Heat stroke is a life-threatening condition characterized by an elevated core body temperature and central nervous system
dysfunction. Despite aggressive lowering of core body temperature and treatment, the pathophysiologic changes associated with
heat stroke can lead to multi-organ dysfunction, which can be fatal.
Recent research has shown that heat stroke results from thermoregulatory failure coupled with an exaggerated acute-phase response
and altered expression of heat-shock proteins. This article will summarize the incidence, thermoregulation, predispositions,
pathophysiology, treatment and outcome of heat stroke.
Definition and incidence
Hyperthermia in dogs can be pyrogenic or nonpyrogenic. Nonpyrogenic hyperthermia can result from exposure to high environmental
temperature (non-exertional heat stroke) or from strenuous exercise (exertional heat stroke).
The classic definition of heat stroke is an elevated core body temperature
> 41 C in dogs, accompanied by central nervous system dysfunction. An alternative definition that might be more appropriate
in veterinary patients is: a form of nonpyrogenic hyperthermia associated with a systemic inflammatory response, leading to
a syndrome of multi-organ dysfunction.
Data on incidence of heat stroke in veterinary patients are lacking, but it is a commonly recognized condition in dogs, especially
in hot, humid environments.
Quick cool-down: The author with a patient, providing treatment aimed at rapid cooling and support of body systems affected
Heat is generated by basal metabolism, muscular activity and oxidative metabolism.
The thermoregulatory center of the body is located in the hypothalamus and receives input from hypothalamic sensor cells that
detect the temperature of the circulating blood and cutaneous sensor cells. A physiologic response is triggered when afferent
sensors throughout the body converge in the hypothalamus and warm blood supplying the hypothalamus stimulates compensatory
There are four modes of heat dissipation: evaporation, conduction, convection and radiation (see Figure 1).
Evaporative cooling involves the loss of water to the environment and cools the tissue/skin surface. Radiative cooling is
the transfer of heat between the animal and the atmosphere. Convective cooling involves the movement of air across a surface
carrying the heat away. Conductive cooling is the exchange of heat between two objects in direct contact with one another.
At ambient temperatures <32 C, convection, conduction and radiation maintain normothermia. Cutaneous vasodilation and increased
cardiac output lead to increased cutaneous circulation, which promotes heat loss through radiation, conduction and convection.
Approximately 70 percent of the total body heat loss in dogs and cats is due to radiation and convection from the body surface.
As environmental temperature increases, evaporative cooling is more important.
The initial compensatory mechanism is activation of the panting center in the brain as the nasal turbinates provide a large
surface area for loss of water from the moist mucous membranes. Some heat loss occurs through sweating (foot pads) and excretion
of feces and urine.
Nonpyrogenic hyperthermia occurs when heat production cannot be adequately dissipated by normal thermoregulatory mechanisms.
Predisposing factors for the development of heat stroke can be categorized into conditions decreasing heat dissipation and
those increasing heat production.
Environmental conditions decreasing heat dissipation include increased ambient temperature, humidity, poor ventilation and
Patient factors include any condition or medication that impairs the ability of the normal homeostatic response mechanism,
such as laryngeal disease, brachycephalic anatomy, cardiovascular disease, central or peripheral nervous system disease, obesity,
hair coat, age and medications (diuretics, B blockers, phenothiazine derivatives). Excessive heat production can occur through
extreme exercise, seizures, hormonal hyperthermia and drugs/toxicities.
Heat stroke causes an altered heat-shock response and an exaggerated acute-phase response that leads to the production of
reactive oxygen species, increased vascular and intestinal permeability, culminating in direct cellular injury and enzyme
The central nervous system changes are characterized by cerebral edema, hemorrhage, infarction and cerebellar dysfunction.
Experimental studies suggest that temperatures as low as 41 C may cause permanent brain damage, which may predispose patients
to subsequent hyperthermic episodes.
The cardiovascular and pulmonary systems are compromised due to the peripheral vasodilation and decreased peripheral vascular
resistance leading to hypovolemia. Excessive panting leads to hemoconcentration, sludging of blood flow and respiratory muscle
Direct cardiac injury may cause myocardial hemorrhage and necrosis. Pulmonary edema may result from cardiac failure, damage
to the vascular endothelium or hypoproteinemia. Damage to the gastrointestinal system is characterized by gut ischemia, which
predisposes to bacterial translocation. Hepatic damage also has been seen and is described as hepatocellular vascular degeneration
with centrilobular necrosis and cholestasis.
Acute renal failure due to tubular necrosis is a result of direct thermal injury, hypoxia and microthrombi. Hyperthermia induces
the platelet activation and coagulation factors; combined with endothelial and platelet damage, this can lead to disseminated
intravascular coagulation. Rhabdomyolysis occurs as a direct result of high temperature and may be increased in patients experiencing
an exertional heat stroke.