Abstract

Although left ventricular dysfunction is the most frequent cause of decreased cardiac output, impaired right ventricular function may also produce low output syndrome. Right ventricular dysfunction can be observed in a number of clinical conditions: right ventricular infarction, acute massive pulmonary embolism, severe primary tricuspid and pulmonary regurgitation, dilated cardiomyopathy, chronic right ventricular outflow obstruction, chronic pre- and postcapillary pulmonary hypertension, congenital right ventricular dysplasia, and infiltrative diseases involving the right ventricle. Of all of these various clinical pathophysiologic disorders, acute right ventricular myocardial infarction is probably the most frequent clinical condition that has the potential to precipitate acute low-output state. Although isolated right ventricular infarction is uncommon, the right ventricle is frequendy involved in patients in whom left ventricular infarction develops. The involvement of the free wall of the right ventricle is frequently seen in patients with left ventricular inferior or inferoposterior wall myocardial infarction. Based on the diagnostic criteria, right ventricular myocardial infarction is observed in up to 40 percent of patients with left ventricular inferior wall myocardial infarction. 1 Sharpe DN Botvinick EH Shames DM et al. The noninvasive diagnosis of right ventricular infarction.. Circulation. 1978; 57: 483-490 Crossref PubMed Scopus (152) Google Scholar The clinical right ventricular myocardial infarction is infrequently observed in patients with left ventricular anterior wall myocardial infarction. A number of complications can be encountered in patients with predominant right ventricular myocardial infarction, although the incidence is comparatively low. Bradyarrhythmias, including sinus bradycardia, sinus arrest, sinoatrial exit block, and various degrees of atrioventricular block are more frequent in patients with right ventricular infarction compared with patients with left ventricular infarction. Right ventricular infarction results most frequently from thrombotic occlusion of the right coronary artery that also provides blood flow via atrioventricular (AV) nodal artery to the AV node in over 90 percent of instances. Thus, AV nodal ischemia and varying degrees of AV nodal block frequendy accompany right ventricular infarction. Occlusion of the right coronary artery, proximal to the origin of the sinoatrial nodal artery, may also produce sinus nodal dysfunction and right ventricular myocardial infarction. Besides bradyarrhythmias, right ventricular myocardial infarction can also produce hypotension and low-output state. The incidence of severe low-output state with clinical features of cardiogenic shock occur in approximately 10 percent of patients with right ventricular infarction. The other complications, such as free wall rupture with or without ventricular septal rupture, pulmonary embolism associated with right ventricular mural thrombosis, and severe tricuspid regurgitation resulting from right ventricular papillary muscle infarction are very infrequently encountered.

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