Physiologic effects of succinylcholine chloride in mechanically ventilated horses anesthetized with halothane in oxygen.

Succinylcholine chloride, administered to horses anesthetized with halothane in oxygen and mechanically ventilated, caused slight but significant (P less than 0.01) increases in heart rate. Significant alteration in mean arterial blood pressure did not occur, and there were clinically insignificant increases in serum K+ and C1- concentration. Cardiac dysrhythmia and myoglobinuria did not occur. Thus, effects of halothane anesthesia and mechanical ventilation prevented cardiac dysrhythmia and hypertension and greatly reduced the tachycardia generally associated with siccinylcholine administration.

Pulmonary hypertension as a cause of atrial fibrillation in young horses: four cases (1980-1989).

Four young horses of various breeds and suffering from atrial fibrillation died of heart failure. All had markedly high pulmonary arterial pressure, right-sided cardiomegaly, and lack of histologic lesions in the right atrium or pulmonary parenchyma. Three horses had hypertrophy and/or necrosis of the tunica media of the pulmonary vasculature. Clinical signs of disease, physiologic data, and pathologic findings indicated that these horses had primary pulmonary hypertension with secondary right-sided cardiac ventricular hypertrophy and dilatation, atrial fibrillation, and heart failure.

Sudden death in training and racing Thoroughbred horses.

We reviewed case records, necropsy reports, and histologic sections from 25 Thoroughbred racehorses that died suddenly at 3 Chicago racetracks. These were young horses ranging in age from 2 to 5 years. There were more females (n = 16) than males (n = 9), and the incidence of death increased slightly in the spring and summer. Twenty-one of the 25 horses died while racing or training. Only 8 of the 25 horses (32%) had lesions sufficient to account for the death. In 6 of those 8 cases, death was caused by massive thoracic or abdominal hemorrhage. The site or nature of the vascular defect in these cases could not be determined. One horse died of severe preexisting pulmonary disease, and one died of encephalitis and cardiac papillary muscle fibrosis. The cause of death was undetermined in 17 horses (68%). Nearly all horses had pulmonary edema, congestion, and/or hemorrhage. We postulate that these unexplained deaths were a result of exercise-induced acute cardiovascular failure.

Cardiovascular effects of amphetamine in the horse.

Each of nine horses was treated with amphetamine alone, with atropine alone, and with amphetamine and atropine in combination. Cardiac effects of these drugs were studied by electrocardiography during resting and exercising states and immediately after exercise. Although each treatment increased heart rate significantly during the resting state, only the amphetamine plus atropine treatment increased heart rate significantly during exercise. Decrease in heart rate immediately after exercise differed significantly for each treatment; the most rapid decrease in heart rate was found after the amphetamine treatment. Amphetamine caused second-degree atrioventricular (AV) block in each horse during the postexercise period. Amphetamine also caused ectopic beats either during or immediately after exercise in six horses. Second-degree AV block was not found when atropine was used alone or when used in combination with amphetamine. Fewer ectopic beats were found when atropine was used with amphetamine. Heart rate responses indicated that the direct effect of amphetamine was greater than the reflex effect at rest and during exercise; the opposite was true during postexercise. Second-degree AV block during the postexercise period was attributed to vagotonia due to baroreceptor stimulation. Release of norepinephrine by amphetamine probably caused many of the ectopic beats by increasing automaticity of subordinate pacemakers.