Myocardial oxygen availability and cardiac failure in hemorrhagic shock.
The relationships between left ventricular function and myocardial O2 availability and metabolism were studied in cats with hemorrhagic shock (AP=30 mm. Hg) with the use of a right heart bypass preparation. Aortic flow and heart rate were held constant. Oxygen-carrying capacity was reduced by diluting donor blood with an equal volume of 5 per cent glucose in saline. Oxygen availability was estimated as the product of arterial O2 content and coronary blood flow. All shock animals showed a progressive metabolic acidemia with time, and a fall in coronary flow concomitantly. Four control animals (AP=75 mm. Hg) as well as two shock animals with high arterial oxygen content and hematocrit showed no significant changes in myocardial O2 metabolism or performance over a period of 90 minutes. Nine shock animals with reduced hematocrit demonstrated a progressive reduction in ventricular function, myocardial O2 metabolism, and O2 availability. As O2 availability fell below 10 ml. per minute per 100 Gm. of heart weight, cardiac failure uniformly appeared and was accompanied by a reduction in O2 extraction and consumption. The correlation between left ventricular dP/dt max and O2 availability was highly significant (r = 0.75, p less than 0.01) in shock animals but not in controls. Thus a close relationship between myocardial O2 metabolism and function during the course of hemorrhagic shock has been demonstrated. Reduced myocardial O2 availability is directly linked with the appearance of cardiac failure.
D000818:Animals; D001011:Aorta; D001794:Blood Pressure; D002415:Cats; D003326:Coronary Circulation; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology; D006400:Hematocrit; D006439:Hemodynamics; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D012771:Shock, Hemorrhagic / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology