Right heart ischemia: pathophysiology, natural history, and clinical management.

Right ventricular (RV) ischemia occurs in 50% of patients with acute inferior myocardial infarction, and may result in severe hemodynamic compromise associated with poor clinical outcome. Acute right coronary artery (RCA) occlusion proximal to the RV branches results in right ventricular free wall (RVFW) dysfunction. The ischemic, dyskinetic RVFW exerts mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function leads to a decrease in transpulmonary delivery of left ventricular (LV) preload, resulting in diminished cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction and septally-mediated alterations in LV compliance, which are exacerbated by elevated intrapericardial pressure. Under these conditions, RV pressure generation and output are dependent on LV-septal contractile contributions, governed by both primary septal contraction and paradoxical septal motion. When the culprit coronary lesion is distal to the right atrial (RA) branches, augmented RA contractility enhances RV performance and optimizes cardiac output. Conversely, more proximal occlusions result in ischemic depression of RA contractility, which impairs RV filling, thereby resulting in further depression of RV performance and more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with right ventricular infarction and hemodynamic compromise often respond to volume resuscitation and restoration of a physiological rhythm. Vasodilators and diuretics should generally be avoided. In some, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover even after prolonged occlusion. Therefore, the term RV infarction appears to be somewhat of a misnomer, for in most patients a substantial proportion of acute RV dysfunction represents ischemic but viable myocardium. Although RV performance improves spontaneously even in the absence of reperfusion, recovery of function may be slow and associated with high in-hospital mortality. Reperfusion enhances the recovery of RV performance and improves the clinical course and survival of patients with ischemic RV dysfunction.