Cardiac Arrhythmias

Cardiac arrhythmias are abnormalities in the normal heart rate, rhythm, or conduction pattern. Arrhythmias result from abnormalities of impulse generation or impulse conduction or a combination of both.

• Horses: 26 to 50 beats/min; 60 to 80 beats/min in foals

• Cattle: 49 to 84 beats/min

• Sheep and goats: 70 to 90 beats/min

Arrhythmias are more common in horses than in other domestic animal species. Up to 25% of horses that have no other signs of heart disease have cardiac arrhythmias during routine examination or electrocardiography.¹ During continuous 24-hour electrocardiography, 44% of normal horses had second-degree atrioventricular (AV) block, 10% had sinus arrhythmia, 3% had sinoatrial (SA) block, 27% had occasional supraventricular extrasystoles, and 15% had occasional ven­tricular arrhythmias.² Cardiac arrhythmias may be present in 40% of horses that have other signs of cardiac disease.¹ The horse may have arrhythmias at rest that are considered benign or functional. Benign, physiologic, or functional arrhythmias are usually bradyarrhythmias and are thought to be the result of increased vagal tone. These arrhythmias disappear at high heart rates (exercise or excitement) or with the administration of atropine 0.01 mg/kg intravenously (IV) or 0.02 mg/kg intramuscularly (IM) or glycopyrrolate (0.003 to 0.006 mg/kg SC or IM). Some examples of benign or functional arrhythmias are as follows:

• Second-degree AV block

• Sinus arrhythmia

• Sinus bradycardia

• SA block

• SA arrest

Other arrhythmias are usually considered to be pathologic, even if there are no other overt signs of cardiac disease.

• Atrial fibrillation/atrial flutter

• Frequent atrial and ventricular premature depolarizations

• Supraventricular or ventricular tachycardia

• Advanced second-degree or third-degree (complete) AV block

The most effective method of identifying the specific arrhythmia is by performing an electrocardiogram (ECG). Resting electrocardiography may not detect arrhythmias that are transient or intermittent. Continuous ECG recordings (Holter or telemetry) are useful for identifying transient arrhythmias and for characterizing the type, frequency, and severity of arrhythmias. Exercising electrocardiography may identify arrhythmias that are absent or clinically insignificant at rest but that may impair performance or affect safety of a rider or driver.

In general, cattle do not have benign arrhythmias like horses, but they are frequently found to have sinus bradycardia and sinus arrhythmia associated with lack of feed intake. These arrhythmias were previously thought to be abnormal and associated with vagal indigestion but have been shown to occur in normal cattle held off feed for 12 to 48 hours.³ Cattle with gastrointestinal disease seem to have increased susceptibility to cardiac arrhythmias, especially atrial premature depolariza­tions and atrial fibrillation. Although the reason for the sus­ceptibility is not established, abnormal electrolyte concentrations, acid-base disturbances, and aberrations in autonomic nervous system function have been proposed.^4,5 Sinus arrhythmia in goats is considered to be a benign arrhythmia and is present in many normal animals. Normal camelids also frequently have sinus arrhythmia.

Mechanisms of Cardiac Arrhythmias

Arrhythmias result from abnormalities of impulse generation or impulse conduction or a combination of both. A variety of mechanisms can cause abnormal impulse generation or

■ BOX 6.3

Causes of Cardiac Arrhythmias in Horses

Common Causes

Excitement

Autonomic imbalance

Fever

Sepsis

Toxemia

Hypoxemia

Colic

Disorders of acid-base or electrolyte homeostasis Congenital defects

Myocarditis

Valvular disease

Idiopathic (presumptive myocardial fibrosis or fibrofatty infiltrate)

Uncommon Causes

Ionophore toxicity

Zilpaterol toxicity Anesthesia

Other drugs Pericarditis

Cardiomyopathy

Cardiac or heart base tumor

Aortic root rupture Aortopulmonary rupture

Atypical myopathy

Aortic regurgitation

Severe hemorrhage

Dynamic upper airway obstruction Rattlesnake envenomation

Cardiotoxic plants

Hyperthyroidism (iatrogenic)

■ BOX 6.4

Causes of Cardiac Arrhythmias in Ruminants Common Causes

Gastrointestinal disease

Lymphosarcoma

Valvular heart disease

Myocardial diseases

Brisket disease

Pericarditis

Cor pulmonale

Excitement

Foot rot

Fever

Sepsis

Toxemia

Disorders of acid-base or electrolyte homeostasis Myocarditis

Uncommon Causes

Ionophore toxicity β-adrenergic agonist (zilpaterol) toxicity

Anesthesia

Hypoxemia

Cardiomyopathy

Autonomic imbalance

Cardiotoxic plants (Rhododendron and Taxus spp.)

conduction (Boxes 6.3 and 6.4).

Automaticity, the ability to initiate action potentials spon­taneously, is a property of cells in the sinus node, some parts of the atria, AV junction, and His-Purkinje system. Cardiac disease can be responsible for the development of automaticity in cells that normally do not have this property. Normal automaticity develops when the membrane potential slowly falls (i.e., becomes less negative) during diastole. When the membrane reaches its threshold potential, an impulse is initiated. The most common clinical arrhythmias caused by the automatic- ity mechanism are sinus tachycardia and sinus bradycardia, which are the result of alterations in autonomic nervous system tone. Enhanced automaticity in another area of the heart that is capable of automaticity (spontaneous depolarization) may be responsible for atrial or ventricular premature beats. Atrial fibrillation is thought to be triggered by rapid firing from one or more foci (in humans, the foci are usually in the pulmonary vein region).

