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Effects of passive heating on central blood volume and ventricular dimensions in humans
Author(s) -
Crandall C. G.,
Wilson T. E.,
Marving J.,
Vogelsang T. W.,
Kjaer A.,
Hesse B.,
Secher N. H.
Publication year - 2008
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.143057
Subject(s) - blood volume , heart rate , medicine , stroke volume , blood pressure , inferior vena cava , ejection fraction , cardiac output , hemodynamics , cardiology , anesthesia , heart failure
Mixed findings regarding the effects of whole‐body heat stress on central blood volume have been reported. This study evaluated the hypothesis that heat stress reduces central blood volume and alters blood volume distribution. Ten healthy experimental and seven healthy time control (i.e. non‐heat stressed) subjects participated in this protocol. Changes in regional blood volume during heat stress and time control were estimated using technetium‐99m labelled autologous red blood cells and gamma camera imaging. Whole‐body heating increased internal temperature (> 1.0°C), cutaneous vascular conductance (approximately fivefold), and heart rate (52 ± 2 to 93 ± 4 beats min −1 ), while reducing central venous pressure (5.5 ± 07 to 0.2 ± 0.6 mmHg) accompanied by minor decreases in mean arterial pressure (all P < 0.05). The heat stress reduced the blood volume of the heart (18 ± 2%), heart plus central vasculature (17 ± 2%), thorax (14 ± 2%), inferior vena cava (23 ± 2%) and liver (23 ± 2%) (all P ≤ 0.005 relative to time control subjects). Radionuclide multiple‐gated acquisition assessment revealed that heat stress did not significantly change left ventricular end‐diastolic volume, while ventricular end‐systolic volume was reduced by 24 ± 6% of pre‐heat stress levels ( P < 0.001 relative to time control subjects). Thus, heat stress increased left ventricular ejection fraction from 60 ± 1% to 68 ± 2% ( P = 0.02). We conclude that heat stress shifts blood volume from thoracic and splanchnic regions presumably to aid in heat dissipation, while simultaneously increasing heart rate and ejection fraction.