ARTERIOVENOUS-SHUNT-MEDIATED INCREASE IN VENOUS RETURN CAUSES APPARENT RIGHT CORONARY ARTERIAL AUTOREGULATION

Objective: Reports of autoregulation in the right coronary vasculature have varied from non-existent to almost perfect. At least some of thi s discrepancy may be due to failure to account for changes in myocardi al metabolism secondary to the method used to vary perfusion pressure. The aim of this study was to determine if the potent autoregulation r eported when right coronary perfusion pressure was lowered by opening a large arteriovenous shunt was due to increased right ventricular myo cardial oxygen consumption (MVO2) induced by augmented preload and aft erload. Methods: Two protocols were used to produce right coronary per fusion pressures of 100, 80, and 60 mm Hg in anaesthetised dogs. In bo th protocols the right coronary artery was cannulated and supplied wit h blood from a pressurised chamber. In protocol 1, right coronary perf usion pressure was decreased independently of aortic pressure, and in protocol 2, aortic pressure was decreased in parallel with right coron ary perfusion pressure by opening a large arteriovenous shunt. Right c oronary blood flow, central venous pressure, and pulmonary arterial pr essure were measured, and right ventricular oxygen extraction and MVO2 were calculated at each level of right coronary perfusion pressure. R esults: In protocol 1, reducing right coronary perfusion pressure alon e resulted in decreased right coronary blood flow and right ventricula r MVO2. Central venous pressure (right ventricular preload) and pulmon ary arterial pressure (right ventricular afterload) did not change. In protocol 2, opening the arteriovenous shunt increased venous return, as shown by increased central venous pressure and pulmonary arterial p ressure. This increased right ventricular MVO2 at the lower right coro nary perfusion pressures and maintained right coronary blood flow at t he level recorded when right coronary perfusion pressure was 100 mm Hg . Conclusions: This apparently potent autoregulation resulted from the shunt induced increase in oxygen consumption at low right coronary pe rfusion pressures, in contrast to the decreased right ventricular oxyg en consumption and right coronary blood flow observed when right coron ary perfusion pressure is selectively decreased.