Feline Shock and Resuscitation
World Small Animal Veterinary Association World Congress Proceedings, 2005
Animal Emergency Center
Milwaukee, WI, USA

Throughout the ages, the cat has mystified mankind. Cats and dogs in crisis share many of the same disease entities, but may not show the same clinical signs. This becomes obvious when attempting to resuscitate the cat from severe shock utilizing techniques and dosages that have been extrapolated from the dog. Pulmonary edema can be a life-threatening consequence.

The physiologic response of the cat to shock, the procedures required for resuscitation, and the parameters that require careful monitoring present specific challenges. Knowledge of these traits specific to the cat is mandatory to optimize our ability to resuscitate without life-threatening complications.

The Shock Triad in Cats

There appears to be a triad of clinical consequences of shock in the cat: hypotension--bradycardia--hypothermia. It becomes apparent that each point of the triangle will cause or contribute to the severity of the other.



The physiologic response to decreased cardiac output in most species is tachycardia due to central sympathetic stimulation mediated by the baroreceptors. In a series of 77 hypotensive cats (blood pressure by Doppler < 80 mmHg systolic) at the Animal Emergency Center, all cats were found to have normal or slow heart rates, even when rectal temperatures were above 100°F (Oncken and Kirby, unpublished data). Schwartz, in 1973, reported that when the baroreceptors have detected inadequate arterial stretch in the cat, vagal fibers are stimulated simultaneously with sympathetic fibers. It is possible that this reported mechanism blunts the typical tachycardic response. Since cardiac output is a function of heart rate and contractility, the compensatory response to shock is blunted. Perfusion to the periphery is impaired and contributes to hypothermia. As the core temperature falls, the heart rate will fall.


Heat is lost when there is a transfer of core heat into the skin with subsequent loss into the environment. Mild to moderate secondary hypothermia is often endogenously triggered in severe metabolic disease as a protective mechanism to decrease energy expenditure and oxygen utilization. This conserves energy during times of extreme energy deficit.

Hypothermia has been used clinically in several species for its protective effects in head trauma, hypovolemic shock, and cardiothoracic surgery. The brain can sustain 5-6 minutes of ischemia in the normothermic state, however this time doubles with each 5°C (13.3°F) drop in core body temperature.Therefore, during periods of low blood flow, the brain is less likely to suffer the effects of hypoxia during hypothermic conditions. Short periods of hypothermia may be advantageous in some cases of trauma-induced hemorrhage by protecting the heart and brain against ischemia until blood volume can be restored.

Although hypothermia can have protective effects during low-flow states, it can also have many deleterious effects. As hypothermia progresses below 34°C (94°F), thermoregulation becomes impaired. Animals with this degree of hypothermia will cease to shiver or seek heat. Peripheral vasoconstriction is replaced by vasodilation, and core heat continues to be lost. Heat production decreases, because the rate of chemical heat production in cells is depressed due to the decreased metabolic rate. Severe hypothermia also depresses the central nervous system, causing the hypothalamus to become less responsive to hypothermia. When the core temperature drops below 31°C (88°F), thermoregulation is completely lost. The increase blood viscosity and metabolic acidosis that accompanies hypothermia can also decrease myocardial function.

A study in rabbits evaluating baroreceptor responses during hypothermia induced by direct blood cooling, showed an increase in sympathetic nervous system (SNS) activity as core temperatures dropped to 28°C (82°F) with little change in the baroreceptor reflex.As temperatures dropped below 25°C (77°F) there was a decrease in the SNS response, and a corresponding decrease in heart rate and blood pressure. By 22°C (71.6°F), the baroreceptor reflex was almost completely abolished


Two separate studies were performed in dogs and cats evaluating the effects of cooling on adrenergic receptor responsiveness. They both demonstrated that α1-adrenergic responsiveness decreases with cooling.Initially, there is a temperature-dependent increase in α1-receptor binding to norepinephrine.This is followed by a decreased receptor affinity for norepinephrine at lower temperatures, accompanied by a subsequent decrease in contractile response.This may indicate a temperature dependent change in receptor conformation, leading to decreased arterial responsiveness to catecholamines. Therefore, normal thermoregulatory induced vasoconstriction is lost at lower temperatures, and arterial vasodilation occurs. The vasodilation with the bradycardia will result in hypotension. The hypotension will compound the hypothermia and bradycardia.

From these studies it appears that there is both decreased receptor responsiveness as well as decreased catecholamine release responsible for the cardiovascular changes seen with hypothermia. The decreased catecholamine release may occur with more severe temperature decreases, due to a decreased baroreceptor response.


