- Consistent hypotensive state 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 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). The pathophysiology leading to shock includes increased systemic vascular resistance to compensate for hypotension, which further worsens the condition. 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 (such as revascularization for ischemia, pacemaker placement for severe bradycardia, or surgical intervention for severe valvular disease, ventricular septal defect, or free wall rupture).
A 2018 study has shown that patients with acute myocardial infarction and cardiogenic shock have a lower risk of death at 30 days following culprit-lesion-only percutaneous coronary intervention (PCI) than with multivessel PCI. However, mortality at 1 year following treatment was not significantly different.
R57.0 – Cardiogenic shock
89138009 – Cardiogenic shock