Effects of passive heating on central blood volume and ventricular dimensions in humans

Abstract

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 degrees 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.

Figure 1. Responses to whole-body heating from a subject and times when the listed procedures were performed

Given the differences in the time necessary to heat each subject to achieve the desired increase in internal temperature, the time line for this subject only approximates the time line for other subjects. MUGA, multi-gated acquisition.

Figure 2. Scintigraphic images of the scanned area in normothermia (upper panels) and heat stress (lower panels) from one subject

Data are analysed from higher resolution images than those displayed.

Figure 3. Percentage change in blood volume from the indicated regions between experimental (i.e. heat stressed) and time control subjects

In each of the indicated regions heat stress significantly reduced blood volume relative to the time control trials. §Outlier data from a time control subject was removed for this analysis due to this subject exhibiting an unexplained pronounced reduction in spleen blood volume that was greater than 5 standard deviations from the mean. See comments in Results regarding the implications of removal of this subject's data point.

Figure 4. Effects of heat stress on left ventricular end-diastolic and end-systolic volumes, as well as ejection fraction

A, percentage change in left ventricular end-diastolic and end-systolic blood volumes as a result of whole-body heat stress and time control conditions derived from multi-gated acquisition (MUGA). Heat stress did not significantly alter left ventricular end-diastolic volume whereas left ventricular end-systolic volume was significantly reduced. B, effects of heat stress and time control conditions on left ventricular ejection fraction. There was no difference in ejection fraction between the groups prior to the heat stress or time control periods. Whole-body heating significantly increased left ventricular ejection, while this value was unchanged at the end of the time control period for this group.