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

Thromboembolic pulmonary hypertension can occur in two different settings: either acute pulmonary embolism or chronic pulmonary thromboembolism. During acute pulmonary embolism, when the heart and lungs are normal, the mean pulmonary artery pressure never excesses 40 mmHg, this is the maximum pressure the right ventricle can stand. During chronic thromboembolism, the right ventricle can adapt to slowly increasing pulmonary artery pressure. The mean pulmonary artery pressure is usually very elevated and right heart failure is delayed. Diagnosis is difficult when an history of acute pulmonary embolism or phlebitis is lacking. At the beginning, the main differential is psychogenic dyspnea. A clue to the diagnosis is given by the pulmonary function test mainly arterial blood gases at rest and exercise and radionuclide perfusion scan. When the pulmonary hypertension is patent the main differential is primary pulmonary hypertension. No definitive clear cut can be made between multiple distal chronic thromboembolism and primary pulmonary hypertension.
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PMID:[Thromboembolic pulmonary arterial hypertension]. 185 24

The authors examined the records of all patients referred for right heart catheterization between 1963-84 because of persistent dyspnoea after one or more episodes of pulmonary emboli. Patients with a history of congestive heart failure, angina, restrictive or obstructive pulmonary disease that could explain their symptoms were excluded. Catheterization was performed 15.8 +/- 24 months after the first suspected episode of pulmonary embolism. Seven of the 29 patients included had resting pulmonary hypertension (PH). All of these had an alveolo-arterial oxygen difference (AaDO2) greater than 25 mmHg. Twenty patients of the group, taken as a whole, had an AaDO2 greater than 25 mmHg. Information was available from 1 month to 5 years later in 6/9 patients with an AaDO2 less than 25 mmHg. In all of them dyspnoea improved or resolved. Information was available in 15/20 patients with AaDO2 greater than 25 mmHg. Three of 8 patients without PH but with an increased AaDO2 on the initial catheterization developed PH within 2 years. Dyspnoea increased in 1 of the remaining five. Four patients who initially had PH developed right heart failure 6 months-3 years later. In the remaining 3, dyspnoea was stable in 1, increased in 1 and one patient died with autopsy evidence of multiple pulmonary emboli. Abnormal oxygenation predicts the presence or subsequent development of PH in patients who are chronically dyspnoeic after pulmonary embolism.
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PMID:AaDO2 as a predictor of pulmonary hypertension resulting from pulmonary emboli. 191 74

Intracardiac echocardiography refers to the method of imaging cardiac structures from intracardiac locations with the use of ultrasound catheters. Advances in catheter-based interventional cardiologic procedures to treat cardiovascular lesions and the problems encountered during those procedures due to inadequate guidance provided by fluoroscopy have given the impetus to develop other guidance modalities. Experimental explorations with intracardiac ultrasound probes have indicated that detailed visualization of cardiac structures in real-time is possible by intracardiac ultrasound. Recent advances in catheter-based ultrasound technology make it feasible to safely pass small-sized catheters in humans into various intracardiac locations and acquire images of valvular structures and various chambers. Experience with 20 MHz ultrasound catheters indicates that high resolution images of normal and abnormal structures can be obtained if the catheter is manipulated close to the region of interest. The problem of the limited depth of field associated with 20 MHz catheters has led to the fabrication of catheters with lower frequency ultrasound elements. Experimental and clinical experience with 12.5 MHz ultrasound catheters points to the capability and potential of intracardiac echocardiography to not only display normal structures but also aid in the identification of valvular abnormalities, chamber dysfunction and pericardial effusions. In addition, aortic disorders such as acute dissection, coarctation and atherosclerotic disease could be delineated. Similarly, abnormalities involving the pulmonary arteries such as pulmonary embolism, organized thrombi, peripheral pulmonary arterial stenoses, and pulmonary hypertension-induced vascular changes could be recognized. Many modifications in the catheter design are being explored. With further work in the area of catheter technology and ultrasound image processing, intracardiac echocardiography is likely to become a clinical tool.
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PMID:Intracardiac echocardiography: current developments. 191 63

More than 10 years ago, thrombolytic therapy with urokinase and streptokinase for pulmonary embolism was found to have considerable advantages over standard heparin therapy. After the introduction of alteplase, a recombinant tissue plasminogen activator, further studies confirmed this benefit. However, thrombolytic therapy for pulmonary embolism has not gained universal acceptance, even though it now has U.S. Food and Drug Administration approval. Clear advantages of thrombolytic therapy over conventional heparin therapy are improved pulmonary capillary blood volume, accelerated clot lysis and accelerated pulmonary perfusion. Earlier reversal of right-sided heart failure, a lower incidence of recurrent pulmonary embolism, a reduced risk of chronic pulmonary hypertension and reduced mortality have been claimed as advantages, but these have not been adequately proved. A recent survey suggests that about half of all patients with pulmonary embolism are potential candidates for thrombolytic therapy. In a subset of patients with hemodynamic compromise, thrombolysis has definite advantages over heparin therapy.
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PMID:Thrombolysis for pulmonary embolism. 192 47

Pulmonary embolus-in-transit represents an important cause of morbidity and mortality in the critically ill patient. Unexplained shock and acute pulmonary hypertension were evaluated with echocardiography. Standard transthoracic echocardiography failed to identify a large embolism-in-transit that was easily visualized by transesophageal imaging. A review of the literature involving emboli-in-transit suggests that early intervention in these patients may be beneficial.
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PMID:Detection of massive pulmonary embolus-in-transit by transesophageal echocardiography. 193 73

