论文部分内容阅读
急性左室功能衰竭可导致威胁生命的肺水肿。患者系统动脉压往往增高,心输出量可正常或降低。左室舒张末期压明显增高,导致肺毛细血管楔压增高,从而引起低氧血症和呼吸窘迫。治疗急性肺水肿旨在迅速降低肺毛细血管压力。常规措施是用利尿剂、静脉切开放血术、旋转止血带或吗啡减少静脉回流。上述措施对缓解肺水肿症状往往有效,但不能立即改善衰竭的左室功能;有时在给予利尿剂或应用止血带后,心输出量锐降,可导致反射性交感神经兴奋,系统血管阻力增加,流出阻力增高和心输出量进一步降低。这种恶性循环可诱致休克。应用利尿剂的另一个
Acute left ventricular failure can lead to life-threatening pulmonary edema. Patients with systemic arterial pressure tend to increase, cardiac output may be normal or reduced. Left ventricular end diastolic pressure was significantly higher, leading to increased pulmonary capillary wedge pressure, causing hypoxemia and respiratory distress. Acute pulmonary edema is designed to rapidly reduce pulmonary capillary pressure. The usual measures are diuretics, phlebotomy, revolving tourniquet or morphine to reduce venous return. These measures to alleviate the symptoms of pulmonary edema tend to be effective, but can not immediately improve the failure of left ventricular function; sometimes given diuretics or tourniquet, cardiac output dropped sharply, can lead to reflex sympathetic excitement, increased systemic vascular resistance, Outflow resistance increased and cardiac output further reduced. This vicious cycle can induce shock. Another use of diuretics