Pulmonary hypertension and the right ventricle in hypoxia

• Published in: Experimental physiology Vol. 98; no. 8; pp. 1247 - 1256
• Main Authors: Naeije, Robert, Dedobbeleer, Chantal
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.08.2013; John Wiley & Sons, Inc
• Subjects: Altitude Sickness - physiopathology; Animals; Heart Ventricles - physiopathology; Humans; Hypertension, Pulmonary - physiopathology; Hypoxia - physiopathology; Ventricular Function, Right - physiology
• ISSN: 0958-0670; 1469-445X; 1469-445X
• DOI: 10.1113/expphysiol.2012.069112

New Findings •  What is the topic of this review? Studies a,contabs,longabsre reviewed showing that hypoxic pulmonary vasoconstriction and subsequent remodelling expose the right ventricle to increased afterload, and that this is occasionally a cause of high‐altitude right heart failure. •  What advances does it highlight? Non‐invasive field studies have shown that hypoxic pulmonary hypertension limits exercise capacity in relationship to increased pulmonary artery pressures in high‐altitude newcomers. This is compensated for by increased lung diffusing capacity, decreased ventilator response and polycythaemia in high‐altitude inhabitants. There is recently reported echocardiographic evidence of altered right ventricular function at high altitudes at rest. These data need to be confirmed with measurements during exercise. Hypoxia causes pulmonary vasoconstriction. Regional hypoxic vasoconstriction improves the matching of perfusion to alveolar ventilation. Global hypoxic vasoconstriction increases right ventricular afterload. The hypoxic pulmonary pressor response is universal in mammals and in birds, but with considerable interspecies and interindividual variability. Chronic hypoxia induces pulmonary hypertension in proportion to initial vasoconstriction. Prolonged hypoxic exposure is also associated with an increase in red blood cell mass, which aggravates pulmonary hypertension by an increase in blood viscosity. Hypoxic pulmonary hypertension in humans is usually mild to moderate, but pulmonary vascular pressure–flow relationships are steep, which corresponds to a substantial afterload on the right ventricle during exercise. A partial recovery of 10–25% of the hypoxia‐induced decrease in maximal oxygen uptake has been reported with intake‐specific pulmonary vasodilating interventions. Hypoxia has been reported to decrease myocardial fibre contractility in vitro. However, the acutely hypoxic right ventricle remains able to preserve the coupling of its contractility to increased afterload in intact animals. Echocardiographic studies of the right ventricle in healthy hypoxic human subjects show altered diastolic function, but systolic function that is preserved or even increased acutely and slightly depressed chronically. These findings are more pronounced in patients with chronic mountain sickness. Their clinical significance remains incompletely understood. Almost no imaging studies of right ventricular function have been reported in a minority of subjects who develop severe pulmonary hypertension and clinical right ventricular failure in hypoxia. No imaging studies of right ventricular function during hypoxic exercise in normal subjects are yet available. Thus, while it is plausible that the right ventricle limits exercise capacity in hypoxia, this still needs to be firmly established.