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

We examined the effects of cyclooxygenase inhibitors on pulmonary hemodynamics and gas exchange after experimental acute pulmonary embolism in 12 intact anesthetized dogs. Pulmonary hemodynamics were evaluated by pulmonary arterial pressure (Ppa)/cardiac output (Q) plots before and 60 min after autologous blood clot embolization and again 30 min after cyclooxygenase inhibition, either by acetylsalicylic acid (ASA, n = 6) or by indomethacin (INDO, n = 6). Gas exchange was assessed using the multiple inert gas elimination technique, at a constant intermediate Q, under each of these experimental conditions. Embolization increased Ppa at all levels of Q studied (p less than 0.001), increased true shunt (p less than 0.05), and shifted perfusion (Q) and ventilation (VA) distributions to lower and higher VA/Q (p less than 0.05), respectively. ASA and INDO further shifted Ppa/Q plots toward higher pressures (p less than 0.05). Concomitantly, the physiologic dead space increased after INDO (p less than 0.001), and the proportion of lung units with a high VA/Q increased and the inert gas dead space decreased after both ASA (p less than 0.05) and INDO (p less than 0.05). We conclude that, in experimental pulmonary embolism, structurally different cyclooxygenase inhibitors aggravate pulmonary hypertension and deteriorate gas exchange by an altered distribution of VA/Q essentially to lung units with a higher than normal VA/Q. These findings may be explained by changes in the distributions of both VA and of Q as a consequence of cyclooxygenase inhibition-associated increases in both bronchial and vascular tone in embolized lung regions.
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PMID:Cyclooxygenase inhibition aggravates pulmonary hypertension and deteriorates gas exchange in canine pulmonary embolism. 155 6

Imaging and Doppler echocardiography permits assessment of right ventricular size and systolic function and of pulmonary arterial pressures, and it may facilitate detection of thromboemboli within the heart or pulmonary artery. In patients with acute pulmonary embolism of sufficient severity to appreciably increase right ventricular afterload, the right ventricle becomes dilated and hypokinetic. Tricuspid regurgitation is generally apparent, but in the absence of preexisting pulmonary arterial or left heart pathology, the regurgitant flow velocity suggests only mild to mild-moderate elevation of pulmonary arterial systolic pressure. The absence of a greater degree of pulmonary hypertension reflects the inability of the previously normal, nonhypertrophied right ventricle to generate a mean pulmonary arterial pressure in excess of about 40 mm Hg. The echocardiographic abnormalities resolve during recovery from pulmonary embolism. Currently being investigated is the question of whether right heart abnormalities resolve more rapidly with thrombolytic therapy than with heparin therapy alone.
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PMID:Echocardiographic evaluation of pulmonary embolism and its response to therapeutic interventions. 155 80

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15

Amrinone, an inotrope with vasodilating properties, is of potential use in managing the right ventricular failure and pulmonary vasoconstriction induced by massive pulmonary embolism (PE). Therefore, to determine the hemodynamic effects of amrinone in a canine model of massive PE, autologous blood clot was infused into ten dogs (eight treated and two control animals) in an amount sufficient to decrease mean systemic arterial pressure (MAP) by at least 25 percent. This resulted in an increase in mean pulmonary artery pressure (MPAP) from 13.4 +/- 3.7 mm Hg to 44.4 +/- 4.8 mm Hg (p less than 0.01), a decrease in MAP from 122 +/- 9.5 mm Hg to 35.6 +/- 9.8 mm Hg (p less than 0.01), and a decrease in cardiac output from 2.73 +/- 0.834 L/min to 1.22 +/- 0.61 L/min (p less than 0.01). Amrinone was administered in an initial bolus of 0.75 mg/kg followed by an infusion of 7.5 micrograms/kg/min, which resulted in significant hemodynamic improvement in all subjects, with a fall in MPAP to 35.3 +/- 5.1 mm Hg (p less than 0.01), an increase in MAP to 98.1 +/- 31.1 mm Hg (p less than 0.01), and an increase in cardiac output to 2.01 +/- 0.7 L/min (not significant) at 5 min. Cardiac output continued to increase to 2.56 +/- 0.16 L/min (p less than 0.01) at 35 min. We conclude that amrinone alleviated pulmonary hypertension, systemic hypotension, and low cardiac output in a canine model of massive PE.
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PMID:Hemodynamic effects of amrinone in a canine model of massive pulmonary embolism. 162 67

A man with Klippel-Trenaunay-Weber syndrome had worsening pulmonary hypertension secondary to recurrent multiple pulmonary embolism despite anticoagulation. Pulmonary thromboendarterectomy was done. However, the patient expired 10 days after surgery due to another bout of pulmonary embolism from his right arm or right chest wall.
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PMID:Klippel-Trenaunay-Weber syndrome with recurrent pulmonary embolism. 164 97

