Abstract

The hemodynamic alterations of septic shock may impair the determinants of cellular O2 supply on all levels. First, myocardial depression and peripheral vasodilation may result in inadequate perfusion pressure and global O2 transport. Second, the distribution of regional blood flow may be mismatched in the face of changes in the regional metabolic demands (i. e. the hepato-splanchnic region). Third, microvascular blood flow and the tissue’s O2 extraction capability may be disturbed for various reasons. The aim of vasoactive drug therapy in septic shock is therefore to correct the cardiocirculatory alterations as far as possible in order to achieve adequate tissue oxygenation. It has to be stressed however that the basic concept for therapy of septic shock is an adequate fluid resuscitation which never can be replaced by any vasoactive drug therapy.

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