Patty Pate, CVT, VTS(ECC), CFE
Ethos Veterinary Health, Woburn, MA
Posted on 2018-05-15 in Emergency & Critical Care.
The body possesses numerous homeostatic abilities in order to maintain an equilibrium. Thermoregulation is just one of the amazing abilities that the canine and feline possess to maintain a core body temperature of 100 – 102.5°F. Though, in the face of disease, thermoregulation may be adversely affected. Patients may become hyperthermic or hypothermic given specific disease processes or as a result to medications used to treat disease. Knowing why the body is altering a patient’s core temperature is essential for veterinary technicians to understand so that they may provide the best care and support needed for their patients.
Thermoregulation is largely controlled by the anterior and preoptic nuclei in the hypothalamus. These areas contain thermoreceptors that can sense the temperature of the blood flowing through that area of the brain, as well as respond to temperature changes throughout the body. In turn, the hypothalamus can trigger mechanisms that will produce and conserve OR dissipate heat as needed.
Thermoregulation is a balance between heat production and heat loss. In cases where heat production and physiologic conservation outweighs that of the body’s ability to dissipate heat, the core body temperature will increase above normal, and the patient will become hyperthermic. The opposite is also true. If the body loses heat at a faster rate than can be produced, the core body temperature decreases, and the patient can become hypothermic.
Mechanisms of heat production
Heat is generated through metabolic and physiologic mechanisms in the body. Hormones such as thyroxine and epinephrine are released in response to the hypothalamus sensing a drop-in body temperature. These hormones serve to increase the metabolic rate of a patient thereby increasing heat production. Major organs in the abdomen are responsible for generating heat as they carry out normal functions. Muscles can also generate heat during exercise or as the patient begins to shiver in response to cold.
While heat production is essential, it is accompanied by physiologic mechanisms and behaviors targeted at conserving heat. As the hypothalamus senses a drop in skin temperature, the sympathetic nervous system is activated causing vasoconstriction. Patients experiencing hypothermia may seek out external heat sources, such as warm sunlight or a furnace, and curl up in a tight ball to conserve heat.
Mechanisms of heat loss
During hyperthermic states, patients will exhibit physiologic changes such as peripheral vasodilation and panting or cooling behaviors such as seeking out cold surfaces to lay on. Patients can dissipate heat through several ways: radiation, convection, conduction, and evaporation. Radiant heat loss happens when patients lose heat into through infrared rays. Heat is lost to cooler objects that the patient is not touching directly. Convection heat occurs as heat is lost into the cooler atmosphere around the patient (blowing air over the patient from a fan). Conduction heat loss happens through the transfer of heat onto cooler surfaces in direct contact with the patient (metal cage floor). Evaporative heat loss occurs through sweating or panting as the moisture accumulating on the surface of the patient’s skin or mucous membranes heats to a point that it is converted to a gas.
Hyperthermia vs. fever
Hyperthermia is defined as a core body temperature above normal values (>102.5°F in non-stressed canines and felines). It can result from inadequate heat dissipation. Heat stroke is a common condition caused by inadequate heat dissipation. Hyperthermia can also be exercise induced, as seen with excessive exercise, hypocalcemic tetany, and seizures. It may be pathologic in nature as seen with malignant hyperthermia, neoplasia, or hypermetabolic disorders, or hyperthermia can be a true fever.
Fevers are classified as a physiologic response to pyrogens. Pyrogens are substances, either exogenous or endogenous, that induce a fever. Exogenous pyrogens have no direct effect on the thermoregulatory set-point of the hypothalamus. Exogenous pyrogens, however, trigger endogenous pyrogens, known as cytokines, throughout the body. These proteins travel to the hypothalamus causing a release of prostaglandins and increase the thermoregulatory set-point, resulting in heat producing and heat-conserving mechanisms to be triggered. The result is a rise in core body temperature.
Fevers can be a patient’s natural defense against pathogens. The increase in body temperature decreases morbidity and mortality as viruses are unable to replicate in warmer environments. Bacterial infections can also be minimized as fevers reduce their ability to utilize iron essential for replication. Interfering with the body’s natural defenses against exogenous pyrogens can only lead to increased morbidity and mortality of the patient.
