult clinical cardiology, combines the convenience of print materials with the instructional capabilities of multimedia technology. This highly interactive CD-ROM program brings you up to date on the most recent developments in your field, then lets you test your knowledge.

ACCSAP 2000 features:

New chapters on hypertension, pharmacology, and cardiac surgery, including preoperative assessment, intraoperative assessment, and postoperative management

425 self-assessment questions—including nearly 200 new questions and 20 new ECGs—all of which have undergone intensive review by a panel of question-writing experts

More than 1,500 teaching images and video clips

Databases of clinical trials and pharmacologic agents (CD version only)

A new evidenced-based medicine chapter that allows users to search on several different fields for—

clinical trials

practice guidelines, and

cardiovascular drug profiles.

Easy-to-use CD-ROM featuring hundreds of images—many in color or full motion

Convenient print version of each chapter

Printed booklets with all self-assessment questions and answers

ACCSAP 2000 topics:

Epidemiology and Prevention of Coronary Heart Disease

Acute Myocardial Infarction

Chronic Ischemic Heart Disease

Heart and Circulatory Failure

Cardiac Arrhythmias and Electrophysiology

Adult Congenital Heart Disease

Valvular Disease

Peripheral Vascular Disease

The Cardiology Consultant and Additional Topics

Echocardiography

Nuclear Cardiology

Intravascular Catheterization and Interventional Cardiology

Basic Science and Molecular Cardiology

Estimating the Predictive Power of Noninvasive Tests

ECG Interpretation

Cardiac Surgery (Preoperative, Intraoperative and Postoperative Care)

Clinical Pharmacology

Hypertension

Evidence-Based Medicine

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VH Dissector Anatomy 4.5.1 + Update to 4.5.2

WinApp | 1 DVD | ISO | 4.45 GB + 5% recovery

ISSUE: 2008

Версия: 4.5.2

Разработчик: Visible Human Project®

System Requirements

Macintosh

* Mac OS X v. 10.3.9 or later

* 800MHz (1.2GHz recommended) or faster processor

* 1024x768 24/32-bit display

Windows

* Microsoft Windows 2000 or later

* Microsoft Internet Explorer 5.5 or later

* 800MHz (1.2GHz recommended) or faster processor

* 1024x768 24/32-bit display

Language: /ENGLISH

The VH Dissector provides access to 3D renderings of photographic anatomy from the Visible Human Project and is a reference resource for life-long learning. The program allows examination of the human body from any combination of traditional views, including cross-sectional, systemic, clinical, surface, regional and surgical anatomy. A unique and remarkable interactive anatomical atlas, combining the power of cadaver dissection with the technology of virtual reality.

Features

* Virtual dissection of the full body anatomy

* 2000 identified anatomical structures

* Structures grouped by region, system or through authored lessons

* Comprehensive index by anatomical structure

* Dissection window synchronised with cross-section window

Dissection window

* Facility to add, remove or add and highlight structures to the dissection window to build up or dissect the anatomical picture

* Structures identified in the relevant window as mouse passes over

* Zoom in to see greater detail or out for orientation and anatomical context

* Rotate the structures to gain greater 3D understanding including position of other structures, their shapes, sizes and systemic relationships

* Overlay skin transparency for complete 3D location and (whole body) referencing context

Cross-section window

* Cross-section navigated as viewed from the inferior position

* Zoom in to cross section for close up details and structure selection

* Structures selected cross-sectionally are displayed fully in dissection window

* Navigate up or down cross sectional images for greater understanding of the shape, size and the relationship of structures

* Useful for improving, understanding and interpreting MRI scans

Lessons

* An authoring and viewing facility allowing tutors to build (using HTML) and then distribute lessons which integrate with the VH Dissector data set and functions

* Allows customisation and structuring of content, whilst benefiting from the full flexibility of the VH Dissector program

* Lessons are separate programs which can be emailed or distributed by CD-ROM which then integrate with the VH Dissector

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AMERICAN COLLEGE OF CARDIOLOGY - Echocardiography - EchoSap III, Volume 1 (CD-ROM) - Обучающая программа
ISBN: 1583970355 | CD-ROM | 11/2000 | Edition Number: 3 | 492.66 Mb + 3% recovery

Improve and test your echocardiography interpretation skills with EchoSAP III, Volume I. This CD-ROM offers a comprehensive overview of echocardiography and is an excellent preparatory tool for examinations that seek to measure echocardiographic interpretation skills

ECHOSAP III features:

Nearly 300 still-frame and full-motion videos
Self-assessment questions with detailed commentary
154 references
Evidenced-based medicine section with databases of guidelines, clinical trials and pharmacologic agents

ECHOSAP III topics:

Standard M-Mode Exam
Standard Two-Dimensional Imaging
Quantitative Structural Measurement
Doppler Exam
Transesophageal Exam
Three-Dimensional Imaging
Stress Echocardiography
Contrast Echocardiography

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Drs Crawford, DiMarco and Paulus"ichael H. Crawford, "Cardiology"
MOSBY | ISBN: 9780323024051 | Edition-2004 | HTML & PDF | 1728 pages | 454.3MB

Having access to up-to-date and authoritative information is essential for any cardiologist. The new second edition of Cardiology, edited by Drs Crawford, DiMarco and Paulus, is your complete cardiology resource, with a practical and user-friendly format that reflects the way you make decisions in practice – enabling you to find and apply definitive guidance quickly.
A team of 250 international experts brings you this thoroughly revised and updated New Edition. Its clinically-oriented coverage integrates basic science, diagnostic investigations, and therapeutic management into a practical, user-friendly reference on all aspects of cardiovascular medicine. A consistent format throughout parallels the clinical decision-making process to make definitive guidance easy to locate and apply. Over 2,360 illustrations, including more than 1,940 full-colour photographs, tables, and diagnostic images make techniques and concepts easy to grasp. Plus, a bound-in CD-ROM features all of the book's illustrations for use in PowerPoint presentations.

Complete your clinic with the new standard in Cardiology!

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==========================

          Healthpointe Is Now Offering Echocardiography Examinations at the Anaheim Clinic.        

Healthpointe’s multidisciplinary team is ready to provide comprehensive and high quality care for patients with cardiovascular needs.

(PRWeb May 28, 2015)

Read the full story at http://www.prweb.com/releases/2015/05/prweb12751712.htm


          Cardiographer (Cardiac Technician) - PRO PERSONNEL - Rustenburg, North West        
Explaining procedures, observing and position patients, and using protective devices to ensure safety and comfort during examination or treatment....
From Indeed - Wed, 28 Jun 2017 10:36:12 GMT - View all Rustenburg, North West jobs
          ECHOCARDIOGRAPHY TECHNOLOGIST - ETOBICOKE CARDIOLOGY CLINIC - Etobicoke, ON        
ADULT &amp; STRESS ECHO:. MUST HAVE 1 YEAR EXPERIENCE IN ADULT &amp; STRESS ECHO. WE ARE LOOKING FOR ECHOCARDIOGRAPHY TECHNOLOGIST TO WORK IN BRAMPTON AND ETOBICOKE...
From Indeed - Fri, 09 Jun 2017 15:36:41 GMT - View all Etobicoke, ON jobs
          Echocardiography Technologist - HART MEDICAL SERVICES INC - Greater Toronto Area, ON        
Hart Medical Services (HMS) is looking to hire *Stress* and *Stress- Echo* technicians for full time and part time employment spanning Monday to Saturday. The...
From Indeed - Thu, 27 Jul 2017 18:24:42 GMT - View all Greater Toronto Area, ON jobs
          ECHOCARDIOGRAPHY TECHNOLOGIST - TORONTO CARDIOLOGY & RADIOLOGY CLINIC - Toronto, ON        
MUST BE ABLE TO DO STRESS ECHO. WE ARE LOOKING FOR ECHOCARDIOGRAPHY TECHNOLOGIST FOR OUR WEST LOCATION....
From Indeed - Thu, 27 Jul 2017 14:23:35 GMT - View all Toronto, ON jobs
          Echocardiography Technologist - Cardiology Lab (153.17) - Women's College Hospital - Toronto, ON        
Performs Doppler Echocardiography, Stress Echo (exercise and dobutamine), Echo Contrast testing in a busy ambulatory setting....
From Indeed - Tue, 25 Jul 2017 21:00:44 GMT - View all Toronto, ON jobs
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          Wimbledon Health Partners’ Findings Make a Sure Fire Case for Echocardiography Testing for Young Athletes        

Every student with a serious cardiac abnormality identified in an echocardiogram had a normal EKG, and all possible abnormalities indicated on EKGs were confirmed false positives from corresponding echoes.

(PRWeb July 14, 2016)

Read the full story at http://www.prweb.com/releases/2016/07/prweb13555511.htm


          Wimbledon Health Partners’ Findings Prove Echocardiograms are Critical to Identifying Serious Abnormalities        

In 94% of the cases where abnormalities were identified through Wimbledon Health Partners’ echocardiography testing, corresponding EKG results were normal, underscoring the importance of using both EKGs and echocardiograms to detect dangerous conditions.

(PRWeb June 14, 2016)

Read the full story at http://www.prweb.com/releases/2016/06/prweb13485608.htm


          Astonishing Number of Heart Abnormalities Identified by Wimbledon Athletics During Recent Testing—a Much Higher Number Than Previously Reported        

Nearly 10% of the student athletes recently tested by Wimbledon Athletics were identified with abnormalities through echocardiography testing, which is significantly higher than studies would indicate. In all but two cases, EKGs for these same athletes were normal, clearly demonstrating the need for both tests.

(PRWeb May 12, 2016)

Read the full story at http://www.prweb.com/releases/2016/05/prweb13411744.htm


          Left Anterior Fascicular Block        
Cardiology Revision Notes - Left Anterior Fascicular Block

Left Anterior Fascicular Block - CardioNotes

Characteristics

Normal activation of the left ventricle proceeds down the left bundle branch, which consist of two fascicles the left anterior fascicle and left posterior fascicle. Left Anterior Fascicular Block (LAFB), which is also known as Left Anterior Hemiblock (LAHB), occurs when a cardiac impulse spreads first through the left posterior fascicle, causing a delay in activation of the anterior and lateral walls of the left ventricle which are normally activated via the left anterior fascicle.
Although there is a delay or block in activation of the left anterior fascicle there is still preservation of initial left to right septal activation as well as preservation of the inferior activation of the left ventricule (preservation of septal Q waves in I and aVL and small initial R wave in leads II, III, and aVF). The delayed and unopposed activation of the remainder of the left ventricle now results in a shift in the QRS axis leftward and superiorly, causing marked left axis deviation. This delayed activation also results in a widening of the QRS complex, although not to the extent of a complete LBBB

 

Criteria for LAFB

  • Left axis deviation (usually between -45° and -90°), some consider -30° to meet criteria
  • QRS interval < 0.12 seconds
  • qR complex in the lateral limb leads (I and aVL)
  • rS pattern in the inferior leads (II, III, and aVF)
  • Delayed intrinsicoid deflection in lead aVL (> 0.045 s)

 

Exceptions

It is important not to call LAFB in the setting of a prior inferior wall myocardial infarction which may also demonstrate left axis deviation due to the initial forces (Q wave in a Qr complex) in leads II, III, and aVF. As opposed to LAHB, the left axis shift is due to terminal forces (i.e., the S wave in an rS complex) being directed superiorly,

 

Effects of LAFB on Diagnosing infarctions and Left Ventricular Hypertrophy

LAHB may be a cause of poor R wave progression across the precordium causing a pseudoinfarction pattern mimicking an anteroseptal infarction. It also makes the electrocardiographic diagnosis of LVH more complicated, because both may cause a large R wave in lead aVL. Therefore to call LVH on an EKG in the setting of an LAHB you should see the presence of a “strain” pattern when you are relying on limb lead criteria to diagnose LVH.

 

Clinical Signficance

  • It can be seen in approximately 4% of cases of acute myocardial infarction
    • It is the most common type of intraventricular conduction defect seen in acute anterior myocardial infarction, and the left anterior descending artery is usually the culprit vessel.
    • It can be seen with acute inferior wall myocardial infarction.
  • It also associated with hypertensive heart disease, aortic valvular disease, cardiomyopathies, and degenerative fibrotic disease of the cardiac skeleton.

 

References

  1. Mirvis DM, Goldberger AL. Electrocardiography. In: Braunwald E, Zipes DP, Libby P, eds. Heart disease: a textbook of cardiovascular medicine, 6th edn. Philadelphia: WB Saunders; 2001:82–125.
  2. Surawicz B, Knilans TK. Chou’s electrocardiography in clinical practice: adult and pediatric, 5th edn. Philadelphia: W.B. Saunders; 2001.

          Dr. Adrian Baranchuk recognized as one of 10 most influential Hispanic Canadians        

One of Canada’s leading experts in cardiology, Queen’s University professor Adrian Baranchuk has been named one of the TD Bank's 10 most influential Hispanic Canadians by the Hispanic Business Alliance. The awards recognize community members who demonstrate influence in education, achievements, volunteerism and/or entrepreneurship.


This is the 10th Anniversary of the award, and this year, the Secretary General of the Organization of American States (OAS), Luis Almagro has been invited to deliver the awards during the ceremony in Toronto.


“This is truly one of the greatest honours I have received in my life,” says Dr. Baranchuk. “To be recognized as a leader is humbling and unexpected. I came to Canada with virtually nothing but I’ve worked very hard to establish myself. Canada, and its health care system have facilitated my integration into a new medical culture and has allowed me to develop into the professional that I am today.”


A native of Buenos Aires, Argentina, Dr. Baranchuk earned his MD from the University of Buenos Aires in 1990. After beginning to build his profile as a cardiologist-electrophysiologist, Dr. Baranchuk immigrated to Canada in 2003. In September 2003, Dr. Baranchuk was appointed as a clinical fellow in electrophysiology at McMaster University. He joined the division of cardiology at Queen’s in June of 2006.


In 2007, he created the Electrophysiology Training Program – a two-year program at Queen’s which teaches physicians from around the world new and sophisticated techniques to treat and cure cardiac arrhythmias. The program has attracted physicians from Canada, the United Kingdom, Chile, Argentina, South Africa, Emirates, Pakistan, Turkey, Dominican Republic and Ireland.


Dr. Baranchuk also founded and led the Broadcasting ECG Rounds to South-eastern Ontario (BESO project) – a program which allows Ontario physicians and students to join weekly training sessions in electrocardiology at Queen’s. His last iBook called Electrocardiography in practice: What to do? was released in iTunes in June 2016. The free application, which has been downloaded more than 1,000 times, is designed to teach electrocardiography in an interactive way.


Through these teaching programs, Dr. Baranchuk has mentored more than 40 medical students, 40 internal medicine residents and many more cardiology residents, fellows and colleagues from Queen’s and overseas. Dr. Baranchuk now serves as the head of the Kingston General Hospital Heart Rhythm Service.


“Being named one of the most influential Hispanic Canadians is a true honour and recognizes Dr. Baranchuk’s talent and drive,” says Dr. Steven Liss, Vice-Principal (Research). “Not only is he a leading cardiologist, Dr. Baranchuk is a motivator in our community and has worked tirelessly to ensure young students and young doctors achieve their potential.”


Dr. Baranchuk is currently the Vice President of the Inter American Society of Cardiology (IASC). He leads the IASC Academy which allows trainees from Latin America to attend courses and observerships in top centers of North America. Dr Baranchuk is the President Elect of the International Society of Electrocardiology and in this role, he engages colleagues and researchers from the region in educational and research activities.


Dr. Baranchuk says his life, both past and present, have driven him to his present successes. “I am obligated to give back because I am truly blessed in my life,” he says with a smile. “About 80 per cent of the people living in Latin America have no chance to pursue their dreams but I represent the 20 per cent that are lucky, that are blessed. This means I need to help others reach their dreams and goals. I am passionate about that.”


The OAS consists of the 35 independent states of the Americas, including Canada and the United States, and constitutes the main political, juridical, and social governmental forum in the Northern Hemisphere. The four main pillars include democracy, human rights, security and development.


