Regional ischemia distal to a critical coronary stenosis during prolonged fibrillation - improvement with pulsatile perfusion

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 decending 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 (PmO ₂) and carbon dioxide (PmCO ₂) tensions and by regional arterial-coronary venous lactate difference. With linear perfusion, regional ischemia in the LAD myocardium had been evidenced by a low PmO ₂ (8± 3 mm Hg), a high PmCO ₂ (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 (PmO ₂ = 21 ± 3 mm Hg, PmCO ₂ = 65 ± 5 mm Hg, P<0.05 vs linear flow study) and lactate consumption was demonstrated (+17.7 ± 2.9 mg/100 ml, P<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<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.