Right ventricular infarction may occur in isolation or with acute inferoposterior left ventricular myocardial infarction. In fact, right ventricular infarction occurs in as many as 30 to 50 percent of patients who have an acute inferior myocardial infarction, and it is hemodynamically significant in approximately one half of these patients. Because the treatment of right ventricular infarction differs from that of the more common left ventricular infarction, it is important for clinicians to be aware of the condition and intervene accordingly.1–5
Classically, right ventricular infarction presents as acute inferior infarction, hypotension and elevated jugular venous pressure, with clear lung fields. However, these findings are seen in fewer than 25 percent of patients with acute right ventricular infarction. Therefore, hemodynamic data, along with an electrocardiogram or echocardiogram/radionuclide angiogram, should be obtained early to confirm the diagnosis.5–8 In this issue of American Family Physician, Horan and Flowers9 describe the diagnosis of right ventricular infarction.
The correct diagnosis is critical in the management of patients who present with low cardiac output and low arterial pressure in the setting of acute myocardial infarction. Right ventricular infarction lowers the compliance of the right ventricle, leading to a reduction in right ventricular filling and a decrease in right ventricular stroke volume. As a result, left ventricular filling and stroke volume would diminish, causing a decrease in arterial pressure. Severe right ventricular dysfunction may be associated with cardiogenic shock. In such cases, conventional treatment may be deleterious. The initial therapy for a patient with acute right ventricular infarction who has hypotension is volume expansion, with the use of normal saline to increase filling of the right ventricle. This will in turn increase filling of the underfilled left ventricle and increase cardiac output.10,11
In some patients with acute right ventricular infarction, volume loading causes dilatation of the right ventricle, which could compromise left ventricular output, because the added pressure in the pericardium does not allow the left ventricle to fill. To avoid this complication, hemodynamic monitoring may be necessary. Positive inotropic support must be considered if the cardiac output does not improve following volume loading.
The administration of dobutamine lowers pulmonary vascular resistance and therefore reduces right ventricular afterload, improving cardiac function.12 Dobutamine can be started at 5 μg per kg per minute, and the dose may be titrated up to 20 μg per kg per minute if required. Diuretics and nitrates, which reduce preload, can diminish cardiac output and induce significant hypotension in the presence of right ventricular infarct. They must be used with caution in this setting.
Patients with inferior myocardial infarction who have associated right ventricular infarction have an increased risk of early morbidity and mortality. Early reperfusion using thrombolytic therapy or primary percutaneous transluminal coronary angioplasty (PTCA) may reduce infarct size and improve the short-term survival in many of these patients.13 In patients with right ventricular infarction, the use of thrombolytic therapy is associated with a 4.2-fold lower incidence of in-hospital mortality and a 2.4-fold lower rate of complications.14 In patients with right ventricular infarction, complete reperfusion of the right coronary artery with PTCA resulted in the dramatic recovery of right ventricular function and an improved clinical outcome. However, unsuccessful reperfusion was associated with a high in-hospital mortality rate.15
Despite the potentially life-threatening acute hemodynamic effects of right ventricular infarction, most patients have spontaneous early hemodynamic improvement and subsequent recovery of right ventricular function. The prognosis after right ventricular infarction is related to the degree of coexisting left ventricular dysfunction. Patients who survive the acute phase tend to show more clinical and hemodynamic improvement of the right ventricle than of the left, in part because of the lower right ventricular muscle mass and the presence of coronary blood flow to the right ventricle during both systole and diastole.10,12