Mechanism of reduced cardiac stroke volume at high altitude.

Two postulates have been advanced to account for reduced stroke at high altitude: (1) diminished venous return secondary to contracted plasma volume and (2) left ventricular (LV) dysfunction secondary to hypoxia. To test these hypotheses, we assessed LV dimensions and contractility indices by M-mode echocardiography and systolic time intervals in 11 young men at sealevel and serially for 10 days at 3100 m altitude. Mean LV end-diastolic dimension fell 16% after 6-8 days, with a 20% decrease in plasma volume reflected by hematocrit rise. Pre-ejection period to LV ejection time (PEP/LVET) ratio was increased after 1-2 days. All indices of contractility were unchanged at rest, and slightly enhanced during exercise. Thus stroke volume falls and PEP/LVET ratio rises at 3100 m because of diminished venous return despite preservation of LV systolic performance.