
Mechanism of reduced cardiac stroke volume at high altitude
Author(s) -
Alexander J. K.,
Grover R. F.
Publication year - 1983
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960060612
Subject(s) - medicine , stroke volume , stroke (engine) , cardiology , altitude (triangle) , mechanism (biology) , effects of high altitude on humans , cardiac output , hemodynamics , heart failure , ejection fraction , anatomy , mechanical engineering , philosophy , geometry , mathematics , epistemology , engineering
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.