We tested the hypothesis that coronary artery blood flow is sufficient to meet myocardial requirements throughout cardiac tamponade in a conscious euvolemic canine model recovered from surgery. Seven mongrel dogs were chronically instrumented to measure ascending aortic blood flow (electromagnetic flowmeter); intrapericardial, right atrial, and aortic blood pressures; regional myocardial blood flow (radionuclide labelled microspheres); and myocardial consumption of lactate, pyruvate, and oxygen. Data were collected during progressive cardiac tamponade induced by intrapericardial saline infusion to the point of hemodynamic decompensation. Decompensated cardiac tamponade (DCT) was defined as a decline in mean aortic blood pressure to 70% of the level present when the pericardia! space was drained of fluid (baseline) and was produced in all animals within 25 minutes. Cardiac tamponade caused a continuous decline in coronary artery blood flow from 1.26 ± 0.35 (baseline, mean ± SD) to 0.53 ± 0.15 ml/min/g (DCT,p<0.01), which was associated with a decrease in myocardial oxygen consumption from 1.26 ± 0.35 (baseline) to 0.74 ± 0.27 ml/min/g (DCT,p< 0.05) and a slight increase in myocardial oxygen extraction from 71 ± 3 (baseline) to 81 ± 4% (DCT,p<0.05). This change in oxygen extraction occurred because of both an increase in arterial and a decrease in coronary venous oxygen content. At all degrees of cardiac tamponade, the lactate-pyruvate ratio did not change significantly from baseline (7.56 ± 2.31), there was no evidence of lactate production, and the normal endocardial to eplcardial blood flow ratio present at baseline (1.41 ± 0.23) was preserved. Although aortic blood pressure was initially well maintained, aortic blood flow declined, and right atrial blood pressure increased continuously as intrapericardial pressure increased. A second group of 2 chronically instrumented animals was prepared to determine whether an adequate coronary vasodilatory reserve was present throughout cardiac tamponade. The reactive hyperemic response to brief coronary artery occlusion (hydraulic occluder) of a large epicardial vessel was measured (Doppler flow probe) in the conscious animal during progressive cardiac tamponade. Although a normal reactive hyperemic response was found at all stages of cardiac tamponade, the peak coronary artery blood flow obtained during reactive hyperemia decreased as intrapericardial pressure increased. Thus, in this conscious canine model of acute progressive cardiac tamponade, despite a continuous decline coronary artery blood flow was always adequate to support aerobic metabolism, and a normal coronary artery vasodilatory reserve was present, even at the time of hemodynamic decompensation. In this euvolemic animal model, myocardial ischemia did not contribute to the deterioration in cardiac function that occurred during acute cardiac tamponade.