• K Werdan, S Hettwer, S Bubel, A Oelke, R S Hoke, R Wimmer, H Ebelt, and U Müller-Werdan.
• Universitätsklinik und Poliklinik für Innere Medizin III, Universitätsklinikum Halle (Saale) der Martin-Luther-Universität Halle-Wittenberg, Ernst-Grube-Strasse 40, 06120, Halle (Saale), Deutschland. karl.werdan@medizin-uni-halle.de
• Internist (Berl). 2009 Jul 1;50(7):799-800, 802-6, 808-9.

AbstractSeptic shock is not only a circulatory shock but is also a cardiac shock, the consequence of a potentially reversible heart impairment known as septic cardiomyopathy. Disturbances of macrocirculation as well as microcirculation, an individually heterogeneous reduction of cardiac function, and an extensive impairment of demand-oriented regulation of heart function characterize the septic shock state. Bacterial toxins, inflammatory mediators, and a disseminated intravasal coagulopathy are responsible for these disturbances; for the impairment of cardiac regulation, the interaction of endotoxin with the cardiac pacemaker current I(f) also plays a role. Circulatory shock as well as septic cardiomyopathy should be quantified: The lowering of systemic vascular resistance characterizes the extent of circulatory shock, and the reduction of relative cardiac output in relation to afterload characterizes the extent of septic cardiomyopathy. The intensity of circulatory as well as of cardiac impairment correlates with an unfavorable prognosis. Treatment of septic circulatory shock and of septic cardiomyopathy is predominantly symptomatic; first causal approaches are under investigation.

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