Hemodynamic spectrum of “dominant” right ventricular infarction in 19 patients

In 19 patients right ventricular infarction was diagnosed on the basis of electrocardiographic features of acute inferior infarction and clinical evidence of elevation of systemic venous pressure and an absence of pulmonary congestion. Right heart catheterization documented elevated right ventricular end-diastolic pressure (mean 15.5 mm Hg) and commensurate right atrial pressure (mean 14.9 mm Hg). In all patients the pulmonary capillary wedge pressure (mean 13.2 mm Hg) was exceeded or equaled by the right ventricular end-diastolic pressure, suggesting a disproportionate reduction in right ventricular compliance or contractile function, or both. Thirteen patients were hypotensive (systolic blood pressure less than 100 mm Hg on admission), including six patients with cardiogenic shock.

Right ventricular infarction is an uncommon and potentially reversible cause of cardiogenic shock;yet, in the experimental model, isolated right ventricular damage is relatively well tolerated. To identify the factors associated with systemic hypotension, data from patients with and without compromised systemic hemodynamic function were compared. In hypotensive patients, the right ventricular end-diastolic pressure was significantly higher (16.8 versus 12.8 mm Hg;p < 0.01) and reflected more extensive right ventricular damage. A pulmonary wedge pressure of 15 mm Hg or more was noted only among the hypotensive patients, and their wedge pressure (mean 14.8 mm Hg) was significantly greater than that of normotensive patients (mean 9.7 mm Hg, p < 0.05). Therefore, in patients with right ventricular infarction, an additional impairment of left ventricular function due to associated infarction of the inferior left ventricle is a significant factor causing hypotension. The elevated wedge pressure may influence right ventricular output by affecting pulmonary arterial diastolic pressure and right ventricular afterload. Right ventricular peak systolic pressure as an index of right ventricular afterload was significantly higher in hypotensive than in normotensive patients (30.5 versus 23.8 mm Hg, p < 0.03), and there was a linear correlation between this pressure and the pulmonary capillary wedge pressure (r = 0.895, p < 0.001).

There was one hospital death (mortality rate 5.3 percent). Clinical management generally consisted of administration of fluids and digitalis and implantation of a temporary pacemaker. This study emphasizes the relatively favorable prognosis of this condition and suggests that aggressive diagnosis and management are appropriate.