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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypotension and shock can be classified as hypotension caused by reduced or maintained left ventricular (LV) ejection. Reduced left ventricular ejection can result from intrinsic left ventricular, aortic valve or mitral valve failure, which includes dilated or ischemic cardiomyopathy, left main trunk disease, acute myocarditis, etc. Acute and subacute severe aortic regurgitation can also cause shock. Echocardiography allows noninvasive diagnosis of infective endocarditis and Takayasu's arteritis to cause severe arotic regurgitation and can also be used to diagnose obstruction of the left ventricular outflow tract. Reduced left ventricular preload can be caused by pericardial effusion and right ventricular ejection failure, and can result from pulmonary embolism, tricuspid regurgitation, right ventricular infarction, tension pneumothorax, hypovolemia and others characterized by a small left ventricle with good ejection fraction. Normal left ventricular ejection may be associated with hypotension. Sepsis, anaphylactic shock and neural disorder are associated with hypotension and normal cardiac output. Pseudohypotension may result from aortic dissection, Takayasu's arteritis, arteriosclerosis obliterans and aortic coarctation. A right parasternal approach enables better visualization of the ascending aorta. Fundamental echochocardiographic scanning allows approximate yet useful diagnosis of hypotension and shock.
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PMID:[Easy echo diagnosis for hypotension and shock]. 1908 1

Approximately 10% of all patients with acute pulmonary embolism (PE) die within the first three months after diagnosis. However, PE is not universally life-threatening, but covers a wide spectrum of clinical severity and death risk. Thrombolytic treatment is indicated patients with acute massive PE who are at high risk for early death, i.e. those patients who present with arterial hypotension and shock. On the other hand, low molecular-weight heparin or fondaparinux is adequate treatment for most normotensive patients with PE. Recombinant tissue plasminogen activator, given as 100 mg infusion over 2 h, is the treatment of choice for patients with PE, although older regimens using urokinase or streptokinase are also efficacious. Beyond the relatively small numbers of patients with massive, high-risk PE as a target population for thrombolysis, there is increasing awareness of the need for risk stratification of normotensive patients and the search for an intermediate-risk group (also called submassive PE). Recent meta-analyses of cohort studies suggest that imaging of the right ventricle or biomarkers of myocardial injury alone may be insufficient for guiding therapeutic decisions. Instead, accumulating evidence appears to support strategies which combine the information provided by an imaging procedure with a biomarker test. These data provide the rationale for a large multinational randomized trial which has set out to determine whether normotensive patients with right ventricular dysfunction, detected by echocardiography or computed tomography, plus evidence of myocardial injury as indicated by a positive troponin test, may benefit from early thrombolytic treatment. This study, which is underway in 13 European countries, will enroll a total of 1000 patients and will be completed in 2012. Together with a parallel trial currently being conducted in the United States, it will hopefully answer the question whether thrombolysis is indicated in submassive PE, thus terminating a 40-year-old debate and filling an important gap in our management concept for acute pulmonary embolism.
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PMID:Thrombolytic therapy for submassive pulmonary embolism. 2295 53