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

Acute circulatory failure is the major complication of acute pulmonary embolism. It may be clinically silent, but sometimes leads to systemic hypotension, shock, or clinical manifestations of right ventricular failure. In these patients, oxygen, inotropic drugs, and fluid loading are indicated. Unless contra-indicated, thrombolytic therapy should be undertaken when clinical signs of circulatory failure occur. Surgical embolectomy is now undertaken in the very few patients not responding to maximal medical treatment. Vena cava interruption is not more often useful in massive pulmonary embolism than in non massive pulmonary embolism.
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PMID:[Treatment of severe pulmonary embolism]. 876 79

Acute massive pulmonary embolism increases pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR), which may lead to early right ventricular failure and subsequent cardiocirculatory deterioration. Inhaled nitric oxide (NO) selectively dilates pulmonary vessels in vivo. Thus, inhaled NO may be useful in preventing cardiocirculatory deterioration following pulmonary embolism. We investigated the effects of inhaled NO in the acute phase of massive pulmonary microembolism in 10 anesthetized and mechanically ventilated piglets (body weight, 18 +/- 2 kg). Microspheres of 300-microns diameter were injected i.v. in an amount sufficient to initially increase mean PAP to 45 mm Hg. Forty-five minutes after pulmonary embolization, the pretreatment control values were recorded. Thereafter, the piglets inhaled 40 ppm NO, and subsequently 80 ppm NO. When 40 ppm NO was inhaled, there was a significant decrease in systolic PAP (-10.3%; 44.5 +/- 2.2 to 39.9 +/- 2.4 mm Hg; p < 0.05) and mean PAP (-9.4%; 32.9 +/- 1.3 to 29.8 +/- 1.3 mm Hg; p < 0.05). PVR was changed by -13.6% (p = 0.07). Administration of 80 ppm NO resulted in a significant decrease in systolic PAP (-12.6%; to 38.9 +/- 1.9 mm Hg; p < 0.05), mean PAP (-11.9%; to 29.0 +/- 1.4 mm Hg; p < 0.05), and PVR (-19.4%; p < 0.05) compared with pretreatment values. Discontinuation of NO inhalation was associated with an immediate return to pretreatment values. Systemic hemodynamics and the arterial and mixed venous oxygen concentrations remained unchanged. We conclude that inhaled NO following acute massive pulmonary microembolism selectively decreases PAP and PVR without influencing systemic hemodynamics in piglets.
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PMID:Inhaled nitric oxide selectively decreases pulmonary artery pressure and pulmonary vascular resistance following acute massive pulmonary microembolism in piglets. 922 5

A 33-year-old man was hospitalized with right heart failure. He was diagnosed as having right atrial mural thrombus complicated with pericarditis on echocardiography, thoracic computed tomography, and cardiac catheterization. Pericardiectomy and thrombectomy with a partial resection of the right atrial wall were performed under extracorporeal circulation. It was suggested that the cause of right atrial thrombus was congestion, atrial fibrillation, and pericarditis. The cause of pericarditis could not be determined by pathologic examination and laboratory data. Surgical treatment should be performed as soon as possible to prevent pulmonary embolism.
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PMID:Right atrial mural thrombus associated with pericarditis. 889 92

Pulmonary hypertension is a severe disorder of the pulmonary circulation and occurs in a variety of vascular and parenchymal lung diseases. It leads to volume and/or pressure overload of the right ventricle and finally to right heart failure. Pulmonary vascular diseases such as chronic pulmonary embolism cause a drastic increase in pulmonary vascular resistance, which results in extremely high pulmonary artery pressures that can even reach systemic levels. On the other hand, moderate pulmonary hypertension can also occur in chronic obstructive and restrictive lung diseases. For a long time, the diagnosis of pulmonary hypertension and cor pulmonale was based upon findings in echocardiography and right heart catheterization. Today modern imaging techniques allow the radiologist to assess right ventricular and pulmonary artery morphology and function. The application of spiral CT, electron-beam CT and MRT permits the diagnosis and differential diagnosis of pulmonary hypertension and also the evaluation and follow-up of underlying vascular or parenchymal lung disorders. In addition, quantification of right ventricular function and calculation of pulmonary hemodynamic parameters are possible.
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PMID:[Pulmonary hypertension and cor pulmonale]. 931 82

Thrombolysis debulks clot and provides primary treatment of pulmonary embolism, whereas intensive anticoagulation is critical for secondary prevention of recurrent pulmonary embolism. The decision to use primary therapy or secondary prevention depends upon the patient's risk of suffering an adverse clinical outcome. We utilize echocardiography to help risk-stratify our patients. The presence of normal right ventricular function portends an excellent prognosis with anticoagulation alone. In contrast, the presence of right ventricular hypokinesis or dilatation may indicate a high likelihood of recurrent pulmonary embolism despite adequate anticoagulation. Among high risk patients, thrombolysis can usually rapidly reverse right heart failure and be life-saving. The procedure for administering thrombolytic therapy has been streamlined to improve efficacy, enhance safety, and reduce costs.
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PMID:Contemporary pulmonary embolism thrombolysis. 970 36

A 32-year-old female is described, who was admitted with symptoms of severe right heart failure. The most likely diagnosis of pulmonary embolism was excluded. Echocardiography and left-right catheterisation confirmed the diagnosis of primary pulmonary hypertension. A possible mediator in the process of PPH could be the appetite suppressants she had taken for some months after her second pregnancy. Before further pharmacologic tests could be performed the patient died in circulatory collapse. Postmortem pathological examination confirmed the diagnosis of PPH by the presence of narrowed pulmonary arterioles, media hypertrophy, thrombotic lesions and normal surrounding pulmonary parenchyma. The literature on primary pulmonary hypertension is revised with special emphasis on diagnosis and treatment algorithms.
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PMID:Primary pulmonary hypertension with fatal outcome in a young woman and review of the literature. 1021 74

