Pathophysiology of aortic cross-clamping.

Arterial hypertension is the most dramatic and consistent component of the hernodynamic response to aortic cross-clamping. Most texts attribute this sign to a sudden increase in impedance to aortic flow and an increase in afterload. Increases in left ventricle endsystolic wall stress and systemic arterial pressure’ are consistent with this notion. However, Caldini, et a12 provided theoretical ground for the following speculations; clamping of the thoracic aorta increases cardiac output by diverting blood away from the longtime constant area, presumably the splanchnic vasculature. In other words, the splanchnic venous vasculature collapses when intramural venous pressure decreases; the latter results from a decrease in blood flow from the arterial to the venous vasculature with a subsequent decrease in venous capacitance, secondary to an elastic recoil. Splanchnic venous collapse, in turn, results in an increase in venous return and cardiac output. There is some experimental sup port for this theory: Occlusion of the inferior caval vein prevented increases in arterial pressure and in enddiastolic myocardial segment length, whereas occlusion of other, smaller veins modified the increases to different degrees, presumably reflecting different amounts of blood volume translocated from various veins, thereby affecting venous return, preload and the degree of arterial hypertension. The authors concluded that blood volume shift from the nonsplanchnic region maintains cardiac output during infraceliac aortic occlusion whereas during occlusion of the thoracic aorta, drainage from the splanchnic area accounts for about 70% of the increase in enddiastolic myocardial segment length.’ Cross-clamping of the thoracic aorta is associated with almost a twofold increase in blood flow through the upper part of the body,‘” and more than a three-fold increase in blood flow though the muscle proximal to the clamp’. These observations are consistent with (but do not prove) the hypothesis of blood volume redistribution. using whole-body scintigraphy with Tc“ -labeled plasma albumin we demonstrated that aortic crossclamping at the diaphragmatic level is associated with a significant increase in blood volume in the organs and tissues proximal to the level of occl~sion.~ Thus, the data presented provide evidence that blood volume shifts from the lower to the upper part of the body during aortic cross-clamping. Variation in the blood volume status of splanchnic vascular tone, resulting from differences in fluid load, depth of anesthesia, pharmacodynamics of an anesthetic, and other factors might affect the degree and pattern of blood volume redistribution. For example, during infrasplanchnic aortic occlusion, the blood volume redistributed from the vasculature below the occlusion might travel to the heart, increasing preload and inducing central hypervolemia, or it might travel to the compliant splanchnic venous vasculature. The distribution of volume between the heart and the splanchnic system would probably depend on the sympathetic discharge to the splanchnic system. Such distribution of blood volume determines the alterations in cardiac output at any particular moment. Crosstlamping of the thoracic aorta is associated with an expected decrease in blood flow distal to the aortic occlusion and a substantial increase in blood flow above the occlusion.’”M Oxygen consumption in the part of the body distal to the aortic occlusion decreases and, paradoxically, so does oxygen uptake in tissues above the occl~sion.~ Our experiments using 31 P nuclear magnetic resonance surface coil spectroscopy, measuring serial changes in the high-energy phosphate of the deltoid muscle, demonstrated a decrease in skeletal muscle creatine phosphate, an increase in glycolytic intermediates, and a decrease in intracellular inorganic phosphate.n These changes are consistent with skeletal muscle hypoxia. The reasons for the reduced oxygen consumption in the muscle tissue above the level of aortic occlusion are unclear. The possible explanations are available elsewhere.’