Physiology, Heat Loss

Issues of Concern

Clinical Manifestations of Insufficient Heat Loss[2]

Heat Stroke:

• Central nervous system dysfunction
• Lack of sweat
• Core body temperature above 40 C
• Skin: Red, hot, dry
• Nausea/vomiting
• Rapid, strong pulse
• Heat syncope

Heat Exhaustion:

• Dizzy or possibly syncope
• Core body temperature between 37 to 40°C
• Excessive sweating
• Skin: Cool, pale, clammy
• Nausea/vomiting
• Rapid, weak pulse
• Heat-associated muscle cramping

Clinical Manifestation of Excessive Heat Loss[3]

Hypothermia:

• Core body temperature below 35°C
• Severe hypothermia: less than 28°C
• Altered mental status
• Loss of consciousness
• Malignant cardiac arrhythmias
• Inability to shiver

 Other Causes of Impaired Heat Loss:

 Hypohydrotic Ectodermal Dysplasia[4]

• Congenital absence or malfunctioning of sweat glands
• Reduced tolerance of high temperatures that require evaporative cooling
• Rely on environmental modifications to control heat exposure

Cellular Level

Heat is generated on a cellular level by metabolism. The basal metabolic rate increases by thyroid hormone, sympathetic stimulation, muscle activity, and chemical activity within cells. When cell metabolism is high, there is a great demand for ATP. During hydrolysis of high energy ATP bonds, part of the derived energy dissipates as heat.[5] To illustrate the effect of environmental temperature on cellular function, in a state of hypothermia (core body temperature lower than 35 degrees C), the rate of cellular heat production decreases by 2-fold per 10 degrees F reduction in body temperature.[6] In hyperthermia, protein denaturation occurs resulting in impaired cellular function and release of inflammatory mediators increases gastrointestinal permeability allowing a release of endotoxins into circulation. Heat loss and production must remain balanced to avoid this pathophysiology. The rate of heat loss is determined by the rate of heat conduction from body tissues to the skin via the blood and the rate of heat transfer from the skin to the surroundings by one of the four mechanisms of heat loss.

Development

Heat Loss in the Newborn[7][8]

Minimizing heat loss in the newborn is central to reducing morbidity and mortality in the neonatal period and is one of the most critical strategies for the optimal development of the infant. Several characteristics of newborn physiology contribute to their increased risk of heat loss. The smaller the size of an infant, the larger the surface area-to-body mass ratio which promotes greater heat loss via conduction. Newborns also have less subcutaneous fat to provide insulation and more body water content. The blood flow in newborns is also altered resulting in peripheral cyanosis. Finally, newborns are unable to activate their muscles to shiver and must rely on the non-shivering thermogenesis in brown fat.

The most significant heat loss occurs immediately after birth. The greatest source of heat loss at birth is when the amniotic fluid evaporates from the skin. Conductive heat loss occurs when the baby gets placed on a cooler surface like a scale or table. The baby can reflexively curl in the fetal position to reduce the surface area in contact with the cooler surface to minimize heat loss. Air flow through the room cases convective heat loss. Radiation is the most significant source of heat loss after birth and throughout the rest of development. If proper measures are not taken to mitigate heat loss immediately after birth, the temperature of the newborn could drop by 2 to 4 degrees C within the first 20 minutes.

Organ Systems Involved

The major organ involved in heat loss is the skin which is responsible for approximately 90% of heat loss. Skin is the largest organ in the human body. Thermoreceptors in the skin consist of free nerve endings with sensory axons that transmit information to the spinal cord. Different types of cation channels activate within nerves depending on the temperature. For example, painfully cold temperatures activate TRPA1 whereas burning pain activates TRPV1/2 channels.[9] The sensory axons are myelinated A-delta fibers for cold temperatures or unmyelinated C-fibers for warm temperatures. Extremely hot temperatures activate nociceptors rather than thermoreceptors. The C-fibers ensure a quick reflex arc in the spinal cord activating a behavioral withdrawal response from the noxious stimulus. The spinal cord sends the temperature signal to the preoptic anterior hypothalamus which is the thermoregulatory center of the brain. Projections from the hypothalamus go to the ventromedial thalamic nucleus and finally to the cortex for conscious perception.[10][11]

Behavior is the most effective response to changes in temperature. Behavioral changes initiated by excessive heat loss include adding layers of clothing, curling up to minimize exposed surface area, or standing near a heat source to enhance heat gain via radiation. To minimize heat production if overheated, the behavioral response would be to reduce physical activity and enhance heat loss by convection by standing near a fan.[12]