Streptokinase, urokinase, tissue plasminogen activator and similar drugs can all cause lysis of venous thrombi and pulmonary emboli, but there is small evidence that accelerated lysis achieves a significantly better clinical outcome, on average, in the shorter or longer term, than heparin alone. Thrombolytic therapy for deep leg vein thrombosis aims to restore flow and to preserve venous valves, and so to prevent chronic post-phlebitic disability, but no trial has convincingly demonstrated that the last can be achieved in more than a few patients. Only a small minority of people with extensive proximal thrombosis develop disabling post-phlebitic venous insufficiency, and there are no good clinical predictors of this outcome. As a result, any widespread use of thrombolytics would bring an immediate risk of major bleeding to many people who will never be destined to develop a clinically important problem. Thrombolytic therapy after venous thrombosis should be avoided except, perhaps, in a few carefully selected patients with severe obstruction. The case for using thrombolytics after recent pulmonary embolism is strongest in the limited number of patients with ongoing hypoxia, respiratory distress, pulmonary hypertension and right heart failure, because thrombolytic therapy often achieves an impressive and almost immediate clinical benefit in this clinical setting. Whether early relief from pulmonary artery obstruction translates into longer-term advantage over heparin remains uncertain, however, because no comparative trial has ever shown these drugs to reduce mortality after pulmonary embolism. In all cases, both the physician and the patient must balance the certainty of an immediate bleeding risk against the uncertainty of a better than marginal real benefit.
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PMID:Thrombolytic therapy for venous thrombosis and pulmonary embolism. 1033 Oct 98

Patients with acute massive pulmonary embolism or primary pulmonary hypertension may develop acute circulatory failure and are therefore admitted in the intensive care. The mortality rate of patients with pulmonary embolism and shock varies between 25 and 35% whereas the corresponding figure in patients with submassive embolism is less than 10%. Spiral computed tomography may be the most convenient test for diagnosing pulmonary embolism in the setting of acute circulatory failure. In the few patients who remain unstable despite adequate symptomatic treatment, transthoracic echocardiography combined with clinical judgement is appropriate. Inotropic support and thrombolytic therapy are clearly indicated for patients with massive embolism and shock. The role of the latter is more controversial in patients with right ventricular distension and normal blood pressure. The optimal duration of anticoagulant therapy for pulmonary embolism remains to be defined. Most patients are adequately treated with a six-month course of oral anticoagulants. A shorter duration may be sufficient when a transient risk factor is the cause of the initial event whereas patients with cancer or antithrombin deficiency may require a life long treatment. Primary pulmonary hypertension is a much more uncommon disease which can also lead to right ventricular failure. Symptomatic treatment combines oxygen, inotropic drugs, as well as the optimisation of right ventricular filling pressure. Specific treatment includes inhaled nitric oxide or intravenous epoprostenol followed by anticoagulants with either calcium channel blockers in patients responding acutely to vasodilators or a continuous infusion of epoprostenol in those who do not respond to acute challenge or who are not improving with calcium channel blockers. Although the long term survival has markedly improved as a result of epoprostenol treatment, some patients with refractory primary pulmonary hypertension remain candidates for lung transplantation.
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PMID:[Acute circulatory failure caused by primary pulmonary hypertension or pulmonary embolism]. 1075 56

In patients with cardiomegaly and signs and symptoms compatible with CHF, unilateral right-sided or bilateral pleural effusions of similar size are likely to be due to left-sided CHF. Isolated right ventricular failure or chronic pulmonary hypertension is not usually associated with pleural effusions, and unrecognized or new-onset left ventricular dysfunction and other causes should be considered when a patient with cor pulmonale presents with a pleural effusion. Unilateral left-sided pleural effusions with cardiomegaly may be due to pericardial disease. Current hypotheses do not adequately explain the laterality of effusions in CHF or pericardial disease. Clinical and radiographic correlation is always required; however, the associations described occur often enough to make them useful in day-to-day clinical practice. When ascribing pleural effusions to CHF, clinicians must be sure the clinical signs and history "fit the picture," because pneumonia and pulmonary embolism may also cause pleural effusions in patients with heart failure. Typical pleural effusions in patients with uncomplicated CHF (demonstrated by small to medium-sized effusions and the absence of fever, leukocytosis, pleuritic chest pain, or marked asymmetry in bilateral effusions) do not require routine diagnostic thoracentesis for evaluation. A reasonable approach in such cases is treatment of the underlying CHF and follow-up radiography to monitor for resolution of the effusions. Prompt diagnostic thoracentesis is indicated whenever atypical features are present and other diagnoses are under consideration.
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PMID:Pleural effusions in cardiovascular disease. Pearls for correlating the evidence with the cause. 1088 42

Echocardiographic demonstration of right ventricular thrombosis is relatively common in pulmonary embolism. There are also reports of right ventricular thrombi in patients affected by right myocardial infarction or dilated cardiomyopathy. In arrhythmogenic right ventricular cardiomyopathy single or multiple aneurysms are often present in the right ventricular free wall. These hypoakinetic areas represent a site for potential development of thrombi especially in advanced disease states. In the literature a single case of a patient affected by arrhythmogenic right ventricular cardiomyopathy with right heart failure and atrial and ventricular thrombi is reported. We report a case of arrhythmogenic right ventricular cardiomyopathy with a right ventricular thrombus located inside a single apical aneurysm in the presence of normal right ventricular systolic function.
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PMID:[Right ventricular thrombosis in arrhythmogenic cardiomyopathy. A case report]. 1093 47


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