Dissociation of Myocardial Contractility and Pump Performance in Hemorrhagic Shock

Abstract

Myocardial performance and contractility were evaluated during standardized hemorrhagic shock in dogs and cats. Myocardial contractility, measured by utilizing V_maχ from the isovolumic force-velocity relation, was maintained despite a decline in cardiac performance and progression to irreversible shock. By contrast, in animals subject to β-adrenergic blockade, there was a significant decline of myocardial contractility, suggesting dependence of V on sympathetic neurohumoral support during shock. Plasma taken at hourly intervals from dogs in shock was assayed for inotropic effect utilizing a cat papillary muscle preparation. Fresh plasma taken during shock caused a small augmentation of contractility, while plasma taken at the same time, but frozen before assay, was depressant. It is concluded that in severe and irreversible hemorrhagic shock there is a dissociation between ventricular function as measured by cardiac output and filling pressure, and contractility as measured by V_maχ. This preservation of V_maχ is probably related to stimulating factors in shock plasma, such as the catecholamines, which overshadow the presence of any myocardial depressant factors.

Initial myocardial adjustments to brief periods of ischemia and reperfusion in the conscious dog.

“…Similarly, in anesthetized animals, hemorrhagic shock depressed cardiac pump performance as reflected by cardiac output and left ventricular diastolic pressure more than it affected V max . 20 In an isolated ventricular septum preparation 21 and in the intact isovolumic heart, 22 ischemia depressed the tension or pressure generated more than their time derivatives, i.e., dT/dt of dP/dt. Finally dL/dt in the anesthetized dog, 23 as well as contractile element velocity (V ce ) in patients, 24 were less sensitive to ischemia than shortening.…”

Production and bioassay of an endogenous myocardial depressant

“…Hemorrhagic shock has been reported by Forrester et al (1972) to decrease pump performance but not necessarily alter the maximum velocity of contraction which is a measure of contractility. Significant reduction of both stroke volume and cardiac output was reported by Siegel and Downing (1970) and Forrester et al (1972) but no long-term effects on either heart rate or left ventricular end diastolic pressure were observed. Goldfarb (1982) and Downing (1933) have reviewed many of the functional changes in shock.…”