ECG Interpretation

The lead II ECG trace revealed sinus rhythm with a mean heart rate of 110 beats/min. Atrial premature complexes (APCs) were frequently detected; these occurred predominantly in a bigeminal pattern. The QRS morphology of the APCs was identical to that of the normal sinus beats. It was not possible to evaluate the ECG trace for noncompensatory pauses because there were no more than 2 consecutive sinus beats. Infrequently, single sinus beats were not followed by an APC. The P′ wave of the APCs appeared to be primarily negative in lead II, suggesting an origin near the atrioventricular junction. The APCs were conducted with a variable coupling interval, and instantaneous rates ranged from 167 to 214 beats/min. All P′ waves were conducted through the AV node. This ECG trace was characteristic of atrial bigeminy.

Discussion

Atrial premature complexes (also known as atrial extrasystoles, atrial premature contractions, and atrial premature impulses) arise from an ectopic focus (or multiple foci) in the atria. They may precede the development of atrial tachycardia, atrial flutter, or atrial fibrillation.² Occasional isolated APCs can be a normal variation in old dogs and have little clinical importance.² Atrial bigeminy is usually, although not always, associated with organic heart disease.³

The conduction of APCs must be considered in relation to intra-atrial conduction, AV nodal conduction, and intraventricular conduction.³ There are several possible intra-atrial conduction sequences. The APC may completely depolarize the atria, activate the sinus node, and reset the sinus cycle. The APC may also completely depolarize the atria, reach the sino-atrial junction, meet an impulse that is leaving the sinus node, and prevent the conduction of that impulse; the APC does not discharge or reset the sinus cycle, and the next sinus beat occurs as expected. A third possibility is that the APC may depolarize the atria and partially penetrate the sino-atrial junction, rendering it refractory. The subsequent sinus impulse occurs as expected but encounters a refractory sino-atrial junction; thus, it is conducted with delay. The APC may also depolarize the atria simultaneously with the sinus impulse. This may cause fusion of the APC and the sinus beat and result in an atrial fusion wave. The P wave morphology of this atrial fusion wave would be intermediate between that of the sinus beat and the APC.³

The APC may encounter the AV node when the node is nonrefractory, partially refractory, or completely refractory. Partial AV nodal refractoriness may occur because the premature APC encounters the AV node when it is still partially refractory from the preceding sinus beat. Thus, conduction through the AV node is slowed, resulting in a prolonged P′-R interval (first-degree AV block). On an ECG recording, this may also appear simply as a P′-R interval that is prolonged, compared with the normal sinus P-R interval, but still within reference limits. Atrioventricular block may develop if the APC reaches the AV node when it is completely refractory. This most often occurs with markedly premature APCs. Electrocardiographically, this atrioventricular block is detected as a P′ wave without an attendant QRS complex. The markedly premature P′ waves are sometimes superimposed on the preceding T wave and become masked, giving the appearance of sinoatrial block. The APC may also enter an accessory pathway as it passes through the AV node and, subsequently, reenter and activate the atria.³ Furthermore, an APC may have normal intraventricular conduction or, because of its prematurity, may encounter a refractory bundle branch, resulting in a bundle branch block pattern.

The 4 main dependent arrhythmogenic mechanisms include altered automaticity, triggered activity, sodium-dependent reentry, and calcium-dependent reentry.⁴ Because of the variable coupling intervals, altered automaticity is the most likely mechanism in this dog. Abnormal automaticity develops in working atrial and ventricular myocardial cells that normally do not undergo spontaneous depolarization. When the transmembrane potential is reduced to < −60 mV, spontaneous depolarization occurs.⁵

The causes of atrial bigeminy are those of any atrial premature depolarization.² The differential diagnoses are numerous and include atrial enlargement secondary to AV valve insufficiency, any atrial disease (ie, right atrial tumors), congenital cardiac defects (ie, tricuspid valve dysplasia, mitral valve insufficiency, and patent ductus arteriosus), infectious causes (ie, viral myocarditis, Chagas disease, and tick-borne diseases), and drug effects (ie, effects of digitalis, anesthesia, and potassium-wasting diuretics).

Treatment for APCs is directed primarily at the underlying condition. If administration of specific antiarrhythmic medication is indicated, the most commonly used drugs include digoxin, B-adrenoceptor blockers, and calcium channel blockers. However, if there is no evidence of organic heart disease (ie, no clinical signs and no detectable pathologic changes), as determined in the dog of this report, no treatment is necessary unless the APCs trigger episodes of supraventricular tachycardia. Twenty-four-hour ambulatory ECG (Holter monitor) was not performed in the dog of this report, but findings of such a procedure would have allowed better characterization of the arrhythmia.

The dog of this report had no echocardiographic evidence of organic heart disease, and no other underlying cause of the APCs was determined. However, the frequency of the dog's arrhythmia suggested that this may become clinically important. At the time of this evaluation, treatment was not recommended; after 1 year, the dog remained clinically unaffected and no arrhythmia was detected during an annual examination performed by the referring veterinarian.