There are four basic mechanisms of heat loss5:
Heat production due to the body's various metabolic processes is directly proportionate to body mass, and, thus, cutaneous heat loss is a function of body surface area.6 Small companion animals have higher surface-area-to-body-mass ratios that make them uniquely susceptible to heat loss. Additionally, cachectic, debilitated, immobile, and critically ill patients have impaired thermoregulatory capabilities and may not be able to retain or seek heat.
Receptors for cold and warm are distributed throughout the body. Cold signals traverse A-delta fibers, and signals from warmth receptors are relayed through C fibers.7 Processing thermoregulatory information occurs through three pathways7: afferent thermal sensing from the periphery, central regulation in the hypothalamus, and efferent responses.
Given these three pathways, peripheral body temperatures are constantly fluctuating while the posterior hypothalamic thermoregulatory center maintains a relatively constant core temperature.8 Cellular metabolism results in heat production by the body, and heat is lost from the body when core heat is transferred through variably conductive tissues to the skin and is subsequently lost to the environment.6 Specifically, heat is transferred from the body's core to the skin through a multitude of blood vessels, including venous plexuses and capillaries, with arteriovenous connections that are under the control of the autonomic nervous system.9,10 The rate of blood flow through these arteriovenous anastomoses varies depending on the degree of vasoconstriction or vasodilation desired.9,10 Increased blood flow leads to increased heat loss, whereas decreased blood flow results in core heat conservation.5
As core body temperature dips below 94 F (34.4 C), thermoregulation is impaired, and animals characteristically cease to shiver or seek heat.11 Peripheral vasodilation rather than vasoconstriction predominates, leading to continued core heat loss.12 Additionally, heat production decreases because of the decreased metabolic rate.4,6 Concurrently, severe hypothermia depresses the central nervous system, ultimately resulting in a hypothalamus that is less responsive to hypothermia.6 Indeed, when the body core temperature drops below 88 F (31.1 C), thermoregulation ceases.5
The prominence of the J wave is related to body temperature, and its genesis is related to dysfunction of the intramyocardial M cells.18 This dysfunction results from a voltage gradient between the epicardium and endocardium that, in turn, produces a prominent epicardial action potential notch.18 This abnormal deflection is more or less present and prominent in each electrocardiographic plane, and the wave occurs as a convex elevation at the junction of the QRS complex and the S-T segment.19
The responsiveness of alpha-1 adrenergic receptors decreases in dogs and cats with decreased core temperatures. Initially, alpha-1 receptor catecholamine binding increases, but with prolonged and progressive hypothermia, there is decreased receptor affinity. Reduced receptor binding results in a diminished contractile response and, ultimately, vasodilation of the cutaneous veins.20 Previous studies have demonstrated hypersensitivity in beta-1 receptors during hypothermia; additionally, alpha-1 adrenoceptor-mediated vasoconstriction was attenuated while alpha-2 adrenoceptor response was unaffected.21,22 Both alpha and beta adrenoceptors are desensitized in people with hypothermia associated with cardiopulmonary bypass.23 Hypothermia around 95 F (35 C) is associated with markedly decreased left ventricular contractility and leads to reduced cardiac output and impaired diastolic relaxation in neonatal pigs.24,25 Cardiac function in dogs with experimentally induced hypothermia is characterized by an initial period of increased ventricular contractility followed by decreased contractility at temperatures less than 68 F (20 C).26 Ventricular fibrillation was documented in 50% of the dogs with temperatures below 74 F (23.3 C).26
Severe hypothermia causes a reduction in both respiratory rate and tidal volume because of decreased cellular metabolism and lowered carbon dioxide production, thus diminishing the stimulation of ventilation.27-29 Patients with subnormal body temperatures also have a blunted response to carbon dioxide, but the degree of oxygen use concurrently decreases, leaving the respiratory quotient unaffected.30 The shifting of the oxygen-hemoglobin dissociation curve to the left, blood sludging, and a decline in alveolar ventilation may lead to hypoxia, pulmonary edema, acute respiratory distress syndrome, or pneumonia.31-33 Patients that experience near-drowning initially hyperventilate secondary to the mammalian dive reflex, potentially resulting in an alkalosis that may exacerbate a left shift of the oxygen-hemoglobin dissociation curve. Severely hypothermic patients may hypoventilate, possibly contributing to the development of acidosis.
