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A guide to differential diagnosis of arrhythmias in horses

Article

It would be highly unusual for clinically significant cardiac disease to be present in a horse without a change in the heart rate, rhythm or the presence of a murmur.

It would be highly unusual for clinically significant cardiac disease to be present in a horse without a change in the heart rate, rhythm or the presence of a murmur.

We provided a "A guide to the differential diagnosis of murmurs in horses" in the November 2007 "In Focus" supplement to DVM Newsmagazine (dvmnews.com). This review offers several key points to assist with correct identification of the most common rate and rhythm disturbances in horses.

Normal sinus rhythm and the ECG

Auscultation is the first clinical tool to detect a rate or rhythm disturbance. Probably one of the most common reasons for missing a rate or rhythm disturbance in a horse is insufficient time in auscultation.

Sustained bradycardia (heart rate < 24 beats/minute) is uncommon in the horse and usually indicates an underlying pathologic etiology. Likewise, sustained tachycardia (heart rate > 50 beats/minute) that cannot be explained by excitement or pain should be further investigated; it could be a sign of underlying cardiac disease.

An arrhythmia simply refers to any change in the time between cardiac cycles that disrupts the regular pattern of systole. Thus the key to detecting an arrhythmia is cardiac auscultation and/or simultaneous palpation of the pulse of sufficient duration to establish a rate, as well as the pattern of systolic events (pulse generation or generation of S1/S2).

When a rate or rhythm disturbance is detected by auscultation, the best way to definitively determine the cause is to perform an electrocardiogram.

Myocardial cells maintain an electric potential, with the inside of the cell carrying a negative potential charge relative to the outside that can rapidly change in response to signals from neighboring cells. This creates the "action potential" that ultimately drives myocardial contraction.

The sinoatrial node (SAN), located in the right atrium, is composed of cells that have an unstable resting potential that drift toward a positive potential. This automatically driven action potential sets the pace of myocardial contraction to normal sinus rhythm.

As each atrial myocyte produces an action potential, calcium is delivered to the intracellular contractile units. As the wave of electrical excitation moves toward the apex, it enters the atrioventricular node (AVN), wherein ventricular contraction is controlled. The AVN sends impulses to the extensive network of the Purkinje cells, that themselves do not contain contractile units. The Purkinje cells serve to disseminate the pace-setting wave of excitation almost simultaneously to the contractile ventricular myocytes. So, ultimately, it is the electrical events of the heart that translate to what we see on an ECG.

By setting both positive and negative electrodes on the body surface, strategically around the heart, the general pattern of the sum of the action potentials created by the drive of the relative ionic charge of the cells can be detected at the body surface.

In other words, as the cells depolarize and become relatively negative on the outside, the surface electrodes detect this wave of change in charge. The ECG recorder generates an "upswing" when the wave of depolarization moves parallel to the surface electrodes, in the direction from the negative electrode to the positive electrode.

Why is this at all meaningful? It tells us that, when trying to optimize the size of the deflections recorded by an ECG unit, the electrodes should be set relatively parallel to the main wave of excitation of the myocardial cells, with the positive electrode set away from the initial site of excitation.

This is exactly what the Base-Apex ECG Lead provides in a horse. In fact, because of the size of a horse's heart and the extensive Purkinje cell system, the Base-Apex Lead typically is the only lead that is needed to record the electrical activity of a horse's heart.

Running a base-apex lead

There are four steps to run a base-apex Lead recording in the horse:

1) The right-arm electrode (frequently the white color-coded one) is clipped to the skin over the right shoulder or right jugular grove.

2) The left-arm electrode (black) is placed over the apex of the left heart slightly above the left elbow.

3) The left-leg (red) electrode serves as a ground and usually is placed on the right side of the neck.

4) The recorder is set to lead I. This will make the left-arm electrode positive and the right arm negative.

If you place your surface electrodes parallel to the main sweep of depolarization (negative charge moving from SAN to AVN to ventricular apex) and set the positive electrode at the left apex of the heart, you will optimize the ECG recording.

This is exactly what happens in lead I. The "base" electrode (top of right heart) is negative and the "apex" electrode (apex of left heart) is positive.

The P-wave represents atrial depolarization. Atrial repolarization is not seen as a separate event on the ECG recording. The QRS complex represents ventricular depolarization.

Technically, the Q-wave is the first negative deflection of the trio, the R-wave is the first positive deflection and the S-wave is the next negative deflection generated by ventricular depolarization. The T-wave represents ventricular repolarization.

The large atria in horses often results in slightly asynchronous depolarization, so the P-wave often appears as biphasic positive deflection in the base-apex recording (i.e., has two small humps). The QRS in horses is depicted mostly as a downward deflection of the ECG recording in the base-apex mode (i.e., mostly the S-wave). The T-wave usually is represented by an upward deflection, but may also be biphasic or negative.

Intrepreting an ECG

There are several steps to interpreting an ECG, but a key step is identification of the QRS complexes.

1) Make sure the horse is standing still and the leads are secure.

2) Find the largest deflections. These should be the QRS complexes or the S-waves.

3) If there was a QRS complex (i.e., ventricular depolarization), there must be ventricular repolarization. So look immediately behind the QRS complex to identify the T-wave.

4) Look in front of the QRS complexes. Is there a P-wave for every QRS? Is there a QRS for every P-wave? If there is no P-wave, it could represent atrial fibrillation or an ectopic junctional or ventricular contraction. If there is a P-wave without a QRS, then the AVN was blocked.

5) Study the intervals from QRS to QRS complex. Are they regular or irregular?

This will help identify normal rhythm, premature beats, and blocked or escaped beats.

6) Do the QRS complexes come earlier (premature) or later (escape or blocked) than expected?

7) Do the configurations of all the QRS complexes and P-waves look the same? This can help you tell if the origin of a complex is normal or ectopic and unifocal or multifocal.

8) Determine the heart rate.When the ECG recorder is set to a paper speed of 25 mm/sec, each of the smallest boxes on the ECG paper grid is equivalent to 0.04 sec. There are five of these boxes in the next larger box on the grid, which is 0.2 seconds.

So if you count the number of QRS complexes over 30 of the larger boxes (six seconds) and multiply by 10, you have the number of ventricular contractions per minute. Some recorders place a large "tick" on the top of the paper that is generated every three seconds. So again, the heart rate can be determined by counting the number of QRS complexes generated over six seconds and multiplying by 10, when the paper speed is 25 mm/sec (Figure 1).

Many newer ECG units will give a heart rate based on the number of QRS deflections, but be careful: Because the equine P- and T-waves are bigger than many other species, these automated counts often are erroneously high, as they mistakenly include the P-and T-waves, as well as the QRS complexes.

9) Are the durations of the complexes normal? In general, this information usually is not critical in making the diagnosis of an arrhythmia in horses, but here are reference intervals:

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.

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).

Figure 1: Second-degree AV block. The period of asystole occurs at the arrowhead, when only a P-wave is generated.

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.

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.

Figure 2: Sinus block. Note the period of asystole between the arrowheads.

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.

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).

Figure 3: Atrial fibrillation with a normal heart rate.

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.

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).

Figure 4: Atrial premature contraction (arrow).

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

3) often a pause or period of asystole after the VPC, if it is isolated (Figure 5)

Figure 5: Ventricular premature contraction (arrow). This patient also has 2nd degree AV block (*).

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).

Figure 6: Sustained ventricular tachycardia (starting at arrow), after four sinus-origin beats.

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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