It is well established that peripheral tissues act as insulators and that the efficacy of this insulation is a strong function of vasomotor status.1For example, surface warming is more effective when humans are vasodilated because vasodilation allows facile flow of heat from the skin surface through peripheral tissues to the core.2Our article again illustrates the importance of thermal insulation provided by peripheral tissues in that the increase in peripheral tissue heat content was many-fold greater than the increase in core heat content during the first hour of warming.
Peripheral tissue temperature was lower than core temperature throughout the study, which precludes direct warming of the core. However, peripheral tissue temperature was consistently greater during circulating-water warming than during forced-air warming. Therefore, less heat left the core with circulating-water warming and core temperature increased approximately 30% faster. Consistent with faster rewarming, our figure 5 shows that the core-to-peripheral tissue temperature gradient was slightly less with circulating water. In both cases, core warming resulted from the combination of metabolic heat production and the insulating effects of warmed peripheral tissues. Such indirect core warming is a well-established phenomenon3and is probably the mechanism by which nearly all clinical warming systems augment core temperature.
We do not understand how Dr. English estimates the core-to-peripheral tissue temperature gradient from core temperature and the change in peripheral tissue temperature without knowing the initial peripheral tissue temperature. Our figure 5 is correct and shows that peripheral tissue temperatures were roughly 0.8°C less than core temperature throughout warming.
Dr. English’s assertion that “above the body, the change in heat content/warmed area was less with air than with water” is curious because it is impossible to attribute observed changes in peripheral tissue heat content to anterior versus posterior warming. Heat transfer rates should therefore be measured with thermal flux transducers rather than estimated from tissue heat content. Despite Dr. English’s assertion to the contrary, this is exactly what we report; anterior heat flux was identical with each tested warmer.4
Dr. English has reported results in terms of h , which is the heat flux divided by the warmer-to-skin temperature difference. As illustrated by his own example, this is a suboptimal measure because the tissue-temperature difference is a function of the heater and tissue characteristics and therefore varies markedly over time. Actual heat transfer rates, the clinically relevant measures of heater efficacy, differ less than might be expected based on h .
We are mystified by Dr. English’s assertion that “the change in heat content/warmed area for water was 1.25 times that of air, not 1.5 times, as the ratio of their h values suggests.” We did not report h or the results that would be necessary to calculate this value. Unlike forced-air warming, the circulating-water system we tested includes a servocontrol algorithm. Because the system was set to 37°C, heating intensity presumably decreased as core temperature approached 37°C. Initial rewarming rates are thus a better indicator of system capability than rewarming rates near normothermia.
We appreciate Dr. English’s assessment that our investigation4“was a sophisticated study of thermoregulatory physiology.” We note, however, that our volunteers were kept anesthetized throughout the protocol specifically to minimize thermoregulatory responses and allow us to isolate heat transfer characteristics that must be known to safely and effectively exploit the full potential of skin-warming systems. Specifically, we evaluated and reported cutaneous heat transfer, regional body heat content, and core rewarming rates—the clinically relevant system characteristics.
* University of Berne, Inselspital, Berne, Switzerland; Outcomes Research™ Institute, University of Louisville, Louisville, Kentucky. email@example.com