This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Goldstein, J. A. Search for Related Content PubMed PubMed Citation Articles by Goldstein, J. A.

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

This article has been cited by other articles:

				C. B. Overgaard and V. Dzavik Inotropes and Vasopressors: Review of Physiology and Clinical Use in Cardiovascular Disease Circulation, September 2, 2008; 118(10): 1047 - 1056. [Full Text] [PDF]

				G. Piazza and S. Z. Goldhaber The Acutely Decompensated Right Ventricle: Pathways for Diagnosis and Management Chest, September 1, 2005; 128(3): 1836 - 1852. [Abstract] [Full Text] [PDF]

				J. A. L. Calbet, G. Radegran, R. Boushel, H. Sondergaard, B. Saltin, and P. D. Wagner Plasma volume expansion does not increase maximal cardiac output or VO2 max in lowlanders acclimatized to altitude Am J Physiol Heart Circ Physiol, September 1, 2004; 287(3): H1214 - H1224. [Abstract] [Full Text] [PDF]

				S. Wasson, G. Govindarajan, H. K. Reddy, and G. Flaker The Role of Nitric Oxide and Vasopressin in Refractory Right Heart Failure Journal of Cardiovascular Pharmacology and Therapeutics, March 1, 2004; 9(1): 9 - 11. [Abstract] [PDF]

				J. A. Goldstein Right versus left ventricular shock: A tale of two ventricles J. Am. Coll. Cardiol., April 16, 2003; 41(8): 1280 - 1282. [Full Text] [PDF]