Cardiac tamponade in dogs with normal coronary arteries. II. Myocardial flow and metabolism with moderate and severe hemodynamic impairment

Summary To determine the effects of cardiac tamponade on myocardial blood flow and its distribution, dogs were prepared with indwelling pericardial catheters. Hemodynamic, myocardial blood flow, and myocardial metabolic data were collected in 5 closed-chest, spontaneously breathing animals with normal blood volumes and hemoglobin concentrations and 6 with acute anemia. Instillation of an average of 89.0±14.9 ml of modified Normosol® into the pericardial space in dogs with normal hemoglobin levels produced mild tamponade with a modest decline in aortic pressure (119.5±14.3 to 96.8±12.1 mm Hg) and significant rises in left and right atrial and pericardial pressures to 7–8 mm Hg. Increasing the pericardial volume to 124.0±13.6 ml produced hypotension (mean aortic pressure 86.2±10.5 mm Hg) and rises in the left and right ventricular filling pressures and pericardial pressure to 10–11 mm Hg. Total myocardial blood flow fell from 1.19±0.18 to 0.73±0.17 ml/min/g (p<0.02) during mild tamponade, and fell further to 0.56±0.17 ml/min/g (p<0.05) with more severe tamponade. Despite these declines, the left ventricular wall inner/outer flow ratio and left ventricular flow as a proportion of total cardiac output were unchanged. In dogs with anemia more severe tamponade was created, with consequently more marked hemodynamic abnormalities. However, the relative changes in myocardial blood flow and inner/outer flow ratio were similar. Myocardial metabolic parameters could be evaluated only in the dogs with less severe tamponade. The coronary arteriovenous oxygen difference changed little during induced tamponade, and, therefore, quantitated myocardial oxygen consumption declined in proportion to the fall in myocardial flow. Furthermore, myocardial lactate extraction and the lactate/pyruvate ratio were not affected by cardiac tamponade. Thus, these experiments cannot support the hypothesis that myocardial ischemia is a pathophysiologic factor in the production of abnormal hemodynamics in cardiac tamponade.Dr. Cohen is the recipient of a Research Career Development Award from the National Heart, Lung and Blood Institute Grant HL-00281.This study was supported in part by National Heart, Lung and Blood Institute Grant HL-17809.