          Oman Pathology Dept__posted__07June2017pdf        
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          WBCS Preliminary(Physics): Sound        
  • Sound is a form of energy and like all other energies, sound is not visible to us. It produces a sensation of hearing when it reaches our ears. Sound can not travel through vacuum.
  • Sound is produced due to vibration of different objects.The matter or substance through which sound is transmitted is called a medium. It can be solid, liquid or gas. Sound moves through a medium from the point of generation to the listener.
  • In longitudinal wave the individual particles of the medium move in a direction parallel to the direction of propagation of the disturbance. The particles do not move from one place to another but they simply oscillate back and forth about their position of rest. This is exactly how a sound wave propagates, hence sound waves are longitudinal waves. Sound travels as successive compressions and rarefactions in the medium. In sound propagation, it is the energy of the sound that travels and not the particles of the medium.
  • There is also another type of wave, called a transverse wave. In a transverse wave particles do not oscillate along the line of wave propagation but oscillate up and down about their mean position as the wave travels. Thus a transverse wave is the one in which the individual particles of the medium move about their mean positions in a direction perpendicular to the direction of wave propagation. Light is a transverse wave but for light, the oscillations are not of the medium particles or their pressure or density – it is not a mechanical wave.
  • To and fro motion of an object is known as vibration. This motion is also called oscillatory motion.
  • Amplitude and frequency are two important properties of any sound.
  • The loudness or softness of a sound is determined basically by its amplitude. The amplitude of the sound wave depends upon the force with which an object is made to vibrate.
  • The change in density from one maximum value to the minimum value and again to the maximum value makes one complete oscillation.
  • The distance between two consecutive compressions or two consecutive rarefactions is called the wavelength, λ.
  • The time taken by the wave for one complete oscillation of the density or pressure of the medium is called the time period, T.
  • The number of complete oscillations per unit time is called the frequency (ν), ν =(1/T). The frequency is expressed in hertz (Hz).
  • Larger the amplitude of vibration, louder is the sound. Higher the frequency of vibration, the higher is the pitch, and shriller is the sound.
  • The frequency determines the shrillness or pitch of a sound. If the frequency of vibration is higher, we say that the sound is shrill and has a higher pitch. If the frequency of vibration is lower, we say that the sound has a lower pitch.
  • A sound of single frequency is called a tone whereas a sound of multiple frequencies is called a note. Of the several frequencies present in a note, the sound of the lowest frequency is called the fundamental tone. Besides the fundamental, other tones present in a note are known as overtones. Of the overtones, those which have their frequencies simple multiple of fundamental frequency, are known as harmonics. All harmonics are overtone but all overtones are not harmonics.
  • The speed of sound is defined as the distance which a point on a wave, such as a compression or a rarefaction, travels per unit time. speed, v = distance / time =(λ/T). Here λ is the wavelength of the sound wave. It is the distance travelled by the sound wave in one time period (T) of the wave. Thus, v = λ ν[Q(1/T)= ν]. or v = λ ν, That is, speed = wavelength X frequency. The speed of sound remains almost the same for all frequencies in a given medium under the same physical conditions.
  • Sound propagates through a medium at a finite speed. The speed of sound depends on the properties of the medium through which it travels. The speed of sound in a medium depends also on temperature and pressure of the medium. The speed of sound decreases when we go from solid to gaseous state. In any medium as we increase the temperature the speed of sound increases. Experiment shows that the velocity of sound in air at 0 0C is about 332 metres per second.
  • The velocity of sound through a gas is inversely proportional to the square root of the density of the gas.
  • The law of reflection of sound states that the directions in which the sound is incident and reflected make equal angles with the normal to the reflecting surface and the three lie in the same plane.
  • If we shout or clap near a suitable reflecting object such as a tall building or a mountain, we will hear the same sound again a little later. This sound which we hear is called an echo. The sensation of sound persists in our brain for about 0.1 second. To hear a distinct echo, the time interval between the original sound and the reflected one must be at least 0.1 second. If we take the speed of sound to be 344 m/s at a given temperature, say at 22 0C in air, the sound must go to the obstacle and reach back the ear of the listener on reflection after 0.1s. Hence, the total distance covered by the sound from the point of generation to the reflecting surface and back should be at least (344 m/s) × 0.1 s = 34.4 m. Thus, for hearing distinct echoes, the minimum distance of the obstacle from the source of sound must be half of this distance, that is, 17.2 m. This distance will change with the temperature of air. Echoes may be heard more than once due to successive or multiple reflections.
  • The phenomenon of prolongation of sound due to successive reflections of sound from surronding objects is called reverberation.
  • Stethoscope is a medical instrument used for listening to sounds produced within the body, chiefly in the heart or lungs. In stethoscopes the sound of the patient’s heartbeat reaches the doctor’s ears by multiple reflection of sound.
  • The audible range of sound for human beings extends from about 20 Hz to 20000 Hz (one Hz = one cycle/s). Children under the age of five and some animals, such as dogs can hear up to 25 kHz (1 kHz = 1000 Hz).
  • Sounds of frequencies below 20 Hz are called infrasonic sound or infrasound. Rhinoceroses communicate using infrasound of frequency as low as 5 Hz. Whales and elephants produce sound in the infrasound range. It is observed that some animals get disturbed before earthquakes. Earthquakes produce low-frequency infrasound before the main shock waves begin which possibly alert the animals.
  • Frequencies higher than 20 kHz are called ultrasonic sound or ultrasound. Ultrasound is produced by dolphins, bats and porpoises.
  • Ultrasounds can be used to detect cracks and flaws in metal blocks. Metallic components are generally used in construction of big structures like buildings, bridges, machines and also scientific equipment. The cracks or holes inside the metal blocks, which are invisible from outside reduces the strength of the structure. Ultrasonic waves are allowed to pass through the metal block and detectors are used to detect the transmitted waves. If there is even a small defect, the ultrasound gets reflected back indicating the presence of the flaw or defect.
  • Ultrasonic waves are made to reflect from various parts of the heart and form the image of the heart. This technique is called ‘echocardiography’.
  • Ultrasound scanner is an instrument which uses ultrasonic waves for getting images of internal organs of the human body. A doctor may image the patient’s organs such as the liver, gall bladder, uterus, kidney, etc. It helps the doctor to detect abnormalities, such as stones in the gall bladder and kidney or tumours in different organs. In this technique the ultrasonic waves travel through the tissues of the body and get reflected from a region where there is a change of tissue density. These waves are then converted into electrical signals that are used to generate images of the organ. These images are then displayed on a monitor or printed on a film. This technique is called ‘ultrasonography’.
  • The acronym SONAR stands for SOund Navigation And Ranging. Sonar is a device that uses ultrasonic waves to measure the distance, direction and speed of underwater objects.Sonar consists of a transmitter and a detector and is installed in a boat or a ship. The transmitter produces and transmits ultrasonic waves. These waves travel through water and after striking the object on the seabed, get reflected back and are sensed by the detector. The detector converts the ultrasonic waves into electrical signals which are appropriately interpreted. The distance of the object that reflected the sound wave can be calculated by knowing the speed of sound in water and the time interval between transmission and reception of the ultrasound. Let the time interval between transmission and reception of ultrasound signal be t and the speed of sound through seawater be v. The total distance, 2d travelled by the ultrasound is then, 2d = v × t. The above method is called echo-ranging. The sonar technique is used to determine the depth of the sea and to locate underwater hills, valleys, submarine, icebergs, sunken ship etc.
  • Again if the speed of any substance, specially of an air-craft, be more than the speed of sound in air, then the speed of the substance is called supersonic speed. The ratio of the speed of a body and that of sound in air is, however, called the Mach number of the body. If the Mach number of a body is more than 1 , it is clear that the body has supersonic speed.

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          CONTOH SOAL UJIAN KOMPETENSI DOKTER        
(Jawaban by Avicenna ‘03 UNHAS)

1.Seorang perempuan berusia 32 tahun yang menderita diabetes mellitus tipe 1 mengalami gagal ginjal progresif dalam kurun waktu dua tahun terakhir. Dialisis belum dilakukan pada pasien ini. Pemeriksaan fisik tidak menunjukkan tanda-tanda abnormalitas. Hasil pemeriksaan laboratorium menunjukkan kadar hemoglobin = 9 dang/dl, hematokrit = 28 %, m3. Apus darah tepi menunjukkan sel-sel eritrosit MCV 94 normositer dan normokromik. Manakah jawaban di bawah ini yang paling mungkin sebagai penyebab kondisi pasien tersebut ?
A) Perdarahan akut
B) Leukemia limfositik kronik
C) Anemia Sideroblast
D) Defisiensi erythropoietin
E) Defisiensi enzim eritrosit

2.Seorang laki-laki berusia 30 tahun yang sebelumnya dalam keadaan sehat, menderita demam dan pruritus, berkeringat malam, serta menemukan benjolan di atas klavikula sinistra selama tiga minggu. Pemeriksaan fisik menunjukkan pembesaran nodus lymphatikus yang tidak nyeri, berdiameter 3 cm, berkonsistensi kenyal dan berlokasi di regio supraklavikula. Pemeriksaan sinar X thoraks memberi kesan adanya limfo-adenopati mediastinal. Manakah jawaban yang paling tepat di bawah ini yang merupakan penyebab penyakit pada pasien tersebut?
A) Tuberkulosis
B) Karsinoma metastatik
C) Penyakit Hodgkin
D) Sarkoidosis
E) Mononukleosis infeksiosa

3.Seorang anak laki-laki berusia 8 digigit oleh seekor lebah. Dalam lima menit terlihat lesi yang membengkak, berukuran 2 cm, dan berwarna merah di tempat gigitan tersebut. Di antara jawaban berikut, temuan manakah yang dominan pada lesi gigitan tersebut ?
A) Reaksi terhadap korpus alienum
B) Perdarahan
C) Infiltrasi limfositik
D) Migrasi neutrofilik
E) Vasodilatasi

4.Seorang laki-laki berusia 80 tahun menderita sebuah karsinoma ulseratif pada kulit skrotum dextra. Grup kelenjar manakah di bawah ini yang pertama kali akan menerima sel-sel metastatik dari karsinoma tersebut ?
A) Iliaka eksterna
B) Iliaka Interna
C) Inguinal superfisialis
D) Inguinal profunda
E) Lumbar (para-aorta)

5.Seorang anak perempuan berusia 4 tahun tidak dapat makan selama dua hari karena penyakit gastro-intestinal. Dari jawaban di bawah ini, manakah yang menjadi sumber utama energi yang akan dioksidasi pada otot rangka penderita tersebut ?
A) Kreatin Fosfat otot
B) Glikogen otot
C) Trigliserida otot
D) Asam lemak serum
E) Glukosa serum

6.Laki-laki, 60 tahun berdebar, badan mengurus, nafsu makan meningkat, mudah emosi, keringat meningkat, sulit tidur.
a.hipertiroid
b.hipotiroid
c.Diabetes Melitus
d.Diabetes Insipidus
e.Sindroma Cushing

7.Laki-laki, 24 tahun, terdapat benjolan di leher depan, tidak sakit. Orang sekampung memiliki sakit yang sama seperti ini.
a.Defisiensi Krom
b.Defisiensi vit B1
c.Defisiensi Iodium
d.Oklusi kelenjar lemak
e.Tumor kelenjar getah bening

8.25 tahun, demam, linu, memakai putow 5 th, 3x/hari dan lemes. 5 jam yg lalu pasien gelisaah, keluar ingus banyak, Keadaan manakah yang sesuai dengan kondisi diatas….
a.Sindroma Withdrawal
b.Overdosis
c.Keracunan kronik
d.Adiksi
e.Toleransi

9.Keadaan manakah yang paling sesuai untuk penggunaan putow pada kasus:
a.Adiksi
b.Toleransi
c.Abstinensia
d.Sugesti
e.Overdosis

10.Seorang laki-laki, 20 tahun mengeluh BAK warna kuning sejak 2 hari. Pada Pemeriksaan fisik terlihat sclera ikterik dan kulit warna kuning. Pemeriksaaan lanjutan apa yang anda usulkan pada pasien ini ?
a.SGOT/PT
b.Ureum/creatinin
c.As. Urat
d.GDS dan GDP
e.Kolesterol total dan LDL

11.Seorang wanita, 30 th dibawa keluarga ke UGD karena muntah darah. Riwayat pasien ini menderita Hepatitis B kronik. Pemeriksaan fisik tampak lemas, TD 140/90, Nadi 90x/mnt, Konjungtiva Palpebra anemis (+), Rambut ketiak (-), ginekomasti (+), spider navi (+), Liver span 5 cm. Apa penyebab hematemesis pada pasien ini?
a.Sind. Mallory Weiss
b.Pecahnya Varises Esofagus
c.Esofagitis
d.Perforasi Ulcus Gaster
e.Perforasi Ulcus duodenum

12.Pemeriksaan Radiologis Rutin pada anak umur 2 bulan:
a.Foto thorax PA
b.Foto thorax lateral kiri
c.Foto top lordotik
d.foto thorax AP

e.Foto thorak lateral kanan

13.Sesak 2hr, batuk, panas tinggi, flu 3hari. Respirasi 53x/menit, t 390C cuping hidung (+).
a.Efusi pleura
b.Bronkopneumonia
c.Pneumonia
d.Sind Schwarte
e.Atelektasis

14.Seorang wanita hamil 29 minggu datang untuk ANC. Tensi 150/90, proteinuri +2. Trombosit , hepar Normal. Yang dilakukan:
a.SC
b.Induksi Persalinan
c.Pemberian Mg S04
d.Pemberian Diazepam
e.KONSERVATIF

15.Wanita G3P2A0 Riwayat SC, hamil aterm, 20 jam inpartu belum lahir, 3 jam dipimpin belum lahir. VT: terapa tangan, letak belakang kepala. CPD relatif Tindakan?
a.SC
b.Partus Percobaan
c.Vacum
d.Forsep
e.Kristeler

16.Laki-laki, 50 th. Hipertensi selama 5 th T= 170/100 mmhg, anjuran anda sebagai dokter keluarga:
a.Pola makan
b.Olahraga aerobik
c.Mengurangi strees
d.Berhenti merokok
e.Mengganti obat

17.Kejadian pada anak usia 5 th dimana ibunya belum pernah vaksinasi TT, pilih salah satu yang benar:
a.epidemik
b.endemik
c.pandemik
d.wabah
e.KLB

18.Anak Perempuan 13 th dibawa ibunya ke poliklinik dengan keluhan panas badan terus menerus sejak 3 hari yll (keringat dingin (+).. ? tulisan ga jelas) nyeri kepala, nyeri otot t.u tungkai,mual muntah, keluar darah dari hidung, bintik2 merah. Px selanjutnya?
a.Tes RL
b.Widal
c.Darah rutin
d.Apus tenggorok
e.mantoux

19.Suntika PP 1,5 jt unit i.m pada laki2 50 th. Tiba2 pasien jatuh ke lantai. PF: kesadaraan menurun, TD 60/ palp, N:120x/mnt, RR=24x/mnt. Penyebab:
a.Ggg pompa jantung
b.Perdarahan hebat
c.Rasa sakit yang berat
d.Hipoglikemi
e.Vasodilatasi hebat

20.laki2 25 th gatal2 seluruh tubuh setelah makan udang. Sejak 5 th yll. Sel apa yang jmlnya meningkat?
a.sel plasma
b.mast cell
c.fibrosit
d.makrofag
e.PMN

21.Perempuan, 35th, hamil anak ke 4, dtng ke RS dengan keluhan cepat lelah dan lesu. PF: tidak ada pembesaran organ, Hb =8, Leu 12 rb, Tr 350rb, mikrositik hiokrom, anisopoikilositosis, eliptosit, Hit jenis dbn, retikulosit dbn. Pemeriksaan Lab yang tepat?
a.kadar besi
b.diff count
c.elektroforesis Hb
d.analisa tinja
e.?? ( tulisan ga jelas)

22seorang pasien tidak sadar di bawa ke UGD stlh menjd korban tabrak lari. N >120 TD turun, kehilangan darah 30-40%. Mnrt ATLS, klasifikasi syok perdarahan?
a. I,
b. II,
c.III,
d.IV,
e.V

23.40 th laki2 henti jantung, resusitasi dan ...?, jika tindakan benar, maka tekanan darah:
a.110/10
b 110/80
c.110/50
d.100/40
e.110/79

24.wanita 40th, berdebar-debar, berat, tertekan, nyeri dada kiri, takut mati.
a.AMI
b.Pneumotorak
c.Perikarditis
d.Kataton
e.Cemas akut

25.Bayi 8 bln, BAB 4-5 x/hari dan sisa makanan yang belum tercerna selama 2 mg. Ibu bekerja memberi ASI 1x sebelum dan 3-4 x setelah kerja. MPASI 3x bubur susu, 1x sari jeruk peras. Ayah tidak bekerja dan nenek membantu mengasuh bayi. Apa yang mendsari BAB tsb?
a.bayi ditinggal kerja ibu
b.nenek membantu nmengasuh
c.bubur susu 3x
d.sari jeruk 1x
e.ayah tidak bekerja

26.Pria 25 th demam 10 hari, mulamula tidak tinggi lalu makin lama makin tinggi terutama di sore hari dan malam. 3hr pertama panas dan mencret, tampak apatis. 3hr mendapat paracetamol dan ampisilin tidak membaik. Pemeriksaan u/ menegakkan diagnosa etiologi?
a.widal, gal/bulyon,kultur darah, serologis
b.inhibisi hemaglutinasi
c.apus darah tebal
d.serologis leptospirosis, widal
e.widal, kultur gal/bulyon, kultur feces

27.Bayi, lubang kencing tidak lazim, pembesarah klitoris, muara uretra ...., rencana?
a.foto rontgen
b.lab darah
c.obserfasi di pusk
d.pasang kateter
e.rujuk poli bedah

28.Bengkak pada mata, kelopak, 2mg timbul pada tungkai dan perut, kencing merah, protein urine 4+
a. GGK
b. SNA,
c.SN,
d. gagal jantung,
e. sirosis hepar,

29.laki2, luka pada kemaluan, 2hr ulcus sekitar gland penis keras, nyeri (-), bersih, rata, PSK 1bln.
a.Ukus banal
b.Ulkus mole
c.Ulkus durum
d.Kompleks primer
e.Ulkus bubanum

30.Bayi laki2 45 th, dibawa ke UGD dengan kel perdarahan yang sulit berhenti di bekas suntikan im hep B. Pada PF: KU baik, perdarahan merembes di paha kiri bekas suntikan, perdarahan tempat lain tidak ada, anemi(-), ikterik (-), hepatomegali (-), splenomegali(-), limfadenopati (-). Lab darah : Hb 11, Leu 8500, trom 170rb, PT PTTK meningkat. Dx?
a.ITP
b. Hemofili A,
C.Hemofili B,
1.Def vit K,
2.DIC

31.manakah dari dibawah ini yang paling mungkin mndasari anemi pada kasus diatas?
a.ggg prod
b.destruksi
c.perdarahan kronis
d.--------”------- akut
e.kongenital


32.Benjolan dirahang bawah kiri, tidak nyeri 5 cm, mendesak daerah telinga keatas, tdk paralise n.7
a.tm. Jinak kel parotis
b.tm ganas kel parotis
c.sialodenitis
d.TBC kel parotis
e.Hemangioma kel parotis

33.laki2 sdh 10th keluar cairan dari telinga kiri, putih, kental, bau busuk. Nyeri telinga (+), demam (+), mulut mencenga kanan, CAE granulasi>
a.OMA
b.OMSK
c.Kolesteatoma
d.Otitis eks maligna
e.Granuloma

34.pasien datang ke dr.A dengan terlambat datang bulan ± 3 bulan. G3P2A0, anak terkecil 7 bulan. Dokter A menolak memberikan terapi dan meyarankan pergi ke dr.B. Dokter B memberi obat dan diminta kontrol setelah 5 hari. Tindakan dr.A adalah…
a. benar, melanggar hukum
b. benar, melawan hukum
c. salah, melanggar hukum
d. salah, melawan hokum

35.Laki-laki, trauma dada, nafas sesak, ngorok. Perkusi dada kiri hipersonor. Saat nafas dada kiri tertinggal. Nadi tak teraba, akral dingin. Apa yang dilakukan di UGD?
a. beri O2 sungkup, nafas spontan & dekompresi jarum
b. beri O2 sungkup, nafas bantu & dekompresi jarum
c. intubasi, O2 sungkup,nafas spontan & dekompresi jarum
d. intubasi, O2 sungkup,nafas bantu & dekompresi jarum
e. langsung dekompresi jarum


36.Laki-laki, 40 tahun, karena mengalami kesakitan tak tertahankan karena menderita tumor ganas, penderita minta euthanasia. Apa alasan dokter memperbolehkan euthanasia?
a. usia tua
b. menghilangkan penderitaan pasien
c. atas permintaan pasien
d. hak manusia untuk emnentukan hak hidup matinya sendiri
e..

37. Laki-laki, sesak, demam 3 hari. Riwayat ayam tetangga mati mendadak dalam peternakan. Rontgen paru : infiltrat luas di lapangan paru. Di bawah ini yang benar :
a. hewan reservoar tidak ada
b. termasuk virus influensa tipe B
c. berkembang biak di sitoplasma sel hospes
d. antigenik variasi pada Ag H dan Ag N

38.umur 7 tahun, perdarahan pervaginam, tanda seks sekunder (+). Riwayat trauma genital disangkal.
a. menarche
b. pubertas dini
c. pubertas tarda
d. klimektarium

39.20 tahun, primi, hamil 37 minggu. T = 180/110, udem anasarka. AKI tinggi selain disebabkan penyakit di atas adalah...
a. DM
b. perdarahan post partum
c. tumor payudara
d. tumor serviks

40.anak 15 tahun. Saat kecil sering demam dan kejang. Sekarang sulit naik kelas dan masih kelas 2 SD. Kemungkinan diagnosanya adalah...
a. retardasi mental
b. deprivasi mental
c. hiperaktif
d. epilepsi
e. deterionasi mental

41.Seorang ibu, bayi perempuan 8 bulan, BAB ± 4 – 5 x/hari disertai sisa makanan yang belum tercerna sempurna sejak 2 minggu terakhir. Ibu bekerja sebagai guru & memberikan ASI 1x sebelum berangkat kerja & sepulang kerja 3-4 x . Makanan tambahan bubur susu 3x/hari & sari jeruk peras 1x sehari. Ayah tidak bekerja, nenek bantu asuh bayi. Anjuran terbaik?
a.Sementara ibu berhenti bekerja
b.Pemberian bubur susu dihentikan
c.Pemberian sari jeruk peras dihentikan
d.Diberikan imunisasi
e.Dikonsultasikan ke puskesmas

42.Balita sesak nafas, badan panas, terdapat nafas cuping hidung, obat apa yang paling tepat ?
A. Ampicillin
B. Amoksisilin
C. Cefotaxim
D. Kotrimoksasol
E. Eritromisin

43.Anak 5 tahun terjatuh, luka robek 2 x 1 cm diberi obat povidon iodine maka jenis penyembuhan lukanya adalah ……….
A. primary intention
B. secondary intention
C. tertiary intention
D. Delayed intention
E. acute intention

44.Seorang pasien laki-laki 18 tahun mengeluh gatal-gatal. Terdapat bercak makulo hipopigmentasi berskuama halus di leher, bahu dan punggung bentuknya macam-macam apabila digaruk akan bersisik, Pemeriksaan dengan KOH 10% terdapat hifa yang pendek, maka diagnosisnya adalah ………
A. Tinea capitis
B. Ptiriasis alba
C. Ptiriasi versicolor
D. Tinea korporis
E. Ptiriasis rosea gilbert

45. Laki-laki dewasa hobi berenang, kemudian mengeluh kram di betis. Struktur yang berperan pada kontraksi otot……..
A. Miofilamen
B. Sarkomer
C. protein aktin dan myosin
D. asam laktat
E. mitokondria

46.Seorang laki-laki 17 tahun diantar ke Puskesmas karena KLL, patah tulang terbuka kedua tungkai, darah mengallir deras. Di Puskesmas penderita tenang, tertidur dan mengeluarkan suara mendengkur seperti berkumur-kumur. Nadi a. radialis cepat dan lemah, ujung jari-jari dingin. Tindakan apa yang harus dilakukan pertama kali ?
A. membebaskan jalan nafas dan mengatur posisi kepala
B. memberi nafas buatan dari mulut ke mulut
C. mengangkat kedua tungkai, badan diberi alas papan keras
D. pasang infuse line cairan koloid dan vasopresor
E. pasang bidai pada kedua tungkai

47.Seorang anak 7 tahun datang bersama adiknya, keduanya dengan keluhan gatal-gatal di seluruh tubuh, sela-sela jari kaki dan tangan. Timbul papul-papul, ada beberapa bentuk vesikel. Lapisan kulit mana yang mengalami patologi pada fase awal penyakit tersebut ?
A. stratum corneum
B. stratum basale
C. stratum granulosum
D. stratum lusidum
E. stratum spinosum

48. Seorang wanita datang, sejak 2 hari terdapat bercak-bercak kemerahan di sekitar mulut, keropeng di bibir. PF : Eritema, vesikel, bula di sekitar bibir dan mukosa mulut. Riwayat minum obat 5 hari yang lalu. Faktor pencetus yang paling mungkin………
A. alergi obat
B. infeksi
C. neoplasma
D. inflamasi
E. Infestasi

49.Komplikasi penyakit tersebut diatas yang dapat menyebabkan kematian……..
A. meningitis
B. hepatitis
C. perdarahan gastrointestinal
D. DIC
E. sepsis

50. Ibu P2A1, setelah KET 1 bln, dtg untuk KB 3 thn. Suami tdk mau kondom/pantang berkala. KB efektif:
a. IUD
b. KB Depoprovera
c. KB Estrogen
d. KB Pil
e. ....

51.Seorang pasien, 40 thn, mengeluh kesemutan di bibir bagian bawah setelah operasi gigi bawah belakang 2 mgg y.l. Apa penyebabnya?
a. Alergi obat anestesi
b. Dosis obat berlebihan
c. Obat anestesi masuk pembuluh darah
d. Kelainan anatomi rahang
e. Trauma jar. Saraf

52. Laki-laki, 26 thn, mudah lelah, keringat >> , mata melotot, tremorpemeriksaan penunjang apa yg perlu dilakukan? T3T4TSH
27. ♀, 22 thn, suntikDM type I. Dasar kelainan metabolik tersebut : insulin seumur hidup
a. Peningkatan proteolisis
b. Peningkatan lipogenesis
c. Peningkatan sekresi kolesterol
d. Penurunan glikogenolisis
e. Penurunan oksidasi ß

53. Laki-laki, 61 thn, pensiun, mengalami gangguan dlm mengingat urutan tgl lahir anaknya. Gangguan tsb?
a. Depresi
b. Delirium
c. Paramnesia
d. Amnesia
e. Demensia

54. Anak 1 bln, putih di tengah mata, stlh dipx Katarak Kongenital. Operasi katarak sebaiknya?
a. 6-8 bln
b. Setelah usia 1 thn
c. Setelah usia 2 thn
d. Setelah usia 5 thn
e. Sebelum usia pendidikan

55. Seorang laki-laki berusia 35 tahun mengalami luka bakar pada seluruh ketebalan kulit pada daerah dorsum manus. Sebuah flap rotasi dari kulit normal dan jaringan subkutaneus dibuat untuk menutupi defek tersebut. Dari jawaban di bawah ini, pada lapisan manakah pembuluh darah arterial yang akan memberikan vaskularisasi pada flap tersebut ?
A) Stratum Basale
B) Dermis bagian dalam
C) Stratum corneum
D) Stratum lucidum
E) Lemak subkutan
Jwb: E

56.Seorang laki-laki berusia 24 tahun dirujuk ke unit gawat darurat rumah sakit setelah tertusuk benda tajam di thoraks anterior pada sisi medial papilla mamae sinistra. Pada saat tiba, diketahui tekanan darah = 70/50 mmHg. Vena-vena leher tampak melebar.Suara pernafasan vesikuler normal pada kedua paru. Dari pilihan jawaban di bawah ini, step pengelolaan berikutnya yang paling tepat adalah:
A) Foto Sinar X Thoraks
B) Intubasi endotracheal
C) EKG
D) Insersi tabung pada cavum thoraks sebelah kiri.
E) Perikardiosentesis
Jwb: A

57.Seorang perempuan berusia 22 tahun berobat ke dokter 3 bulan setelah menemukan sebuah benjolan pada kuadran lateral bawah mammae dextra. Pemeriksaan fisik menunjukkan massa berdiameter 2 cm, berbentuk oval, padat, halus, dan mobil pada mamae tersebut. Tidak ditemukan pembesaran kelenjar getah bening axilla. Jika biopsi eksisi di lakukan pada benjolan tersebut, maka kemungkinan besar akan menunjukkan tanda-tanda penyakit:
A) Nekrosis lemak
B) Fibroadenoma
C) Kelainan fibrokistik mammae
D) Karsinoma intraduktal
E) Papilloma intraduktal
Jwb: B

58.Seorang wanita berusia 54 tahun dibawa ke unit gawat darurat oleh keluarganya karena baal dan lemah pada tangan kiri dan kedua kakinya selama 2 jam. Dia memiliki riwayat tekanan darah tinggi dan penggunaan alkohol serta merokok sebanyak 2 bungkus rokok setiap hari selama 30 tahun. Rasa pada tangan kiri dan kedua kaki menurun dan kekuatan otot adalah 0/5. Terdengar bruit pada arteri karotid kanan.
Manakah dari pemeriksaan di bawah ini yang paling tepat untuk penegakan diagnosis awal?
A) Electroencephalography
B) Carotid duplex scan
C) CT scan kepala
D) Echocardiography
E) Carotid angiography
Jwb: C

59.Satu hari setelah perbaikan terhadap ruptur aneurisma aorta yang dilakukan dalam keadaan emergensi, seorang pria berusia 66 tahun menghasilkan urine sebanyak 35 mL selama perioda 4 jam, sebuah kateter foley masih terpasang. Dia menerima 14 unit darah selama operasi. Suhu C (100 F), tekanan darah 104/68 tubuhnya 37.8 126x/menit. Pemeriksaan fisik menunjukkan adanyammHg, dan nadi edema perifer yang luas. Suara jantung normal. Pada pemeriksaan dengan auskultasi suara paru terdengar bersih. Perut teraba lunak. Hasil pemeriksaan laboratorium menunjukkan: Hematocrit 27%, Serum Na+ 143 mEq/L, K+ 5.0 mEq/L, Urine Na+ 6 mEq/L. Manakah dari pernyataan di bawah ini yang merupakan penyebab oliguria yang paling tepat untuk pasien tersebut?
A) Gagal jantung
B) Hypovolemia
C) Occluded Foley catheter
D) Renal artery thrombosis
E) Transfusion reaction
Jwb: B

60.Pria, 38 th, 2 mgg ini merasakan kaki kirinya terasa sangat nyeri saat tidur. sebenarnya dirasa sakit sejak 1 tahun belakangan, namun hanya dirasakan bila berjalan. Penderita mengeluh jarak tempuh makin lama makin pendek dan sering berhenti karena nyeri. Bila istirahat nyeri hilang. Penderita seorang perokok berat. PF secara umum normal, pada eks. inf. sinistra tidak teraba pulsasi a. dorsalis pedis dan tibialis posterior. pemeriksaan lab normal.
Manakah diagnosis yg paling mungkin?
A. Acute arterial occlusion -> tdk mgkn akut sdh 1 thn
B. Thromboangitis obliterans
C. Diabetic arteriopathy
D. Chronic arterial thrombosis
E. atherosclerotic peripheral arterial occlusive disease
Jwb: B

61.pria, 31 th, menderita Buerger's disease. mengeluh ujung kelingking kaki kanannya kehitaman dan bau. juga dirasakan sangat nyeri. PF umum normal, status lokalis: tampak gangren kering pd ujung digiti V pedis dex. Lab: Hb 13,1 Leu 12.100 lab lain normal Tindakan pd pasien:
A. Nekrotomi & debridement, kemudian disiapkan u/ amputasi elektif
B. Nekrotomi & debridement, kemudian diberi analgetik, antibiotik, & vasodilator oral
C. insisi & drainase, --> analgetik, antibiotik, vasodilator oral
D. tidak nekrotomi & debridement --> tapi analgetik, antibiotik, vasodilator oral ?
E. amputasi dgn anestesi lokal --> antibiotik, analgetik, vassodilator oral
Jwb: B

62. wanita 35 tahun, tungkai kanan bengkak sejak 2 thn lalu, tidak nyeri. diagnosa paling mungkin?
A. deep vein thrombosis
B. Lipedema
C. Limfedema
D. Edema statis
E. Edema
Jwb: C

63. perempuan 18th, nyeri diujung kaki kiri sejak 5 hari yll, jari tsb tampak pucat dan dingin dibanding kaki kanan. pulsasi hanya jelas teraba di inguinal tetapi lemah. sejak 1bln yll sakit kepala terus menerus. TD di lengan kiri-kanan sama, tetapi TD di tungkai kiri lebih lemah dr yg lain.
diagnosis paling mungkin?
A. Arterioskelosis
B. Aterosklerosis obliterans
C. Tromboflebitis
D. Tromboangitis obliterans
E. Arteritis takayasu
Jwb: E

64.Apa tanda dan gejala terpenting dari Volkmann's ischemic:
A. Pallor
B. Coolness
C. Swelling
D. Numbness
E. Pain
Jwb: E

65.seorang gadis cantik datang ke praktek saudara mengharapkan tinggi badan bertambah karena dia bercita2 jd pramugari. dr menyarankan / Rontgen daerah lutut. apa yg terutama dilihat dari hasil Ro pd kasus diatas?
A. Periosteum
B. Epiphysis
C. Metaphysis
D. Epiphyseal plate
E. Perichondrium
Jwb: E

66. Laki2, 25th, kecelakaan lalu lintas (KLL) --> sepeda motor, dibawa ke dukun tulang. 1mgg kemudian dibawa ke UGD & trnyata mengalami patah tulang (Fx) terbuka 1/3 atas tibia grade 3A. Tindakan?
A. pemberian antibiotik (AB) dan anti tetanus serum (ATS)
B. Dilakukan imobilisasi dgn plaster cast
C. dilakukan pemeriksaan kultur dan resistensi test kuman dr lukanya
D. Dilakukan debridement, fiksasi eksternal, AB yg sesuai
E. Amputasi kakinya
Jwb: D

U/ 3 soal berikut gunakan skenario dibawah ini
67. pada saat dilakukan pertolongan di UGD terhadap korban KLL, didapat primary survey: A clear, B clear. Pada saat C, cairan apa yg sebaiknya diberikan pada pasien ini?
A. larutan D5%
B. larutan Hemasel
C. larutan NaCl 0,9% ?
D. larutan HES 5%
E. larutan RL
Jwb: E

68. bila dicurigai pd pasien ini mengalami obstruksi partial jalan napas yg disebabkan pangkal lidah, pada pemeriksaan bunyi apa yg terdengar?
A. Snoring
B. Crowning
C. Gurgling
D. Wheezing
E. Grunting
Jwb: A

69.apakah pada pasien ini perlu dipasang nasopharyngeal airway?
A. Tidak, karena bukan trauma oro-maxillofacial hebat
B. Tidak, karena tidak ada gangguan koagulasi
C. Perlu, karena terjadi fx basis kranii
D. Perlu, karena terjadi fx os nasale
E. Perlu, karena akan dilakukan operasi didaerah hidung
Jwb: A

untuk soal2 dibawah gunakan skenario berikut:
70.seorang pengendara mobil mengalami KLL di jalan tol. Penderita mengalami trauma multiple. Di UGD, primary survey stabil. saat secondary survey, saudara akan membuat foto Ro pertama

71.Pemeriksaan Ro di daerah mana yg saudara usulkan?
A. Kepala, leher, toraks, pelvis
B. Daerah persendian dan ekstrimitas
C. Kepala dan leher
D. Toraks dan abdomen
E. Pelvis
Jwb: A

72.Jika pada pasien (px) ini ditemukan jejas pada kepala dan dada, tindakan airway management apa yg boleh dilakukan?
A. Head tilt
B. Chin lift
C. Jaw thrust -> ACLS
D. Fleksi kepala
E. Ekstensi kepala
Jwb: C

73.tiba2 ada pasien mengalami henti jantung sehingga perlu dilakukan kompresi jantung luar pada RJP, bila kompresi dilakukan dengan benar berapa tekanan darah yg dihasilkan?
A. 100/10 mmHg
B. 120/80 mmHg
C. 100/50 mmHg
D. 100/40 mmHg
E. 110/70 mmHg
Jwb: A

74. Berapa perbandingan kompresi jantung luar dan bantuan napas saat pasien belum diintubasi, dengan 2 penolong?
A. 5:2
B. 5:1
C. 15:1
D. 15:2
E. Boleh tidak teratur
Jwb: D

75.Pasien ini perlu dilakukan intubasi. Berapa lama batas waktu prosedur pemasangan yg paling baik?
A. Tidak lebih dari 30 detik
B. Sampai timbul sianosis
C. Sampai timbul bradikardi
D. Sampai penderita mulai bangun
E. Sama dengan lama kita menahan napas
Jwb: A

76.Bayi perempuan, 4 bulan. terdapat benjolan kebiruan di temporal kiri. Benjolan muncul pd usia 1 minggu dan semakin membesar lambat. Bayi tampak tidak terganggu. Kadang benjolan membesar saat pasien menangis. Saat ini diameter benjolan 4cm.
Apakah terapi yg paling sesuai?
A. Observasi
B. Eksisi massa
C. Ekstirpasi
D. Injeksi sklerosan
E. Injeksi kortikosteroid
Jwb: C

77. anak laki2, 5 tahun. jatuh dari sepeda 5 hari yll. terdapat luka sobek di lengan kirinya ukuran 2x1 cm yg diobatinya dgn povidone iodine
termasuk penyembuhan luka mana pd kasus diatas?
A. Primary intention
B. Secondary intention
C. Tertiary intention
D. Delayed intention
E. Acute intention
Jwb: B

78.bayi baru lahir dgn labiognatopalatoschizis. Bayi sehat, BB 3500g. tidak ada kelainan bawaan pd organ lain. Orang tua adlh pasangan yg sehat, tidak ada cacat bawaan, demikian juga kakek & nenek dr kedua pihak.
apa yg paling mungkin menjadi faktor penyebab kelainan bawaan tersebut?
A. Trauma pada kehamilan trimester kedua
B. Faktor genetik
C. Kekurangan vitamin A dan E selama kehamilan
D. Kekurangan asam folat
E. terjadinya radiasi dari sinar X pada kehamilan muda ibunya
Jwb: E

u/ 4 soal dibawah gunakan skenario berikut:
Pria, 46th, ke UGD dgn keluhan muntah dan buang air besar berdarah sejak satu hari yll. Kejadian itu diawali dgn nyeri mendadak pada ulu hati, muntah jg mengandung sisa makanan, tetapi lebih banyak muntah seperti ter. riwayat nyeri ulu hati berulang sejak setahun yll. biasanya nyeri dirasakan bbrp jam setelah makan
Pada pemeriksaan fisik ditemukan Keadaam umum lemah, kedua tungkai teraba dingin. pada pemeriksaan abdomen tidak terdapat nyeri tekan, nyeri lepas, maupun kekakuan otot. Perut tidak kembung dan bising usus meningkat. Tidak ditemukan tanda2 gagal hati. TD 90/60 mmHg, Nadi 110x/mt lemah dan tidak teratur.

