The normal horse's heart rate varies with exercise up to a maximum of 200 - 240 beats/ minute. The exercising horse should
have a sinus tachycardia with a heart rate of 70-120 beats/minute trotting, 120-150 beats/minute cantering, 150-180 beats/minute
at the hand gallop, and 180-240 at the gallop. The horse's heart rate should recover quickly if the horse is fit, dropping
below 100 beats/minute in the first 5 minutes following maximal exercise and returning to baseline within 30-45 minutes following
exercise. Cardiac arrhythmias are the most common cardiovascular cause of poor performance.
Arrhythmias are frequently detected in the normal horse at rest and immediately post exercise. Exercising electrocardiography
needs to be performed to determine the significance of cardiac arrhythmias on performance.
Atrial fibrillation is the cardiac arrhythmia most frequently associated with poor performance. The degree of exercise intolerance
is dependant upon the presence, type and severity of the horse's underlying cardiac disease and on the individual's resting
vagal tone. Although horses with atrial fibrillation usually have normal resting heart rates, they have higher than normal
heart rates during exercise, usually 40-60 beats/minute higher for each exercise level. The cardiac output of exercising horses
decreases significantly at high work loads due to marked increases of heart rate resulting in shortened ventricular filling
time and the lack of the atrial contribution to ventricular filling. Thus atrial fibrillation causes a marked drop in performance,
resulting in race times that decrease by 15-30 seconds or more. Conversion from atrial fibrillation to sinus rhythm usually
results in the return of the horse to its previous level of performance.
The large atrial myocardial size and high vagal tone of the normal horse are two criteria necessary for the development of
atrial fibrillation. In most instances it is suspected that an atrial premature contraction initiates the arrhythmia. Potassium
depletion also predisposes horses to the development of atrial fibrillation and can occur associated with furosemide administration,
bicarbonate administration and/or excessive sweating. Horses with atrial fibrillation often have a decrease in resting systolic
left ventricular function that is manifested echocardiographically as a decrease in fractional shortening. This usually returns
to normal within several days of conversion to sinus rhythm. Persistent left ventricular dysfunction following conversion
also suggests the presence of underlying myocardial disease.
Ventricular and Supraventricular Premature Depolarizations
Occasional premature depolarizations may be detected post exercise and are clinically insignificant if infrequent. Ventricular
premature depolarizations and paroxysms of ventricular tachycardia have been observed in horses quitting or fatiguing while
exercising on the treadmill. Supraventricular extrasystoles are observed less frequently during an exercising ECG. Paroxysmal
ventricular tachycardia detected at peak exercise, or as the horse is tiring, indicates an exercise-induced myocardial problem.
Exercising ventricular arrhythmias have been associated with arterial hypoxemia in horses with upper respiratory dysfunction,
particularly those with severe upper respiratory tract obstruction. Problems with myocardial perfusion or a pre-existing myocarditis
or cardiomyopathy must also be considered. Exercise-induced electrolyte and metabolic disturbances may also be involved in
the pathogenesis of some of these arrhythmias. The premature depolarizations may decrease race times by 2-3 seconds for horses
with occasional exercising premature depolarizations to 20-30 seconds or more for horses with sustained ventricular tachycardia.
Sustained ventricular tachycardia has also been associated with collapse and sudden death. The detection of frequent ventricular
or supraventricular premature depolarizations during peak exercise or in the immediate post exercise period should prompt
further cardiac evaluation.
Advanced Second-degree A-V Block
Severe bradyarrhythmias are uncommon and associated with severe exercise intolerance and/or collapse. Advanced second degree
atrio-ventricular block or third degree heart block are usually associated with an inflammatory focus and may respond to aggressive
treatment with large doses of corticosteroids. If no response to the steroids is seen, there are probably degenerative changes
in the A-V node and the horse's prognosis is poor to grave.
Echocardiography is the technique of choice for evaluating horses with suspected myocardial dysfunction. Exercise-induced
myocardial dysfunction can be diagnosed with stress echocardiography. Stress echocardiography is very useful in assessing
the cardiovascular component of poor performance in horses with normal resting left ventricular function or borderline myocardial
dysfunction at rest and a vague history of exercise intolerance. Global assessments of left ventricular function should be
made pre and post exercise to evaluate the myocardial response to peak exercise. No change or a decrease in systolic thickening
of the left ventricular free wall and interventricular septum following strenuous exercise is abnormal.
Clinical signs of myocarditis/cardiomyopathy vary but most horses present with exercise intolerance or signs of congestive
heart failure. Arrhythmias and/or murmurs of mitral and tricuspid regurgitation are often detected. Atrial and ventricular
premature depolarizations are common in less severely affected horses. Murmurs of valvular regurgitation are usually associated
with clinically insignificant, mild or moderate atrioventricular valvular regurgitation. The echocardiogram is normal or a
mild decrease in shortening fraction (20-30%) is detected, occasionally with segmental wall abnormalities. These horses have
a fair to good prognosis for recovery and return to performance with rest and/or corticosteroid therapy.