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Equine cardiology cases (Proceedings)
As in all species, cardiac examination involves cardiac auscultation for rate, rhythm, heart sounds, and murmurs, palpation of peripheral pulses, and examination of peripheral veins and edema.
The following information on equine cardiac examination will form the basis for our discussion of equine cardiology cases. As in all species, cardiac examination involves cardiac auscultation for rate, rhythm, heart sounds, and murmurs, palpation of peripheral pulses, and examination of peripheral veins and edema. The points for equine cardiac auscultation are as follows:
• Mitral - left 5th ICS halfway between shoulder and sternum
• Aortic - left 4th ICS just below point of shoulder
• Pulmonic - left 3rd ICS just below point of shoulder
• Tricuspid - right 3rd - 4th
There are normal variations in rhythms in horses. The most common rhythm is sinus rhythm. However, physiologic arrhythmias can result in horses from the effects of high resting vagal tone. The characteristics of these rhythms are that they disappear with exercise or excitement. The most common vagal-induced rhythm in horses is second degree AV block (ausculted in 15 to 18% of horses; detected by Holter monitor in 44% of horses). Sinus arrhythmia and sinus block occur in horses but are uncommon. Vagal-induced second degree AV block must be differentiated from pathologic AV block due to AV nodal disease. Pathologic AV block should be suspected if there is more than 1 in dropped beat in a row, if there is less than 3 normal beats between each block, and if the block fails to convert to sinus rhythm with exercise. All four heart sounds (S1, S2, S3, S4) are audible in healthy horses. Intensity varies with duration of diastolic filling and sympathetic stimulation. S1 is early ventricular contraction, AV closure, ejection w/semilunar opening. S2 associated with closing of semilunar valves and back flow of blood. Splitting of S1 and S2 can be normal. S3 is associated with vibration of ventricular wall during passive filling of ventricle and is best heard over the apex with the bell of the stethoscope. S3 may become very loud with volume overload of the ventricle (e. g. Mitral regurgitation). S4 is the atrial sound and is detected in most horses and is often mistaken for a split S1. Other sounds in horses include a systolic "click" over semilunar valves that is considered normal. In contrast, a systolic "click" over MV may be due to prolapsed.
Physiologic murmurs commonly occur in horses due to the size of the heart and volume of blood flow. These murmurs do not alter heart function and are not attributed to cardiac pathology. These physiologic murmurs are grade 1 to 3/6 and do not create a palpable thrill. They are localized to a single valve area and do not radiate. They are short in duration and do not occur throughout systole (not holo or pansystolic). The most common physiologic murmurs in horses are systolic ejection murmurs over the aortic and pulmonid valve. Less commonly early diastolic murmur (protodiastolic) between S2 and S3 can occur physiologically. These sometimes "squeak" and do not occur throughout diastole.
The common murmurs that resolve from heart disease in horses are tricuspid regurgitation, mitral regurgitation, ventricular septal defect, and aortic regurgitation. These generally result from valvular or myocardial disease and are evaluated by use of echocardiography.
Jugular vein pulsation occurs in horses with cardiac failure and tricuspid regurgitation. Normal pulsation occur ⅓ the way up the jugular vein with the head in a normal position. Abnormal pulsation is beyond the ⅓ point of the neck. Cardiac failure, cranial mediatinal masses, and pericardial disease can lead to jugular vein distention.
The response of the heart to exercise can be an important part of cardiac assessment in horses and may be done with a rider (if deemed safe in the face of possible cardiac disease), on a lounge line, or on a treadmill. Heart rate monitors or telemetric ECG are useful to assess the heart rate in response to exercise. Heart rates of 70-120 are normal at a trot. Heart rates of 120-150 normal at canter. Heart rates of 150-180 normal at hand gallop and heart rates may exceed 180 at gallop. The heart rate usually falls to less than 100 per minute upon cessation of exercise. Heart rate abnormalities detected during exercise testing may be from lack of fitness or cardiac disease which can usually be demonstration via cardiac examination. Pulmonary, URT disease, musculoskeletal disease, and other illness may lead to heart rate abnormalities during exercise. Telemetric electrocardiogram, pre and post exercise echocardiogram, and cardiac enzymology are important techniques for assessment of cardiac disease in some cases.
