Pulmonary Hypertension and the Heart: a Complex Interaction

Pulmonary hypertension primarily affects the heart by increasing right ventricular (RV) afterload. The initial response of the RV is an increased contractility soon followed by hypertrophy, with little or no increase in dimensions. When this “homeometric” adaptation fails, in case of rapid and/or severe increase in pulmonary artery pressure, the RV also uses a “heterometric” adaptation at the price of increased dimensions, higher filling pressures, systemic congestion and decreased exercise capacity. Dilatation of the RV impairs left ventricular (LV) filling. This diastolic interaction eventually alters systolic interaction, or contribution of LV contraction to the strength of RV contraction, which further deteriorates RV function. Too high or low lung volumes may increase pulmonary vascular resistance. Excessive decrease in pleural pressures be a cause of LV failure and worsening of pulmonary hypertension by upstream transmission of filling pressures. The complexity of heart-lung interactions in pulmonary hypertension needs understanding to optimize treatment strategies.