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STATE-OF-THE-ART PAPER

Pathophysiology and management of right heart ischemia

^* Division of Cardiology, William Beaumont Hospital, Royal Oak, Michigan, USA

Manuscript received December 27, 2001; revised manuscript received April 26, 2002, accepted May 24, 2002.

^* Reprint requests and correspondence: Dr. James A. Goldstein, Director, Research and Education, Division of Cardiology, William Beaumont Hospital, 3601 West Thirteen Mile Road, Royal Oak, Michigan 48073, USA.
jgoldstein{at}beaumont.edu

Acute right coronary artery occlusion proximal to the right ventricular (RV) branches results in right ventricular free wall dysfunction, exerting mechanically disadvantageous effects on biventricular performance. Depressed RV systolic function decreases 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 and performance, resulting in more severe hemodynamic compromise. Bradyarrhythmias limit output generated by the rate-dependent noncompliant ventricles. Hemodynamic compromise may respond to volume resuscitation and restoration of physiologic rhythm. Vasodilators and diuretics should generally be avoided. In some patients, parenteral inotropic stimulation may be required. The right ventricle appears to be relatively resistant to infarction and recovers even after prolonged occlusion. The term RV "infarction" appears to be somewhat of a misnomer, for in most patients acute RV dysfunction represents ischemic but predominantly 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 recovery of RV performance and improves the clinical course and survival.

Abbreviations and Acronyms   AV   atrioventricular   JVP   jugular venous pressure   LV   left ventricular   MI   myocardial infarction   RA   right atrial   RCA   right coronary artery   RV   right ventricular   RVFW   right ventricular free wall   RVI   right ventricular infarction

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