A guide to differential diagnosis of arrhythmias in horses - DVM
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A guide to differential diagnosis of arrhythmias in horses


DVM360 MAGAZINE


Reference intervals

In normal sinus rhythm, the SAN fires and sets the pace of systole by sending the wave of depolarization through the atria and to the AVN to the ventricles.

Common nonpathologic variations of normal sinus rhythm are second-degree atrioventricular (AV) block, sinus block and sinus arrhythmia.


Figure 1: Second-degree AV block. The period of asystole occurs at the arrowhead, when only a P-wave is generated.
Second-degree AV block occurs with high resting vagal tone that slows conduction of impulses from the SAN to the AVN. Thus the SAN fires, causing atrial contraction and generation of a P-wave, but no conduction through the AVN. Systole, S1, S2 and the QRS complexes do not occur (Figure 1).

Typically second-degree AV block is detected as a fairly rhythmic (regularly irregular) loss of the sounds of S1 and S2. During these periods of asystole, occasionally the sole sound of atrial contraction (S4) is audible. Because second-degree AV block is physiologically associated with increased parasympathetic tone, it should dissipate with exercise or excitement. If it does not go away with exercise and the heart rate does not increase with exercise, it should be considered pathologic.


Figure 2: Sinus block. Note the period of asystole between the arrowheads.
Sinus block is less common. Auscutation sounds very similar to second-degree AV block, as there are periods of asystole, but S4 is never audible during the periods of asystole. Sinus block also is due to high vagal tone that blocks the pacing cells of the SAN. So here, the atrial do not contract (thus no S4) and the ECG shows a period during which neither P-waves or QS/T complexes are generated (Figure 2). Like second-degree heart block, sinus block should dissipate with exercise.

Sinus arrhythmia is less common in horses than people, but it is a normal physiologic response to the changes in parasympathetic and sympathetic tone with the respiratory cycle. During inhalation, the sympathetic nervous system is stimulated, thus the heart rate may increase slightly. During exhalation, parasympathetic tone is greater, thus the heart rate slows.

Common pathologic arrhythmias

Atrial fibrillation is caused by inhomogeneity of depolarization of the atrial myocytes. Coordinated atrial contraction does not occur; thus the sound of S4 is never heard during atrial fibrillation. The conduction of impulses from the atria to the ventricles is not in a directed path as it is with normal sinus conduction, so the random event of an atrial impulse firing the AVN accounts for the irregularly irregular rhythm of atrial fibrillation.

Another audible characteristic of atrial fibrillation is that the intensity of S1 and S2 often varies from beat to beat. Because horses can have a normal heart rate while in atrial fibrillation, not surprisingly atrial fibrillation frequently is confused with second-degree AV block on auscultation.


Figure 3: Atrial fibrillation with a normal heart rate.
The irregularly irregular rhythm can be hard to detect if the heart rate is faster, so the ECG is the best way to confirm (Figure 3).

The classic ECG findings of atrial fibrillation are:

1) no definitive P-waves

2) flutter in the baseline

3) normal-appearing QS complexes at irregular intervals.

Atrial fibrillation is not normal and, if documented, further evaluation of the heart with an echocardiogram is recommended.

Atrial premature contractions (APC) may be normal in horses if they are rare in occurrence or occur following exercise.

An APC occurs when a focus in the atria, other than the SAN, fires an impulse that sets off atrial conduction. In auscultation, systole is heard "sooner than expected," may be of different intensity than beats originating from the SAN and the premature beat is not followed by a pause.

If there are four or more premature atrial contractions in a row or it is sustained, it is referred to as atrial tachycardia. Atrial tachycardia (not normal) is almost impossible to distinguish from sinus tachycardia by auscultation alone.


Figure 4: Atrial premature contraction (arrow).
On the ECG, APCs are identified by a normal-looking QS complex that appears sooner than expected and is preceded by a P-wave that may be of different conformation than SAN origin beats (Figure 4).

Frequent APCs or those that result in an increased heart rate are not normal and require further investigation into their cause. Even with an ECG, atrial tachycardia can be difficult to distinguish from sinus tachycardia. Atrial tachycardia should be suspected if tachycardia is sustained and cannot be explained by pain or excitement.

Ventricular premature contractions (VPC) are less common than APCs, but are less worrisome if they are rare in occurrence. A VPC represents an impulse that originates from the ventricles, resulting in ventricular depolarization and contraction without atrial conduction or contraction.

On auscultation, S1 and S2 occur "sooner than expected," often are quieter than SAN-origin beats and are followed by a pause, as the SAN resets.

Ventricular tachycardia is never normal and represents four or more VPCs in a row. Because the impulses originate from the ventricles, on the ECG the characteristic findings of VPCs are:

1) a bizarre-shaped QRS complex that occurs sooner than normal

2) the QRS is not preceded by a P-wave


Figure 5: Ventricular premature contraction (arrow). This patient also has 2nd degree AV block (*).
3) often a pause or period of asystole after the VPC, if it is isolated (Figure 5)


Figure 6: Sustained ventricular tachycardia (starting at arrow), after four sinus-origin beats.
Ventricular tachycardia is difficult to distinguish from nonpathologic sinus tachycardia. An ECG will distinguish ventricular tachycardia as a series of rapid, bizarre-shaped QRS complexes (Figure 6).

Dr. Barton is the Josiah Meigs Distinguished Teaching Professor at the University of Georgia's College of Veterinary Medicine, where she is a large-animal internist in academic practice. She received her DVM from the University of Illinois in 1985, her PhD in physiology at the University of Georgia in 1990 and became an ACVIM diplomate in 1990.


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