[Pulmonary hypertension].

G. Schuler
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Abstract

Depending on their size pulmonary emboli are responsible for an abrupt rise in pulmonary artery pressure. Not only mechanical obstruction, but also liberation of vasoactive substances from platelets trapped within the emboli represent the underlying mechanism. Intrapulmonary shunts, caused by vaso- and bronchoconstriction, may result in arterial hypoxemia. Although this clinical finding is encountered in most cases, normal arterial blood gases do not rule out significant pulmonary embolism. Even a small rise in pulmonary artery pressure causes significant reduction of right ventricular stroke volume and a decrease in left ventricular filling pressure. Impaired left ventricular filling is aggravated by biventricular interdependence. Elevated pulmonary artery pressures during rest and exercise are normalized by effective fibrinolytic therapy.
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(肺动脉高压)。
肺栓塞的大小不同,可导致肺动脉压突然升高。不仅是机械性阻塞,栓塞内血小板中血管活性物质的释放也代表了潜在的机制。由血管和支气管收缩引起的肺内分流可能导致动脉低氧血症。虽然这种临床表现在大多数病例中都遇到过,但正常的动脉血气并不能排除明显的肺栓塞。即使肺动脉压小幅升高,也会导致右心室卒中容量的显著减少和左心室充盈压力的降低。左心室充盈受损因双心室相互依赖而加重。休息和运动时肺动脉压升高可通过有效的纤溶治疗恢复正常。
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[Pulmonary hypertension]. [History of atrial fibrillation]. Plasma levels of NT-pro-BNP in patients with atrial fibrillation before and after electrical cardioversion. Experience with INR self-management: patient selection and complication rates. Slow pathway ablation in children with documented reentrant supraventricular tachycardia not inducible during invasive electrophysiologic study.
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