Under certain circumstances, conduction abnormalities allow a propagating impulse, which has already excited the heart, to persist and reexcite the atria or ventricles after the end of the refractory period. This can occur in an ordered or random fashion. Random reentry occurs over reentrant pathways that continuously change in size and location with time, whereas ordered reentry occurs over a relatively fixed reentrant pathway. Impulse propagation may be slow enough that reentrant circuits can be established in small areas of myocardium. In large animals the size of the myocardial circuit is large enough that relatively mild alterations in impulse propagation may make reentry feasible and may account for the relatively greater frequency of arrhythmias in these species.

Under clinical conditions, cardiac arrhythmias may be associated with disturbances in electrolyte concentrations, especially potassium and calcium; in acid-base balance; and in autonomic nervous system function. These conditions can precipitate cellular changes conducive to the development of arrhythmias by any of the previously mentioned mechanisms.

Approach to Diagnosis of Cardiac Arrhythmias

It is important to distinguish between abnormal arrhythmias that are primary and those that are secondary. Most abnormal arrhyth­mias of horses and cattle are tachyarrhythmias. Primary arrhythmias are caused by pathologic conditions of the heart (myocarditis, valvular disease, conduction system abnormalities, and pericarditis). Secondary arrhythmias develop in the absence of heart disease and can be caused by excitement, fever, sepsis, hypoxemia, acid-base disorders, electrolyte homeostasis, gastrointestinal disturbances, anemia, severe hemorrhage, anesthesia, ionophores, other drugs, or toxemia. The treatment and prognosis for the two types of arrhythmias can be very different, and examination and laboratory tests are used to assist in making the distinction.

1. Take history. Determine the diet, feed additives, or medica­tion (including thyroid hormone, furosemide, bicarbonate, or other prerace medications); note whether there has been exercise intolerance, syncope, fever, coughing, or edema; inquire about gastrointestinal problems, diarrhea, or colic; inquire about access to cattle feed (containing ionophores or beta adrenergic agonists), poultry feed (containing ionophores), or feed supplements (containing kelp) and about previous respiratory tract infections in this animal or stablemates.

2. Perform a physical examination to determine whether there is primary cardiac disease. Record the animal's vital signs. Determine whether this is a bradyarrhythmia or tachyar­rhythmia. Careful auscultation should note which heart sounds are present and should characterize the arrhythmia. There may be irregularities in the basic rhythm, added sounds, or long pauses; classification of heart rate by regularity of rhythm can distinguish one arrhythmia from another (see Chapter 30). Note whether a pulse deficit is present by simultaneous auscultation and palpation of the peripheral arterial pulse; note the strength of the peripheral arterial pulse; observe the jugular vein for pulsations and distention; examine peripheral veins for distention; and examine mucous membrane color and capillary refill time. Careful auscultation of the lungs with and without a rebreathing bag should be performed.

3. Record an ECG. The base-apex lead can be used to screen for arrhythmias; it is attached using positive, negative, and ground leads as follows:

a. Positive lead is attached to skin over the left fifth inter­costal space at the point of maximal intensity (PMI) of the apex beat; using lead I, this is the left arm electrode; using lead II or lead III, it is the left leg electrode.

b. Negative lead is attached to the skin of the right jugular furrow two thirds of the distance from the ramus of the mandible to the thoracic inlet; using lead I or lead II, this is the right arm; using lead III, it is the left arm. ECG interpretation is discussed in Chapter 30.

4. If there is a cardiac murmur, perform an echocardiogram (including 2D, M-mode, and Doppler). Look for evidence of ventricular dysfunction, myocardial failure, chamber dilation, valvular abnormalities (such as prolapse, thicken­ing, ruptured chordae tendineae, or endocarditis), congenital defects, aortocardiac fistula, aortopulmonary fistula (Friesian horse), pericardial effusion, and tumor.

5. Obtain feed for analysis if ionophore (monensin, lasalocid, salinomycin) or β-adrenergic agonist (zilpaterol) exposure is suspected.

6. Determine if horse is grazing on pasture containing seeds of Acer pseudoplatanus or Acer negundo species in the late fall or early spring⁶ or other cardiotoxic plants.

7. Obtain whole blood for the following:

a. CBC

b. Selenium and vitamin E concentrations if cardiomy­opathy suspected

c. Blood gas determinations and acid-base status

7. Test serum or plasma for the following:

a. Electrolyte (Na, K, Cl, Ca, Mg, P) concentrations

b. Vitamin E (α-tocopherol) concentration

c. Cardiac troponin-I (cTnI) or cTnT⁷ if myocardial inflammation, injury, or necrosis is suspected

8. Test urine for the following:

a. Electrolyte (Na, K, Cl) concentrations

b. Creatinine determination for fractional clearance calculations

c. Myoglobin and hemoglobin

9. Calculate fractional excretion of potassium in the urine. This will be variable, depending on the diet, but a low value indicates the need for supplementation.

10. Treat the arrhythmia if:

a. Patient is hemodynamically unstable (e.g., poor cardiac output, weak peripheral pulses, cold extremities, syncopal)

b. There is ventricular tachycardia with a rapid rate (heart rate >120 beats/min)

c. There are multifocal ventricular ectopic beats

d. A QRS is detected in the preceding T wave (R on T)

e. There is advanced second-degree or complete (third- degree) AV block

f. The primary problem is cured or the condition is stabilized, and the patient is symptomatic with the cardiac arrhythmia

g. If the arrhythmia is performance limiting, such as atrial fibrillation in horses performing high-intensity exercise