[Septic shock and regional circulations]

Owing to the scarcity of clinical studies on this subject, one must turn to experimental data, with reservations concerning their extrapolation to human beings. Septic shock, a distributive shock, results from a homogeneous decline of vascular tone and therefore regional blood flows. Direct vasodilators, such as nitric oxide and prostaglandins, and indirect vasodilators, such as cytokines, produce vasodilation with hypocontractility. During hyperkinetic shock in animals, dilatation of the mesenteric and coronary arteries is observed, with reduction of pancreatic and skin muscle flows. Two clinical studies have confirmed this coronary vasodilatation without increase in myocardial oxygen consumption. In the liver the hepatic artery buffer response is altered, the portal flow rate is reduced without changes in portal vein pressure, and the hepatic vein saturation is less than that of the pulmonary artery, thus testifying to an increase of oxygen extraction, mainly in the liver. The hepatic flow rate is also influenced by the liver glucose content. The mesenteric and pancreatic circulations are particularly threatened, their flow rate being reduced by 50% due to vasoconstriction. In the kidney the flow rate is biphasic: high first, then low. Treating hypovolaemia does not prevent the renal function from being altered, even when the flow rate is maintained. Blood flow is reduced in the respiratory muscles, despite an increase in work and oxygen consumption. Finally, treatment with vasopressors does not seem to correct the disorders observed in cardiac output distribution and has little increasing effect on arterial blood pressure.