79.Mana diagnosis yg paling tepat u/ pasien ini?
A. Syok hemorhagik e.c. perdarahan varices esophagus akut
B. Syok hemorhagik e.c. perdarahan ulkus peptikum
C. Syok hemorhagik e.c. perdarahan varises fundus lambung akut
D. Syok hemorhagik e.c. perdarahan kanker lambung
E. Syok hemorhagik e.c. perdarahan vascular malformation
Jwb: B

80.Mana penanganan paling awal yg harus dilakukan pd pasien ini
A. Resusitasi cairan, pengawasan ketat tanda vital, --> pemberian obat maag
B. Resusitasi cairan dan transfusi darah, oksigenasi, pasang NGT, --> obat maag
C. Resusitasi cairan dan transfusi darah, oksigenasi, pasang NGT, AB broad spectrum, laparotomy
D. Resusitasi cairan dan transfusi darah, oksigenasi, pasang NGT, pengawasan ketat thd tanda2 vital, endoscopy
E. Resusitasi cairan, oksigenasi, pasang NGT, AB broad spectrum, bilas lambung
Jwb: E

81.Apakah cairan resusitasi yg paling tepat u/ pasien ini?
A. Packed Red Cell
B. Whole Blood
C. Larutan RL
D. Larutan HES
E. Larutan Normal Saline

82.Setelah pasien diresusitasi, tampak perbaikan hemodinamik. endoscopy GI tract atas terlihat sumber perdarahan, tetapi gagal menghentikan perdarahan, dan dibutuhkan 750cc darah u/ menjaga tekanan darah cukup selama 8 jam
Mana penanganan lanjut yg paling tepat?
A. Injeksi Adrenalin IV
B. Laparotomy Explorative u/ mengontrol perdarahan
C. Lebih banyak transfusi u/ menjaga Hb
D. Proton-pump inhibitor IV (omeprazole)
E. IV Pitressia drip

83.pria 55th, ke UGD dgn nyeri seluruh perut sejak 2 hari yll. nyeri dimulai di ulu hati kemudian menyebar ke seluruh perut. Pasien tampak berkeringat dan lethargic. Nyeri tekan, nyeri lepas, dan kram otot ditemukan. Perut tampak kembung dan bising usus menurun. Batas paru-hepar menghilang, TD 100/60 mmHg, nadi 100x/mt, suhu 38C, punya riwayat nyeri ulu hati berulang selama setahun ini. dia selalu makan aspirin u/ keluhan nyeri kepalanya
mana yg merupakan penyebab paling sering penyakit ini?
A. Primary peritonitis
B. Secondary peritonitis
C. Tertiary peritonitis
D. Faecal peritonitis
E. Foreign body peritonitis

U/ 3 soal berikut gunakan skenario ini
anak 2 bln --> ke UGD, perut kembung, muntah, tidak buang air besar sejak 4hr yll. Ada riwayat diare menyemprot. Pada pemeriksaan ditemukan pergerakan meconium yg lambat dan obstipasi berulang

84.Mana diagnosis yg paling tepat?
A. Intussuception
B. Diare akut
C. Enterocolitis
D. Hirschprung's disease
E. Ulcerative colitis

85.mana penanganan thd pasien yg paling tepat?
A. NGT dapat mengurangi distensi abdomen
B. Rectal biopsy harus dilakukan secepatnya u/ diagnosis pasti
C. Pemeriksaan yg paling akurat u/ diagnosis pasti adl CTscan abdomen
D. Abdominal X-ray dan barium enema harus dilakukan setelah kondisi akut ditangani
E. Rectal biopsy dapat dilakukan pada keadaan akut

86. Mana tindakan penanganan yg paling tepat?
A. rectal biopsy, plain X-ray, Barium enema, NGT insertion, resusitasi cairan dan warmed saline enema
B. NGT & resusitasi cairan, AB, diikuti warmed saline enema, Rectal biopsy dan Ba enema
C. Rectal biopsy, resusitasi cairan dan warmed saline enema, Foto polos abdomen, Ba enema, NGT
D. NGT dan resusitasi cairan, Rectal biopsy, barium enema, Foto polos abdomen, warmed saline enema
E. Rectal biopsy, NGT, resusitasi cairan, warmed saline enema, foto polos abdomen, Ba enema

u/ 2 soal, gunakan skenario berikut
bayi perempuan 9 bln --> UGD, sering buang air besar berdarah dan berlendir. Sehari sebelumnya bayi tampak gelisah dan menangis melengking, hal ini terjadi berulang2. Tidak ada demam sebelumnya, pada pemeriksaan ditemukan massa di epigastrium dan tidak ada portio-like appearance pada colok dubur
87.mana diagnosis paling tepat?
A. Disentri amuba
B. Intussuception
C. Haemorrhoid
D. Ulcerative colitis
E. Perforated Meckel's diverticulum

88.Mana yg paling mengarahkan diagnosis?
A. buang air besar berdarah dan colok dubur
B. Intussuception triad
C. Nyeri kolik dan colok dubur
D. BAB berdarah tanpa demam
E. Masa teraba tanpa portio-like appearance

skenario u/ 2 soal berikut
wanita 30 th --> UGD, penurunan kesadaran 3 jam setelah tabrakan bermotor kecepatan tinggi. saat masuk UGD RR 25x/mt, TD 120/70 mmHg, HR 98x/mt. Penderita masih membuka mata dgn rangsangan nyeri dan dapat melokalisasi nyeri yg diberikan tetapi tidak dapat mengeluarkan suara

89.apa tindakan saudara pertama kali?
A. melakukan pemeriksaan foto kepala u/ mencari adanya fraktur
B. melakukan CT-scan kepala
C. menjamin airway (intubasi) dgn kontrol cervical
D. melakukan resusitasi cairan
E. Pemeriksaan thd adanya trauma ditempat lain

90. Setelah kondisi pasien stabil, pemeriksaan fisik menemukan adanya hematom di parietal kiri, laserasi pada dada kanan dan abdomen
pemeriksaan pendukung apa yg dilakukan?
A. foto polos kepala, cervical, thorax, abdomen
B. CT scan kepala, foto cervical, thorax, pelvis
C. CT scan kepala, foto thorax, pelvis
D. Foto kepala AP dan lateral, cervical, thorax, pelvis
E. CT scan kepala, cervical, thorax, foto pelvis, USG abdomen

91.laki2 27th --> UGD krn KLL. penderita melakukan gerakan menarik angg badan dila dirangsang, suara tidak jelas, dan tidak dapat membuka mata biarpun dirangsang. berapa GCS?
A. 8
B. 9
C. 6
D. 7
E. 5

92.wanita 65 tahun --> terpeleset di kamar mandi dia menahan tubuh dengan tangan kanan. kemudian dia merasa nyeri di pergelangan tangan kanan. sendi tangan tampak seperti garpu
manakah tulang yg mungkin patah?
A. metacarpal I
B. Radius
C. Ulna
D. Humerus
E. Clavicula

93.pria 35th, dirujuk ke klinik mata dari klinik endokrin. dia menderita DM sejak 10th yll, kadar gula darah normal. pemeriksaan visus maupun luar mata normal. funduskopi: media jernih, papil normal, retina datar, tidak ada neovascularization, dot haemorrhages (+), hard exudates (+), macula edema (-), foveal reflex normal
apa diagnosis paling mungkin?
A. proliferative diabetic retinopathy
B. nonproliferative diabetic retinopathy
C. Central retinal vein occlution
D. Central retinal artery ocllution
E. Retinal detachment

94.anak 9th --> klinik mata, mata gatal, blepharospasme, fotofobia, sekret mata yg copious mucoid, visus (N), slit lamp --> cobblestone pada palpebra superior
penatalaksanaan?
A. antibiotik topikal
B. antimetabolik topikal
C. acyclovir topikal
D. antihistamin topikal
E. Topical artificial tears

skenario 2 soal:
pria 35th, mata gatal, merah, sekret sperti susu pada konjungtiva. slit lamp --> pappilla di konjungtiva tarsal superior dan inferior. riwayat keluarga dgn penyakit atopik

95.diagnosis?
A. vernal conjunctivitis
B. Atopic conjunctivitis
C. Acute conjunctivitis
D. Flictenularis conjunctivitis
E. Follicle conjunctivitis

96.reaksi hipersensitif mana pada kasus diatas?
A. type I
B. II
C. II
D. IV
E. I & IV

skenario 2 soal dibawah:
wanita 40th, penurunan penglihatan sejak 3hr yll disertai nyeri, mata merah berair. didiagnosis dr.umum sebagai pasien TBC. pemeriksaan --> injeksi siliar, flare bilik mata depan (+), keratic presipitat (+)

97.diagnosis?
A. uveitis akut
B. Vitritis
C. Choroiditis
D. Endophtalmitis
E. Pars planitis

98. terapi
A. kortikosteroid dan sikloplegic (kort. u/ reaksi radangnya (cuz etiologi blm jelas bgt), sikloplegia u/ mencegah sikatrik)
B. beta bloker topikal
C. antihistamine topikal
D. Topical mast cell stabilizer
E. Antibiotik topical

skenario 2 soal:
pria 50th, mata merah, nyeri, keluar air mata. pada pemeriksaan ditemukan ulkus kornea periferal

99.diagnosis?
A. Bacterial ulcer
B. Herpetic ulcer ?
C. Geographican ulcer
D. Fungal ulcer
E. Mooren's ulcer

100. terapi utama?
A. AB oral
B. anti-fungal
C. kortikosteroid topikal
D. Antihistamine
E. AB topikal

skenario 2 soal:
pria 55th, --> klinik mata, mata kiri kabur. pemeriksaan VOS 3/60 konjungtiva tenang, kornea jernih, COA sedang, pupil bulat rx (+), lensa jernih, TIO 15 mmHg, funduscopy Cup/Disc ratio 0,9, gonioskopi --> sudut terbuka

101.pemeriksaan apa lagi yg saudara lakukan?
A. Retinometer
B. Octopus perimetry
C. Streak retinoscopy
D. USG
E. Refractometry

102.diagnosa paling mungkin?
A. Glaukoma sudut tertutup primer
B. Glaukoma sudut terbuka primer
C. Glaukoma sudut terbuka sekunder
D. Glaukoma sudut tertutup sekunder
E. Serangan glaukoma akut

skenario 2 soal
pria 70th --> klinik 24jam, keluhan penurunan pendengaran pada telinga kiri sejak 6 bulan yll. anda melakukan pemeriksaan audiometric

103. u/ mengetahui derajat gangguan dengar anda melakukan
A. tes Rinne
B. tes Webber
C. tes Swabach
D. tes tone decay
E. tes BERA


104.setelah melakukan tes weber ternyata suara lebih keras pada telinga kiri, apa artinya
A. telinga kanan --> tuli konduktif
B. telinga kiri --> tuli konduktif
C. telinga kanan --> tuli sensorineural
D. telinga kiri --> tuli sensorineural
E. kedua telinga tuli konduktif

105.anak 3 tahun diantar ibunya krn belum bisa komunikasi
mana hal berikut yg menunjukkan dampak pada anak?
A. ketulian memberi hal yg sangat bermakna pd anak usia sekolah (6-9th)
B. ketulian mempengaruhi 'educational performance' dan perkembangan sosial
C. ketulian pd anak memberi dampak yg sama spt ketulian pd dewasa
D. ketulian pd usia dini (0-3) tidak mempengaruhi perkembangan bicara
E. ketulian pd usia skolah (6-9) mempengaruhi perkembangan bicara

106.anak laki2 5th --> poliklinik, otore telinga kiri sejak 3hr yll. diawali dgn infeksi saluran napas atas. kesadaran CM, febris (39), membran timpani bulging dgn supurasi telinga tengah
diagnosis?
A. Miringitis bulosa
B. Otitis media supuratif kronik
C. Mastoiditis akut
D. Otitis media akut
E. Mastoiditis kronis

skenario 2 soal
bayi perempuan 8bln, --> UGD sesak napas sejak 3hr yll, stridor saat inspirasi dan retraksi ringan di suprasternal. sesak berkurang bila penderita tidur miring atau memakai bantal. tidak ada febris, tidak disertai gangguan makan/minum. pemeriksaan radiologis soft tissue leher memperlihatkan penyempitan di daerah laring. keluhan seperti ini dirasakan sejak 2 bulan yll tetapi sembuh sendiri
Dx: LARYNGOMALACIA

107.pemeriksaan penunjang?
A. naso-endoskopi
B. Rhinoskopi posterior
C. Rontgen thorax AP dan Lat
D. Laringoskopi -> OMEGA SHAPED EPIGLOTTIS
E. Esofagoskopi


108.pada anak, apakah upaya preventif penyakit diatas? GA ADA LAH, KONGENITAL GITU LOWH..CUMA HINDARI ISPA, JGN TIDUR TERLENTANG, JGN NANGIS (GMN CARA MENCEGAH ANAK KCIL NANGIS COBA???)
A. kortikosteroid dosis rendah jangka menengah
B. Vaksinasi Haemophillus influenza tipe B
C. Oksigenasi yg adekuat
D. AB dosis rendah jangka lama
E. hindari makanan dan minuman dingin dan es

109.anak perempuan 9th, dtg dgn hidung tersumbat sejak 2bln yll. keluhan terutama pada pagi hari disertai bersin dan sekret hidung yg tertelan. rinoskopi anterior --> mukosa dan konka hidung yg livide dan sekret yg serous.
apa pengobatan rasional?
A. membiasakan pasien kontak dgn alergen dari konsentrasi rendah
B. meningkatkan kebugaran jasmani dgn olahraga 1x/mgg
C. obat H1-receptor antagonist
D. dekongestan topikal selama 2 mgg
E. mengupayakan pengobatan yg mampu menekan gejala pada fase cepat maupun lambat

110.anak laki2 8th --> poliklinik, keluhan tidur mengorok sejak setahun yll hilang timbul. pem.fisik --> pembesaran tonsil dgn tonsil tidak hiperemis, kripta melebar, dan detritus
PF mana yg memperlihatkan adanya tonsilitis kronis?
A. Pembesaran tonsil
B. tidak hiperemis
C. detritus minimal
D. tidur mengorok
E. kripta melebar

111.wanita 29th --> poli tht timbul benjolan di pipi kiri sejak 3th yll, nyeri tekan (-), diameter 5cm, dan mendorong daun telinga keatas. tidak ada tanda2 paralisis N VII, kulit tampak normal. diagnosis?
A. tumor ganas kelenjar parotis
B. tumor jinak parotis
C. Sialoadenitis
D. TBC pada kelenjar parotis
E. Hemangioma di kelenjar parotis

112.anak perempuan 5th --> nyeri pada telinga kiri. 2mgg sebelumnya menurut ibunya, anaknya pernah ke poli THT dgn keluhan otitis media akut supuratif bilateral tetapi sudah sembuh. Ditemukan kolesteatoma pada telinga kiri. pasien ini direncanakan u/ operasi pengangkatan kolesteatoma.
Apa tujuan dilakukan operasi?
A. perbaikan pendengaran
B. menjaga penurunan pendengaran
C. mengangkat seluruh jaringan patologis
D. mempertahankan keutuhan dinding posterior canal
E. rekonstruksi dari membran timpani

113.Seorang wanita, 32 tahun, G2P1A0, hamil 12 minggu.
Hb 10, mcv dan MCHC normal
a. tidak perlu diberi apa2
b. Br Fe 100 mg/hari -> masih mual (12minggu)
c. Kadar ferritin diperiksa
d. Beri Vit C
e. Nasehat makanan mengandung besi

114.Seorang wanita, 25 tahun mengeluh diperkosa 5 hari
yl. 2 hari kemudian Polisi minta VeR, sikap dokter
a. VeR berdasarkan rekam medis sebelumnya
b. Laporan medis berdasarkan rekam medis sebelumnya
c. Meminta Polisi membawa pasien kembali
d. VeR berdasarkan rekam medis sesuai tanggal
pemeriksaan
e. Menolak VeR

115.Jika pada pasien itu tidak dijumpai luka, selaput
dara berwarna merah, berarti
a. 5 hari yl benar diperkosa
b. Tidak benar diperkosa
c. Dibuat pingsan dulu baru diperkosa
d. Trauma selaput dara
e. Bersetubuh

116.Sepasang pemuda-pemudi akan melangsungkan pernikahan 5 bulan lagi, adapun si calon perempuan menderita nyeri pinggang kronis, setelah menjalani pemeriksaan di diagnosa TB tulang VT 7 & VT 8. Dokter telah melakukan pengobatan dengan inj. Streptomisisn sebanyak 60x dan kombinasi pengobatan oral. Apakah yang anda sarankan terhadap pernikahannya?
a. Membatalkan pernikahan
b. Tetap nikah, dengan menunda kehamilan sampai pengobatan selesai
c. Tetap menikah saja

117.Seorang bapak umur 50th dahulu rajin olah raga saat ini sdh tidak rajin olah raga lagi, akhir-akhir ini kepikiran tetangga yang menderita dm, tapi bapak tersebut tidak terdapat klinis DM, riwayat Keluarga DM (+). Apa saran anda?
a. Cek GDS
b. Lanjutkan olah raga rutin lagi
c. Langsung berikat OAD oral

118.Seorang pelanggan praktek anda yang menderita asma sedang pergi keluar kota, ternyata sakit asmanya kambuh, pasien tersebut menelpon anda apa yang harus dilakukan karena posisi tidak ada obat, anda sedang merencankan piknik dengan keluarga, sikap anda?
a. Menyuruh pasien anda segera pulang dan periksa ke anda
b. Kirim resep via fax
c. Menyuruh membeli obat asma yang dijual bebas
d. Menyuruh ke IGD setempat

119.Pasien trauma kepala radiologi tampak SOL, dengan hematoma epidural pembuluh darah yang terkena?
a. Bridging vein
b. A. Meningea media
c. A. Serebral anterior
d. A. Serebral posterior

120.Smith Antigen (+) dengan nyeri sendi
a. OA
b. SLE
c. RA

121.Anak 4 tahun demam tinggi, menggigil dan delirium, 1 minggu sebelumnya gangguan miksi sedikit sedikit dan nyeri, hipotensi + hiperventilasi. Mikoroskopis urin bakteri batang gram negative, substansi dibawah
a. Kolagen
b. Hyaluronid
c. Lipopolisakarid
d. Peptidasakarid

122.Interaksi Aspirin (nyeri kepala) & salah satu obat diabet. Efek samping?
a. Hipoglikemia
b. Perdarahan
c. Emboli
d. Perforasi lambung

123.Wanita 28 tahun menyendiri afek datar
a. Psikopat
b. Schizoid
c. Paranoid
d. Antisocial
e. Depresi

124.11 tahun timbul bercak darah pada vagina, kemungkinan
a. Menstruasi
b. Tumor
c. Hamil ektopik
d. Kehamilan
e. Infeksi vagina

125.Neonates premature lahir merintih nafas cuping hidung retraksi subkostal (+), sianosis (+)segera setelah lahir. Ibu pecah ketuban 36 jam sebelum lahir pervaginam demam (+). Diagnois
a. Penyakit membrane hyaline
b. Asfiksia berat
c. Sindrom aspirasi mekonium
d. Bronkopneumonia
e. Transcient tachy pneumonia of the newborn

126.Anak 3 th, 5 hari demam batuk pilek tp sudah sembuh. sekarang pada telinga kanan sakit pendengaran berkurang. Px tht yang perlu dilakukan adalah
a. Rhinoskopi anterior
b. Rhinoskopi posterior
c. Garputala
d. Otoskopi
e. Pemeriksaan faring

127.Anak 4 tahun demam 2 hari Nampak sakit dilingkungan rumahnya endemis aedes aegepty sdh 2 tahun. Px penunjang yang dilakukan
a. LED
b. Apusan darah
c. Trombosit
d. Urine

128.Pria, 76 tahun, ugd, ngorok, kesadaran menurun tensi 60/30, N: 110 r 28, tindakan :
a. Px darah
b. ABC
c. Respirator
d. Sa

129.Wanita, Ca servik, sikap?
a. Simpatik
b. Empatik
c. Naturalistic
d. Antisipatik

130.primi hamil 5 minggu dip x anti toxo. Hasil IgM (+) IgG 1/100. 3 minggu dip x ulang, IgM (-), IgG 1/400. Obat paling tepat
a. Sulfonamide
b. As folinik
c. Pirimetamin
d. Spiramisin

131.Wanita, pengecapan lidah tidak bias merasakan rasa pahit sejak 3 bulan, def. mineral.
a. Cuprum
b. Ferum
c. Selenium
d. Zinc
e. Mangan

132.Laki-laki, 30 th tumit sakit dan bengkak, Ro tulang tumitnya patah dan tulang kaki lain : radiolusen
a. Osteoporosis
b. Osteomalasea
c. Osteodistrofi
d. Osteolisis
e. Osteofit

133.Seorang wanita 30 tahun sudah menikah 6 tahun, haid terlambat 2 bulan. KU= pucat, lemas, akral dingin dan mengeluh nyeri perut tiba2. TD: 90/50 mmhg, nadi 100x/ menit, RR= 24x/menit, Hb: 7 g/dl. Keadaan yg paling mungkin pada pasien :
a.KET
b.Appendicitis acute
c.Kolestitis akut
d.Pankreatitis
e.Cystitis

134.Seorang wanita 44 tahun mengeluh nyeri abdomen kanan bawah tiba2. Pada pemerikasaan ditemukan nyeri tekan dan nyeri lepas abdomen kanan bawah. Pemeriksaan lab Hb: 11 g/dl, Leuko 12.000, diagnosa sementara ?
a.Appendicitis acute
b.Kolestitis acute
c.Pankreatitis
d.KET
e.Cystitis