Clinical pathology effects
Hypoglycemia and hypothermia frequently occur concurrently, and low blood sugar may exacerbate a decrease in metabolic activity that may perpetuate hypothermia.34,35 Hypokalemia is commonly documented in patients with hypothermia and is a result of intracellular shifting (rather than true loss) that is thought to be due to a temporary depression in the function of the potassium pump mechanism in the cell membrane.36,37 Potassium derangements secondary to hypothermia must be monitored for and carefully corrected to avoid the development of dysrhythmias or perfusion abnormalities, particularly during rewarming.36-39
Hypothermia-induced coagulation abnormalities include reversible platelet sequestration and decreased platelet thromboxane production, granule secretion, and von Willebrand factor expression leading to decreased platelet aggregation, as well as enhanced fibrinolytic activity and slowing of enzymatic activity required for clotting.40 One study showed surface cooling to 89.6 F (32 C) induced reversible platelet dysfunction, and another study showed bleeding time in pigs doubled at 86 F (30 C).41,42 Coagulation abnormalities may be easily missed in the clinical setting because most coagulation tests are conducted at 98.6 F (37 C), potentially preventing identification of a coagulopathy present at hypothermic temperatures. Hypothermia-induced coagulation disorders rapidly reverse once normothermia is reestablished.41
Hypothermia induces diuresis and a reduction in glomerular filtration rate, which is secondary to both a reduced release of vasopressin and a reduction in renal medullary hypertonicity.43 With progressive hypothermia, hypovolemia and subsequent mild increases in hematocrit and blood viscosity develop.44 Hemoconcentration and low microcirculatory flow increase blood viscosity by 4% to 6% for each one degree Celsius that body temperature declines.44 Suppression of antidiuretic hormone and core-directed shunting of peripheral blood induce diuresis in hypothermic states that may contribute to hypovolemia.45,46
Cerebral blood flow and cerebral autoregulation are adversely affected by declining body temperature, most frequently resulting in mentation changes.31 Cerebral metabolic rate and cerebral blood flow decrease about 5% for each one degree Celsius drop in body temperature.47 Severe hypothermia is associated with abnormal neurologic signs ranging from depression to coma. Hypothermia also results in decreased metabolism of anesthetic agents, potentially prolonging recovery and affecting mentation in postoperative patients.31 A previous study showed mild hypothermia conveyed a cerebral protective benefit against ischemia during resuscitation without inducing cardiovascular consequences; interestingly, moderate hypothermia resulted in cardiovascular decompensation despite conferring neurologic benefits.48
Immune system effects
Hypothermia causes vasoconstriction and a left shift of the oxygen-hemoglobin curve that leads to impaired oxygen delivery to tissues and may be associated with a diminished resistance to infection.49,50 Tissue hypoxia is associated with impaired oxidative killing by neutrophils, and decreases in body temperature cause a reduction in phagocytosis, impaired chemotaxis, and pancytopenia, as well as a depression of the production of cytokines and antibodies.51
People with postoperative hypothermia have poor wound healing and increased incidence of infection.52 Wound healing is further impaired by tissue hypoxia because hydroxylases required for granulation tissue depend on adequate oxygen tension.51 A previous study clearly showed wound cultures were significantly more often positive in patients with mild perioperative hypothermia compared with normothermic patients.52 However, a retrospective veterinary study showed no difference in infection rates in patients experiencing perioperative hypothermia.53
Anesthetic and surgical effects
General anesthesia and surgery readily result in primary and secondary hypothermia. Intubated patients inspire cold, dry air delivered directly to the lungs. Routine aseptic preparation of surgical sites promotes evaporative heat loss, and cold table surfaces and open body cavities will exacerbate heat loss through conduction and radiation, respectively. Anesthetic agents affect the hypothalamic thermoregulatory center in such a way that thermogenic responses are not triggered until low temperatures are reached.6 Centrally mediated thermoregulatory vasoconstriction is directly inhibited to cause peripheral vasodilation. Anesthesia decreases the metabolic rate by 15% to 40% and inhibits muscular activity to cause decreased heat production.4,6,54-56
Coagulopathy and platelet dysfunction logically represent serious complications in surgical or posttraumatic patients at risk for hemorrhage. Hypothermia delays anesthetic recovery and may lead to surgical complications such as dysrhythmias, hypotension, respiratory depression, bradycardia, coagulopathy, altered blood viscosity, and anesthetic drug overdose.57 Minimizing the duration of anesthetic and surgical procedures may reduce the incidence of secondary hypothermia.
Consequences following trauma
Hypothermia after trauma is common in people.58 Although there is a correlation between hypothermia and mortality, there is no threshold below which mortality is assured.58,59 A markedly hypothermic patient may initially appear deceased because of poor cardiac contractility, bradycardia, increased blood viscosity, and cold or stiff limbs. For this reason, you must thoroughly evaluate a patient with severe hypothermia, potentially using advanced diagnostic tests, such as electrocardiography, to ensure rapid identification and to afford rapid intervention.
Hypothermia in trauma patients is often proportional to the degree of shock and severity of tissue damage.24,60 Previous laboratory studies suggest that patients with hemorrhagic shock have increased survival with concurrent mild hypothermia compared with those whose resuscitation protocols included rewarming interventions, thus underscoring the potential benefit of hypothermia during low perfusion states.39,61
In Part 2 of this series, Cold critters: Assessing, preventing, and treating hypothermia, I describe three common rewarming methods, and I discuss when to apply these different methods and what rewarming complications you need to watch out for.
Christopher G. Byers, DVM, DACVECC, DACVIM (small animal internal medicine)
MidWest Veterinary Specialty Hospital
9706 Mockingbird Drive
Omaha, NE 68127
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