Purpose of review
The ultimate goal of therapy for cardiogenic shock is to restore microcirculatory function and thereby restore the oxygen supply to sustain cellular function. Therapeutic measures mainly focus on improving pressure-derived macrocirculatory parameters. However, it is increasingly clear that to achieve significant progress in treatment, microcirculatory physiopathological mechanisms must be considered.
Microcirculatory function deteriorated during cardiogenic shock and improved after treatment. Postcardiogenic shock microcirculatory disturbances, both myocardial and peripheral, were a prognostic factor for the long-term outcome. Hypothermia, whether pharmacologically or physically induced, improved postresuscitation myocardial and cerebral function, an effect associated with improved postresuscitation microcirculation. The impact of cardiogenic shock on cerebral and myocardial microcirculation could be evaluated with MRI. In severe heart failure, pharmacological interventions improved microcirculation. An assessment of the microcirculation was often performed using handheld video microscopy for direct observation of the sublingual microcirculation, which proved to be useful for evaluating the effects of interventions during cardiogenic shock. A large multicenter study on critically ill patients is now being conducted using this technique.
Cardiogenic shock induces microcirculatory disorders that can be monitored and influenced in various manners, both pharmacologically and physically. In addition to global hemodynamic optimization, interventions must also ameliorate the microcirculation.