An Analysis of Cardiopulmonary Hemodynamics During Hemorrhagic Shock in Dogs

Utilizing the standard Wiggers' method, hemorrhagic shock was induced in ten anesthetized dogs by bleeding to a mean arterial pressure (MAP) of 50 mmHg for 2 hr and then to 30 mmHg for 1 hr, followed by reinfusion of the shed blood. The experimental protocol was designed to evaluate the effect of hemorrhagic shock on sequential pulmonary hemodynamic changes in relation to those of cardiac and systemic circulation. All selected cardiopulmonary hemodynamic parameters were recorded throughout the experiment on a multi-channel poly-oscillograph monitor. Total pulmonary resistance (TPuR) started rising early in hemorrhagic shock and was found to rise to a level that was 10-fold greater than pulmonary arteriolar resistance (PAR). This meant that, 90% of TPuR came from the venous side of the pulmonary vascular bed. Persistently raised TPuR even after reinfusion was linked to early death of the experimental animals. Myocardial contractility (max dp/dt mmHg/sec) which is one of the indices for cardiac performance was found to be severely depressed at terminal stage (p<0.001). Both total pulmonary and peripheral resistances were found to have an inverse relationship to ventricular performance which was measured by left ventricular stroke work (LVSW) and right ventricular stroke work (RVSW). There is a high suspicion that reinfusion or resuscitation following prolonged hypovolemic shock may aggrevate the hemorrhagic shock effects by facilitating the distribution of accumulated blood-borne toxic substances to various target organs and that, this has been linked with the early and sustained pulmonary hemodynamic disturbance found in these experiments.