Hot times, hot dog

Hot times, hot dog

Jul 01, 2006

Q. Please review heat-illness problems in dogs.

A. Dr. Kenneth J. Drobatz at the 2005 American College of Veterinary Internal Medicine Forum in Baltimore gave a lecture on pathophysiology and treatment of heat-induced illness. Some relevant points in this lecture are provided below.

Heat illness may represent a continuum from the least to the most severe form. Heat cramp is characterized by muscle spasms resulting from sodium and chloride depletion. When signs such as fatigue, weakness, muscle tremors, vomiting and diarrhea occur, heat prostration/exhaustion may be diagnosed. The heatstroke is severe central nervous system disturbance and is often associated with multi-organ dysfunction. Generally, owners seek veterinary attention when their dogs demonstrate signs consistent with heat prostration/exhaustion or heatstroke.


Thermal homeostasis is maintained by a balance between heat load and heat-dissipating mechanisms controlled by temperature-sensitive centers in the hypothalamus. Environmental as well as metabolic heat are the major contributors to heat load. Body temperature increases when heat load exceeds heat dissipation. As the body temperature increases, heat loss via radiation and convection from the skin is facilitated by increased cutaneous circulation as a result of increased cardiac output and sympathetic mediated peripheral vasodilation. The shunting of blood to the periphery is a trade off with blood supply to the viscera (intestines and kidneys). Significant heat loss also occurs as a result of evaporation from the respiratory tract through panting.

A warm, humid environment and exercise are the most common heat loads that dogs experience and may cause extreme hyperthermia even in individuals with functional heat dissipating mechanisms. Respiratory evaporative heat loss may be diminished by humid climactic conditions, closed confinement with poor ventilation and upper respiratory abnormalities such as brachycephalic conformation, laryngeal paralysis or masses, or collapsing tracheobronchial tract. Diminished radiation and convective heat loss from the skin may occur as a result of hypovolemia due to any cause, poor cardiac output, obesity or lack of acclimatization to heat. Situations that combine high heat load and diminished heat dissipation may result in a rapid and extreme rise in body temperature.

Most heat illness in dogs usually presents during late spring or early summer when the warm humid weather begins. Despite progressively warmer days later in the summer, heat-induced illness becomes less frequent unless dogs are left in cars. This may be due to a lack of time for acclimatization to the change in environmental temperature. Acclimatization to heat can take two weeks or more and is associated with enhanced cardiac performance, salt conservation by the kidney and sweat glands through activation of the renin-angiotensin-aldosterone axis, an increased capacity to sweat, plasma volume expansion, increased GFR and an increased ability to resist exertional rhabdomyolysis.

Thermoregulation failure

Heat stroke occurs due to a combination of events, which primarily include failure of thermoregulation, an exaggerated acute phase response, and alteration of heat-shock proteins. The reaction of the body during heat stroke involves many of the same mediators as sepsis.

The physical findings of dogs suffering from heat-induced illness vary with the intensity and duration of the increased body temperature. The rectal temperature may be decreased, normal or increased depending upon tissue perfusion and whether cooling measures have been implemented already. The pulse is often weak due to hypovolemia and fast as a result of compensatory sinus tachycardia. The respiratory rate is very rapid usually to improve heat dissipation rather than as a result of respiratory disease. Most dogs present in a hyperdynamic state. The mucous membranes are usually hyperemic, and the capillary refill time is short. The pulses are often weak due to hypovolemia secondary to evaporative fluid loss, vomiting, diarrhea and vasodilation. Sinus tachycardia is common. Some dogs have occasional ventricular arrhythmias. ECG evaluation should be performed on all dogs with severe heat-associated illness.

Evaluation of the respiratory system is warranted because evaporation through the respiratory tract is a major route for heat dissipation. Loud or noisy breathing that is heard without the stethoscope suggests an upper airway problem, such as laryngeal paralysis/edema, obstruction or tracheobronchial collapse. Many dogs with heat-induced illness have been vomiting, and aspiration pneumonia should be considered. Dogs suffering from disseminated intravascular coagulation may have pulmonary parenchymal hemorrhage resulting in crackles or harsh airway sounds.

Mentation may range from alert to comatose. Depression is the most common abnormality. The severely affected dog will be comatose or stuporous at presentation. Pupils can range from dilated to pinpoint but usually are responsive. Some dogs may be cortically blind at presentation. This may resolve after several hours. Ambulatory dogs may be ataxic. The cause of these neurologic abnormalities may be poor cerebral perfusion, direct thermal damage, cerebral edema, CNS hemorrhage or metabolic abnormalities such as hypoglycemia or hepatoencephalopathy.