Biventricular function at high altitude: implications for regulation of stroke volume in chronic hypoxia

Abstract

The myocardium is well protected against chronic hypoxia. In chronic hypoxia stroke volume falls both at rest and on exercise. The fall in stroke volume is associated with reduction in left ventricular dimensions and filling pressure. An obvious explanation for this is the reduction in plasma volume observed at high altitude, but this does not appear to be the whole story. Neither is left ventricular systolic function abnormal even at the summit of Mount Everest. Hypoxia itself may have a direct effect on impairing myocardial relaxation. Increased pulmonary vascular resistance leads to right ventricular pressure overload. This may impair right ventricular function, and reduce stroke volume and venous return to the left atrium. Interaction between the right and left ventricles, which share a common septum and are potentially constrained in volume by the pericardium, may impair diastolic left ventricular filling as a consequence of right ventricular pressure overload, and hence reduce stroke volume. It is questionable how clinically significant is this left ventricular diastolic dysfunction. The relative importance of different mechanisms which reduce stroke volume probably depends whether hemodynamics are measured at rest or on exercise. Intervention with sildenafil to ameliorate hypoxic pulmonary vasoconstriction is associated with both an increase in exercise capacity and stroke volume in hypoxia. Whether these have a causal association remains to be demonstrated.