Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications

Abstract

Acute PE may lead to right ventricular dilatation and failure. Through ventricular interdependence and decreased left ventricular filling, cardiac output and systemic circulation also may be compromised. The associated decrease in coronary perfusion pressure to the acutely overloaded right ventricle may produce ischemia and worsening right heart failure. This downward cycle of right ventricular failure and ischemia may ultimately progress to right ventricular infarction, circulatory arrest, and death. Certain clinical findings, hemodynamic values, and, particularly, echocardiographic signs can identify right ventricular dysfunction after PE. Detection of right ventricular hypokinesis helps to stratify patients' risk, because right ventricular dysfunction confers a worse prognosis than does normal right ventricular function after PE. The concept of "hemodynamic instability" after PE should be expanded to include right ventricular dilatation and wall motion abnormalities, even among normotensive patients. Aggressive intervention with thrombolytic therapy, vasoactive agents, or mechanical embolectomy may improve right ventricular function and clinical outcome.