Other changes made by the hypothalamic efferent output include adjusting sympathetic outflow through the intermediolateral column to subcutaneous vessels. There is decreased sympathetic outflow to vessels causing vasodilation to avoid heat loss. Vasodilation results in the opening of arterioles and arteriovenous anastomoses which markedly increases blood flow to facilitate a greater transfer of heat to the skin surface. The thermal gradient between the relatively cooler environment drives radiation of heat from the skin surface into the surrounding air. Additionally, a reduced sympathetic outflow through the reticular formation to the ventral horn of the spinal cord and skeletal muscle results in shutting down thermogenesis by shivering. Sweat glands have muscarinic receptors activated by acetylcholine to enhance evaporative heat loss and other thermogenic signalers like thyroid hormone, and adrenal release of catecholamines will decrease to reduce metabolic activity.[13][14]

Function

Humans are warm-blooded animals which means we can alter our metabolism to maintain equal heat production and heat loss; this is clinically significant because all organ systems depend on a stable core body temperature to operate well on a cellular level. At extremes of temperature, enzyme efficiency and diffusion capacity decrease which reduces cellular energy availability and membrane ion fluxes that drive cellular activity. Clinically this manifests as a reduced level of consciousness and behavioral disorganization.[5][15]

Environmental and hormonal influences exist that cause less extreme temperature variation such as circadian rhythm causing diurnal variation with the lowest temperature being between 3:00 and 6:00 AM and peak temperature 12 hours later. Children have a greater diurnal variation than adults.[16][17] During the estrogen phase of the menstrual cycle, the core temperature falls, whereas progesterone increases body temperature. The body can handle these physiologic variations and more extreme variations of temperature due to autonomic thermoregulation of the core body temperature. The core body temperature remains constant whereas the outer body temperature varies with the environment. The shell consists of the skin and subcutaneous fat. In a warm environment, the shell is closer to the core temperature. In a cold environment, there is a larger temperature gradient between the shell and the core, so the shell “thickens.” The thickness of the shell is the result of the proximity of subcutaneous blood flow to the surface. In a cold environment, the vessels vasoconstrict, so the blood flow to the skin reduces which allows it to cool to the ambient temperature. As the temperature of the shell equilibrates with the environmental temperature, the thermal gradient is diminished thus preventing heat loss. The thickness, or insulating capacity, of the shell, is varied based on the heat exchange needs of the body since the skin is the main heat exchanger.[18][19]

Mechanism

Heat loss occurs through four mechanisms: evaporation, convection, conduction, and radiation. The heat generated by the core body tissues travels to the vasodilated skin surface capillaries, and the temperature gradient between the limbs and environment drives transfer of heat to the surrounding air, mainly by radiation. Radiation is the most significant source accounting for approximately 60% of heat loss. Core body tissues transfer heat in subcutaneous blood vessels which emit infrared rays from the skin surface to lose heat by radiation. Evaporation is the next major source accounting for about 22% of heat loss. Water vaporization requires energy and consumes heat facilitating heat loss. This process occurs even when the body is not sweating. The body depends on evaporation for heat dissipation when the environmental temperature is warmer than the skin or when convection and radiation are insufficient. Finally, conduction and convection contribute roughly 15% of heat loss. Conduction is the loss of molecular kinetic energy in the form of heat from the skin to the surroundings. Different mediums transfer heat by conduction at different rates. For example, the conductive transfer of water is 100 times that of air. Radiation and conduction can facilitate heat loss as long as skin temperature is greater than the surroundings. At extremely high skin temperature (over 43°C), evaporation is the only mechanism of heat dissipation.[5]

Pathophysiology

Diminished Thermoregulatory Capacity of the Elderly[20]

During the aging process, the sympathetic response to a cold environment is blunted reducing the discharge rate of sympathetic nerves to the cutaneous vasculature. Additionally, due to the increase in reactive oxygen species (ROS) there is a decrease in availability of BH, which is an essential co-factor in the production of norepinephrine, so the sympathetic neurotransmitter itself is in shorter supply. Vasodilatory response to heat is also impaired due to ROS which may limit nitric oxide synthase function. The elderly are therefore at risk for both hypothermia and hyperthermia.

