Pathophysiology and clinical management of right heart ischemia

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Abstract
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. Right coronary artery occlusion proximal to the RV branches results in RV systolic dysfunction, which decreases transpulmonary delivery of left ventricular (LV) preload and diminishes cardiac output. The ischemic right ventricle is stiff, dilated, and volume dependent, resulting in pandiastolic RV dysfunction. Under these conditions, RV pressure generation and output depend on LV-septal contractile contributions. 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 and performance, leading to more severe hemodynamic compromise. Bradyarrhythmias limit the output generated by the rate-dependent noncompliant ventricles. Patients with RV ischemia and hemodynamic compromise often respond to volume resuscitation and restoration of a physiologic rhythm. In some patients, parenteral inotropic stimulation may be required. The ischemic right ventricle appears to be relatively resistant to infarction and has a remarkable ability to recover. The term RV infarction appears to be a misnomer, as RV performance improves spontaneously even in the absence of reperfusion. Reperfusion, however, enhances the recovery of RV performance and improves the clinical course.

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