Patients suffering from septic shock often present with not only severe reduction of afterload induced by vasodilation but are also affected by sepsis-induced cardiac dysfunction. Elevated troponin levels, which are typically not caused by coronary ischemia, may indicate septic cardiomyopathy which is characterized both by altered systolic function as well as by disturbances in the regulation of heart rate and heart rate variability. The latter findings are based not only on the dysfunction of the autonomous nervous system but are also the result of the direct interaction of endotoxins with cardiac pacemaker cells. In order to quantify the extent of septic cardiomyopathy, cardiac output has to be considered in the light of the existing afterload, i.e., by the parameter 'afterload-related cardiac performance' (ACP). Therapy of septic shock (and thereby septic cardiomyopathy) is based on the well-known causative, supportive, and adjunctive strategies. Stabilization of cardiac function is assured by volume resuscitation (including blood transfusion) and inotropic support (dobutamine). Further specific therapeutic approaches have not yet been established.