Diagnosis and Treatment of Cardiogenic Shock

Abstract

Cardiogenic shock is the leading cause of death in patients hospitalized with acute myocardial infarction [1, 2]. Cardiogenic shock is characterized by a state of inadequate tissue perfusion due to cardiac dysfunction and is classically manifested by systemic hypotension and end-organ hypoperfusion in the setting of adequate or elevated left ventricular fi lling pressures. The hemodynamic defi nition includes sustained hypotension (systolic blood pressure 30 mm Hg or more in mean arterial pressure from baseline for at least 30 minutes) and a reduced cardiac index (<2.2 L min m) [3]. In the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) Trial [4], tissue hypoperfusion was defi ned as cold peripheries (extremities colder than core), oliguria (<30 mL/h), or both. Subjects requiring pharmacological or mechanical circulatory support to maintain blood pressure are also included in this category. In the setting of an acute myocardial infarction, hypotension, tachycardia, peripheral vasoconstriction, decreased urine output, and altered mentation are all manifestations of the syndrome, which can range from “preshock” to fully developed pump failure. It is important to recognize the preshock syndrome because early investigation of its etiology and early intervention may reduce the development of frank cardiogenic shock. In this state, systolic blood pressure may be normal to borderline without pressors, but this “stability” occurs at the expense of an elevated peripheral resistance and elevated heart rate that support a borderline stroke volume. The signs of peripheral hypoperfusion may be obvious or subtle. This is also known as nonhypotensive cardiogenic shock and is associated with ineffective tissue perfusion and a severely depressed cardiac index. The preshock syndrome is associated with a high in-hospital mortality (43%), which is lower than that in patients with classic cardiogenic shock (66%) [5]. This syndrome predominately occurs in the setting of a large anterior wall myocardial infarction (MI). Recognition of this “preshock state” is important to avoid potentially cardiodepressant medications and to identify patients who might benefi t from aggressive revascularization strategies.