Cardiogenic shock is a clinical state of acute circulatory failure secondary to a reduction in cardiac output to a level that is inadequate to supply tissues with sufficient oxygen for cellular metabolism. The vast majority of cases of cardiogenic shock are due to acute myocardial infarction (AMI) and subsequent LV dysfunction. Cardiogenic shock can also be caused by ventricular wall rupture, acute mitral valve regurgitation, valvular heart diseases, dysrhythmias or cardiomyopathy.

The critical care management of cardiogenic shock remains challenging, as reflected in the mortality rates of up to 50% of patients with AMI (Theile et al., N Engl J Med 367:1287–1296, 2012). Common pharmacological agents used to improve cardiac output and reverse tissue malperfusion, by definition, increase the myocardial oxygen demand with potentially deleterious consequences (Samuels et al., J Card Surg 14:288–293, 1999). For this reason it is critical to employ a strategy of augmenting cardiac output just enough to realise adequate organ perfusion without further exacerbating the supply/demand mismatch that the failing heart represents. The attainment of this balance point remains extremely difficult, exacerbated by the inherent inadequacies of our current technologies and biological markers that poorly, if at all, determine this endpoint. Consequently there is a fundamental requirement to develop technologies and treatment strategies with tissue perfusion at their core.