Hypertension and Clinical Hemodynamics Section, Veterans Administration Hospital, Washington, D. C. 20422.
J Clin Invest. 1969 Nov;48(11):2008-18. doi: 10.1172/JCI106166.
Left ventricular end diastolic (LVEDP) and mean right atrial (RAP) pressures were recorded simultaneously in 30 patients with shock (14 acute myocardial infarction, 10 acute pulmonary embolism or severe bronchopulmonary disease, and 6 sepsis). Myocardial infarction was characterized by a predominant increase in LVEDP, pulmonary disease by a predominant increase in RAP, and sepsis by a normal relationship between LVEDP and RAP. In all three groups a significant positive correlation was noted between RAP and LVEDP, with the regression line in cor pulmonale deviated significantly toward the RAP axis and the regression line in myocardial infarction exhibiting a zero RAP intercept at an elevated LVEDP.Low cardiac outputs with elevated LVEDP in myocardial infarction indicated severe left ventricular failure. Low outputs with elevated RAP in cor pulmonale were consistent with right ventricular overload. Although cardiac outputs often were normal in sepsis, low outputs with elevated cardiac filling pressures in some patients were consistent with a hemodynamic or humoral-induced generalized depression of cardiac performance.Vasoconstrictor and inotropic drugs often produced a functional disparity between the two ventricles, with the gradient between LVEDP and RAP increasing, apparently because of an increase in left ventricular work or an inadequacy of left ventricular oxygen delivery. Acute plasma volume expansion with dextran in patients with pulmonary vascular disease resulted in a somewhat more rapid rise in RAP than in LVEDP. In septic and myocardial infarction shock, however, LVEDP and RAP usually rose proportionally, with the absolute rise of LVEDP surpassing that of RAP. Although the absolute level of the central venous pressure thus may not be a reliable indicator of left ventricular function in shock, changes in venous pressure during acute plasma volume expansion should serve as a fairly safe guide to changes in LVEDP.
30 例休克患者(14 例急性心肌梗死、10 例急性肺栓塞或严重支气管肺病、6 例败血症)同时记录左心室舒张末期(LVEDP)和平均右心房(RAP)压力。心肌梗死的特点是 LVEDP 明显升高,肺部疾病以 RAP 明显升高为主,败血症则是 LVEDP 和 RAP 之间的关系正常。在这三组患者中,RAP 和 LVEDP 之间均存在显著正相关,肺心病的回归线明显偏向 RAP 轴,而心肌梗死的回归线在 LVEDP 升高时截距为零。心肌梗死时 LVEDP 升高伴心输出量降低表明严重左心室衰竭。肺心病时 RAP 升高伴心输出量降低与右心室超负荷一致。虽然败血症时心输出量通常正常,但一些患者在充盈压升高时心输出量降低,与心脏功能的血液动力学或体液诱导性普遍抑制一致。血管收缩剂和正性肌力药物常导致两个心室之间出现功能差异,LVEDP 和 RAP 之间的梯度增加,显然是由于左心室工作量增加或左心室氧供不足。在肺血管疾病患者中用右旋糖酐进行急性血浆容量扩张导致 RAP 升高速度比 LVEDP 稍快。然而,在败血症和心肌梗死性休克中,LVEDP 和 RAP 通常呈比例升高,LVEDP 的绝对升高超过 RAP。虽然中心静脉压的绝对值可能不是休克时左心室功能的可靠指标,但急性血浆容量扩张期间静脉压的变化应作为 LVEDP 变化的相当安全的指南。