Approach to patients with heart failure and pulmonary hypertension

Pulmonary hypertension (PH), defined as a mean pulmonary artery pressure greater than 25 mm Hg, is not a diagnosis, but rather the physiologic consequence of the interaction between pulmonary blood flow, pulmonary vascular impedance, and downstream pulmonary venous pressure. The diagnosis and appropriate treatment of PH in patients with or without heart failure (HF) requires an understanding of the underlying pathogenesis, whether it be due to increased pulmonary venous pressure, increased pulmonary vascular resistance (PVR), increased pulmonary blood flow, or a combination thereof. Furthermore, an explanation for the underlying cause must also be sought. For example, a rise in pulmonary venous pressure may relate primarily to an increase in left ventricular end-diastolic pressure in a patient with a known cardiomyopathy; however, it may be complicated by severe mitral regurgitation. Similarly, an increased PVR may reflect reactive changes in the pulmonary vasculature due to long-standing pulmonary venous hypertension, concomitant hypoxemia/hypercapnia, or it may be the harbinger of chronic thromboembolic disease. It is imperative that reversible causes of PH be considered. Although most often diagnosed by Doppler echocardiography, full hemodynamic characterization of PH requires right heart catheterization to measure biventricular filling pressures and PVR. Integration of invasive pulmonary hemodynamics with an assessment of right ventricular function is essential to appreciate the clinical and prognostic significance of PH of an individual patient. Right heart catheterization is not practically feasible in all patients with HF and PH; however, at a minimum it should be performed in patients with a Doppler-estimated pulmonary artery pressure greater than 60 mm Hg, those who present clinically with predominant right HF, significant mitral valve disease, and in particular, patients with impaired right ventricular function.