Get PulmCCM’s Weekly Email Update
Stay up-to-date in pulmonary and critical care. No spam.
“Study hard what interests you the most in the most undisciplined, irreverent and original manner possible.”
Heat-related illness is a very common form of environmental injury. Like many insults, it may be modelled by ‘diathesis-stress.’ In other words, heat-related illness materializes at the cross-roads of inherent patient characteristics [e.g., age, co-morbidities, genotype, that is, one’s diathesis] and external stress [e.g., ambient temperature, humidity, exertion]. Thus, those with multiple, chronic co-morbidities, the elderly and children may be more susceptible because they are less able to dissipate heat and maintain oral hydration.
Ultimately, heat-related illness evolves as the body accrues positive heat balance as a function of the law of energy conservation. While the body has multiple thermoregulatory, homeostatic mechanisms to maintain constant internal temperature, these can be overwhelmed leading to many of the common, non-specific symptoms of heat-related illness: malaise, nausea, dizziness, irritability. With heat exhaustion, this is uncommonly accompanied by an internal temperature more than 40 degrees Celsius, but may be significantly higher in heatstroke – as considered later.
But how, specifically, does the body amass positive heat balance? What are the compensatory mechanisms to maintain neutral heat balance? How does heat-related illness [e.g., heat exhaustion and heatstroke] evolve and what are some of the cardiovascular consequences?
Energy and temperature
First, the average tissue specific heat is 3.47 kilojoule per kilogram x degree Celsius. What does this mean? This piece of physiological trivia helps us relate the amount of heat energy absorbed by the body to the average rise in body tissue temperature – how ‘heat energy’ is measured clinically. So, if the amount of heat energy and the mass of tissue are both known, then we can calculate the rise in temperature.
What’s an example of heat energy experienced by the body? If an 85 kg human were to run the pace of a 6-minute mile for 30 minutes, this person would burn about 700 Calories or 167 kilojoules [i.e., 1 Calorie = 4.2 kJ]. So, if all 167 kJ were absorbed by this running human, without any heat dissipation, then average body temperature would rise by 0.7 degrees Celsius [e.g., 36.3 to 37.0 Celsius or 97.3 to 98.6 degrees Fahrenheit] based on the average tissue specific heat noted above.
The aforementioned example also underscores the difference between total metabolic rate and metabolic heat production in the body. The amount of heat production can be determined by taking the entire metabolic rate and subtracting from it the external work performed. Interestingly, the human body is quite inefficient at performing external work, so the vast majority [i.e., greater than 80%] of the total metabolic rate is elaborated as metabolic heat. In fact, running approaches 0% external efficiency! Thus, in the example above, the rise in total metabolic rate with running is expressed almost entirely as metabolic heat.
As above, while metabolic heat energy is elaborated into the body with rising metabolic rate, the body has a number of mechanisms by which heat energy is dissipated into the atmosphere; this prevents heat storage and maintains constant body temperature.
If we abbreviate heat storage as S, then it can be expressed as a balance between the addition of heat as per above [i.e., metabolic rate, less external work] and the subtraction of heat by dry transfer, evaporative heat transfer [e.g., sweating] and heat lost via respiration.
S = [(Metabolic rate – external work) – (transferdry + transferevaporative + transferrespiratory)]
If S is zero, then there is balanced heat exchange and body temperature is constant. At resting room temperature, metabolic heat production is dissipated primarily by dry heat transfer. However, in the example of the running individual above, roughly 167 kJ over 30 minutes of heat is added – assuming most of the metabolic rate is converted to metabolic heat [i.e., low external work efficiency]. If heat transfer processes cannot dissipate those 167 kJ over the same time period, then S > 0, and the patient is moving towards heat exhaustion and heatstroke. Note that all of the above terms are expressed in energy over time [e.g., Watts] and with respect to the body. How might this equation explain the development of heat-related illnesses, that is, S > zero?
Dry transfer has 3 basic components: conduction, convection and radiation. Thinking about how this equation explains the evolution of heat exhaustion requires conceptualizing negative heat transfer, that is, mechanisms that increase S above zero.
Conductive heat transfer occurs by direct contact; therefore, negative conductive heat transfer is an uncommon cause of heat-related illness unless a person is found down on a hot surface [e.g., asphalt]. Convection is heat transfer by liquid moving over a surface. For a human, it is proportional to the temperature gradient between the atmosphere and the skin or clothing surface as well as the velocity of the liquid [e.g., air] moving heat away. Negative convective heat transfer [i.e., rising S above], therefore, occurs when there is little air movement, when the ambient temperature is greater than or equal to the skin or clothing surface temperature and when homeostatic mechanisms prevent the skin from warming. Because the gradient is relative to outer clothing temperature, heavy, insulated materials block convective losses and raise the risk of heat storage over time.
Finally, radiant heat transfer is an electromagnetic energy transfer between warm and cool bodies. Solar radiation is the most common form of radiant heat exposure that raises S. Like convection, this transfer is proportional to the gradient between the mean, ambient radiant temperature and the body surface. Note that humans are also a source of radiant heat, which can be visualized with infrared technology.
Heat transfer by evaporation is driven by the gradient between ambient humidity and the surface of the skin [e.g., sweating]. Evaporative transfer is therefore related to body surface area and the fraction of the area that is covered in sweat – normally this is about 6% but can increase to 85% in non-acclimatized individuals. Evaporative transfer also has a convective component and is a relatively inefficient means of heat transfer despite being capable of eliminating roughly 140 – 150 kJ per hour under optimal conditions. Sweating is usually engaged once dry losses cannot keep pace with heat production. Sweating is clearly an adaptive mechanism meant to push S downwards and negative evaporative loss [i.e., condensation on the skin] would contribute to heat-related illness only in special conditions such as a steam room.
Heat transfer via respiration is a special mechanism made up of both dry and evaporative transfer described above. The convective component relates to the specific heat capacity of the inspired gas and the minute ventilation moving said gas in and out of the respiratory tree; therefore, minute ventilation plays some role in total body heat transfer with the atmosphere. Similarly, evaporative, respiratory heat transfer occurs as a function of minute ventilation and the humidity difference between the inspired gas and the upper airways. As above, respiratory heat transfer normally pushes S downwards and clinical scenarios in which respiratory transfer contributes to heat-related illness would require very hot and humid external conditions interacting with high minute ventilation.
Why first principles?
On first blush, the heat balance equation described above appears unnecessarily complicated for clinical medicine. Nevertheless, thinking about heat transfer with an objective framework of independent and dependent variables conceptualizes patients at risk for heat-related illness and especially prevention and treatment. In other words, how does the clinician lessen heat storage over time [i.e., S < 0] in patients with heat exhaustion and heatstroke?