135.Seorang peternak kambing di lengan kanannya ada ulkus bewarna hitam, kuman yg paling mungkin :
a.Streptococus pyogenes
b.Stafilokokus aureus
c.Bacilus anthracis
d.Clostridium perfringens

136.Anak dengan tungkai bengkak foto rontgen terdapat Codman triangle, diagnosa?
a.Osteosarcoma
b.Osteoblastoma
c.Chondroblastoma

137.Wanita hamil 25 minggu ditemukan anemia gizi, apa yg menyebabkan?
a.Defisensi vit A
b.Def. Vitamin c
c.Def. Zn
d.Def. Zat besi
e.Def. Fe

138.Wanita 45 tahun timbul benjolan pada payudara makin lama makin besar, batas
tidak jelas, nampak peau’d orange, diagnosa?
a.Tumor philoides
b. FAM
c. Fibrokistik
d. Intraductal Ca invasive
e. Intraductal Ca insitu

139.Wanita 30 tahun datang dengan keluhan keluar cairan hilang timbul, pendengaran menurun, panas(-), nyeri pada telinga. Pada otoskopi tidak tampak perforasi membrane timpani, terdapat jaringan granulasi, sedikit cairan dan kolesteatoma. Diagnosa?
a.Otitis media supuratif akut
b.Otitis media kronis maligna
c.Otitis media kronis benigna
d.Miringitis bulosa
e.Otitis media serosa

140. Pria 35 tahun pilek, bersin-bersin, hidung buntu diikuti sakit kepala. Pilek mula-mula encer tetapi setelah beberapa hari kental. PF hidung terdapat cairan kental, konka hiperemi dan udem. Diagnosa?
a. rhinitis vasomotorika
b. rhinitis alergi
c. rhinitis akuta
d. sinusitis maxillaries
e. sinusitis frontalis

141.Wanita 35 tahun, hidung buntu. Sejak 1 tahun terpapar debu bersin-bersin, pilek encer banyak, badan tidak panas. PF hidung cairan encer, konka pucat. Diagnosa?
a. rhinitis vasomotorika
b. rhinitis alergi
c. rhinitis akuta
d. sinusitis maxillaries
e. sinusitis frontalis

142.Pria 12 hari masuk RS karena ikterik, BBL 2800gr, lahir merah cukup bulan, ibu tidak ada riwayat abortus, PF dbn, ikterik Kramer III. Diagnosa?
a. ikterik patologis
b. ikterik fisiologis
c. sepsis neonatorum
d. hepatitis
e. kolelithiasis

143.Seorang pria ditemukan meninggal di lading, kondisi badan sudah kaku, sendi tidak dapat digerakkan. Bilakah terjadi hal tersebut?
a. tidak adanya asetilkolin pada celah sinaps
b. Adanya penghambatan pelepasan Ca++ dari RES
c. tidak ada produksi ATP lagi
d. terputusnya asetilkolin pada celah sinaps

144.Pria 75 tahun masuk RS 3 hari karena kaki bengkak, perut terasa besar dan padat. Pada PF tes undulasi positif, hepar teraba 3 jari bawah arcus costae, udem 2 tungkai. Terapi simptomatik yang paling cocok untuk pasien ini?
a. aldosteron reseptor bloker
b. Angiotensin II bloker
c. beta bloker
d. loop diuretic
e. diuretic tiazid

145.Minuman yang tepat dan murah untuk pelari marathon 10 km
a. air putih
b. air teh
c. air jeruk
d. air gula
e. air garam

146. Pasien 55 tahun dtang ke UGD pk 08.00, sejak 5 jam yll mengeluh nyeri kepala kiri, kaki dan tangan lemas dan tidak dapat digerakkan, vertigo dan pelo. TD+190/100, N=100x/menit, RR+20x/menit Kelainan pembuluh darah yang ditemukan pada CT Scan:
a. A. cerebralis anterior sinistra
b. A. cerebralis posterior sinistra
c. A. cerebralis media
d. A. carotid interna
e. A. basilaris

147.Pasien 48 tahun merasa tangan kanan tidak dapat memegang sapu. Pada malam hari siku terasa sakit walaupun tidak ada aktivitas. Sakit terasa setelah bermain tennis 5 hari yll. PF: edema dan eritema pada siku. Otot mana yang terkena?
a. flexor digitorum ulnaris
b. extensor carpi radialis
c. flexor carpi ulnaris
d. pronator teres
e. triceps brachii

148. RO: tulang tumit radioluscent, Lab218. Laki-laki 30 thn, jatuh calciferol menurun
a. Osteoporosis
b. osteomalacia
c. osteolisis
d. osteofit
e. osteodistrofi

149.Lidah tidak merasakan pahit sejak 3 bulan, kekurangan mineral:
a. Cu
b. Fe
c. Selenium
d. Zn
e. Mg

150. Anak 9 tahun telinga kanan keluar cairan, pendengaran menurun, perforasi subtotal membrane timpani. Diagnosa?
a. OMA
b. OMSK
c. OM efusi
d. OM

151.Pria 75 tahun datang ke UGD dengan keluhan bengkak pada kedua tungkai sejak 3 hari yang lalu. Pada autoanamnesa dikatakan bahwa pasien menghabiskan sebagian besar waktunya berbaring di tempat tidur, makan sedikit-sedikit dan ada riwayat hipertensi. Tes undulasi +, atrofi otot tungkai, hepar teraba 3 cm di bawah arcus costae, JVP meningkat, kadar albumin normal. Diagnosa?
a. gagal jantung
b. gagal hati
c. gagal ginjal
d. malnutrisi
e. imobilitas umum

152.Seorang pasien usia 20 tahun dirujuk ke RS karena tidak sadarkan diri. Pasien seorang mahasiswa asal Kupang NTT yang telah tinggal di Jakarta selama 1 tahun. Satu bulan yang lalu, penderita pulang kampong dan baru kembali ke Jakarta 1 minggu yang lalu. PF Nadi: 100x/menit, TD 120/80, suhu axilla 39,90C dan GCS 3. Pada hapusan darah ditemukan bentuk parasit Plasmodium falcifarum. Bagaimana respon imun pada kasus di atas?
a. Imunitas seumur hidup
b. Imunitasnya bersifat protektif
c. Didominasi imunitas humoral
d. Imunitas yang terbentuk cepat hilang
e. Pembentukan imunitas sangat cepat

153.Pria 52 tahun menderita DM tipe 2 datang ke dokter untuk pemeriksaan rutin. Selama ini pasien mendapatkan terapi diet dan latihan yang dijalankan dengan patuh. PF tidak menunjukkan tanda-tanda abnormalitas. Hasil pemeriksaan lab menunjukkan peningkatan kadar HbA1C. Penyebab paling mungkin?
a. Pemasukan glukosa ke dalam sel otot menurun
b. Kecepatan absorpsi usus menurun
c. Kecepatan absorpsi usus meningkat
d. Sekresi insulin pancreas menurun
e. Sekresi insulin pancreas meningkat

154.Wanita 44 tahun, terdapat benjolan payudara kanan. Pada mammografi tampak focus-fokus densistas irregular ukuran 0,5-1 cm. Pada biopsy fine needle aspiration pada payudara kanan dan kiri terdapat sel-sel maligna. Diagnosa?
a. Infiltrating ductal Ca
b. maligna pyloides
c. Colloid Cs
d. Medullary Ca
e. Infiltrating lobular Ca

155.Wanita 44 tahun didiagnosa Ca payudara. Dokter menganjurkan periksa imunohistokimia untuk reseptor estrogen dan progesterone. Untuk mengetahui apa pemeriksaan di atas?
a. respon kemoterapi
b. stadium tumor
c. kehadiran metastasis
d. derajat keganasan
e. resiko kanker payudara familial

156.Wanita 40 tahun ke dokter umum dengan badan lemas 1 minggu yang lalu. Keluhan disertai wajah pucat dan jantung berdebar-debar tapi tidak demam, nyeri bagian tubuh lain tidak ada. Apa yang paling mungkin?
a. Leukemia
b. Anemia
c. Trombositopenia
d. Polisitemia
e. Pansitopenia

157. Bayi 2 hari datang ke UGD dengan keluhan muntah-muntah, belum BAB. PF: anus normal, perut tampak distensi dan peristaltic meningkat. Colok dubur: meconium menyemprot lalu obstipasi lagi. Diagnosa?
a. Meconium plug syndrome
b. Meconium ileus
c. Penyakit Hirschprung
d. Rectal stenosis
d. Anal membrane stenosis

158.Pria 25 tahun syok datang ke UGD. Baju pasien tampak kotor dan berdasarkan alloanamnesa pasien KLL. Pinggang kiri terdapat echimosis, ekskoriasi dan teraba massa. Apa yang terjadi pada pasien tersebut?
a. trauma limpa
b. trauma colon descendent
c. trauma ginjal kiri
d. trauma ureter kiri
e. trauma lambung

159.Pria 55 tahun di ICU tampak tidur pulas, reflek pupi (-). PF: tampak kurus, kedua mata kuning, spider naevy (+), perut buncit. Bibir pasien terdapat bercak darah dan mulut bau amandel. Riwayat alcohol umur 30 thaun. Sepuluh tahun yll pasien gemuk kemudian lama-lama makin kurus Karena tidak nafsu makan. 2 tahun terakhir pasien kurus, lemah dan mudah lelas. Dua hari yll pasien muntha darah. Kenapa kedua mata pasien kuning?
a. Penumpukan etanol di kornea
b. Meningkatnya bilirubin direk di serum
c. Meningkatnya pigmen penuaan di kornea
d. Penumpukan bilirubin di sclera

160.Wanita, rambut rontol, bibir pecah-pecah dan minum vitamin banyak buat kanker dan infeksi. Kelebihan vitamin apakah?
a. A
b. C
c. D
d. E
e. K

161.Wanita 25 tahun, amenore 2 bulan, menderita DM tergantung insulin. Kadar glucagon normal, kemungkinan diagnosa?
a. kehamilan
b. Hipopituitari
c. polikistik ovarium disease

Bayi menengok kanan kiri jika dipanggil, tertawa jika diajak bermain, mengoceh tidak ada arti, duduk belum kuat.
a. 1 bulan
b. 3 bulan
c. 6 bulan
d. 9 bulan
e. 12 bulan

162.Pria datang ke PKM dengan luka-luka kecil di kemaluan disertai rasa perih dan gatal, setelah berhubungan dengan PKS. 4 bulan yll juga mengalami hal yang sama setelah 10 hari berhubungan dengan PKS. Terdapat ulkus kecil, multiple, vesikel di korpus penis dan vesikel ada yang ditutup pus. Ada demam dan sakit pinggang. Diagnosa?
a. ulkus mole
b. ulkus durum
c. herpes genital rekuren
d. liken planus

163.Seorang laki-laki berusia 45 tahun datang ke dokter dengan keluhan jantung berdebar. Keluhan ini dirasakan setelah minum obat sesak nafas yang diberikan oleh dokter 2 hari yll. Saat itu pasien didiagnosa mengidap asma bronchial. Dari hasil pemeriksaan fisik ditemukan takikardi dan TD: 160/95 mmHg. Obat mana yang paling mungkin menyebabkan keluhan pasien di atas?
a. Salbutamol
b. Terbutalin
c. Efedrin
d. Fenilpropanolamin
e. Ritodrin

164.Seorang pasien pria berusia 50 tahun, pasien TBC datang ke dokter dengan keluhan nyeri sendi pangkal jari kaki dan jempol kaki kanan sejak semingggu yang lalu. Pasien minum OAT secara rutin sejak 3 minggu yll. Pada PF ditemukan peradangan pada sendi metatarsofalangeal dan interfalang I. Hasil pemeriksaan lab menunjukkan kadar asam urat 9,5 mg%. Obat manakah yang paling mungkin berperan menimbulkan keluhan pada pasien di atas?
a. INH
b. Etambutol
c. Rifampisin
d. Streptomisin
e. PAS

165.Seorang mahasiswi berusia 21 tahun datang ke dokter dengan keluhan gatal-gatal di bagian muka dan leher beberapa saat setelah makan makanan laut. Pada pemeriksaan ditemukan bercak kemerahan dan udem lokak di daerah muka dan leher, kelopak amta sedikit bengkak 2 hari yang akan datang ia akan menghadapi ujian. Obat antihistamin apa yang paling tepat?
a. CTM
b. Difenhidramin
c. Siklizin
d. Loratadin
e. Dimenhidrat

166.Pria HIV (+) datang dengan candidiasis oral (+), hasil apa yang diharapkan?pemeriksaan KOH
a. Spagheti dan meatball
b. hifa panjang bersekat
c. pseudohifa

167.Pria 23 tahun, keluhan gatal malam hari di glans dan batang penis ada papul eritem multiple. Diagnosa?
a. scabies
b. tinea kruris
c. herpes genital
d. sifilis

168.Pria 34 tahun, kantoran. DM dan diberi terapi insulin. BB turun 2 kg tapi nafsu makan naik. GD di rumah 280-320. Apa yang harus dilakukan?
a. tambah dengan metformin
b. ganti jenis insulin
c. meningkatkan kalori
d. menurunkan kalori
e. meningkatkan dosis insulin

169.Wanita 25 tahun DM tipe I terkontrol dibawa ke RS karena ketoasidosis setelah 2 hari sebelumnya terkena infeksi saluran kemih. Hormon apa yang berpengaruh?
a. androastenedion
b. kortisol
c. T4
d. Leptin
e. Glukagon

170.Wanita 60 tahun atrofi adrenal bilateral, Kenapa bisamenderita sindroma Cushing. CT Scan terjadi keadaan ini?
a. Addison
b. terkena terapi kortikosteroid
c. Waterhowen sindrom

171.Wanita 35 tahun datang pusing, penglihatan gelap bila berganti posisi sejak 1 bulan lalu. Hb 9 Ht 27 Trombo 250.000 Leuko 7000. Defisiensi apakah?
a. asam folat
b. B1
c. B6
d. B12
e. Zat besi

172.Pria 3 hari datang dengan demam dan tidak mau minum sejak kemarin, didapat apatis BB 2100gr, T 39, ikterus. Diagnosa?
a. asfiksia neonatorum
b. tetanus neonatorum
c. sepsis neonatorum
d. ikterus neonatorum

173.Wanita gatal di bawah kutang, riwayat gatal dari kecil, terdapat likenifikasi, ekskoriasi, dan periorbital darkness. Terapi?
a. Loratadin
b. Prednison
c. Dexametason
d. Cimetidin

174.Pria usia 50 tahun tidak mempunyai anak setelah menikah selama 5 tahun ditemukan tanda-tanda pubertas sekunder, penis berukuran normal, teraba 1 testis pada scrotum kanan, teraba benjolan ukuran 3x4 di inguinal kiri. Diagnosa?
a. Kriptokismus

175.Karyawan sulit tidur, bagun terasa lelah. TD: 120/70.
a. insomnia primer
b. gangguan ansietas
c. gangguan psikosomatis
d. gangguan psikosis

176.Pria 60 tahun mual, nyeri perut. PF hepar membesar karena terbungkus massa, vena-vena membesar, umbilicus menonjol. Walaupun keluarga pasien sangat percaya pada perawatan anda tapi anda merujuk, sikap dokter?
a. mengabaikan kepercayaan
b. melinpahkan tanggung jawab kepada dokter lain
c. merasa keterbatasan kemampuannya
d. tidak dapat mendiagnosa

177.Bapak usia 45 tahun kecelakaan lalu lintas, pingsan, nafas putus-putus, yang dilakukan pertama kali?
a. foto thorax, leher, kepala
b. foto thorax, abdomen, pelvis
c. ABC/ airway breathing circulation
d. foto kepala, leher, thorax, abdomen
e. foto persendian dan ekstremitas

178.Wanita usia 22 tahun minta divisum setelah diperkosa. 2 hari kemudain polisi mendatangi dokter dan menyuruh mengeluarkan surat visum, yang anda laukan?
a. visum sesuai rekam medis
b. visum sesuai yang sudah ada
c. menyuruh penyidik untuk mengantarkan ke korban dan diperiksa lagi
d. tidak melakukan visum
e. menolak melakukan pemeriksaan

179.Laki-laki usia 65 tahun datang ke Puskesmas dengan sesak nafas dan bengkak di kedua tungkai sejak 2 hari yll, minum obat hipertensi sejak 5 tahun yll, sejak 1 hari yll kencing berwarna agak merah dan sedikit. Pemeriksaan penunjang yang mendukung pemeriksaan kea rah diagnosa?
a. SGPT
b. kreatinin
c. ureum
d. clearance creatinin
e. CPK MB

180.Wanita 12 tahun BB 40 kg keluhan berkeringat, mata melotot, tangan gemetaran. Pemeriksaan yang perlu dilakukan?
a. bikarbonat
b. T3, T4 dan TSH
c. Asam urat
d. glukosa darah puasa
e. darah dan urin rutin

181. Ibu memebawa anaknya berusai 8 bulan ke Puskesmas dengan demam sejak 3 hari, tidak nafsu makan, demam pada malam hari. Diagnosa?
a. DBD
b. typhoid
c. malaria tropikana
d. malaria tertiana
e. demam biasa

182.Seorang anak menderita gatal-gatal pada punggung, kaku di tangannya setelah diteliti ternyata anak-anak (teman-temannya) menderita keluhan yang sama. Kemungkinan diagnosa?
a. tinea pedis
b. tinea kruris
c. dermatitis kronik
d. dermatitis kontak
e. skabies

183.Wanita 20 tahun mata kanan sukar dibuka, mulut mencong ke kiri, Diagnosa?
a. Bells palsy
b. stroke hemoragik
c. stroke akibat penyumbatan
d. emboli

184.Wanita 30 tahun G3P2A0 mengeluh mulas-mulas sejak 20 jam. Kehamilan cukup bulan, sudah dipimpi
          Muerte súbita en el atleta        

Instituto de Investigación de Ciencias Aplicadas
a la Actividad Física y del Deporte
Universidad de Guadalajara
 

Dr. Gustavo Pineda Nava 
(México) 


Resumen    La muerte súbita en el atleta se define como el fallecimiento no traumático, durante ejercicio, que se presenta dentro de la primera hora de haber iniciado los síntomas. Se estima que se tienen cuatro muertes de estas características, por cada millón de atletas por año en los Estados Unidos. Las entidades nosológicas que la causan son diferentes de acuerdo al grupo de edad al cual nos referimos; en menores de 35 años, la principal causa es la Miocardiopatía hipertrófica, y en mayores de 35 años, la causa es enfermedad ateroesclerótica coronaria. Existen otras menos frecuentes como las anormalidades congénitas de las arterias coronarias, displasia arritmogénica del ventrículo derecho, enfermedades valvulares, etc. La mejor forma de disminuir la incidencia de este evento es la prevención, utilizando medidas de evaluación a deportistas en forma general, incluyendo exámenes médicos y de gabinete. Ésto es, interrogatorio y exploración física completos, radiografía de tórax y electrocardiograma. Existen cuestionarios enfocados para valorar signos, síntomas y antecedentes cardiovasculares, que deben aplicarse a toda aquella persona que inicie con un programa de ejercicio físico, sea niño o adulto, y así encontrar en ellos, factores de riesgo que pongan en peligro su vida durante la práctica deportiva.   

