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Treatment of hyperthermia: is assessment of cooling efficiency enough?

Exercise-induced heatstroke is a potentially dangerous consequence of performing physical activity in hot conditions. In order to avoid central nervous system dysfunction and organ damage or failure, the primary goal of treating the hyperthermic patient has traditionally been to lower core body temperature (T c) to below 40◦C as fast as possible (Casa et al. 2007). The effectiveness (i.e. cooling rate) of several cooling techniques has been studied extensively, with cold (ice) water immersion currently regarded as the most powerful method (Casa et al. 2007). Nevertheless, because cold water immersion facilities may be limited in the field setting, other treatment techniques, such as evaporative cooling, ice pack application or cold saline infusion methods, may be more suited (Leicht et al. 2009). Both experimental and empirical evidence would suggest that there is no perfect method, since most techniques are not likely to be well tolerated by the patient, with discomfort, excessive shivering (ice water immersion or ice pack application), as well as numbness and parasthesiae (infusion) sometimes being reported. Moreover, exposure to cold sometimes results in a ‘cold shock’ (Datta & Tipton, 2006), which has the potential to be a precursor to drowning or adverse pulmonary/cardiovascular problems. A ‘cold shock’ is generally accompanied by a sympathetic overdrive, responsible for inspiratory gasp, hyperventilation, hypocapnia, tachycardia, heart rhythm troubles, peripheral vasoconstriction and hypertension (Datta & Tipton, 2006). Given the possible adverse effects of cardiac electrical instability and increased sympathetic background during recovery from exercise (Billman, 2002), evaluation of the effects of cooling techniques on cardiovascular control and heart rhythm is important in susceptible individuals. As shown by Leicht et al. (2009) in this issue of Experimental Physiology, some cooling treatments applied to hyperthermic individuals can result in different levels of postexercise cardiovascular control. While cooling efficiency over a 40 min period after exercise-induced hyperthermia was similar amongst cold intravenous infusion, ice pack and fan misting conditions, parasympathetic reactivation, as evidenced by heart rate (HR) variability (HRV) analysis, was clearly different. This study is important because it suggests that the cooling rate per se is not the only important criterion to consider when assessing the appropriateness of a cooling strategy. While the exact contribution of T c to the autonomic response is unknown, it is worth noting that T c exerts a direct local (nonautonomic) effect on sino-atrial node firing rate (i.e. the higher the temperature, the higher the HR). However, it does not alter arterial baroreflex sensitivity (Gorman & Proppe, 1982). Thus, T c is likely to affect HR (i.e. autonomic tone), but not necessarily HRV (i.e. autonomic modulation). The consistent (linear) relationship between T c and HR, but not HRV, as shown by Leicht et al. (2009; Fig. 1, redrawn from Table 1 in their paper), confirms the view that differences in HRV are probably not directly related to internal body temperature. Even in the case of the saline infusion conditions, in which HR was shifted towards higher values due to the presumed reflex tachycardia and sustained sympathetic overactivity (see next paragraph), the relationship between HR and T c (identity line) remained similar to that observed for the other two conditions. Taken together, these data suggest that: (1) continuous HR monitoring could be used in the field as an easy and affordable means of assessing cooling efficiency (i.e. to follow T c); and (2) assessment of HRV might represent a valid tool to reveal perturbations in cardiovascular autonomic modulation caused by a given cooling strategy. This latter point could potentially identify a dangerously hidden situation in the patient (i.e. depressed parasympathetic background). An understanding of the physiological mechanisms which are likely to interfere and affect cardiovascular autonomic modulation during the postexercise period following exertional hyperthermia (Fig. 2) might assist us in choosing the most appropriate cooling strategy. Except for individual factors, such as low fitness levels or ageing, that are spontaneously associated with depressed/delayed parasympathetic reactivation, pressureand temperaturerelated inputs inherent with each cooling procedure are mostly responsible for the postexercise autonomic state. Since sympathetic activity is involved in the abolishment of postexercise hypotension, methods likely to accelerate plasma volume restoration, such as appropriate rehydration, might prevent excessive sympathetic stimulation. Methods expected to increase central venous pressure (CVP) modestly, such as saline infusion or application of hydrostatic pressure through water immersion, are likely to activate (cardiopulmonary/baro)receptors responsible for triggering parasympathetic and inhibiting sympathetic control of HR. Thus, interventions that increase CVP will, in turn, increase parasympathetic modulation. Likewise, techniques (e.g. air fanning) that effectively (but not excessively) stimulate cold receptors (i.e. skin, subcutaneous tissue and venous receptors) are also likely to increase parasympathetic modulation. When these types of stimuli are simultaneously applied, as is the case with cold (14◦C) water immersion, a cumulative effect is observed, so that HRV indices are greatly increased (Buchheit et al. 2009). Conversely, techniques that induce extreme changes in CVP, such as those observed with the cold saline infusion conditions in the study