A guide to differential diagnosis of arrhythmias in horses

A guide to differential diagnosis of arrhythmias in horses

Feb 01, 2008

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 ( http://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.