Rewarming prior to resuscitation has been shown in one study to decrease an animal's ability to withstand hemorrhagic shock.This study was done on two groups of ratsin which phlebotomy was used to induce hypotension. The control rats were allowed to autoregulate their own temperatures during the shock period. The experimental rats were warmed to temperatures between 34° and 36°C throughout several hours of shock, prior to onset of resuscitation. Survival during shock and post-resuscitation was significantly higher in the control group compared to the experimental group.

Rapid rewarming of human trauma patients, in combination with fluid resuscitation, has a marked effect on decreasing the mean ICU stay, decreasing blood loss and blood product requirements, decreasing fluid requirements, and reducing mortality. This information and the suspected pathophysiologic mechanisms of shock in the cat have been instrumental in the formation of our hypovolemic shock resuscitation guidelines for the cat.

The cat is first assessed for evidence of cardiac disease by careful auscultation for a heart murmur or gallop. If heart disease is suspected, small volume resuscitation using only crystalloids is performed. When there is no historical or clinical evidence of heart disease, titration of crystalloids with colloids is recommended.

The doppler indirect measurement technique may not detect an audible pulse in a peripheral vessel in the initial evaluation of the hypotensive cat. An infusion of warm isotonic crystalloids is given IV at 10-15 ml/kg. Hetastarch is then administered at 5 ml/kg given over 5-10 minutes. The blood pressure is checked. Once the blood pressure is above 40-60 mmHg systolic by doppler, then only maintenance crystalloids are given while the cat is aggressively warmed.

Rewarming a hypothermic cat can be accomplished by several different methods: passive surface rewarming, active surface rewarming, and active core rewarming. During external heating, care must always be taken to prevent skin burns by controlling the temperature of the external heating devices or placing a barrier between the heat source and the patient. External heating devices can be constructed out of fabric filled with uncooked dried beans or rice. These packets are then warmed in the microwave. However, the temperature should be tested prior to placing these or any warming device in contact with the animal's hair coat or skin. Smaller animals can be placed inside heated pediatric incubators. A tent can be constructed out of blankets to trap heat and warm air from hot water bottles or warm air blowers near the animal. It is important to remove warm water bottles once they reach body temperature to prevent heat loss to the bottles by conduction.

When using aggressive surface rewarming in hypovolemic animals, the heat source should be applied to the thorax and abdomen, and the extremities should remain cool to prevent peripheral vasodilation. In addition, the warm periphery can decrease neuronal feedback to the thermoregulatory center, therefore decreasing the thermoregulatory response.

Once the cat's rectal temperature has risen to 98 F, the blood pressure is rechecked. The hetastarch can then be repeated at 5 ml increments over 15 minutes until the systolic blood pressure > 90 mmHg and the CVP is 6-8 cm of water (with adequate cardiac and renal function). The rectal temperature must be maintained as needed by hot water bottles and warm fluids. Both colloids and crystalloids are administered at the minimum amount required to maintain pressure and volume. Should volume overload occur, decreasing crystalloid rate of infusion, stopping colloid infusion, and administering furosemide at 2-7 mg/kg IV can help eliminate signs.

Efforts to avoid rewarming complications should be made. Restoring an adequate circulating volume is essential during the rewarming period. The authors' recommendations are to only actively rewarm until a rectal temperature of 37°C (98°F) is reached. At these mildly hypothermic temperatures coagulation and cardiovascular functions are restored without overwhelming the circulatory system. This also may help prevent the "afterdrop" phenomenon by reducing the core to periphery temperature gradient. Once intravascular volume is replaced, and the major consequences of hypothermia are reversed, passive surface rewarming should be sufficient to allow slow return of normothermia as the patient's cardiovascular system recovers. It is vital to monitor the patient carefully for hypotension, arrhythmias, acid-base and electrolyte abnormalities, CNS depression, and pulmonary complications during rewarming and in the immediate period following. Any ongoing abnormalities should be treated aggressively.

Pain control

It is vital to the maintenance of cardiovascular function and the mental well being of the cat to provide pain control. In the critically ill cat, it is best to titrate analgesics and sedatives to effect, as responses are variable and can be affected by underlying renal and hepatic dysfunction. For mild to moderate pain control, butorphanol 0.2-0.8mg/kg IV q 2-6 hrs is given initially. For control of severe pain, the combination of injectable opioids oxymorphone (DuPont) 0.05-0.1mg/kg IV or morphine (Steris Labs) 0.1mg/kg IM with diazepam (Steris Labs) 0.2mg/kg IV is effective and reversible.


1.  Oncken, A, Kirby R, Rudloff E. Hypothermia in the Critically Ill Dog and Cat. Comp of Cont Ed. June, 2001.

Speaker Information
(click the speaker's name to view other papers and abstracts submitted by this speaker)

Animal Emergency Center
Milwaukee, WI

MAIN : Critical Care : Feline Shock & Resuscitation
Powered By VIN