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The effect of pulsatile cardiopulmonary bypass on intramyocardial gas tensions and regional myocardial blood flow was studied in 10 mongrel dogs. Following application of a critical stenosis to the circumflex coronary artery (CIRC), animals were placed on total bypass with vented, fibrillating hearts. During three 45 minute periods of perfusion, animals alternately received pulsatile or linear flow with perfusion pressure carefully maintained at 80 mm. Hg. In myocardium supplied by the stenosed CIRC, intramyocardial oxygen tension (PO2) rose from 13 +/- 3 to 19 +/- 5 mm. Hg when a period of linear flow was followed by a period of pulsatile flow (p less than 0.025). Similarly in the CIRC-supplied area, intramyocardial carbon dioxide (PCO2) decreased from 128 +/- 12 to 99 +/- 12 mm. Hg (p less than 0.005) with conversion from linear to pulsatile flow. Myocardial blood flow (microsphere technique) to endocardial and epicardial layers of the CIRC-supplied area was significantly greater (p less than 0.05) during pulsatile than during linear perfusion. In contrast, when periods of pulsatile bypass were followed by periods of linear perfusion, myocardial PO2 fell from 25 +/- 6 to 9 +/- 3 (less than 0.02) and myocardial PCO2 rose from 82 +/- 12 to 154 +/- 12 mm. Hg (p less than 0.001). These data suggest that (1) fibrillation-induced regional ischemia distal to a critical coronary stenosis can be reduced by pulsatile perfusion during bypass and (2) the mechanism for the reduction in regional ischemia is improved myocardial blood flow.

In a previous study from this laboratory, regional myocardial ischemia developed distal to a critical coronary stenosis in the fibrillating heart on cardiopulmonary bypass when myocardial perfusion was non-pulsatile. To assess the effect of pulsatile perfusion on the development of the fibrillation-induced ischemia, 10 dogs were placed on total cardiopulmonary bypass with the heart in the vented fibrillating state. A critical stenosis was applied to the left anterior descending artery (LAD). Pulsatile perfusion with a pulse pressure of 35 mm Hg and a pulse rate of 100/min was produced by a new method developed in this laboratory. During the 2 hours of bypass, ischemia in the LAD-supplied myocardium was assessed by changes in intramyocardial oxygen (PmO2) and carbon dioxide (PmCO2) tensions and by regional arterial-coronary venous lactate difference. With linear perfusion, regional ischemia in the LAD myocardium had been evidenced by a low PmO2 (8 +/- 3 mm Hg), a high PmCO2 (170 +/- 25 mm Hg) and regional lactate production (9.2 +/- 4.2 mg/100 ml). In contrast with pulsatile perfusion intramyocardial gas tensions remained stable during the 2 hours on bypass (PmO2 = 21 +/- 3 mm Hg, PmCO2 = 65 +/- 5 mm Hg, P less than 0.05 vs linear flow study) and lactate consumption was demonstrated (+17.7 +/- 2.9 mg/100 ml, P less than 0.001 vs linear flow group). With linear perfusion, myocardial blood flow to the LAD area had decreased 56 +/- 8% in the subendocardial layer and 46 +/- 7% in the subepicardial layer. In the dogs receiving pulsatile flow during bypass, regional LAD blood flow remained unchanged over the 2-hour bypass period and was significantly higher than the flow with linear flow (P less than 0.05). These data indicate that fibrillation-induced regional myocardial ischemia distal to a critical stenosis can be prevented by maintaining pulsatile perfusion during cardiopulmonary bypass.

The effect of a critical coronary artery stenosis on myocardial blood flow and metabolism in the fibrillating heart was assessed by placing 10 dogs on cardiopulmonary bypass, venting the ventricle, inducing ventricular fibrillation, and applying critical stenosis to the left anterior descending coronary artery (LAD). Endocardial and epicardial blood flows were measured by the radioactive microsphere technique prior to the application of the stenosis and after one hour and 2 hours of fibrillation. Intramyocardial oxygen tension (PO2) and carbon dioxide tension (PCO2) were continuously monitored in the LAD-supplied myocardium by a mass spectrometer probe inserted at midmyocardial depth. Selective arterial-coronary venous lactate differences were determined at control, one hour, and 2 hours. At the end of the 2 hour period, vital dye injection defined the distribution of the LAD. Endocardial flow to the myocardium of the stenosed LAD was reduced by 50 per cent after one hour and by 70 per cent after 2 hours (p less than 0.05). Epicardial flow fell 40 per cent after one hour and 50 per cent after 2 hours (p less than 0.05). Endocardial and epicardial flow in the distribution of the unstenosed circumflex coronary artery remained unchanged. Changes in myocardial PO2 and PCO2 in the LAD-supplied myocardium indicated the development of severe ischemia in all 10 dogs and suggested myocardial infarction in 5. There was a conversion from lactate extraction to lactate production during the 2 hour period of ventricular fibrillation. From this study, it is concluded that the myocardium distal to a critical stenosis suffers a progressive reduction in flow during ventricular fibrillation which does not occur in regions supplied by unstenosed coronary arteries. Thus prolonged fibrillation in the presence of a flow-limiting coronary stenosis may play a role in the pathogenesis of myocardial infarction during coronary bypass surgery.

A new method for producing pulsatile flow during cardiopulmonary bypass is described. The method requires only the addition of a dilated segment in the tubing which passes beneath the arc of a standard roller pump. Preliminary studies demonstrate that pulsatile flow and pressure with physiologic contours can be produced by this "bubble tube" system. Furthermore, the new tubing causes less hemolysis than standard pump tubing.