Once thought to be rare, right ventricular infarction is known to occur at approximately 30% of patients with myocardial infarction with Q wave. In most patients, the amount of right ventricular myocardium affected by infarction is small and therefore, signs or symptoms of right ventricle failure appear rarely. Mild right ventricular dysfunction can be demonstrated in patients with transmural inferior infarction, through sensitive cardiac diagnostic techniques, non-invasive (echocardiography, radionuclide angiography). The diagnosis is suggested if there is elevation of the ST segment in the right precordial leads.
Sometimes, patients with acute myocardial infarction of the inferior wall present severe right ventricular failure, which suggests that there was an extensive right ventricular infarction. The means of non-invasive cardiac evaluation in such patients frequently show an almost normal left ventricular function and marked dysfunction of the right ventricle.
In patients with predominant right ventricular infarction, there is an array that can mimic hemodynamic cardiac tamponade or constrictive pericarditis. Sometimes, just the volume expansion therapy may be effective in the treatment of low cardiac output and hypotension occurring in a predominantly right ventricular infarction. Other patients with right ventricular infarction show refractory hypotension and more aggressive treatment is indicated. Thrombolytic therapy, mostly efficient, often interrupts the clinical syndrome of right ventricular infarction.
Protocol in right ventricular infarction
1. The diagnosis of right ventricular infarction is suggested predominantly in patients with inferior infarction with Q wave that show hypotension, jugular venous distension, usually in the absence of pulmonary congestion. Right precordial derivations of the ECG frequently show elevation of the ST segment in patients with right ventricular infarction.
a. Confirmation of the diagnosis is obtained using ultrasonography, radionuclide angiography (low ejection fraction and increased right ventricular volume) or right heart catheterization.
b. Confirming a certain diagnosis and the indication of management of therapy are obtained by right heart catheterization with a flow directed catheter. Predominant hemodynamic characteristics of the right ventricular infarction include: pressure in the right atrium and telediastolic pressure in right ventricle increased, which is equal to or greater than the pressure in the pulmonary artery or pulmonary capillary pressure; normal pulmonary arterial systolic pressure; normal pulmonary vascular resistance; paradoxical pulse greater than 10 mm Hg in the blood pressure and sometimes, inspiratory decrease in right atrial pressure (Kussmaul’s sign). These last two features, together with diastolic pressure equalization of the right heart (right atrium, right ventricle, pulmonary artery, pulmonary capillary) may suggest misdiagnosis of cardiac constriction or compression. Scintigraphic and ecographic exams of the right ventricle can differentiate the right ventricular infarction from cardiac tamponade or constrictive pericarditis. Increased pressure in the right atrium may suggest acute pulmonary embolism. Normal pulmonary pressures and, if necessary, normal pulmonary perfusion exclude pulmonary embolism.
Right Ventricular Infarction Treatment
Patients who meet the criteria which were highlighted for the predominantly right ventricular infarction are treated as follows:
a. in the absence of hypotension and severe bradyarrhythmias, the right attitude is to wait.
b. In the presence of hypotension, bradyarrhythmias must be corrected.
In some patients with right ventricular infarction, refractory bradyarrhythmias and hypotension administration of atropine respond quickly to sequential atrioventricular stimulation. Isolated ventricular stimulation is usually ineffective in correcting hypotension in these patients. Consideration should be given to increasing the intravascular volume with dextran or colloidal solutions. Volume expansion should be continued until the right atrial pressure reaches a level of at least 14 to 15 mm Hg (often higher pressures are required to remedy systemic hypotension).
c. If hypotension persists after correction of bradyarrhythmias and plasma volume expansion, dopamine or dobutamine infusions are recommended. Intra-aortic balloon counterpulsation was also sometimes used in these patients, but it is unclear if the intent is beneficial for patients with right ventricular infarction.
d. If the systemic arterial pressure is adequate, but there are signs and symptoms of marked right ventricular failure (hepatic congestion with increased serum enzymes and bilirubin, cardiac output decreased with increasing urea and creatinine), patients can be treated with simultaneous infusions of nitroprusside and plasma volume replacement solutions.
e. Efficient thrombolytic therapy can lead to the disappearance of the signs of right ventricular infarction. Such therapy should be started as soon as possible after the onset of stroke. Pharmacological or mechanical thrombolytic therapy (angioplasty) may result, each of them, to a marked improvement in the patient’s clinical status.