Augmented venous return: protection of the ischemic myocardium during endotoxemia.

The effects of gram-negative endotoxin (Escherichia coli 4 mg/kg) induced myocardial failure in the pentobarbital-anesthesized dog were examined by monitoring its influence on coronary and systemic hemodynamics and correlating these results with myofibrillar ATPase activity. An identical series of studies was performed incorporating a femoral-femoral arterial-venous shunt to augment venous return. Over a five-hour period, gram-negative endotoxemia was associated with a progressive fall in arterial pressure, stroke volume, cardiac output, coronary flow, and a rise in total peripheral resistance and diastolic coronary vascular resistance. Augmenting venous return by 313 +/- 71 ml/min significantly increased cardiac output, stroke volume, and coronary flow and substantially reduced total peripheral resistance and coronary vascular resistance. Myofibrillar ATPase activity from both endocardium and epicardium was significantly depressed in the endotoxin-shocked preparations. However, with the augmentation of venous return with the A-V shunt in the endotoxin-treated animal, myofibrillar ATPase activity is normal. It appears that endotoxin causes a decrease both in venous return and in cardiac contractility by increasing total peripheral resistance, coronary vascular resistance, and impedance to left ventricular ejection. Augmenting venous return by optimizing preload and reducing afterload prevents any significant increase in total peripheral resistance, coronary vascular resistance, or impedance to left ventricular ejection. This is manifested by a rise in cardiac output, stroke volume, and coronary flow and the preservation of myocardial function. This is the first successful application of left ventricular afterload reduction in noncardiogenic shock.