- Consistent hypotensive state (≥ 30 minutes) with systolic blood pressure of < 90 mm Hg and mean arterial blood pressure of 30 mm Hg below the baseline.
- Normal or elevated cardiac filling pressures (left ventricular end-diastolic pressure > 18 mm Hg and/or right ventricular end-diastolic pressure > 10-15 mm Hg).
- Severely reduced cardiac output (< 1.8 L/min/m2 and < 2.2 L/min/m2 without and with support, respectively).
Etiologies for cardiogenic shock include cardiomyopathy (primarily due to myocardial ischemia / infarction or dilated cardiomyopathy), arrhythmia (including tachyarrhythmias such as sustained ventricular tachycardia and severe bradyarrhythmias such as complete heart block), and mechanical causes (eg, severe aortic or mitral valve disease, severe ventricular septal defects, and left ventricular free wall rupture). Typically, severe depression of myocardial contractility leads to decreased cardiac output and low blood pressure and worsens coronary ischemia. The pathophysiology leading to shock includes the compensatory increase in systemic vascular resistance to compensate for inadequate stroke volume and hypotension, which further exacerbates the issue. Systemic inflammation has also been theorized to play a role by release of interleukins, tumor necrosis factors, and nitric oxide.
Treatment includes establishing adequate circulation with inotropes (eg, dopamine or dobutamine), vasopressors (eg, norepinephrine or dopamine), and/or mechanical support (eg, intra-aortic balloon pump or left ventricular assist device) as well as treatment of the underlying cause (eg, revascularization for ischemia, pacemaker placement for severe bradycardia, or surgical intervention for severe valvular disease, ventricular septal defect, or free wall rupture).