Thermoregulation Flashcards
Explain the mass balance characteristics of the control of internal body temperature
the internal body temperature remains stable despite wide changes in atmospheric temperature because homeostatic mechanisms match heat production & loss (mass balance).
four modes of heat transfer from the skin to the environment
Radiation, conduction, convection, & evaporation.
Explain the feedback control of internal body temperature
Up to 44 - 46C, the firing rate of the warmth receptor fibers increases. As the temperature decreases below the set point of 37C, the firing rate of the cold receptor fibers increases. These action potentials, firing at temperature-dependent frequencies, travel up afferent fibers via the spinal cord to the hypothalamic regulatory center.
The hypothalamic center integrates thermal information from the skin and central temperature receptors, and directs changes in efferent activity resulting in vasoconstriction to conserve heat or shivering to produce more heat, or vasodilation and sweating to increase loss of heat.
A decrease in body temperature activates cold receptors in the skin to increase their firing rate. This is carried to the hypothalamic integrating center (set point comparator) by afferent nerves which alter their rate of firing. Efferent sympathetic nerves are activated to decrease heat loss and increase heat production.
If the preoptic area of the hypothalamus is heated in experimental subjects, heat sensitive neurons/receptors in the hypothalamus are activated, the skin sweats profusely and the skin vessels vasodilate.
List the short-term responses to heat and cold, as well as adaptations to warm and cold environments
The sympathetic nervous system (SNS) supplying the skin vasculature is inhibited (less vasoconstriction=vasodilation) when the body temperature rises, and activated (vasoconstriction) when the body temperature falls.
Acclimatization to hot weather (1-6 weeks) involves a change in the sweat glands to increase sweating capability (up to 2-3L/hr).
With acclimatization, there is also a DECREASE in the LOSS of NaCl in the sweat to CONSERVE body salt. This is mainly due to ALDOSTERONE secretion from the adrenal cortex.
frostbite
freezing of surface areas. The most vulnerable areas are the extremities. Necrotic damage can occur and is followed by gangrene. Cold induced vasodilatation is the last response.
heat exhaustion
failiure of cardiovascular homeostasis in a hot enviornment. There is hypovulemia due to vasodialation & sweating. Collapse may occur due to blood pooling in the limbs. Treat with rehydration in a cool enviornment.
heatstroke
Elevated core temperature with neurological disturbances. Sweating ceases in patients with true heatstroke, most likely because the high temperature itself causes damage to anterior hypothalamic-preoptic area. Either environmental stress overwhelms an impaired thermoregulatory system or there is too high of metabolic heat production. Same treatment as heat exhaustion.
Patients with heatstroke commonly exhibit tachypnea and hyperventilation caused by direct central nervous system stimulation, acidosis, or hypoxia. The blood vessels in the skin are vasodilated, and the skin is warm.
Radiation
transfers heat as electromagnetic waves between objects that are not in contact— the rate of temperature transfer is proportional to the temperature difference between the body surface and the environment.
At rest indoors ~60% of body heat is lost by radiation as infrared rays–most important heat loss mechanism @ rest.
Conduction
is intermolecular thermal heat transfer between solid objects in direct contact (e.g., lying on hot sand causes a body to gain heat by conduction, whereas placing an ice pack on a sore muscle causes conductive heat loss). Normally, heat exchange by conduction is minimal in a person wearing shoes and clothing = conduction is very low amount of heat transfer.
Convection
is loss or gain of heat by movement of air or water over the body. Because heat rises, air carries heat away from the body by convection (this is why a fan keeps one cool on a hot day—the ―wind chill‖ factor). A body immersed in water exchanges most heat by convection. Around 15-20%.
Most heat is transferred from the core to the skin by convection in the blood, where it is then lost to the air & surroundings.
Evaporation
of water from the skin and respiratory tract can carry large amounts of heat generated by the body because of the amount of heat required to transform water from liquid to gas phase (insensible loss is ~650ml/day) = 20%. Air circulation improves the rate of evaporation of sweat from skin, and high humidity makes it less effective.
Evaporative losses from the surface of the skin by
sweating normally dissipate nearly all of the heat produced during exercise. However, inadequate heat loss upon excessive heat exposure can lead to heat exhaustion, in which the body core temperature rises to 39oC (102.2°F), or in severe cases to heat stroke when the core temperature reaches 41oC (105.8°F) or higher.
If evaporation cannot occur or is difficult because the air is saturated with water vapor, sweating is not an effective means of heat loss.
During exercise about almost all of body heat is removed by sweat evaporation (in low humidity).
How does the feedback control of internal body temperature change with fever versus exercise
See pg. 51
At the onset of exercise, the rate of heat production increases in proportion to the exercise intensity and exceeds the current rate of heat dissipation. This causes heat storage and a rise in core temperature. Hypothalamic thermoreceptors sense the increase in core temperature. The hypothalmic integrator/comparator detects an error signal and activates heat dissipation effectors. After the beginning of exercise, evaporative heat loss from sweating is normally a much more important means of eliminating heat than convective or radiative loss of heat.
Fever is an increase in temperature set point and core temperature, and is usually due to a pathological process such as infection by a pyrogen. When the set point is raised, the mechanisms for raising body temperature are engaged, thereby enhancing heat conservation and heat production. When pyrogens cross the blood brain barrier, they increase the set point (endogenous pyrogens are sensed by hypothalamic control neurons, possibly via local release of prostaglandins–asprin & acetominophen inhibit prostoglandin synthesis & reduces fever). Since the set point is raised, the body thinks that is is cold so fever is really an adjustment (it stays only as long as the pyrogen is present). The person develops chills, and effectors that elevate body temp are activated. Vasoconstriction conserves heat by reducing blood flow to the skin; the skin feels cold; shivering generates heat; curling up conserves heat. When the pyrogen is removed, the set point returns to normal. The lower set point activates mechanisms to dissipate heat leading to hot skin, intense sweating, and vasodilation to counteract the higher body temp.
See pg. 51
Increased body temperature
engages skin vasodilation, sweating, and decreased heat production to reduce body heat.
Decreased body temperature
engages skin vasoconstriction, piloerection (important in lower animals, not humans), and thermogenesis/heat production (shivering, sympathetic/chemical excitation, thyroid hormone production).
Sympathetic/chemical excitation involving epinephrine and norepinephrine may be relevant in infants.
Malignant hyperthermia
A massive increase in metabolic rate, oxygen consumption, & heat production in skeletal muscle can be lethal. Can occur due to genetic defect by mutation of the ryanodine receptor or inhalation of anaesthetics.
