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Regulation of cardiac output in hypoxia
Author(s) -
Siebenmann Christoph,
Lundby Carsten
Publication year - 2015
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/sms.12619
Subject(s) - cardiology , hypoxia (environmental) , afterload , medicine , stroke volume , cardiac output , heart rate , tachycardia , baroreflex , anesthesia , hemodynamics , blood pressure , chemistry , oxygen , organic chemistry
This brief review addresses the regulation of cardiac output (Q) at rest and during submaximal exercise in acute and chronic hypoxia. To preserve systemic O 2 delivery in acute hypoxia Q is increased by an acceleration of heart rate, whereas stroke volume ( SV ) remains unchanged. Tachycardia is governed by activation of carotid and aortic chemoreceptors and a concomitant reduction in arterial baroreflex activation, all balancing sympathovagal activity toward sympathetic dominance. As hypoxia extends over several days a combination of different adaptive processes restores arterial O 2 content to or beyond sea level values and hence Q normalizes. The latter however occurs as a consequence of a decrease in SV whereas tachycardia persists. The diminished SV reflects a lower left ventricular end‐diastolic volume which is primarily related to hypoxia‐generated reduction in plasma volume. Hypoxic pulmonary vasoconstriction may contribute by increasing right ventricular afterload and thus decreasing its ejection fraction. In summary, the Q response to hypoxia is the result of a complex interplay between several physiological mechanisms. Future studies are encouraged to establish the individual contributions of the different components from an integrative perspective.