Can recovery from mild hypothermia be accelerated so much by mechanically distending locally heated blood vessels?

The following is the abstract of the article discussed in the subsequent letter:

	ABSTRACT

Grahn, Dennis, John G. Brock-Utne, Donald E. Watenpaugh, and H. Craig Heller. Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand. J. Appl. Physiol. 85(5): 1643-1648, 1998.Peripheral vasoconstriction decreases thermal conductance of hypothermic individuals, making it difficult to transfer externally applied heat to the body core. We hypothesized that increasing blood flow to the skin of a hypothermic individual would enhance the transfer of exogenous heat to the body core, thereby increasing the rate of rewarming. External auditory meatus temperature (T_EAM) was monitored in hypothermic subjects during recovery from general anesthesia. In 10 subjects, heat (45-46°C, water-perfused blanket) was applied to a single forearm and hand that had been placed in a subatmospheric pressure environment (30 to 40 mmHg) to distend the blood vessels. Heat alone was applied to control subjects (n = 6). The application of subatmospheric pressure resulted in a 10-fold increase in rewarming rates as determined by changes in T_EAM [13.6 ± 2.1 (SE) °C/h in the experimental group vs. 1.4 ± 0.1°C/h in the control group; P < 0.001]. In the experimental subjects, the rate of change of T_EAM decreased sharply as T_EAM neared the normothermic range.

	LETTER

Can recovery from mild hypothermia be accelerated so much by mechanically distending locally heated blood vessels?

To the Editor: Grahn et al. (1) pose some puzzling questions in their claim to be able to accelerate rewarming from mild hypothermia by heating the forearm and hand under negative-pressure conditions.

They quote a mean maximum rate of change of external auditory meatus temperature (T_EAM; taken to represent "core" temperature) of 13.6°C/h, compared with 1.4°C/h for their control group (see Table 2 in Ref. 1). Using the latter number to (overgenerously) represent the contribution to rewarming from the rest of the body, this suggests that their new technique was capable of a maximum rate of rewarming of ~12°C/h, on average. For an average body mass of 70 kg and a specific heat of 3.5 kJ · kg¹ · K that represents 2,940 kJ/h, or 0.8 kW.

For a subject with an initial core temperature of 34°C, i.e., forearm arterial temperature of 34°C, and assuming a remarkably high warmed forearm venous temperature of 40°C, the arteriovenous temperature difference would be 6°C, i.e., a heat gain of 21 J/ml of blood. To achieve the above mean maximum rate of rewarming would require a unilateral forearm and hand blood flow of 800/21 = 38 ml/s, i.e., 2.3 1/min, close to one-half the expected total cardiac output.

Alternatively, assuming a unilateral forearm and hand blood flow of just 1 l/min, or 16.7 g/s, the venous blood would have to be warmed to 13.7°C higher than arterial, i.e., to 47.7°C.

These numbers become still more remarkable when it is noted that at least one subject (the experimental subject whose data are shown in Fig. 1 of the paper) achieved a rate of rise of T_EAM of 24°C/h. This would require a unilateral forearm and hand blood flow of 4.6 l/min with a venous temperature assumed to be 40°C, or a venous temperature of 61.4°C if the unilateral forearm and hand blood flow was only 1 l/min.

These expectations contrast with the body of literature, which shows that local application of negative pressure of greater absolute magnitude than 30 mmHg results in arteriolar constriction, in what is widely known as the venoarteriolar response (2-5).

I would be interested to know whether the authors can account for any of these apparent conflicts or have measured blood flow within the sealed chamber held at negative pressure.

	REFERENCES

1.   Grahn, D., J. G. Brock-Utne, D. E. Watenpaugh, and H. C. Heller. Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand. J. Appl. Physiol. 85: 1643-1648, 1998[Abstract/Free Full Text].

2.   Blair, D. A., W. E. Glover, A. D. M. Greenfield, and I. C. Roddie. The increase in tone in forearm resistance blood vessels exposed to increased transmural pressure. J. Physiol. (Lond.). 149: 614-625, 1959.

3.   Wolthius, R. A., S. A. Bergman, and A. E. Nicogossian. Physiological effects of locally applied reduced pressure in man. Physiol. Rev. 54: 566-595, 1974[Free Full Text].

4.   Henriksen, O. Local sympathetic reflex mechanism in regulation of blood flow in human subcutaneous adipose tissue. Acta Physiol. Scand. Suppl. 450: 1-48, 1977[Medline].

5.   Henriksen, O. Sympathetic reflex control of blood flow in human peripheral tissues. Acta Physiol. Scand. 143, Suppl. 603: 33-39, 1991[Medline].

E. Howard N. Oakley, Environmental Medicine Unit Institute of Naval Medicine Alverstoke, Gosport Hampshire PO12 2DL, United Kingdom

	REPLY

To the Editor: Oakley states that our paper poses "... some puzzling questions in [our] claim to be able to accelerate rewarming from mild hypothermia." We appreciate the opportunity to respond to these puzzling questions for two reasons. First, since we present not just a claim but hard data, it is nice to emphasize that when data do not fit a model it is time to reexamine the model. Second, a reexamination of the model Oakley uses in his letter illustrates a common but wrong assumption that frequently enters into considerations of whole body heat exchange.

Traditionally, it has been assumed (as Oakley assumes) that it is necessary to heat the entire body mass to treat hypothermia, and most technologies in use actually do that because they transfer heat to the body surface. In our paper, we report on a means of delivering heat preferentially to the body core of a hypothermic individual. Oakley's calculations illustrate the value of our rewarming methodology. If we had to heat the entire body mass, our method would not work. However, since we are able to deliver heat directly to the much smaller mass of the body core, our method does work as demonstrated.

At rest, 80% of the cardiac output is distributed to the body core. Therefore, any heat added to venous blood will preferentially affect the body core. The body core, however, is only ~10% of the total body mass. So, the mass of the body core of a 70-kg person would be 7 kg or less. Increasing the temperature of such a mass at a rate of 12°C/h requires only 294 kJ/h and not 2,940 kJ/h, as calculated by Oakley.

The blood flow requirements for rewarming the body core fall within a physiologically reasonable range. Increasing body core temperature at a rate of 12°C/h with an arteriovenous temperature gradient of 6°C would require a unilateral forearm and hand blood flow of 0.228 l/min, or ~5% of the total cardiac output. Subcutaneous heat-exchange vascular structures are localized in the nonhairy skin surfaces. With maximal vasodilation, blood flow through the heat-exchange vasculature can be as great as 30% of the total cardiac output. Assuming an equal distribution of blood flow through the various heat-exchange surfaces, the maximum blood flow capacity of a single heat-exchange vascular bed would be 6% of the total cardiac output (0.3 l/min). The blood flow capacity of the heat-exchange vasculature of a hand is greater than the blood flow required to achieve the results reported by us (1).

We are somewhat puzzled by the statement "these expectations contrast with the body of literature, which shows that local application of negative pressure ... , results in arteriolar constriction ..." Grahn et al. (1) cite the appropriate references to show that 1) blood vessels in the hand can be distended by exposing the distal portion of the limb to subatmospheric pressure, and 2) the application of heat to the distended tissues increases blood flow through the hand.

	REFERENCES

1.   Grahn, D., J. G. Brock-Utne, D. E. Watenpaugh, and H. C. Heller. Recovery from mild hypothermia can be accelerated by mechanically distending blood vessels in the hand. J. Appl. Physiol. 85: 1643-1648, 1998.

Dennis Grahn, H. Craig Heller, Department of Biological Sciences Stanford University Stanford, California 94305