The clinical picture of pulmonary embolism (PE) ist remarkably unspecific and one has to rely mainly on imaging techniques to obtain a reliable diagnosis. PE is not a primary disease but the complication of deep venous thrombosis (DVT), and thus there is a strong correlation between pulmonary embolism and venous thrombosis. Radiologic screening of these diseases is based on invasive and noninvasive tests. Chest X-ray has a low predictive value of 63% and helps mainly in ruling out other diagnoses such as pneumothorax or pneumonia. Chest computed tomography scanning with contrast may occasionally be useful in detecting large central emboli. Magnetic resonance imaging in PE has not yet been shown to be of great clinical value. Digital subtraction angiography has the potential advantage of allowing injections of smaller contrast volumes and is particularly useful in pulmonary hypertension. Cardiac and respiratory motion blur images and render interpretation difficult. Conventional pulmonary angiography is required for definitive diagnosis in a significant number of patients, especially when V/Q scan is non-diagnostic. Its morbidity and mortality is nowadays negligible. If these facilities are not available, they can often be obviated by venous studies searching for the presence of venous thromboses. Alternative modalities include contrast phlebography and venous ultrasound imaging. This last, newly developed technique combined with compression Doppler is safe and accurate, at least in the femoral and popliteal veins. Contrast phlebography remains the standard imaging method, is widely available, and demonstrates floating clots or thromboses with minor complications using non-ionic contrast media.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Diagnostic and interventional radiology in pulmonary embolism]. 194 62

A 68-year-old man with remote history of previous myocardial infarction presented with a four-week history of intermittent dyspnea. After developing hypotension during an exercise tolerance test, he underwent cardiac catheterization, revealing significant pulmonary hypertension and two-vessel coronary artery disease. Pulmonary angiography confirmed the presence of pulmonary emboli which partially resolved after thrombolytic therapy. Subsequent treadmill testing confirmed the absence of exercise-induced hypotension two months following treatment. This case underscores the importance of considering pulmonary embolism as a potential cause of exercise-induced hypotension, since it can be successfully treated with thrombolytic agents weeks after the initial onset of symptoms.
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PMID:Pulmonary embolism presenting as exercise-induced hypotension. 198 18

Thrombolytic therapy has been used fairly extensively in the management of acute proximal deep-vein thrombophlebitis of the extremities, acute pulmonary embolism, and acute peripheral arterial thrombosis and embolism in addition to acute thrombotic coronary events. In the presence of acceptable indications and a favorable benefit to risk ratio, this form of therapy, when successful, has served as a useful adjunct in the management of these disorders. In deep-vein thrombophlebitis, lysis of the thrombus before permanent pathological changes (eg, organization, scarring) have occurred can prevent venous valvular dysfunction and postural venous hypertension and its complications, especially the postphlebitic syndrome. In the more severe forms of acute pulmonary embolism, thrombolytic therapy, when applied early after symptom onset, decreases morbidity and is likely to prevent a chronic increase in pulmonary vascular resistance and persistent pulmonary hypertension. In peripheral arterial thrombo-occlusive events, early restoration of flow through thrombolysis has been shown to limit ischemic damage and serve as a useful supplement to angioplasty or surgery. Thrombolytic therapy has been used less extensively in acute strokes. Here the danger of reperfusion causing bleeding into a softened area of brain undergoing infarction has slowed its evaluation for this disorder; its application to stroke remains experimental.
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PMID:Thrombolytic therapy for noncoronary diseases. 200 69

In 4 consecutive patients admitted for multiple pulmonary embolism 2-dimensional echocardiography showed large right atrial migrant thromboemboli in transit, floating and prolapsing into the right ventricle in diastole. This pattern was always associated with the echocardiographic signs of pulmonary hypertension. All the patients were treated with intravenous infusion of 100 mg of rt-PA in 3 hours. rt-PA determined the dissolution and disappearance of the right atrial thromboemboli (it took 4 hours in 2 patients and 5 hours in the remaining 2), and the concomitant disappearance of the echocardiographic signs of pulmonary hypertension. During and after the rt-PA therapy there was no evidence of further pulmonary embolism. The fibrinolytic treatment for right atrial thromboemboli during multiple pulmonary embolism is a promising alternative to right atrial thrombectomy: our results indicate that rt-PA acts rapidly and is effective and safe; if these results will be confirmed in a larger group of patients, rt-PA could become the first-choice therapy of right atrial thromboembolus.
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PMID:[Thrombolytic therapy in the treatment of thromboembolism of the right cardiac cavity during pulmonary embolism: our experience with rt-PA and review of the literature]. 212 90

A 79-year-old woman was admitted with general fatigue. Chest roentgenogram showed diffuse reticular shadows and bilateral pleural effusion. Peripheral blood studies revealed an elevation of platelet count (203.3 X 104/mm3). The case was diagnosed as essential thrombocythemia and treated with ACNU. The platelet count decreased. Bilateral pleural effusions increased gradually and their characteristics changed from bloody exudate to transudate. Biopsy of her pleura and thoracoscopy were carried out without significant results. Later, systemic edema, which suggested right heart failure, developed. The diagnosis of pulmonary hypertension and right heart failure was made by echocardiogram and right cardiac catheterization. Because perfusion scan of the lung revealed some perfusion defects, complication of pulmonary embolism was suspected. Bilateral pleural effusion and pulmonary artery pressure decreased with treatment by nifedipine, furosemide and isosorbide dinitrate. This is the first case report of essential thrombocythemia, pulmonary hypertension, right heart failure and bilateral pleural effusion.
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PMID:[A case of essential thrombocythemia with pulmonary hypertension and bilateral pleural effusions]. 221 92


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