Efficacy of right ventricular unloading during right coronary artery occlusion in an experimental model.

This investigation examined the efficacy of right atrial-pulmonary artery bypass (RA-PA) during acute ischemia of the right ventricle. The right coronary artery (RCA) was ligated in 25 open chest, open pericardium sheep. Control animals (n = 15) were resuscitated with only intravenous fluids. In the experimental animals (n = 10) RA-PA bypass was initiated 5 minutes after right coronary occlusion. Sixty percent (9/15) of the control animals died within 90 minutes of RCA occlusion from refractory ventricular arrhythmia or right ventricular failure. Four of 10 RA-PA animals died within 2 hours of RCA occlusion from severe pulmonary hemorrhage and arterial oxygen desaturation when high flow rates (2.5 to 3.5 L/min) were initially instituted. In these animals, lung histologic findings demonstrated extensive hemorrhage into the alveolar spaces. After 6 hours of RCA occlusion in the six surviving control animals, there were significant increases in central venous pressure and right ventricular end-diastolic cord length (relative ventricular volume change measured by ultrasonic crystal analysis), and a significant decrease in the cardiac output. In contrast, during RCA occlusion in the six surviving animals on RA-PA bypass, cardiac output was well maintained, and there was a significant decrease in central venous pressure and end-diastolic length. The percent of change from baseline in end-diastolic length correlated inversely with the percent of change from baseline in cardiac output (r = -0.81, p less than 0.01). By crystal violet and triphenyltetrazolium chloride dye techniques, the mean percentage area of necrosis to area of risk was significantly less for the RA-PA group compared with the control group (5.6% versus 67.1%, p less than 0.0001). In this experimental model, RA-PA bypass effectively unloaded the acutely ischemic right ventricle, maintained systemic cardiac output, and significantly reduced right ventricular infarction size. Further investigations with this ventricular support modality are needed to determine its effects on pulmonary pathophysiology.