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“I believe that the very process of looking can make a thing beautiful.”
With the basics of temperature, heat and heat transfer described previously, this section turns to some select physiological aspects of heat-related illness. While this is clearly a very broad topic with multiple, intersecting avenues of discussion, focus is placed on basic physiology, cardiovascular response, individuals at risk and how these factors relate back to the heat transfer equation. For more in depth reading on this topic, this review is an excellent primary source.
As described in the first portion of this primer, heat-related illness may be viewed as an interplay of diathesis and stress. Much of the physiology elaborated below describes phenotypes, or diatheses, at accentuated risk for a given heat stress. In a manner analogous to preload being matched by the Frank-Starling mechanism, one might think of heat stress as an energetic preload that must be met by mechanisms needed to ‘unload’ heat energy from the body. When there is mismatch between heat loading and unloading in a given patient, the risk of heat-related illness rises; per the heat transfer equation, this is realized with S > 0.
Given that convective transfer of heat from the body requires a ‘counter-current exchange’ from flowing cutaneous blood to moving ambient air, diminished perfusion of the skin retains heat. Thus, any insult to the cardiovascular system – whether acute or chronic – retards heat exchange for any given metabolic state. The body then relies more upon evaporative transfer [e.g., sweating] which can enhance volume loss and, therefore, venous return and cardiac output; a vicious cycle is kindled.
Very generally in those without significant underlying cardiopulmonary disease, heat stress alone [i.e., without additional exercise] raises cardiac output primarily as a function of heart rate, though when coupled with orthostatic stress, stroke volume does fall. Heat stress alone also raises splanchnic vascular resistance and shifts blood away from this bed to the central venous circulation. A similar pattern is observed in the liver, spleen and thorax; cutaneous blood volume rises.
If significant aerobic exercise is added to the mix, then there are further increases in heart rate and stroke volume tends to rise initially as venous blood volume shunts to exercising muscles – vascular beds with diminished venous capacitance – augmenting venous return. With additional exercise, blood flow to muscles diminishes vascular resistance such that other vascular beds limit blood flow to compensate. Tissues that are ‘robbed’ of blood to pay the muscles include the kidneys, gut and skin. With heat stress alone, the skin first removes vasoconstriction and then later actively vasodilates. The addition of exercise blunts that latter mechanism; importantly, falling cutaneous blood flow retards heat exchange with the environment. As exercise continues to exhaustion, stroke volume begins to fall, especially if hydration is not maintained; falling cardiac output emphasizes diminishing cutaneous blood.
Recall from the first section that exercise increases metabolic heat to the body, thus external heat stress alone raises S by impairing heat loss mechanisms while additional metabolic work in hot surroundings accentuates S by adding metabolic heat to the body. Yet per the above, exercise to exhaustion also impairs heat loss mechanisms, especially via cutaneous blood flow deficiency. Accordingly, the aforementioned hemodynamic changes seen in the face of heat stress alone, or heat stress with exertion, lend themselves to the classification of severe heat-related illness [i.e., heatstroke] as ‘exertional’ or ‘classic,’ described later.
Highlight on hydration
The role of hydration is particularly important as evaporative heat transfer becomes a dominant mechanism for heat unloading. Notably, working in hot conditions can cause more than 3 litres of sweat production per hour! Even if one were to maintain oral hydration at a rate of 1.5 litres per hour, the sweating individual can quickly lose 2-5% of his or her body weight within hours. Such volume loss further degrades heat transfer because skin blood flow is impaired which, in turn, diminishes conductive and evaporative heat transfer as sweating diminishes with time. Further, volume depletion raises the core temperature at which adaptive heat transfer mechanisms are triggered and also heightens blood osmolality which blunts cutaneous vasodilation and the sweat response.
Patient risk factors
Increasing age is a clear risk factor for heat-related illnesses such as heat exhaustion and heatstroke. While there is no clear threshold above which this risk takes hold, it is probably somewhere in the 6th decade of life. Though this risk can span life from the mid-30s to, certainly, above 75 years of age.
The mechanisms by which age predisposes individuals to inadequate heat transfer are manifold, but may hinge upon diminished convective and evaporative losses. First, age blunts both the thirst response and recovery from dehydration, such that the attendant risks of volume depletion are more likely, as described above. In addition to the risk of hypovolemia, older individuals have weakened capacity to enhance skin blood flow and because sweating is impaired as a function of falling anti-cholinergic responsivity of the sweat glands [and potentially anti-cholinergic medications], older individuals are more susceptible to S > 0 conditions.
Reduced blood flow to the skin in elderly individuals is of multifaceted etiology and related to any or all of the following : 1. Impaired thermoregulatory vasodilatory response [independent of medications], 2. Structural changes in the cutaneous vasculature and 3. Diminished cardiovascular reserve and stroke volume. Older individuals have less blood flow redistribution from the splanchnic circulation with heat stress which may contribute to diminished venous return and therefore stroke volume.
In addition to age, autonomic dysfunction observed with chronic diabetes yields similar susceptibility to heat stress as both sweating and regional blood flow are dysregulated. Chronic hypertension and common anti-hypertensive medications are also known to attenuate heat exchange as is underlying cardiac dysfunction.
The cursory description of general hemodynamic changes consequent to both heat stress and heat stress coupled with exertion help explain the diathesis-stress of heat-related illness. In other words, older, medicated patients with perturbed hemodynamics and with limited cardiovascular reserve are disposed to adverse events during warm weather, even in the context of limited exertion.