We investigated interactions between cardiac output, VA/Q distribution pattern, pulmonary gas exchange, O2 transport, and tissue oxygenation in 16 patients during the acute phase of pulmonary embolism (PE). The effects of breathing room air, O2 therapy (FIO2 = 0.40) (11 patients), and dobutamine (four patients) were studied after right catheterization using the multiple inert gas elimination technique. The pattern of VA/Q ratio distributions was found to depend essentially on cardiac output level. The individual blood flow perfusing ventilated areas was found to be inversely related to the mean VA/Q ratio of blood flow distribution. PVO2 was directly related to cardiac index (p less than 0.02), and negatively related to the mean VA/Q of blood flow distribution. In view of the influence of low VA/Q ratios and PVO2 on arterial hypoxemia, our results showed that the heart's response to PE conditioned the strategy of pulmonary gas exchange and O2 transport. Oxygen breathing led to a slight but consistent fall in cardiac output (-0.6 +/- 0.5 L/min, p less than 0.01). However, although PaO2 remained normal and PVO2 was slightly improved, we found no evidence for a role of hypoxic pulmonary vasoconstriction in the pulmonary hypertension observed during the acute phase of PE. Administration of dobutamine improved O2 transport and tissue oxygenation, although PaO2 remained constant or even fell in some cases because of increased VA/Q mismatch.
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PMID:Influence of cardiac output on oxygen exchange in acute pulmonary embolism. 173 76

Abnormalities of the plain chest radiograph of 123 patients with acute pulmonary embolism (PE) and no prior cardiac or pulmonary disease were related to the pulmonary arterial mean pressure, the partial pressure of oxygen in arterial blood, and the alveolar-arterial oxygen gradient. Patients with either a prominent central pulmonary artery or cardiomegaly had higher pulmonary arterial mean pressures than did patients with atelectasis, a pulmonary parenchymal abnormality or pleural effusion (p less than 0.001). These radiographic findings give clues to the severity of pulmonary hypertension in acute PE and suggest that pulmonary infarction or hemorrhage is associated with less severe PE.
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PMID:Relation of plain chest radiographic findings to pulmonary arterial pressure and arterial blood oxygen levels in patients with acute pulmonary embolism. 173 55

Two patients with protein C deficiency developed symptomatic pulmonary hypertension secondary to chronic pulmonary embolism. They were successfully treated by thromboendarterectomy.
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PMID:Surgical treatment of pulmonary hypertension in protein C deficiency. 177 14

For the treatment of massive pulmonary embolism thrombolytic therapy is efficient in reducing late mortality and complications from chronic pulmonary hypertension. Best results are achieved if treatment is started as soon as possible. Even after days or weeks after pulmonary thromboembolism, however, thrombolytic therapy is beneficial. In life threatening conditions due to right heart failure an initial bolus of 2,000,000 U urokinase should be administered. The number of contraindications can be markedly reduced due to the well controlled thrombolysis with urokinase.
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PMID:Thrombolytic therapy in fulminant pulmonary thromboembolism. 178 41

Pulmonary hypertension due to recurrent thromboembolism is a rare disease but life-threatening. We evaluated 18 patients (11 female, 7 male) with this pathology between 1973 and 1991. We compared clinical features and evolution of our patients with the ones of the literature. The mean interval between beginning of symptoms and diagnosis was 5 years (range 1-10 years) and the most frequent symptom was increasing dyspnoea. In 2 of our patients there were well definite predisposing causes for thromboembolism (intracardiac catheters), 6 of the others had a previous episode of acute pulmonary embolism. Mean pulmonary arterial pressure was 50 mmHg and low output was present in 8 of these. Lung perfusion scintigraphy was diagnostic in 98% of cases showing segmental defects and pulmonary angiography confirms diagnosis revealing abrupt cut-off of cases showing segmental defects and pulmonary angiography confirms diagnosis revealing abrupt cut-off a major pulmonary artery. Angiographic evaluation of thrombus extent and location was difficult. In a small number of patients was found lupus anticoagulant, deficiency of protein C, of protein S and of antithrombin III. Mortality in medical treatment was 39% at a mean follow-up of 4-5 years. Progression of pulmonary hypertension was due to recurrent pulmonary embolism only in 30-40% of cases. The role of caval filter is not well established. Thromboendarterectomy shows immediate good results at short time but the long-term results are not known.
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PMID:[Thromboembolic pulmonary hypertension]. 184 71


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