Palabras clave: Muerte súbita. Ejercicio. Enfermedad cardiovascular.  Abstract    Sudden cardiac death in the athlete is defined as non-traumatic death during exercise, within the first hour of the initiating symptoms. It is estimated that there are four deaths for every million athletes per year in the United States with these characteristics. The causes of the untimely death are different with regard to the age group that is being referred to; in < 35 years old, the principal cause is hypertrophic cardiomyopathy and in > 35 years old, the cause is coronary arteriosclerosis. There are other causes that are less frequent, like congenital disorders of the coronary arteries, arrhythmic dysplasia of the right ventricle, valvular diseases, etc. The best way to diminish the incidence of this event is prevention, using methods to evaluate the athletes, including clinical and laboratory exams. This is, a complete physical exploration and patient interrogation, thoracic x-ray and electrocardiogram. There is the existence of questioners focused to evaluate sings, symptoms and a cardiovascular history, that should be applied to everyone that starts an exercise program, whether it's a child or an adult, to find the risk factors that place in danger their lives during sports participation.  
Keywords: Sudden death. Exercise. Cardiovascular disease. 

Se tiene conocimiento de la Muerte Súbita relacionada con actividad física, desde el año 490 a. C. cuando el soldado griego Pheidippides murió al llegar a Atenas, después de haber corrido desde Maratón (1). La Muerte Súbita, constituye un suceso muy dramático, ya que involucra el fallecimiento de una persona activa y en la mayoría de los casos, en plena juventud.

Inicialmente fue tomado el término, para designar aquellos fallecimientos súbitos e inexplicables, simbolizados por la inocencia de la comunidad médica; en el atleta, se define como aquel deceso inesperado, no violento ni traumático, que se presenta instantáneamente o dentro de la primera hora de haberse iniciado los síntomas cuando se está realizando actividad física deportiva o inmediatamente después. Algunos autores prolongan el tiempo de evolución del cuadro hasta 6 horas después de haberse iniciado (2).

I. Presentación y frecuencia
    La Muerte Súbita en población general, se presenta alrededor de 400,000 casos anualmente en los Estados Unidos (3,4). La presencia de este evento en el atleta es afortunadamente, poco frecuente y de acuerdo a las estadísticas reportadas, y tomando en cuenta los grupos estudiados, podemos concluir que en los Estados Unidos se observan 100 casos de muerte súbita durante ejercicio en atletas por año; con 25 millones de participantes en deportes competitivos en esa nación, corresponde entonces a 4 muertes por millón de atletas por año. En los estudiantes a nivel bachillerato, se tiene estimado que ocurra con un rango de 1:100,000 a 1:300,000 por año académico (2,5). En actividad física de forma recreativa, se tienen reportes de que se presenta una muerte por cada 887,526 horas de participación en actividades físicas (6); en otro estudio, en Rhode Island, entre corredores recreativos masculinos entre 30 a 64 años de edad, se observó un fallecimiento por cada 396,000 horas, o una por cada 7,620 corredores por año (7). En lo que se refiere a los corredores de maratón, se tiene estimado que existe de una a dos muertes anualmente en una población de 15,000 a 25,000 sujetos de esta disciplina (6). Se tiene el reporte de esquiadores y caminata en montaña en Austria y se observa una muerte súbita por cada 780,000 horas de caminata y 1'630,000 horas de esquiar (8). En cuanto al género, podemos decir que en los hombres es más frecuente que en las mujeres a razón de 0.75 y 0.13/100,000, respectivamente (9-11).

II. Clasificación
    De acuerdo al mecanismo etiológico, la muerte súbita se puede clasificar de la siguiente manera (2, 12):
  1. Certera: aquellos casos en los cuales, durante la necropsia se identifique una evidencia anatómica obvia como su causa; por ejemplo un infarto al miocardio agudo o ruptura de aorta.
  2. Probable: en los sujetos en los cuales se encuentra un cambio anatómico que pudiera causar alteraciones secundarias, tales como la Hipertrofia concéntrica del ventrículo izquierdo o la Arteriopatía coronaria.
  3. Presumible: Aquellos casos en los cuales no se identifica una causa que directamente este involucrando a la muerte súbita; por ejemplo, Prolapso de la válvula mitral.
    Existe otra forma de clasificar a los sujetos que presentan muerte súbita, y es de acuerdo a la edad de presentación; a saber, se divide en dos grandes grupos: a) menores de 35 años, y b) mayores de 35 años. Lo anterior es debido a que la frecuencia de patologías causantes es diferente. En el primer grupo, las enfermedades cardíacas congénitas constituyen la mayor proporción de causa de muerte, mientras que en el segundo grupo, la enfermedad coronaria ateroesclerótica es la principal etiología (2,3,13-20). Hay que tomar en cuenta que en la población general, el 80% de las muertes súbitas son atribuibles a una arritmia cardíaca, la cual puede ser causada por variados sustratos etiológicos (21).

III. Causas en menores de 35 años
    Como ya se mencionó, las enfermedades cardíacas congénitas, son la causa principal de muerte súbita en menores de 35 años, siendo la Miocardiopatía hipertrófica asimétrica la que con mayor frecuencia es observada en dichos sujetos. También se encuentran otras patologías como: Displasia arritmogénica del ventrículo derecho, anomalías coronarias congénitas, Hipertrofia idiopática del ventrículo izquierdo, entre otras (Cuadro I).

a) Miocardiopatía hipertrófica
    La Miocardiopatía hipertrófica es una enfermedad caracterizada por la alteración idiopática del miocardio que incluye la presencia de hipertrofia ventricular izquierda y/o derecha en ausencia de una causa cardíaca o sistémica, y que suele predominar la afectación sobre el tabique interventricular (22-24). La enfermedad es frecuentemente familiar y se caracteriza por la desorganización de miocitos y miofibrillas, el aumento de la matriz colágena y las alteraciones de las arterias coronarias intramiocárdicas. Algunos pacientes presentan gradientes intraventriculares y son frecuentes las alteraciones de la función diastólica ventricular, la isquemia miocárdica y las arritmias (22,25,26). Recientemente se han identificado mutación de nuevos genes causantes de la enfermedad, aparte de las ya encontradas en la cadena pesada de la  - miosina (14ql), están las de  tropomiosina (15q2), en el gen de la troponina T cardíaca (1q3), así como en el locus 11 p13-q13 (24).
    Clínicamente puede cursar asintomática o manifestarse por disnea, angina, síncope y muerte súbita. En el 47% de los pacientes, cursa asintomática antes de presentarse muerte súbita, y sólo el 7% presentan síncope previamente (27). En algunos casos, la enfermedad progresa hacia el deterioro de la función sistólica e insuficiencia cardíaca (23).
    En un inicio, la Miocardiopatía hipertrófica era reconocida solo por sus características hemodinámicas, especialmente el gradiente en el tracto de salida ventricular izquierdo; sin embargo, el espectro de la enfermedad se ha ido ampliando con la identificación principal de dos formas de presentación: la obstructiva (de la eyección del ventrículo izquierdo) y la no obstructiva caracterizada principalmente por disfunción diastólica del mismo ventrículo (23, 28). La peor manifestación de la Miocardiopatía hipertrófica es la muerte súbita la cual es la principal causa de muerte condicionando más de la mitad de la mortalidad de estos pacientes, con una incidencia anual del 2-4% en adultos y del 4-6% en niños y adolescentes (27). Cuando se trata de la muerte súbita en atletas, la Miocardiopatía hipertrófica es causa en el 36% (29). Se identifican ciertos factores de riesgo para muerte súbita, en los que se encuentran: I) la edad, pues el riesgo de muerte súbita es significativamente mayor en niños y jóvenes, disminuyendo en etapas posteriores de la vida; II) así mismo, la historia familiar con miocardiopatía hipertrófica presenta una alta incidencia de muerte súbita precoz (30). No existe correlación entre el grado sintomático de los pacientes y el riesgo de muerte súbita, únicamente el síncope recurrente parece tener significado en niños y jóvenes con miocardiopatía hipertrófica (30). En algunos estudios se ha identificado el ejercicio como factor desencadenante de muerte súbita por diferentes mecanismos: I)aumento del tono adrenérgico, con mayor "obstrucción" del ventrículo izquierdo; II)taquicardia y vasodilatación periférica, con mayor dificultad al llenado diastólico, y III)inestabilidad eléctrica; es importante recalcar que la mitad de las muerte súbitas en atletas jóvenes se deben a la Miocardiopatía hipertrófica (23,27,30). Como consecuencia de estudios realizados en pacientes con Miocardiopatía hipertrófica considerados como de alto riesgo, se han podido identificar varios mecanismos potenciales que solos o combinados, pueden dar lugar a muerte súbita; estos mecanismos no son los mismos en todos los pacientes y probablemente son diferentes en niños y en adultos. Así mismo, algunos pueden tener una base hemodinámica mientras otros son arrítmicos. Entre los diferentes mecanismos que se han propuesto están: a)arritmias ventriculares, b)arritmias supraventriculares (como la fibrilación auricular) causantes de colapso cardíaco, c)bradicardias, d)isquemia severa (debida en parte a la escasa reserva coronaria secundaria a las alteraciones en los pequeños vasos coronarios intramiocárdicos), e)conducción aurículo-ventricular rápida (debida a la presencia de vías accesorias o no) y trastornos de la conducción (27,30,31). Por otra parte, en el estudio de Yoshida y cols.(32), proponen una relación entre los cambios electrocardiográficos sugestivos de isquemia subendocárdica durante el ejercicio y una respuesta anormal en la presión arterial, también durante la actividad física.
    Las consecuencias hemodinámicas de estas anomalías electrofisiológicas pueden verse aumentadas por la presencia de obstrucción subaórtica, alteraciones de la función diastólica, por la respuesta a una arritmia ó a la propia taquicardia sinusal fisiológica que puede estar modulada por la anormal respuesta vascular periférica identificada en un 30-40% de los pacientes jóvenes, que presentan hipotensión de esfuerzo a pesar de aumentar normalmente el gasto cardíaco (30). Además de los factores hemodinámicos, la inestabilidad eléctrica del miocardio es un determinante importante de muerte súbita, esto influenciado probablemente por el grado de desorganización de las fibras miocárdicas (23,27,30,31,33). Frecuentemente existen además, anormalidades en las coronarias intramurales hasta en el 80% de los casos estudiados en necropsias. Las arterias tienen engrosadas las paredes (por aumento de la íntima y de la media) y su luz está reducida, siendo ésto, en grandes zonas miocárdicas (27). Se han podido identificar algunas alteraciones electrocardiográficas en este tipo de pacientes, tales como datos de crecimiento ventricular izquierdo, alteraciones de la repolarización con ondas T isoeléctricas, PR corto, arritmias ventriculares y supraventriculares (25, 34).
    Existe una gran relación entre la actividad física y muerte súbita en los sujetos que padecen cardiomiopatía hipertrófica (27,28,30,31,33,35-38). Por lo anterior, se debe de diagnosticar en forma oportuna esta enfermedad y poder prevenir la muerte, limitando los riesgos de acuerdo a los lineamientos propuestos por la 26ª Conferencia de Bethesda (39,40).

b) Anomalías congénitas de las arterias coronarias
    En lo que se refiere a las anomalías congénitas de las arterias coronarias, que constituyen la segunda causa en frecuencia de muerte súbita en atletas menores de 35 años, dichas anomalías pueden ser en su origen así como en su trayecto (cuadro II), además de que encontrar esta enfermedad in vivo, es desafortunadamente raro, ya que de lo contrario, podríamos actuar en consecuencia para prevenir la muerte (41). Se presenta con una frecuencia de 0.2 a 1.4% de la población sometida a coronariografía (18), pero en estudios de necropsia general se aprecia con un aumento hasta del 2.2% (20), con más alta frecuencia en hombres, encontrándose en un 81% (13). Es causante de muerte súbita en deportista con un porcentaje variable; puede ser según reportes que hablan desde el 12 al 14% (2), hasta un 19% de acuerdo como lo reporta Maron (29). De los casos con anomalías de la coronaria izquierda, el 57% presenta muerte súbita, en contraste con las anomalías de la coronaria derecha que solamente el 25% presentan muerte inesperada (42).
    La anomalía más frecuentemente observada en este grupo de patologías, es el origen de la coronaria izquierda y derecha a partir del seno de Valsalva derecho (43). Existen otras formas de presentación enlistadas en el cuadro I, en donde también se observan como causas de muerte súbita, las arterias coronarias en túnel, las hipoplásicas y las que se encuentran con fístulas (43). En un estudio de Steinberg (44) se presentó una asociación de las anormalidades de las coronarias con la miocardiopatía hipertrófica en un 16%, en personas de 1-21 años de edad, que murieron súbitamente.
    Aunque no se ha identificado totalmente el mecanismo de muerte súbita en los deportistas que presentan este tipo de anormalidades coronarias, se ha propuesto varias teorías: I) compresión de la coronaria entre la aorta y el tronco de la arteria pulmonar, II) el acodamiento de la coronaria, y III) espasmo arterial, llevando todo lo anterior a la presentación de arritmias ventriculares secundarias a isquemia miocárdica aguda (43,44).

c) Hipertrofia idiopática del ventrículo izquierdo
    La hipertrofia idiopática del ventrículo izquierdo es la tercera causa de muerte súbita dentro de los deportistas y se identifica por presentar un exagerado crecimiento de las paredes ventriculares, teniendo una hipertrofia concéntrica con disminución de la cavidad ventricular, en forma simétrica (12). Ésta, puede ser una variante de la miocardiopatía hipertrófica, y en algunas ocasiones se le ha asociado a una hipertensión no diagnosticada previamente (43). En un estudio realizado por Maron y cols. (45), en atletas que murieron súbitamente, encontraron una frecuencia de presentación del 10%, que se asemeja a lo reportado por Maron y la Asociación Americana de Corazón (29), aunque existen reportes desde el 3.2% de frecuencia como causa de muerte súbita en atletas (46), hasta el 18%, reportado por Salem (47). Hay que hacer diferencia de la hipertrofia encontrada como una adaptación al ejercicio (48), y la observada en esta forma de patología; aunque la originada por actividad física también es importante por las dimensiones que puede alcanzar, el grado de hipertrofia encontrada en la idiopática, es hasta de 600gr, superando lo previsible por un alto nivel de entrenamiento (43,49-53). De igual manera, Maron (19) relaciona diversos criterios para distinguir entre la hipertrofia encontrada en el "corazón del atleta" y en la miocardiopatía hipertrófica, en donde valora los patrones inusuales de hipertrofia ventricular izquierda, dimensión de la cavidad ventricular izquierda, patrones electrocardiográficos, dimensión de la aurícula izquierda, género femenino, disminución de la hipertrofia con el desacondicionamiento y la historia familiar de la miocardiopatía hipertrófica, dejando una "zona gris" entre los dos grandes grupos, constituyendo un círculo de riesgo aumentado para poder definir entre lo patológico y lo fisiológico. Típicamente, presentan un grosor del séptum interventricular mayor de 15mm con disminución de la cavidad ventricular izquierda, no congruente con el otro parámetro (54).

d) Displasia arritmogénica del ventrículo derecho
    Por otra parte, esta enfermedad es una importante causa de muerte súbita en el mundo, sobre todo en Europa, y especialmente en Italia. Existe un estudio del norte de Italia, en donde analizan las causas de muerte súbita en menores de 35 años de 1979 a 1996, y encuentran que la Displasia arritmogénica del ventrículo derecho es la patología más frecuente con el 22.4%, por encima de la Miocardiopatía hipertrófica (2.0%) y las anomalías del origen de las arterias coronarias (12.2%) (15). En contraparte, en el estudio realizado por Aguilera y cols. (55) en España, encuentra que esta causa de muerte súbita en menores de 35 años, representa solo el 6.8% de los casos revisados de los años 1991 a 1997. En dicho estudio, se encontró una predominancia muy marcada sobre el género masculino (95.2%), con una relación aproximada de 2:1.
    La Displasia arritmogénica del ventrículo derecho es una enfermedad del músculo cardíaco de etiología desconocida caracterizada por inestabilidad eléctrica, debido a la presencia de atrofia muscular y remplazo del miocardio ventricular derecho por tejido adiposo o fibroadiposo (56,57). Aunque la etiología es desconocida, se ha encontrado una relación de tipo familiar, por lo que algunas investigaciones han podido identificar un defecto dentro del cromosoma 14q23-q24 (56,57).
    Las características anatómicas en estudios autópsicos han observado disminución de los elementos contráctiles de la pared ventricular derecha y su sustitución por tejido adiposo, apareciendo fundamentalmente en el subepicardio del ápex, el infundíbulo y la zona subtricuspídea del mismo ventrículo, formando el llamado "triángulo de la displasia". Se han distinguido dos tipos histopatológicos: la lipomatosa y la fibrolipomatosa, esta última asociada a dilataciones aneurismáticas, cicatrices y adelgazamiento de la pared (57).

IV. Causas de muerte súbita en mayores de 35 años
    Los atletas mayores de 35 años de edad, representan una población diferente en cuanto a las causas de presentación, aunque prácticamente son las mismas etiologías, la incidencia es disímil. En éstos, la enfermedad ateroesclerótica coronaria es con mucho, el principal motivo, observándose con menor porcentaje de presentación otras enfermedades como la miocardiopatía hipertrófica, enfermedad valvular e identificación de arritmias cardíacas (cuadro I). Esta causa representa aproximadamente el 80% de las muertes súbitas durante ejercicio en atletas de la edad antes mencionada (58). Generalmente se les observa, una enfermedad ateroesclerosa grave subyacente (43), es decir, lesiones obstructivas mayores del 75%.
    Existen otras causas menos frecuentes de muerte súbita en atletas de este grupo de edad, como son: Prolapso de la válvula mitral (39,59), Estenosis aórtica (5,46,60) Miocarditis (45,61), Síndrome de Marfán (62), Síndrome células falciformes (63-66), trastornos del sistema de conducción cardíaca y arritmias (67-77), uso de la cocaína (5,78,79), uso de esteroides (80-84), Sarcoidosis (12,43), Conmoción cardíaca (85-87), enfermedad de Kawasaki (16), accidentes cerebro-vasculares (88,89), golpe por calor (88,90), enfermedades pulmonares incluyendo asma (91,92) y tumores intracardíacos (93).

V. Cuadro clínico
    La poca frecuencia de síntomas prodrómicos, hacen que la muerte súbita aparezca como evento inicial, lo que hace más difícil su prevención (15,94). Alrededor de la tercera parte de los pacientes que sufren de muerte súbita, presentan algún tipo de síntomas prodrómicos (95), entre éstos, podemos encontrar: dolor precordial, palpitaciones, mareos, disnea, pre-síncope y síncope (45,96). Este último, es la manifestación en que mayor atención debemos de poner, ya que se relaciona muy estrechamente con muerte súbita (97).
    Las dos categorías principales en que se puede clasificar al síncope son: el reflejo (vasovagal, ortostático, etc) y el cardíaco (mecánico o eléctrico) (98). Existe un tercer grupo, menos común, en que se contemplan las causas no cardiovasculares e inexplicables. Por otra parte, se calcula que alrededor de 0.16% al 4.7% de corredores de larga distancia, tienen síncope durante la competencia, debido a diversos factores tales como la deshidratación, obesidad, entrenamiento inadecuado, sobreentrenamiento, lesiones previas y la inadecuada aclimatación al momento de la carrera (99). Hablando de causas cardiovasculares, en la miocardiopatía hipertrófica, uno de sus principales síntomas es el síncope (27,37,100). No cabe duda, que siempre que se presenta este evento es dramático y deberá de evaluarse correctamente y en forma completa, para poder diagnosticar la causa desencadenante y prevenir la muerte súbita.

