• H Ebelt and K Werdan.
• Klinik und Poliklinik für Innere Medizin III, Universitätsklinikum Halle (Saale), Ernst-Grube-Strasse 40, Halle, Germany. henning.ebelt@medizin.uni-halle.de
• Internist (Berl). 2010 Jul 1; 51 (7): 844-9.

AbstractIn patients suffering from severe sepsis an impairment of cardiac function is seen constantly. Patients with septic shock often show a transient reduction of cardiac ejection fraction. Besides, a tremendous impairment of heart rate variability corresponding to a poor prognosis is often found. Endotoxin might play a pivotal role in the conjunction of inflammation and the disturbance of heart rate regulation. Experimental studies show that the complex interactions of endotoxin, the cardiac pacemaker current I (f), and the autonomous nervous system lead to an increase of resting heart rate and in parallel to a decrease of heart rate variability - as typically seen in patients with severe sepsis. The method of choice to quantify the degree of septic cardiomyopathy at the intensive care unit certainly is to determine cardiac output in relation to systemic vascular resistance. Unfortunately, clinical trials aiming to influence the causal pathogenesis of septic cardiomyopathy (inhibition of excess formation of nitric oxide, suppression of cytokine release etc.) were rather disappointing so far. Positive effects might be assumed for the administration of activated protein C thereby underlining the role of microcirculatory alterations in the development of septic cardiomyopathy.

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