Hyperthermia can have deleterious effects on a patient. An increase in body temperature will result in increased metabolic rates and oxygen consumption. Hyperthermia also leads to an increase in caloric needs of the body as reserves are utilized in response to increasing metabolic rates. In addition to increased caloric needs, water requirements are increased by 7% for every degree above normal. Many times the requirements exceed the patient’s water consumption leading to dehydration. More serious conditions can ensue at higher temperatures (>107°F): hyperkalemia, hypocalcemia, myoglobinemia, myoglobinuria, rhabdomyolysis and disseminated intravascular coagulopathy to name a few.
Hypothermia is defined as a core body temperature below normal values (<100°F). It can be classified as either a primary or secondary condition. Primary hypothermia is caused by prolonged exposure to the cold. Secondary hypothermia can result from several different causes, including shock, disease, trauma, surgical exposure, and anesthesia or other drug-related causes. The body’s willingness to tolerate hypothermia is dependent on the cause. Patients experiencing a primary hypothermia have shown to be more resistant to the deleterious effects of hypothermia, while patients suffering from secondary hypothermia have little tolerance and clinical manifestations of hypothermia can be noted in these patients at higher temperatures. (Table 1) A number of deleterious side effects affecting the cardiovascular, respiratory, renal, hepatic, immune and coagulation systems have been associated with prolonged and severe hypothermia.
Caring for patients with thermoregulatory derangements
Treatment of hyper- or hypothermic patients should be focused on the primary disease process contributing to the derangement. Patient’s may require additional nursing support allowing time for treatments take effect.
Active cooling of hyperthermic patients with a core body temperature greater than 105.7°F can be performed in order to accelerate heat dissipation mechanisms. Bathing patients in tepid water, placing ice packs on major vessels, and utilizing fans are all ways to actively cool patients externally. Patients should be cooled slowly, and active cooling should be removed once the patient reaches 103°F to avoid rebound hypothermia.
Mildly hypothermic patients should be supported in order to prevent any continued heat loss while their intrinsic mechanisms work to catch up. Wrapping them in warm blankets to conserve heat and ensuring that they are on warm, dry bedding is the first step in treating these patients. In cases of moderate to severe hypothermia, active warming can be initiated, with a focus on slowly warming the patient’s trunk of their extremities. Aggressively warming the patient’s extremities can lead to rewarming shock. This can happen when a patient’s extremities are rewarded too quickly causing vasodilation. This, in turn, will cause pooling of warmer blood from the core. The much cooler blood from the extremities is then carried to the heart causing hypotension and bradycardia. Focusing rewarming efforts on the trunk of the patient will allow the extremities to warm slowly through natural circulation.
Once a patient’s hyperthermia or hypothermia has been corrected, close monitoring should be performed to ensure that body’s hemostatic mechanisms have kicked back in and they are able to maintain their own normal body temperature. In some cases, such as malignant hyperthermia, patients will continue to exhibit thermoregulatory derangements and need continued support.
- Byers, CG. Cold Critters: Understanding hypothermia. Veterinary Medicine. February 2012.
- Byers, CG. Cold Critters: Assessing, preventing, and treating hypothermia. Veterinary Medicine. February 2012.
- Guyten, AC & Hall, JE. Body Temperature, Temperature Regulation, and Fever, Textbook of Medical Physiology, 11th Edition. Philadelphia, PA: Elsevier, Inc.; 2006: 889-901.
- Miller, JB. Hyperthermia and Fever, In: Silverstein, DC & Hopper, K (Eds), Small Animal Critical Care Medicine. St. Louis, MO: Elsevier, Inc.; 2015: 21-26.
- Powell, LL. Heatstroke. Clinicians Brief. August 2008: 13-16.
- Todd, J & Powell, LL. Hypothermia, In: Silverstein, DC & Hopper, K (Eds), Small Animal Critical Care Medicine. St. Louis, MO: Elsevier, Inc.; 2015: 720-722.
About the author
Patty Pate, CVT, VTS (ECC), CFE has nearly 20 years’ experience in the veterinary field with the last 16 years focused on emergency and critical care working at Massachusetts Veterinary Referral Hospital, Bulger Veterinary Hospital and Port City Veterinary Referral Hospital. In her current role of Technician Clinical Educator for Ethos Veterinary Health (East Region) Patty provides educational opportunities to 400 veterinary technicians, was instrumental in the development of the Ethos AVA Program and is a primary instructor for the program. Patty is the Secretary of the NHVTA and lectures frequently on emergency, critical care, and compassion fatigue.