At high altitude, as hypoxia induces pulmonary vasoconstriction and increases ipulmonary arterial pressure, right ventricular (RV) function will be affected. The right ventricular function may be affected directly by the hypoxaemic challenge or indirectly through a pressure overload due, in turn to changes in the pulmonary circulation. Both animal and human studies show that moderate or transient hypoxia results in adaptive changes in right ventricle that are reversible with re-exposure to normoxic conditions and RV dysfunction is mainly due to mechanical overload from the pulmonary circulation. When hypoxia is more severe or more prolonged, it may directly impact ventricular diastolic or systolic function through mechanisms that remain to be unraveled. Chronic exposure to hypoxia in high-altitude natives suffering from Monge's disease may lead to RV hypertrophy, RV failure and overall cardiac failure. The adrenergic system may be involved, as well as HIF, PKC or phospholamban. More studies using the latest imaging technology should give us a better understanding of RV systolic and diastolic function in humans exposed to altitude hypoxia including acute, chronic or chronic intermittent hypoxia.