RV Infarction - A Tale of Two Ventricles: Key Points
The following are key points to remember from a JACCFocus Seminar, which presents an in-depth, contemporary understanding of the pathophysiology, clinical consequences, and management of right ventricular (RV) myocardial infarction (MI):
- RV infarction occurs in about one half of patients with acute inferior ST-segment elevation MI (STEMI) and leads to higher in-hospital morbidity and mortality. In patients who survive the initial complications, RV function eventually recovers even in the absence of RV recanalization, due to the low oxygen supply-demand profile of the RV.
- The culprit is usually a proximal right coronary artery (RCA) occlusion impairing RV branch flow and RV free wall perfusion, resulting in RV systolic dysfunction. Left ventricular (LV) preload, cardiac output, compliance, and filling are ultimately impaired through several mechanisms, including a leftward shift of the intraventricular septum.
- Right-sided electrocardiography (ECG) should be routine practice for all patients with inferior MI. ST-segment elevation and loss of R wave in V3R and V4R are sensitive indicators for RV infarction.
- Bradycardia, hypotension, and high-grade atrioventricular block are red flags that RV infarction may be present. Ventricular tachyarrhythmias are not uncommon and ventricular tachycardia storm may occur.
- Complications may include ventricular septal rupture, RV free wall rupture, reopening of a patent foramen ovale resulting in right-to-left shunt, and severe tricuspid regurgitation.
- Clinical presentation can include chest discomfort (most common), nausea, vomiting, diaphoresis, elevated jugular venous pressure, or systemic hypotension. Biventricular heart failure may occur in patients with pre-existing LV dysfunction.
- Useful noninvasive imaging tests include echocardiogram, cardiac magnetic resonance imaging, and cardiac computed tomography; the latter can help distinguish acute pulmonary embolism with RV shock from RV infarction. Hemodynamic assessment with right heart catheterization can confirm the diagnosis if echocardiography is insufficient.
- In the emergency department:
- Right-sided ECG and prompt bedside echocardiogram should be obtained.
- Intravenous nitroglycerin and beta-blocker should be avoided.
- Atropine or transcutaneous pacing may be necessary.
- RV preload should be optimized.
- Norepinephrine and dopamine should be the initial agents of choice if vasopressor support is needed.
- Reperfusion-induced reflex bradycardia-hypotension may occur following recanalization of the proximal RCA, and can be profoundly destabilizing. Pre-emptive placement of a venous sheath should be considered to facilitate transvenous pacing or vasopressor administration. RCA reperfusion produces immediate improvement and later recovery of the RV free wall. Failure to reperfuse the major RV branches impairs recovery and reduces in-hospital survival.
- Mechanical circulatory support, as a bridge to recovery, should be considered for patients with persistent hemodynamic compromise. Early institution of biventricular mechanical support is essential in patients with severe hemodynamic compromise exacerbated by concomitant severe LV systolic dysfunction. In patients with severe multivessel coronary disease, more complete revascularization may be beneficial.