Considering that thermoregulation involves more than the adaptations of cutaneous blood flow to changing ambient temperatures, it is essential to consider the other physiologic limitations of the elderly that place them at risk for insufficient thermoregulation. The expected increase in cardiac output in response to heat has decreased in the elderly due to reduced sensitivity of the beta adrenoreceptors in the heart. Less renal and splanchnic blood flow is redirected to the skin as well due to the reduced sympathetic tone. The dermal thinning that occurs with age reduces vascularization and limits the efficacy of the skin as an insulator or heat exchanger. Sweat glands are less productive, and the morbidity of dehydration exacerbates this problem in the elderly population. Thermogenesis has reduced due to reduced skeletal muscle mass involved in shivering, atrophy of brown tissue mass, endocrine deficiencies, and cardiopulmonary problems restricting the available oxygen for consumption in heat production. Peripheral nerve fiber loss and lower conduction velocity contribute to reduced thermal sensitivity that develops in a distal to proximal fashion. For uncertain reasons, behavioral thermoregulation seems to be impaired in the elderly as well, and they tend to favor warmer environments.

The average difference between the core body temperature of a young adult and a geriatric adult is approximately 0.4°C; this is an important clinical consideration when evaluating an older adult for fever since their baseline temperature is lower. One study of nursing home patients found an increase in the incidence of infectious fever in the elderly when the fever threshold was lowered to 37.2 degrees C/99 degrees F, or 1.1 degrees C/2 degrees F above baseline. It is therefore clinically relevant to keep in mind the physiologic differences in thermoregulation between the elderly and young adults patient populations.

Heat acclimatization[21]

Humans who live in tropical regions demonstrate a higher heat tolerance than those living in more temperate regions. Their core body temperature is similar, but their threshold for a thermoregulatory response to heat is about 0.5°C higher; this is due to the adaptation of the sweat glands. Heat loss by evaporation gradually increases, and so does aldosterone secretion. The result is an increased level of less salty sweat and resultant thirst from the increased NaCl plasma concentration.

Clinical Significance

Perioperative Hypothermia[22][21]

General and regional anesthesia produce hypothermia which is the most common perioperative thermal disturbance. Volatile anesthetics promote heat loss through vasodilation and direct impairment of hypothalamic thermoregulation. Opioids contribute by depressing sympathetic tone and therefore reducing the ability to thermoregulate via vasoconstriction. Hypothalamic depression results in an increased interthreshold range between the temperatures at which the thermoregulatory system induces a response to cold or heat. An increased interthreshold range results in a reduced ability to adjust to the increased heat loss from drug-induced vasodilation. Due to the effect of hypothermia on drug metabolism, an important clinical consideration is the reduction of the minimum alveolar concentration of the volatile anesthetics by 5% for each degree C below normal.

Three phases of temperature decline following induction of general anesthesia:

• Phase 1
  • Within the first 30 minutes
  • Redistribution of body heat to the skin from the core
  • The greatest decline in temperature mediated by radiation
• Phase 2
  • Approximately 1 hour
  • Core temperature decreases linearly at a slower rate
• Phase 3
  • Approximately 3 to 5 hours
  • Heat loss equals heat production
  • Thermoregulation restored

Due to the previously mentioned consequences of hypothermia, precautions in the perioperative setting against heat loss are essential. These include temperature monitoring, prewarming, maintaining an OR temperature of lower than 24 degrees C during induction, patient positioning with extremities tucked when possible, and warming of IV fluids.

Heat Stroke[21]

Heat stroke is an emergent clinical condition that requires immediate removal of the patient from the heat, ATLS protocol activation, and implementation of cooling measures while awaiting transportation. External cooling methods include evaporative cooling with misting water on the patient’s skin while fanning warm air. Immersion in an ice bath or application of ice packs on the axilla, groin, neck, and head are also effective. Considerations when performing immersive cooling include induction of shivering when the skin cools below 30 C and difficulty in accessing the patient if the cold water induces reflexive bradycardia. Internal cooling methods include gastric, bladder, and rectal lavage or even cardiopulmonary bypass. Cooling measures should terminate when the core temperature is 38 degrees C.

The pathophysiology of heatstroke involves the insufficiency of the body’s heat loss mechanisms. At extremes of heat, the body relies on evaporative cooling because an insufficient thermal gradient exists between the skin and environment to facilitate conduction or radiation. However, if the humidity is also extremely high, evaporation is also limited. The amount of work exerted in a given environment is another contributor to heat stroke risk. For example, when a person is doing heavy work, the environmental temperature can be as low as 29.4 degrees C to cause heat stroke. Therefore, heat stroke results from an unfavorable balance of environmental temperature, humidity, and level of physical work. One can avoid heat stroke with appropriate precautions and care is necessary with exposure to hotter climates.