Low cardiac output abolishes cardiovascular responses to infra‐renal aortic cross‐clamping in the pig

Background: Previous data suggest that preoperative myocardial dysfunction is associated with an altered cardiac response to infra-renal aortic cross-clamping (AXC). This study was designed to further explore how acute reductions in stroke volume and cardiac output influence the systemic, preportal and renal circulatory responses to AXC. Methods: In chloralose-anesthetized normoventilated pigs, graded increases in pericardial pressure (P PERICARD ) were obtained by local infusions of dextran. Measurements included cardiac output (CO, thermodilution), mean blood pressure proximal to the aortic clamping site (MAP PROX ) and ultrasonic flowmetry for portal (Q PORT ) and renal (Q REN ) blood flows. In all animals, measurements were made a) prior to AXC, b) at the end of a 5 min AXC period and, c) 5 min following declamping. These recordings were repeated during control (P PERICARD 0 cmH 2 O) and during stages with increased P PERI- CARD (4 and 8 cmH 2 O, respectively). Results: Pericardial infusions of dextran produced hemodynamic responses that in magnitude were proportional to P PERI CARD levels. Stroke volume, CO and mean arterial pressure decreased, while systemic vascular resistance (SVR) increased. In the preportal tissues, vascular resistance increased and Q PORT decreased. Similarly, in the kidney, vascular resistance and Q REN decreased, but only at a P PERICARD of 8 cmH 2 O. At control, AXC increased SVR, MAP PROX, Q PORT and both renal and preportal vascular resistances. When P PERICARD was increased to 4 cm H 2 O, the responses to AXC concerning SVR and MAP PROX were not significantly altered, while renal and preportal circulatory responses were blunted. At stages with a P PERICARD of 8 cmH 2 O, we could not demonstrate any circulatory responses to AXC. Conclusions: AXC-induced systemic, preportal and renal circulatory responses are inhibited during a condition of acutely lowered cardiac output.