Mesenteric hemodynamic response to circulatory shock

Abstract

Purpose of review: The mesenteric hemodynamic response to circulatory shock is substantial and asymmetrical; the vasoconstrictive response disproportionately affects the mesenteric organs. The cardiac output is sustained partially, at no cost in nutrient flow to the mesenteric organs, by vasoconstriction of the mesenteric veins, resulting in the "autotransfusion" of up to 30% of the circulating blood volume into the systemic circulation.

Recent findings: Hemorrhagic or cardiogenic shock also results in decreased perfusion pressure, prompting selective vasoconstriction of the mesenteric arterioles to maintain perfusion pressure of the vital organs, here at the selective expense of the mesenteric organs. Septic shock may be associated with increased or decreased mesenteric blood flow but is characterized by increased oxygen consumption, exceeding the capability of mesenteric oxygen delivery.

Summary: The response to any of these conditions can, variably and unpredictably, cause hemorrhagic gastric stress erosions, nonocclusive mesenteric ischemia of the small bowel, ischemic colitis, ischemic hepatitis, acalculous cholecystitis, and/or ischemic pancreatitis. Injury to the mesenteric organs can also initiate the systemic inflammatory response syndrome and, consequently, multiple organ failure.