VI. Prevención
    De lo anteriormente expuesto se deduce la necesidad de un examen exhaustivo a cada atleta, además de una meticulosa historia clínica para encontrar posibles factores de riesgo que predispongan la muerte súbita (27).
    La realización de exámenes periódicos y completos a deportistas, para diagnosticar procesos morbosos que los pongan en riesgo a muerte súbita, es la única forma de poder prevenir tal evento. El propósito de estas valoraciones es encontrar sujetos con riesgo para presentar eventos cardiovasculares durante el ejercicio. Se han propuesto diferentes cuestionarios fáciles de realizar entre los grupos participantes de cualquier actividad física, de diferentes edades, aplicado por médicos y personal paramédico encargados de la atención directa de los deportistas, y en los que se pueden identificar cuales presentan riesgo alto y entonces derivarlos a especialistas.
    Entre éstos, se encuentran principalmente el PAR Q & YOU, de la Sociedad Canadiense de Fisiología del Ejercicio (101), y la propuesta por la Asociación Americana de Corazón (AHA) y el Colegio Americano de Medicina del Deporte (ACSM) (cuadro III) (102). En dichos cuestionarios, el interrogatorio se enfoca a determinar la presencia de signos y síntomas cardiovasculares, que nos orienten al diagnóstico temprano de enfermedades y factores de riesgo para muerte súbita. Son 13 las preguntas recomendadas por el AHA, enfocadas a encontrar antecedentes de importancia cardiovascular, tales como: dolor de pecho, síncope/presíncope, falta de aire inexplicable, fatiga inexplicable asociada con el ejercicio, detección de soplo cardíaco, incremento de la presión arterial, historia familiar de muerte prematura, enfermedades cardiovasculares en parientes relativamente cercanos menores de 50 años, miocardiopatía hipertrófica, miocardiopatía dilatada, síndrome de QT largo, síndrome de Marfán, arritmias clínicamente importantes (29,103).
    Simons (104) en su artículo de Prevención de Muerte Súbita, menciona que la disminución en la incidencia de ésta en atletas jóvenes, se debe a la implementación de la medicina preventiva, tal como lo refiere R. C. Cantu expresidente del Colegio Americano de Medicina del Deporte en Indianápolis.
    Sobre la evaluación periódica de los atletas, se ha discutido mucho al respecto y en l996, se publicaron las recomendaciones por parte del AHA (29) y en 1998 un anexo (105), en donde se especifica que las valoraciones por medio de una historia clínica personal y familiar, así como la exploración física completa y detallada para atletas colegiales, deben realizarse por personal calificado antes de comenzar el entrenamiento y competencias y continuar con revisiones cada año en los siguientes 3-4 años. En los atletas a nivel universitario, cada 2 años deberá de efectuarse la evaluación posterior a la basal. Cuando se obtengan cambios en el estado médico o alguna anormalidad, se tendrá entonces la evidencia para enviar a especialista o solicitar exámenes de apoyo (105). El electrocardiograma y la radiografía de tórax, siguen siendo elementos muy importantes para valorar de primera intención a los deportistas (106).
    Cuando se detectan anormalidades que pueden poner en riesgo la vida del deportista, nos debemos de apoyar en lo propuesto por el AHA y el ACSM en la 26ª Conferencia de Bethesda, en relación a cada uno de los task force.
    Sigue constituyendo un gran dilema para el deportista el aceptar cuando se le niega la participación competitiva en su actividad favorita, pero tenemos que convencerlo de los dictámenes médicos, ya que contamos con la experiencia del basquetbolista Reggie Lewis' que tuvo muerte súbita sobre la duela, cuando previamente ya se le había notificado que debía restringir su actividad física (107).
    Otro gran grupo de personas en las cuales debemos enfocar la prevención, son aquellas que siendo aparentemente sanas, están realizando o van a realizar un programa de acondicionamiento físico para mejora de su peso corporal, como coadyuvante en su apariencia física, o solamente en forma recreativa. Sobre todo, si se tratan de varones mayores de 40 años, o mujeres mayores de 50 años, de acuerdo a la Clase IIb de sujetos asintomáticos y Clase I en estudios pediátricos con factores de riesgo y que van a iniciar un programa de ejercicio (108). Los riesgos de complicaciones o de muerte súbita son mayores cuando la actividad física es vigorosa; ésto hay que tomarlo en cuenta para poder solicitar la prueba de esfuerzo o algún otro estudio complementario (109). Nunca hay que olvidar los procesos por los que pasa un sujeto en el momento de la práctica deportiva, que pueden aumentar el riesgo de muerte súbita por un mal entrenamiento, tales como la deshidratación, desequilibrio electrolítico, aumento de la presión arterial, etc. Es por ello que siempre deben de ser apoyados por un entrenador calificado, además de tener una revisión médica, para poder disminuir el riesgo de complicaciones precipitadas por el ejercicio, y aprovechar los beneficios del ejercicio en personas con enfermedad cardíaca en prevención primaria y secundaria (110). En un estudio realizado en 10,540 atletas, estudiantes en la ciudad de Iowa, encontraron que 20 personas tenían razones cardiovasculares para impedirles el ejercicio físico; además, en 442 sujetos se les restringió su actividad (111). Ésto demuestra la facilidad de descubrir factores que ponen en riego la vida del deportista durante el ejercicio físico. Los deportistas más jóvenes son más difíciles de convencer que aquellos de edad madura para que disminuyan o suspendan la actividad física, por diversas razones que envuelven al joven (112).
    El tomar una decisión como la antes mencionada, requiere de tener conocimientos amplios de la medicina del deporte, porque involucra aspectos médicos, psicológicos, legales, económicos y sociales, y cada persona o grupo relacionado con el deportista debe de asumir el rol que le corresponde para el cuidado médico integral del atleta (113-116). Las contraindicaciones que se pueden tener ante un deportista para que realice ejercicio físico, son muy específicas y atañen directamente a factores que ponen en riesgo su vida, que hablando de aspectos cardiovasculares, las principales son las enfermedades congénitas o la coronaria ateroesclerótica, las cuales, identificándolas, se deben enviar los pacientes a manejo por un especialista (117-121). Es muy importante tener en cuenta que las consideraciones que se hagan sobre un atleta en relación con la disminución o cese de la actividad física, son sólo recomendaciones, y deberán de ser valoradas por el propio atleta, su familia, su entrenador, y en su caso, la escuela a la que pertenece, para determinar entonces, que actitud tomar más adelante con el sujeto afectado (122).
    En forma similar a lo que se realiza en otras partes del mundo, por ejemplo en Italia y España (123), en nuestra institución llevamos a cabo dos tipos de valoración médico deportiva para la autorización de realización de actividad y física y deportes: el primario, en el cual se le realiza historia clínica general basándonos en la exploración física completa y en un cuestionario escrito sobre antecedentes patológicos de importancia principalmente cardiovascular; elsecundario, en el cual se aplica una revisión cardiológica especializada, electrocardiograma de reposo y prueba de esfuerzo. En grupos de deportistas de alto rendimiento, se les agrega ecocardiograma a la batería de estudios practicados. Solamente cuando es necesario y de acuerdo a los hallazgos en las revisiones, se les solicita monitoreo electrocardiográfico Holter, prueba de mesa basculada, angiografía coronaria o estudio electrofisiológico. Cuando una persona es inicialmente revisada en forma primaria, y se le encuentran alteraciones sugestivas de cardiopatía, o datos de riesgo para muerte súbita, es enviado a la valoración secundaria.
    Un aspecto muy importante es el implementar el equipo médico de apoyo para resucitación cardiopulmonar dentro de la institución deportiva que se trate, para que sepan actuar eficaz y eficientemente en el momento de presentarse un problema médico mayor. Este equipo médico consiste en el personal y el material adecuado y completo para poder suministrar una resucitación oportuna (124-126).

VII. Conclusión
    La muerte súbita es un fenómeno con baja incidencia de presentación, pero que debemos de poner mucha atención en la prevención de ella, por medio de los exámenes médicos a toda persona con actividad física que presente síntomas, para ir limitando aún más su aparición. Creemos que la utilización de cuestionarios enfocados para la detección de antecedentes y/o síntomas cardiovasculares son fundamentales, para evaluar a grandes grupos de personas, como lo son en escuelas o asociaciones deportivas, en las que es necesario dejar al descubierto posibles factores de riesgo, para después evaluar clínicamente y en forma integral al sujeto que presente probabilidades de sufrir eventos mayores.
    Es muy importante, que cuando encontremos alguna alteración en el sujeto, valoremos la necesidad de enviarlo con un especialista para su manejo integral, apoyándonos en las recomendaciones propuestas en la 26ª Conferencia de Bethesda.

Figura 1
Causas de muerte súbita < 35 años

Figura 2
Causas de muerte súbita > 35 años


Cuadro 1
Causas de Muerte Súbita en el Atleta

Cuadro 2
Anomalías Congénitas de las Arterias Coronarias

Cuadro 3
Cuestionario del AHA/ACSM para evaluación preparticipación
en instalaciones para el acondicionamiento físico/salud



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          ASUHAN KEPERAWATAN PADA KLIEN DENGAN KELAINAN KATUP JANTUNG        
ASUHAN KEPERAWATAN PADA KLIEN DENGAN KELAINAN KATUP JANTUNG Katup merupakan pintu yang mengalirkan darah di dalam jantung antara atrium dan ventrikrl serta antara ventrikel dan aorta/arteri pulmonalis. Pergerakan membuka dan menutupnya pasif tergantung pada tekanan dari atrium dan ventrikel jantung. Beberapa katup (valvula): 1. Katup atrioventrikuler (katup antara atrium dan ventrikel) a. Valvula trikuspidalis : antara atrium kanan dan ventrikel kanan b. Valvula bikuspidalis: antara ventrikel kiri dengan atrium kiri Kedua katup tersebut memungkinkan darah mengalir dari masing-masing atrium ke ventrikel pada saat diastole ventrikel dan mencegah aliran balik pada saat diastole ventrikel. 2. Katup semilunar (katup antara ventrikel dengan aorta/arteri pulmonalis): a. Katup aorta b. Katup pulmonal Masing-masing memiliki 3 daun katup yang simetris dan menonjol seperti corong yang dikaitkan dengan cincin serabut. Pembukaan katup terjadi pada waktu masing-masing ventrikel berkontraksi (tekanan ventrikel lebih tinggi daripada tekanan yang ada dalam pembuluh darah arteri/aorta. Hal ini memungkinkan darah mengalir dari masing-masing ventrikel ke arteri pulmonalis dan aorta selama systole ventrikel dan mencegah aliran balik sewaktu ventrikel diastole. Dalam keadaan normal, luas permukaan katup 4-6 cm. PENYAKIT KATUP Ada dua jenis penyakit katup yaitu: 1. Stenosis katup: katup menyempit, Katup menjadi lebih tebal sehingga menurunkan fleksibilitas katup 2. Insufisiensi katup (regurgitasi): katup mengalami kekakuan akibat scar dan retraksi sehingga tidak dapat menutup dengan sempurna. MITRAL STENOSIS yaitu terhambatnya aliran darah dalam jantung akibat perubahan struktur katup mitral yang menyebabkan tidak membukanya katup mitral secara sempurna pada saat diastolic. ETIOLOGI: 1. PENYAKIT JANTUNG REMATIK (99%) 2. Pembentukan thrombus, penumpukan kalsium, dan atrial mixoma. Patofisiologi: Perubahan yang terjadi pada mitral stenosis adalah: 1. Komisura saling melengket satu sama lain dan bentuk berubah 2. Cup daun katup menjadi lebih tebal membentuk jaringan fibrosis 3. Chordate tendinae menebal, memendek dan saling melekat Tingkatan stenosis 1. Sedang: bila luas pembukaan katup 1,5 – 2 cm. Sudah menimbulkan perubahan hemodinamik. Aliran darah dari atrium kiri ke ventrikel kiri dengan tekanan abnormal 2. Berat: Bila luas pembukaan katup <= 1 cm. Darah mengalir dari atrium kiri ke ventrikel kiri dengan tekanan yang tinggi, terjadi peningkatan tekanan vena pulmonal tekanan onkotik terganggu terjadilah edema paru. Akibat lain: Darah yang dialirkan dari atrium ke ventrikel berkurang, deficit aliran darah ke aorta ----- gangguan hemodinamik GEJALA KLINIK 1. Sesak saat aktivitas 2. Cepat lelah 3. Lemah 4. Palpitasi, keringat dingin 5. Batuk, pada kongesti vena ada orthopnea, hemoptisis, PND 6. Disfagia, tidak napsu makan 7. Kadang-kadang chest pain 8. Edema perifer (mulai terjadi gagal jantung kanan) 9. Cianosis 10. BJ Jantung 1 keras, murmur sistolik 11. kekuatan nadi melemah, takikardi 12. Gangguan pada EKG Pemeriksaan penunjang 1. EKG 2. Echocardiography 3. Thoraks foto Penatalaksanaan medis 1. Perbaikan katup/penggantian katup dengan mitral valve replacement (MVR) 2. Obat-obatan: antibiotic, digitalis, diuretic, antikoagulan, anti aritmia 3. Diet rendah garam STENOSIS MITRAL PENINGKATAN TEKANAN ATRIUM KIRI VENA PULMONALIS DAN DILATASI ATRIUM PENINGKATAN TEKANAN VENA ARTERI PULMONALIS DILATASI VENTRIKEL KIRI PERUBAHAN TEKANAN ONKOTIK PLASMA HIPERTENSI PULMONAL HIPERTROPI VENTRIKEL KIRI KONGESTI PARU EDEMA PARU KEGAGALAN VENTRIKEL KIRI PEMBESARAN ATRIUM DAN VENTRIKEL KANAN GAGAL JANTUNG KIRI GAGAL JANTUNG KANAN DISTENSI VENA JUGULARIS ASCITES EDEMA PERIFER MITRAL INSUFISIENSI Keadaan dimana terjadi aliran darah balik (regurgitasi) dari ventrikel ke atrium selama sistolik yang disebabkan oleh kebocoran katup mitral. Insiden minsufisiensi mitral lebih sedikit daripada mitral stenosis ETIOLOGI: 1. MITRAL INSUFISIENSI AKUT a. Perforasi karena terjadi infeksi pada jantung b. Rupture chordate tendinae c. Ruptur muskulus papilaris, seiring dengan infark miokardium 2. MITRAL INSSUFISIENSI KRONIK a. Penyakit jantung rematik (RHD) b. Anomaly congenital c. Endokarditis d. Cardiomioplasty Patofisiologi: Katup mengalami pemendekan, kekakuan, deformitas dan retraksi pada 1 atau 2 katup mitral, terjadilah pemendekan dan saling melekatnya chordate tendinae dan otot papilaris. Selama periode systole, tekanan lebih banyak di ventrikel kiri. Akibat penutupan yang tidak sempurna dari katup mitral mengakibatkan darah kembali ke atrium kiri yang mengakibatkan distensi pada vena pulmonal. Akibatnya atrium kiri akan bekerja lebih keras untuk memompakan darah. Akibat kerja yang berlebihan tersebut terjadilah dilatasi dan hipertropi atrium kiri. Peningkatan atrium kiri dapat menyebabkan kongesti pulmonal dan memicu terjadinya gagal jantung kanan. GEJALA KLINIK: Ssesak saat olahraga, aktivitas, stress, hamil Lelah, pusing, palpitasi, suara serak/parau. Batuk Hemoptisis (jarang), chest pain (jarang) Sistolik murmur, BJ 1 melemah, JVP meningkat Bunyi napas rhonkii, cyanosis, diaphoresis Nadi melemah (bisa normal), irama tidak teratur Tekanan darah normal/menurun PEMERIKSAAN DIAGNOSTIK 1. EKG 2. THORAKS FOTO PENATALAKSANAAN 1. Non surgical: a. Mengurangi aktivitas b. Mengurani intake garam, diuretic c. Pemberian digitalis d. Pemberian vasodilator----mengurangi resistensi, pengosongan ventrikel kiri-----mengurangi regurgitasi e. Anti koagulan -----mengurangi risiko emboli f. Oksigen 2. Surgical: (pada mitral inssufisiensi berat) Diagnose keperawatan 1. Penurunan curah jantung b.d. peningkatan tekanan atrium, kongesti vena 2. Gangguan perfusi jaringan b.d. terganggunya lairan darah arteri dan vena 3. Berlebihnya volume cairan b.d. retensi natrium dan air 4. Intoeransi aktivitas b.d. tidak adekuatnya suplai oksigen 5. Cemas b.d.perubahan status kesehatan, dampak hospitalisasi STENOSIS TRIKUSPID Penyebab terbesar adalah penyakit jantung rematik (RHD). Biasanya tidak berdiri sendiri tetapi umumnya bersama-sama dengan stenosis mitralis. PATOFISIOLOGI Darah dari atrium kanan sedikit tertahan karena penyempitan katup trikuspid Atrium kanan akan menekan lebih kuat atrium kanan mengalami dilatasi dan hipertropi. Curah jantung juga akan berkurang akibat adanya hambatan sirkulasi pada tingkat katup tricuspid. GEJALA KLINIS Peningkatan tekanan atrium kanan akan diteruskan ke vena kava superior dan vena cava inferior perasaan berdenyut pada leher, kepala juga adanya perasaan perih diperut akibat adanya hepatomegali. Keadaaan curah jantung yang rendah akan mengakibatkan mudah lelah, sesak napas dan gejala lain seperti halnya stenosis mitral PEMERIKSAAN DIAGNOSIS 1. Ecg 2. Thoraks foto 3. Echocardiography 4. Kateterisasi jantung PENATALAKSANAAN 1. Kurangi Aktivitas fisik 2. Obat diuretic 3. Operasi valvotomy, tetapi paling baik tricuspid valve replacement (TVR) INSUFISIENSI TRIKUSPID Dapat terjadi atas dua sebab: 1. Fungsional disebabkan dilatasi ventrikel kanan yang menyebabkan dilatsi tricuspid yang akhirnya menyebabkan insufisiensi tricuspid. Timbul sebagai akibat adanya decompensasio cordis kanan 2. Organic, disebabkan RHD dan atau kelainan congenital PATOFISIOLOGI Insufisiensi Trikuspid Memungkinkan Adanya Darah Yang Kembali Ke Atrium Kanan Pada Saat Ventrikel Sistolik Dan Pada Saat Ventrikel Diastolik Volume Darah Yang Sampai Atrium Kanan Dan Ventrikel Kanan Mengalami Dilatasi Dan Hipertropi GEJALA: Sama Dengan Stenosis Trikuspid PEMERIKSAAN DIAGNOSTIK 1. ECG 2. Echocardiography 3. Thoraks foto 4. Kateterisasi PENATALAKSANAAN KONSERVATIF - ISTIRAHAT, PEMBATASAN AKTIVITAS FISIK - OBAT-OBATAN: DIGITALIS, DIURETIK OPERATIF - VALVULOPLASTY BERSAMAAN PADA KATUP MITRAL YANG TIMBUL BERSAMA - TVR BILA ADA KERUSAKAN OGANIK YANG BERAT
          Newborn Foundation Research, Programs and Advocacy Highlighted at WCPCCS in Barcelona        

Saint Paul, MN (rushPRnews) 08/06/17 — Newborn Foundation Research, Programs and Advocacy Highlighted at World Congress of Pediatric Cardiology & Cardiac Surgery in Barcelona

The Newborn Foundation, an international nonprofit leveraging process innovations and medical technologies to improve outcomes and reduce disparities for infants, presented two sessions during The 7th World Congress of Pediatric Cardiology & Cardiac Surgery (WCPCCS) at the Centre Convencions Internatcional de Barcelona in Barcelona, Spain in July.