The first case is a 3 year old Thoroughbred gelding with exercise intolerance. The horse raced successfully 5 weeks ago and then developed coughing and fever. He was rested for a few days and then training resumed. Substantial reduction in performance has been noticed during training. He does not cough or exhibit respiratory noise. Complete blood count and chemistry were normal. Thoracic auscultation (cardiac and pulmonary; at rest and on rebreathing bag) and thoracic ultrasound (pulmonary and echocardiography) were normal. Electrocardiogram at rest was normal. Exercise testing on a treadmill was performed. For the treadmill examination, the horse was fitted with telemetric ECG electrodes. Computer recordings were monitored and collected during exercise. Endoscopic and echocardiographic equipment were prepared for examination during and after exercise, respectively. Blood gas analysis at rest was normal. The treadmill speed was incrementally increased as tolerated by the horse. Electrocardiogram was monitored during a gallop while an endoscopic examination was performed. No endoscopic abnormalities were visualized. Electrocardiogram revealed atrial premature contractions. Post exercise echocardiography was performed with a heart rate of 90 beats per minute and revealed normal diastolic and systolic dimensions of the left ventricle and an increase in the fractional shortening compared to baseline. Pre and post exercise muscle enzymes and blood gas were normal. The diagnosis for the poor performance is myocardial disease leading to exercise induced atrial premature contractions. The premature contractions result in reduced diastolic filling which reduces cardiac output. The differential diagnosis for myocardial disease in horses includes: electrolyte abnormalities, viral disease (influenza), endotoxemia, ionophores, ischemia, Se deficiency, tumors, bacterial embolism, and idiopathic cardiomyopathy. With the history of respiratory disease, influenza was suspected and paired serology was performed. The horse demonstrated a 3 fold rise in influenza titer over 7 days suggesting viral myocarditis. Cardiac troponin I was mildly elevated at 0.043 mg/L suggesting active myocardial disease. Forty five days rest (and longer if troponin still elevated) was recommended. Post exercise ECG should be repeated before resuming training.
A seven year old Paint gelding presented with acute onset of severe dyspnea and intermittent collapse. Body temperature was normal and heart rate (200 beats per minute) and respiratory rate (56 breaths per minute) were greatly elevated. The horse was extremely week with cyanotic mucous membranes and when he lowered his head, white frothy fluid (pulmonary edema) poured from both nostrils. Ecletrocardiogram revealed ventricular tachycardia. A bolus of quinidine gluconate injectable (2 mg/kg) were administered intravenously and the rhythm converted to sinus rhythm transiently and began to revert back to ventricular tachycardia after a ten minutes. A second bolus of quinidine gluconate was administered a constant rate infusion prepared. In 24 hours the horse was changed to quinidine sulfate (20 mg/kg) twice daily for two weeks. Strict stall rest was enforced. Acute myocarditis was diagnosed. Echocardiogram, complete blood count, and serum chemistry performed to look for an underlying cause of myocarditis but were normal. Feed analysis did not reveal ionophore contamination of feed. The quinidine was discontinued and the arrhythmia did not recur so the horse was discharged. The owner allowed the horse to run the fence line chasing another horse and he collapsed. Reexamination revealed that the arrhythmia recurred. Quinidine sulfate therapy was reinstituted and rest enforced. The arrhythmia again resolved and quinidine therapy was discontinued. The horse recovered after 60 days rest. Alternative antiarrhythmic therapies for ventricular tachycardia in horses include: Lidocaine (0.25 mg/lb every 10 minutes), quinidine gluconate, propranolol. Procainamide, and amiodarone.
A 7 year old Thoroughbred race horse presented for prepurchase examination. Exercise intolerance was not reported by the current owner. Auscultation revealed a grade III/VI systolic crescendo murmur over the mitral valve that radiated toward the base of the heart. Temperature, heart rate, and respiratory rate were normal. Pulse pressure, rate, and rhythm were normal. Complete blood count and serum chemistry were normal. Echocardiogram did not reveal left heart enlargement. Doppler echocardiography revealed moderate mitral regurgitation into the left atrium. Mitral valve leaflets appeared normal. Fractional shortening was normal. The presence of mitral regurgitation reduces the value of the horse due to reduced resale value. Moderate mitral regurgitation can significantly reduce exercise tolerance due to increased pulmonary pressure. However, the ability of this horse do perform in the prospective buyers desired function can only be determined by evaluation in work on a trial basis. Progression of mitral regurgitation in the absence of demonstrable lesions is generally slow.