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

12 patients with pulmonary hypertension, primary pulmonary hypertension 3, secondary to recurrent pulmonary embolism 4, chronic obstructive pulmonary disease 2, and complicated with congenital heart disease 3, inhaled nitric oxide (NO). The NO concentration was adjusted in the range between 20-160 ppm to get a maximum hemodynamic effects. On inhaling NO, pulmonary artery pressure decreased in all patients. The maximum hemodynamic effects showed that pulmonary systolic, diastolic and mean artery pressure dropped by 22.9%, 21.0% and 20.3% (P < 0.001) respectively. Total pulmonary resistance decreased by 32.7% (P < 0.01). Cardiac index and oxygen delivery increased by 33.2% and 24.8% (P < 0.01) respectively. The ratio of pulmonary systolic artery pressure and systemic systolic artery pressure changed from the baseline 0.73 to 0.54. It is indicated that NO dilated pulmonary artery selectively in patients with hyperkinetic, obliterative and hypoxic pulmonary hypertension.
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PMID:[Hemodynamic effects of inhaled nitric oxide in patients with pulmonary hypertension]. 765 63

In this review, the second of a two part series, the analytic techniques introduced in the first part are applied to a broad range of pulmonary pathophysiologic conditions. The contributions of hypoxic pulmonary vasoconstriction to both homeostasis and pathophysiology are quantitated for atelectasis, pneumonia, sepsis, pulmonary embolism, chronic obstructive pulmonary disease and adult respiratory distress syndrome. For each disease state the influence of principle variables, including inspired oxygen concentration, cardiac output and severity of pathology are explored and the actions of selected drugs including inhaled nitric oxide and infused vasodilators are illustrated. It is concluded that hypoxic pulmonary vasoconstriction is often a critical determinant of hypoxemia and/or pulmonary hypertension. Furthermore this analysis demonstrates the value of computer simulation to reveal which of the many variables are most responsible for pathophysiologic results.
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PMID:Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. 2. Pathophysiology. 793 36

Pulmonary hypertension caused by acute pulmonary embolism has been attributed to mechanical obstruction of the pulmonary arteries and also to vasoconstriction. We examined the role of nitric oxide in the vasoreactivity associated with pulmonary microembolism. Two kinds of microemboli of similar size were used: thorny microemboli (lycopodium spores, LP) and smooth microemboli (latex microspheres, MS). In isolated rat lungs perfused with blood, five injections of LP or MS into the pulmonary artery each caused a rapid increase in mean perfusion pressure, followed by a slow fall to a new, higher base line. Vasoconstriction was significantly greater after embolization with LP than after embolization with MS. Preadministration of L-NMMA, a nitric oxide synthase inhibitor, enhanced the increase in mean perfusion pressure caused by embolization with LP, but not the increase caused by embolization with MS. Before embolization, acetylcholine caused slight vasodilation. After embolization with MS, acetylcholine caused vasodilation; but after embolization with LP, acethlcholine caused vasoconstriction. Thus, we conclude that repeated embolization with LP may cause endothelial injury, and that nitric oxide may protect against pulmonary hypertension induced by LP emboli.
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PMID:[Role of nitric oxide in vasoreactivity caused by experimental pulmonary microembolism]. 882 95

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

This report illustrates the rare occurrence of a pulmonary embolus in a neonate during cardiac catheterization. The patient was a term newborn who underwent repair of obstructed infradiaphragmatic total anomalous pulmonary venous connection. Postoperative risk factors for pulmonary embolism included severe pulmonary hypertension unresponsive to nitric oxide therapy, an indwelling venous catheter, and young age. Successful management was achieved by initial mechanical fragmentation with streptokinase infusion and monitoring by serial lung perfusion scans.
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PMID:Acute pulmonary embolism in a neonate: precipitation during cardiac catheterization and successful treatment. 970 74

A 29-year-old woman with mixed connective tissue disease presented with signs of progressive pulmonary hypertension. After admission to the hospital her condition worsened rapidly and she developed a cardiac arrest resistant to cardiopulmonary resuscitation. Therefore, emergency extracorporeal assist was performed. No pulmonary embolism was found. Right heart catheterisation showed severe pulmonary hypertension, which was treated with nitric oxide ventilation. She was weaned from the extracorporeal assist with high doses of inotropic agents. Because of suspicion of exacerbation of her underlying disease, which led to pulmonary hypertension, immunosuppressive treatment was started with high doses of corticosteroids and plasma exchange. This resulted in slow recovery over the next four weeks. Control echocardiography showed complete normalisation of cardiac function without signs of pulmonary hypertension. Two months after admission she was discharged from the hospital in good condition.
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PMID:Vanishing pulmonary hypertension in mixed connective tissue disease. 1008 49

We describe a 66-year-old woman with right-sided heart failure and cardiogenic shock resulting from severe pulmonary embolism. Her hemodynamic status improved dramatically with the use of inhaled nitric oxide. A proposed mechanism of action and a review of the literature are presented.
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PMID:Inhaled nitric oxide in a patient with severe pulmonary embolism. 1078 15

Acute massive pulmonary embolism carries a high mortality with the majority of deaths occurring during the early phase. We describe a case of massive pulmonary embolism resulting in severe cardiovascular collapse and cardiac arrest which was treated successfully with inhaled nitric oxide.
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PMID:Use of inhaled nitric oxide in pulmonary embolism. 1047 Apr

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

We studied the antithrombotic activity of 2-acetoxybenzoate 2-[1-nitroxy-methyl]-phenyl ester (NCX 4016), a novel nitric oxide (NO)-releasing aspirin derivative, in vivo in different animal models of platelet-dependent and independent pulmonary thromboembolism and compared it with that of aspirin. NCX 4016 protected mice from death induced by the intravenous (i.v.) injection of collagen plus epinephrine, of 9,11-dideoxy-11alpha, 9alpha-epoxymethano-prostaglandin F(2alpha) (U46619) and of thrombin while aspirin was only active against collagen plus epinephrine. The drop in platelet count and number of lung emboli were reduced by NCX 4016 more effectively than aspirin. NCX 4016 protected mice also from mechanical pulmonary embolism (i.v. injection of hardened rat red blood cells) while aspirin was ineffective. In rabbits, NCX 4016 significantly reduced the accumulation of [111In]oxine-labeled platelets in the pulmonary vasculature induced by collagen and by thrombin while aspirin produced reductions which were significant only versus collagen. In conclusion, NCX 4016 exerts a more pronounced antithrombotic activity than aspirin in vivo in two different animal species, largely due to a deeper inhibitory effect on platelets. NCX 4016 may represent a better antithrombotic agent than aspirin.
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PMID:Prevention of pulmonary thromboembolism by NCX 4016, a nitric oxide-releasing aspirin. 1084 12


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