Embolism pulmonary

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). 

Indications for treatment with streptokinase include acute occlusion of arteries, deep vein thrombosis, and pulmonary embolism. Streptokinase therapy in coronary thrombosis, which is the usual cause of myocardial infarction (54,71,72), has proved to be valuable. In this frequently fatal condition, the enzyme is adrninistered intravenously at a dose of 1.5 million units over 60 min, or given by intracoronary infusion at a 20,000- to 50,000-unit bolus dose followed by 2000 to 4000 units/min for 60 min therapy must be instituted as soon as practicable after the diagnosis of heart attack is made. For deep vein thrombosis, pulmonary embolism, or arterial occlusion, streptokinase is infused at a loading dose of 250,000 units given over 30 min, followed by a maintenance dose of 100,000 units over a 60-min period. 

Pulmonary embolism. A blood clot trapped in the blood vessels of the lungs. 

In general, arterial thrombi are platelet-rich ( white clots ) and form at ruptured atherosclerotic plaques, leading to intraluminal occlusion of arteries that can result in end-organ injury (e.g., myocardial infarction, stroke). In contrast, venous thrombi consist mainly of fibrin and red blood cells ( red clots ), and usually form in low-flow veins of the limbs, producing deep vein thrombosis (DVT) the major threat to life results when lower extremity (and, occasionally, upper extremity) venous thrombi embolize via the right heart chambers into the pulmonary arteries, i.e., pulmonary embolism (PE). 

Therapeutically t-PA and urokinase are the most important drugs for fibrinolytic therapy (myocardial infarction, stroke, massive pulmonary embolism). This treatment is associated with an enhanced risk of bleeding complications. 

Occurs as a result of circulatory insufficiency associated with overwhelming infection Occurs when obstruction of blood flow results in inadequate tissue perfusion. Examples include a severe reduction of blood flow as the result of massive pulmonary embolism, pericardial tamponade, restrictive pericarditis, and severe cardiac valve dysfunction Occurs as a result of blockade of neurohum oral outflow. Examples include from a pharmacological source (ie, spinal anesthesia) or direct injury to the spinal cord. This type of shock is rare. 

Many serious health problems result from abnormally located blood clots heart attacks (clots in coronary arteries), pulmonary embolism (clots in the lungs), and peripheral arterial occlusion and deep vein thrombosis (clots in the limbs). Each year heart attacks alone afflict over a million people in the United States, and almost half of them die as a result. 

Tissue plasminogen activator 530 amino acids, glycosylated E. coli Yeast Animal cells Acute mycocardial infarct Pulmonary embolism Approved for sale Animal cell culture most effective way of producing active enzyme... 

Streptokinase is administered by intravenous or intra-arterial infusion in the treatment of thrombo-embolic disorders, e g. pulmonary embolism, deep-vein thrombosis and arterial occlusiorrs. It is also used in acute myocardial irtfarclioa... 

Cl 0.08-0.96) and symptomatic pulmonary embolism (PE) (OR 0.34, 95% Cl 0.17-0.69), but an increase in major extracranial hemorrhage when compared to placebo (OR 2.17, 95% Cl 1.10. 28). Nonsignificant reductions in combined death and disability, as well as increases in case fatality and sICH were also observed. The authors concluded that insufficient evidence existed to support the routine use of LMWH in the management of patients with ischemic stroke. 

In stroke patients presenting to the ED, the first goal of treatment is immediate cardiac and respiratory stabilization. The systemic blood pressure is most often elevated in the setting of an acute stroke as the result of a catecholamine surge, and if the patient is hypotensive, the clinician should consider a concomitant cardiac process, such as myocardial infarction (MI), congestive heart failure (CHF), or pulmonary embolism (PE). 

Kamphuisen PW, Agnelli G. What is the optimal pharmacological prophylaxis for the prevention of deep-vein thrombosis and pulmonary embolism in patients with acute ischemic stroke Thromb Res 2007 119(3) 265-274. 

Management of Deep-Vein Thrombosis and Pulmonary Embolism... 

Low cardiopulmonary reserve (i.e., right-ventricular hypokinesis on echocardiogram) where an initial or repeat pulmonary embolism would be catastrophic... 

The current values for ruling out a cardiac etiology for dyspnea are a BNP less than 100 pg/mL (100 ng/L) or an NT-proBNP less than 300 pg/mL (300 ng/L or 35.4 pmol/L). BNP measurements require cautious interpretation, as numerous conditions can also elevate BNP concentrations. These include older age, renal dysfunction, pulmonary embolism, and chronic pulmonary disease. Nesiritide, a recombinant BNP drug, has an identical structure to native BNP and will interfere with the commercial BNP assay, resulting in a falsely elevated level. Therefore, blood for BNP determination should be obtained 2 hours after the end of a nesiritide infusion, or alternatively the NT-proBNP assay should be utilized. 

Streptokinase + 35% +++/+ Infusion over 60 minutes 613 Pulmonary embolism, deep vein thrombosis, arterial thromboembol ism, clearance of an occluded arteriovenous catheter... 

Mitral stenosis or regurgitation Mitral valve prolapse Chronic obstructive pulmonary disease Pulmonary embolism Idiopathic ("lone" atrial fibrillation) Thoracic surgery ... 

Identify risk factors and signs and symptoms of deep vein thrombosis and pulmonary embolism. 

Venous thromboembolism (VTE) is one of the most common cardiovascular disorders in the United States. VTE is manifested as deep vein thrombosis (DVT) and pulmonary embolism (PE) resulting from thrombus formation in the venous circulation (Fig. 7-1).1 It is often provoked by prolonged immobility and vascular injury and is most frequently seen in patients who have been hospitalized for a serious medical illness, trauma, or major surgery. VTE can also occur with little or no provocation in patients who have an underlying hypercoagulable disorder. 

DVT, deep vein thrombosis HIT, heparin-induced thrombocytopenia PAI-I, plasminogen activator inhibitor PE, pulmonary embolism SERM, selective estrogen receptor modulator VTE, venous thromboembolism. 

Venous thromboembolism most commonly develops in patients with identifiable risk factors (Table 7-1) during or following a hospitalization. Many, perhaps the majority of patients, have asymptomatic disease. Patients may die suddenly of pulmonary embolism. 

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