The conference is held once every 4 years and convened more than 3,500 experts in pediatric cardiology, cardiothoracic surgery, researchers, and other professionals and advocates involved in the care of children with heart disease. The sessions highlighted advocacy and humanitarian efforts to combat congenital and childhood heart diseases, with a focus on newborn screening and emerging technologies for low-resource settings.

 Additionally, the Newborn Foundation presented two posters, including one presenting interim data from the largest newborn pulse oximetry screening project in the world, the BORN Project. Based in China and the Philippines, the pilot studies are screening more than 100,000 newborns and is the first in the world to use mobile phone- based pulse oximetry to screen newborns in resource poor and remote birth settings.

“We are honored to be participating for the second time, in the largest gathering of pediatric cardiac experts in the world,” said Annamarie Saarinen, co-founder and CEO of the Newborn Foundation, who also served on the faculty of the World Congress of Pediatric Cardiology & Cardiac Surgery.

“It was particularly inspiring to see the growing interest in the use of technologies such as automated echocardiography, telemedicine and pulse oximetry to earlier detect and treat babies with hidden, but deadly heart defects and other serious medical conditions. It’s a privilege to be playing a role in advancing these innovations to benefit babies everywhere.”

 

The Newborn Foundation also presented another session on the development of automated echocardiography to democratize access to high quality heart and lung imaged in low resource settings. Access to automated echocardiography can contribute to faster diagnosis of serious medical conditions, improved access to care and increased newborn and pediatric survival rates.

About the Newborn Foundation

The Newborn Foundation is an international nonprofit working specifically to leverage policies, programs and medical technologies to improve access and outcomes while reducing disparities for newborns. Co-founded by the mother of a child diagnosed with critical congenital heart defects as a newborn, the organization has been integral in the policy development, adoption and implementation of technologies for early detection, intervention and care of the youngest patients, including the landmark addition of universal newborn pulse oximetry screening for heart defects and other serious health conditions.

Facebook.com/newbornfoundation

Twtter.com/newbornfdn (@newbornfdn)


          MIT Externships; not your everyday job search opportunities.        
With the winter term nearing a close, the hunt for students to find a employer and/or internship in the coming months is becoming increasingly intense.

OIT has a very unique niche in the job market hunt, specifically for the Medical Imaging students. Rather than attempt to wax on the subject myself, Chin (Silver) Chan volunteered some of his time to elaborate on the unique opportunities provided by the MIT Department. Enjoy!!

For All current and Prospective
OIT Medical Imaging Students:

My name is Chin Silver Chan and I am a student office aide for the Student Success Center at the library. I was asked by my supervisor to write some blog entries and as it has been a long time since I have written a blog I’ll have to ask you to bear with me.

Here at OIT I am a junior and a teaching assistant for the Radiologic Science (x-ray) program.  Lately I have been asked a lot of questions by my sophomores and “Pre-MITers” about senior externship. Even though a lot of people are interested or were already admitted to the imaging programs, they actually have no idea what awaits them senior year. I guess they have some powerful blind faith then?   ;)

All Medical Imaging Technology (MIT for short) students in their senior year have to extern out to a hospital in another city. This is because our local hospital could not possibly handle the large number of students that rotate every year. Yet at the same time our students need a certain amount of clinical experience by law before we’re allowed to take the registry exam with our governing board and become certified to work in the US.  It’s similar to how lawyers need to take the BAR exam in order to practice.

Where you extern at is highly variable - pretty much if any hospital is willing to work out the contract with OIT and your program director then it could be a potential extern site so long as you can fulfill your clinical competencies there. For x-ray, the vast majority of our sites are in Oregon. Usually a hospital in every major city here will take one of us every year.  I know we currently have established sites in Eugene, Salem, Medford, Bend, Portland, La Grande, etc. However for the other medical imaging programs the sites are more diverse.  My friends in Echocardiography have told me that their sites are all over the country: New York, Ohio, Texas, and more.

Note: If you have friends in higher places at a hospital, you could have them sponsor you and, with the help of your program director, you can establish your own personal extern site.

So how do you know which site you get?
Well that is determined by the infamous “draw”.

In order to be fair to all juniors (such as yours truly) who are about to extern next year, they will do a drawing for extern sites. Before the draw your program director will have gathered enough hospital contracts that will be equal or slightly greater than the current juniors. Be advised that these contracts are extremely fickle and could change even the minute before the draw.

Anyways, all of the students in your program gather together with your professors and they call out an extern site at random. For example they’ll say like “Oregon Health Science University in Portland”, and then whoever is interested in that site will throw in a piece of paper with their name on it into a bucket. They will draw a name at random from that bucket and that person gets that site. They will keep drawing until everyone has a site. What this means is if you have just enough sites for juniors then someone will HAVE to be stuck with an extern site that potentially no one wanted. However fear not, for at the end of the draw you’ll be allowed to trade each other sites if desired. With some shrewd bargaining you’ll be able to get somewhere that you will remotely like…hopefully.

So what are the advantages to each site?
Besides the location, some sites have more advantages than others such as a stipend, paid health insurance, child care, etc. However, students are usually not aware of the perks of each site until AFTER the draw is over - in order not to influence their choices. Some sites are better than others to learn certain specialties, for example if one wanted to specialize in the Catheterization Lab and other interventional type procedures, they would be best served by externing to a place like OHSU, which is a level 1 trauma center and could provide more learning opportunities. Also, it is likely that your extern site will become your first job for at least a few years since they have already seen what you can do during externship.

So all of this is a simple process right? Basically, everything is determined by luck but a lot of people have trouble agreeing with it. I can’t say I blame them as I like to plan out my own future. However, you need to get use to the idea that the draw is really an illusion of choice so don’t have your heart set on any particular site or you might suffer. Before joining a program you need to be willing to move wherever for a year and do what it takes to succeed.  Some of the previous juniors I have talked to have said that they didn’t even draw what was on their top 10 choices on their list.

Externship is really all about showing off what you’ve learned in school and making your own opportunities. Even though the x-ray program has a 99% pass rate on our registry, no amount of quality training will absolutely guarantee success. Only you can determine that, and with that said I want to wish everyone good luck and hope you enjoy the ride!

          Cardiograph aplicacion android para saber tus latidos        
¿Alguna vez ha querido conocer como de rápido late tu corazón en ese momento? Pues ahora es más fácil que nunca, porque puedes usar tu teléfono móvil para conseguir los datos rápidamente en cualquier sitio y en cualquier momento.


Cardiograph es una aplicación android con la cual se puede medir tu ritmo cardiaco usando el teléfono móvil de forma fácil, eso sí, el teléfono debe tener un cámara pues las mediciones se realizan poniendo el dedo índice sobre la lente.  Si tiene flash es mejor, pues las mediciones necesitan una buena iluminación para hacer los cálculos.

Se puede obtener desde el mercado androide gratis, pero con publicidad, es una aplicación curiosa para nuestro Samnsung Galaxy Mini o cualquier otro teléfono.
No se puede decir que la medida sea  totalmente fiable, pero se acerca, puede dar una idea y es muy curioso compartirlo con los amigos.

El sonido que produce al detectar una pulsación es similar al de las máquinas  de hospitales, lo cual no hace creer que estamos en un centro médico.

Esta diseñado con una interface visual muy apañada inspirada en equipo médico real. Visualiza cada latido como dibujado por una aguja sobre un papel y da el número total de pulsaciones en una pantalla simulada similar a una digital LCD.

También muestra varias hechos, noticias y curiosidades sobre asuntos relativos al corazón, siempre mientras lo tienes encendido.

Un simple manual es este:

Paso 1) Activar el boton start / stop.

Paso 2) Colocar el dedo índice sobe la cámara y cubrir la lente completamente.

Paso 3) Las lecturas aparecerán en unos pocos segundos, la barritas sobre el corazón muestra la precisión de las medidas.

Si estas tomando lecturas erróneas, intenta ajustar la posición de tu dedo sobre la lente y también recuerda hacerlo en un lugar con buena iluminación.


          Ø¶Ø±Ø¨Ø§Ù† زندگی ...        

نام دستگاهی که ضربان قلبمان را نمایش می دهد Cardiograph است. 
کارش نشان دهنده وضعیت تپش قلب ماست.
روایت من اما معرفی نام و کار این دستگاه نیست.
موضوع آگاهی ما در زمانی است که به این نمودار نگاه می کنیم.
با بالا و پایین رفتنش به ما می گوید که هنوز زنده ایم.
سوال من این جاست که چگونه زنده ایم یا چگونه زندگی می کنیم؟
بعضی از قسمت ها بالای نمودار مانند بخشی از زمان های ماست که در اوج ناراحتی
یا خوشی هستیم و قسمتی از نمودار در پایین ترین نقطه قرار دارد همانند بخشی از زندگی که در نهایت کمبود و نیازیم.
آن چه مهم است روند ادامه دار آن است که به ما می گوید در جریان هستی و هم چنان زنده.
زندگی سراسر بالا و پایین دارد و این معنای درست و حقیقت محض زندگیست که گاه بالا نشینی و گاه نه،
گاه خوش حالی و گاه نه،
گاه همراهی و گاه نه،
گاه داری و گاه نه،
گاه دیده می شوی و گاه نه،
گاه لذت می بری و گاه نه،
گاهی دل می دهبم و گاه نه،
گاه منطقی هستیم و گاه احساسی،
گاهی جوری گاه ناجور،
گاه تکیه گاهی و گاه تیکه می دهی،
گاه مصممی و گاه شک داری،
گاه دوست داری و گاه بی تفاوت می شوی،
گاه می خواهی و گاه فرقی برایت نمی کند،
گاه به دنبالش هستی و گاه به دنبالت،
گاه اراده می کنی و نمی شود،
گاه آرزو می کنی و مستجاب نمی شود،
گاه می بخشی و گاه نمی بخشند،
گاه هست انکار می کنی،
گاه نیست روایت می کنی،
گاه دست می گیری گاه پشت پا می خوری،
گاه بر زبان می آوری گاه خاموش می شوی،
گاه می خوابی، خوابت نمی برد،
گاه بیداری، خوابت برده است،
گاه شروع نشدی تمام می شوی،
گاه تمام شده، تمام نمی شوی،
و گاه و گاه و گاه ...
همه این را گفتم که بگویم زندگی تا ضربان دارد فرصت داری.
من زندگی را دوست دارم ...

          Philips Showcases Data-Driven Cardiology Solutions at ACC.17        
Philips, cardiology solutions, ACC.17, Azurion angiography system, iFR outcomes results, IntelliSpace Cardiovascular

March 24, 2017 — At the 2017 American College of Cardiology's Annual Scientific Session & Expo (ACC.17), Philips showcased a broad range of integrated, patient-centric solutions designed to address the prevention, diagnosis, minimally invasive treatment and chronic care at home of cardiac conditions.

Philips exhibited the company's advanced, connected health offerings in the cardiology space at ACC.17, including:

  • Azurion – The company’s recently launched, next-generation image-guided therapy platform allows clinicians to easily and confidently perform a wide range of routine and complex procedures, helping them to optimize interventional lab performance and provide superior care. Azurion is powered by ConnectOS, a new operating system that provides a seamless integration of real-time information from all relevant technologies in the interventional lab.
  • Evolution 3.0 – Philips introduced the X8-2t Live 3D TEE (transesophageal echo) transducer, which allows for new levels of live 3-D imaging with new 3-D TEE features, including a new acoustic design with higher frequencies and bandwidth to provide increased resolution and tissue filling. Fast, easy and confident transthoracic and transesophageal echo allows clinicians to diagnose surgical pathology in real time.
  • HeartModel AI – The company’s Anatomical Intelligence Ultrasound (AIUS) application brings advanced automated quantification, 3-D views, robust reproducibility and significant time-savings to echocardiography quantification.
  • IntelliSpace Cardiovascular – Provides access to advanced cardiovascular informatics applications, brings multimodality images and clinical tools together in a single workspace for integrated clinical decision support. It seamlessly integrates with the IntelliSpace Portal advanced visualization solution, IntelliSpace ECG (electrocardiogram) data management solution, and the Philips Xper Information Management cath lab workflow solution.
  • DreamStation BiPAP autoSV Advanced – Designed to deliver optimal ventilation with minimal intervention for patients with central sleep apnea, complex sleep apnea and periodic breathing. Philips' clinically proven algorithm provides support when needed to help reduce events and normalize ventilation, and works with the patient's breathing pattern to minimize applied pressure, pressure support and machine breaths which can help patients experience comfortable, restful sleep.

Philips also highlighted new iFR (instant wave-Free Ratio) outcome results from over 4,500 patients. The data, which represent the largest randomized coronary physiology outcome studies to date, has the potential to help shape revascularization guidelines.

Read the article “Easier to Use iFR Equal to Outcomes of FFR in Coronary Lesion Evaluation.”

In addition to presenting data around the benefits of iFR technology, Philips hosted "Cardiology Talks," a program of short talks and conversation on key findings, trends and ideas impacting the cardiology specialty today. During the 20-minute sessions, clinicians, scientists and thought leaders shared their experiences and perspectives, discussed innovations, and invited attendees to join in the conversation.

For more information: www.usa.philips.com/healthcare


          (USA-MS-Jackson) Health Technician (Telemetry)        
Job Overview ## Job Overview ### Summary About the Agency **Health Technician (Telemetry), GS-0640; 1 vacancy; Jackson, MS** **Announcement Number: VA-17-DET-1991083-T5-BU** **OPEN TO CURRENT AND PERMANENT DEPARTMENT OF VETERANS AFFAIRS EMPLOYEES ONLY** **OUR MISSION**: To fulfill President Lincoln's promise – "To care for him who shall have borne the battle, and for his widow, and his orphan" – by serving and honoring the men and women who are America's Veterans. How would you like to become a part of a team providing compassionate care to Veterans? "As a VA professional, your opportunities are endless. With many openings in the multiple functions of VA, you will have a wide range of opportunities and leadership positions at your fingertips. Not only is it the largest, most technologically advanced integrated health care system in the Nation, but we also provide many other services to Veterans through the Benefits Administration and National Cemeteries. VA professionals feel good about their careers and their ability to balance work and home life. VA offers generous paid time off and a variety of predictable and flexible scheduling opportunities. For more information on the Department of Veterans Affairs, go to http://www.vacareers.va.gov/" Special Employment Consideration: VA encourages persons with disabilities to apply, including those eligible for hiring under 5 CFR 213.3102(u), Schedule A, Appointment of persons with disabilities [i.e., intellectual disabilities, severe physical disabilities, or psychiatric disabilities], and/or Disabled veterans with a compensable service-connected disability of 30% or more. Contact the Agency Contact on the last page of the JOA for information on how to apply under this appointment authority via the Selective Placement Coordinator. For more information on the "Who may apply" eligibility requirements, please refer to the OHRM Status Candidates and Other Candidate Definitionsdocument. ### Duties One (1) vacancy existed, in Jackson, Mississippi for a Health Technician (Telemetry), Nursing/Patient Care Services. This position will be assigned to work in the Telemetry Centralized Monitoring Room and involves monitoring, gathering, and reporting of standard electrocardiographic (EKG) tracings from a centralized monitoring station. Specific duties of the position include but are not limited to the following: * Performs telemetry monitoring activities including: initiation, recording, documenting, interpreting and discontinuing telemetry. * Performs ongoing visual observations of dynamic telemetry monitoring. Measures and interprets telemetry readings on hard copy printouts. Recognizes and reports changes in patient's telemetry reading outside the established parameters to appropriate personnel. * Recognizes, records, and rapidly reports potentially dangerous dysrhythmias to appropriate nursing staff. * Maintains records related to telemetry. * Maintains telemetry equipment and supplies. Contacts biomedical or engineering personnel for troubleshooting in identified potential * Equipment malfunction. * Maintains cleanliness if central telemetry monitoring room equipment. * In collaboration with personnel, maintains adequate levels of disposable supplies. Answers telephone and replies or refers calls appropriately. * Recognizes any potentially emergent situation; responds appropriately by seeking assistance as necessary. Initiates and/or performs CPR as needed. * Other duties as assigned with appropriate instructions and supervision. **WORK SCHEDULE:** Primarily Days (7:30 am – 4:00pm) with evening rotation (3:30 pm – 12:00 midnight) including weekends and holidays (This could change at the agencies discretion) **POSITION DESCRIPTION TITLE/PD#:** Health Technician/586-8890-0 **RELOCATION INCENTIVE:** Not authorized for this position. ### Supervisory Status No ### Travel Required * Not Required ### Relocation Authorized * No ### Who May Apply #### This job is open to… OPEN TO CURRENT PERMANENT DEPARTMENT OF VETERANS AFFAIRS EMPLOYEES ONLY Questions? This job is open to 2 groups. Job Requirements ## Job Requirements ### Key Requirements * MUST be an employee of the Department of Veteran Affairs. * Subject to a background/suitability investigation. * Designated and/or random drug testing may be required. * Require 1 year time in grade at the GS-5 level. * Selective Service Registration is required for males born after 12/31/1959. * Must pass a pre-employment physical upon selection. ### Qualifications **To qualify for this position**, applicants must meet all requirements by the closing date of this announcement Tuesday, August 22, 2017 **AREA OF CONSIDERATION (WHO MAY APPLY):** Open to Current, Permanent Department of Veteran Affairs Employees Only (1st Area of Consideration – current permanent G.V. (Sonny) Montgomery VAMC employees; 2nd Area of Consideration – current permanent VA Nationwide employees.) **MINIMUM QUALIFICATIONS:** ******EDUCATION AND EXPERIENCE AS INDICATED:** ******SPECIALIZED EXPERIENCE:** MUST have one (1) year of specialized experience equivalent to at least the next lower grade level (GS-05). Experience that equipped the applicant with the knowledge, skills and abilities (KSAs) to perform successfully the duties of the position, and that is typically in or related to the work of the position to be filled. Examples of specialized experience would typically include performing telemetry monitoring; demonstrate advanced knowledge of cardiac rhythms; recognizing potential dangerous dysrhythmias; maintaining telemetry equipment and supplies, etc. **OR** **EDUCATION:** Graduate education or an internship meets the specialized experience required above the GS-5 only in those instances where it is directly related to the work of the position. **(Unofficial Transcripts Required if using education to qualify for this position.)** **PREFERRED EXPERIENCE:** * Completion of a rhythm recognition course, provide certificate of completion * Two (2) years of telemetry experience Experience refers to paid and unpaid experience, including volunteer work done through National Service programs (e.g., Peace Corps, AmeriCorps) and other organizations (e.g., professional; philanthropic; religions; spiritual; community; student; social). Volunteer work helps build critical competencies, knowledge, and skills and can provide valuable training and experience that translates directly to paid employment. You will receive credit for all qualifying experience, including volunteer experience. **Note:** Only education or degrees recognized by the U.S. Department of Education from accredited colleges, universities, schools, or institutions may be used to qualify for Federal employment. You can verify your education here: http://ope.ed.gov/accreditation/. If you are using foreign education to meet qualifi