Although right ventricular infarction has been described for many years at autopsy, the hemodynamic impact was not well recognized until the report of Cohn et al in 1974. Since it is essential to recognize early signs of predominant right ventricular infarction because it may require a unique form of therapy, several clinical and electrocardiographic studies have attempted to detect right ventricular involvement in acute myocardial infarction. Necrosis of a large proportion of the right ventricle causes a hemodynamic derangement characterized by systemic hypotension and disproportionate elevation of right ventricular filling pressure compared to left ventricular filling pressure. This in turn causes an elevation of the central venous pressure (jugular venous pressure), one of the hallmarks of the bedside diagnosis of right ventricular infarction. pilocarpine-eyedrops.com
In addition, patients frequently develop Kussmauls sign due to decreased ability of an infarcted right ventricle to handle the increased volume load caused by inspiration. The understanding of the hemodynamics of right ventricular infarction is important not only to institute the appropriate treatment, but to avoid mismanagement such as giving drugs (nitrates, diuretics) that can reduce even further the ventricular filling pressure. Volume expansion by either crystalloid or colloid solutions is the primary therapy in order to maintain adequate right ventricular output. However, in case of severe right ventricular damage, this chamber may operate at the “flat” part of the ventricular function curve and fluid replacement alone does not necessarily increase right ventricular stroke volume.
In the case we have described, the clinical presentation was typical of an inferior wall myocardial infarction with significant right ventricular involvement. This was further substantiated by the coronary anatomy, the site of occlusion and the hemodynamic findings. In addition, ST-segment elevation in precordial leads, as in this patient, has been described in patients with right ventricular infarction.
Mechanical reperfusion techniques have proved to be useful, when applied early to salvage left ventricular myocardium and in the management of electrical complications. Duration of ischemia and the presence of even minimal perfusion to jeopardized tissue are the most important variables for recovering ventricular function. This case indicates that reperfusion may also be useful in managing hypotension due to predominant right ventricular infarction. Although there was some degree of left ventricular dysfunction, it is unlikely that the rapid hemodynamic improvement after percutaneous transluminal coronary angioplasty was related to left ventricular reperfusion. We believe that in this patient the rapid reperfusion of the right ventricle achieved by coronary angioplasty, in addition to a brief volume load, brought an immediate beneficial effect in restoring normal hemodynamic parameters without the need for prolonged expansion of intravascular volume or use of inotropic agents. To our knowledge, the use of PTCA in right ventricular infarction has not been described previously in the literature.