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.
D000531:Altitude; D002302:Cardiac Output; D004452:Echocardiography; D004562:Electrocardiography; D006321:Heart / Q000502:physiology*; D006439:Hemodynamics; D006801:Humans; D010701:Phonocardiography; D005082:Physical Exertion; D013318:Stroke Volume; D016276:Ventricular Function