Page 107 - Rapid Review of ECG Interpretation in Small Animal Practice, 2nd Edition

Answer 39 ECG Cases

Answer 39
VetBooks.ir 1 ECG 39a shows an SVT converting into sinus rhythm.

2 • The initial section of ECG 39a shows a narrow complex tachycardia at a rate of 300 bpm. The QRS
complexes are tall and narrow and therefore the arrhythmia is presumed to be supraventricular in origin,
despite the fact that P waves cannot be readily identified. The heart rate is rapid enough that any P waves
will be buried in the preceding T wave. Diltiazem, a calcium-channel blocker, was administered and the
SVT terminated abruptly followed by a sinus rhythm with a heart rate of 125 bpm.
• This ECG demonstrates the difficulty in discerning VT from SVT when the heart rate is very rapid.
A differential diagnosis for the arrhythmia is VT, as the QRS complexes during the tachycardia do
not look exactly like the QRS complexes during sinus rhythm. The response to diltiazem, however,
strongly suggests that this was a SVT, as calcium-channel blockers are effective at terminating SVTs
but are not effective at treating ventricular arrhythmias.

The cat from ECG 39a was stabilized and a subsequent ECG was recorded several hours later (ECG 39b).
The ECG shows sinus rhythm with a heart rate of 200 bpm. The PR interval is unusually short (40 ms;
normal: 50–90 ms), resulting in a P wave that appears very close to the QRS complex. This finding
(ventricular pre-excitation) coupled with the history of SVT is suggestive of the presence of an accessory
AV pathway. Accessory pathways (APs) are extra-AV nodal pathways situated between the atria and the
ventricles and allow the cardiac impulse to travel directly from the atria to the ventricles while bypassing
the AV node. Normal conduction via the AV node is also present. In ventricular pre-excitation, the AP
reaches the ventricle prior to AV nodal impulses and “pre-excites” the ventricle, causing early activation
and a short PR interval. The normal conduction via the AV node fuses with the pre-excitation impulse and
can result in a QRS complex with a slurred upstroke, called a delta wave.
Pre-excitation by itself has little clinical consequence; however, the presence of the AP along with
the AV node creates a circuit of conduction tissue that promotes development of SVT. SVT as seen in
ECG 39a is often triggered by an atrial premature contraction. The tachycardia utilizes the AV node for
forward conduction and the AP for conduction back to the atria. Drugs that block AV nodal conduction,
such as diltiazem, can terminate the SVT by blocking impulse conduction through the AV node. Other
antiarrhythmic drugs can selectively slow conduction in the AP and can also be effective at terminating the
tachycardia. Cessation of tachycardia that is resistant to medical therapy requires interventional procedures
such as catheter ablation using radiofrequency energy to destroy (ablate) the accessory pathway.

39b
I

II

III

aVR

aVL

aVF

94