ECG Interpretation

Electrocardiography had been performed as a routine part of patient monitoring during anesthesia. The cat’s heart rate was 160 beats/min with a P-wave duration and amplitude of 0.02 seconds (reference range,¹ < 0.35 seconds) and 0.1 mV (reference range,¹ < 2 mV), respectively. The QRS-complex duration and amplitude were 0.02 seconds (reference range,¹ < 0.40 seconds) and 0.2 mV (reference range,¹ < 0.9 mV), respectively. The T-wave amplitude was also within the reference limit for cats.¹ In the ECG tracing obtained during anesthesia, the first complex appeared as a normal sinus complex and was followed by a single ventricular premature complex. However, the P wave moved through the subsequent QRS complex, suggesting that the atria and ventricles were beating independently of each other and at similar rates. This finding was suggestive of type I isorhythmic atrioventricular dissociation (IAVD). There were 2 apparently independent rhythms present. The first rhythm was an underlying sinus rhythm with a P-wave mean electrical axis of +90° (reference range, 0° to +90°). The normal mean electrical axis indicated a normal superior-to-inferior, anterior-to-posterior, and right-to-left axis, which resulted in a P wave that had positive polarity in the inferior leads. The second rhythm was a junctional rhythm that depolarized the ventricles in an antegrade direction and resulted in the apparently normal morphology and duration of the QRS complexes.

When the cat’s abnormal rhythm was detected, the surgical procedure and anesthesia were discontinued. The cat’s recovery from anesthesia was unremarkable. The next day (24 hours after anesthesia), ECG was repeated (Figure 2). At this time, the cat’s heart rate was 240 beats/min with a normal sinus rhythm and an apparent right-axis deviation as indicated by the prominent S waves. There was no evidence of the previously identified IAVD. Measurements of the P and T waves and QRS complexes were all within reference intervals.¹ An echocardiogram was also obtained and evaluated by a board-certified cardiologist; no abnormalities were noted.

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Six-lead ECG recording obtained from the cat during an examination 24 hours after anesthesia. There is a normal sinus rhythm, and no IAVD is noted. Paper speed = 50 mm/s; 1 cm = 2 mV.

Citation: Journal of the American Veterinary Medical Association 259, 8; 10.2460/javma.259.8.849

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Discussion

Isorhythmic atrioventricular dissociation is rarely reported in the veterinary medical literature and appears to occur more commonly in dogs than in cats.^2,3,4,5,6 Isorhythmic atrioventricular dissociation is the presence of 2 concurrent but independent rhythms: one that is a sinus rhythm and another that is of ventricular or junctional origin. There are 2 patterns of IAVD.^2,7 Type I IAVD is characterized by fluctuation in the P-QRS complex as the P waves move across the QRS complexes, thereby creating a variable PQ interval. In type II IAVD, the P waves and QRS complexes are in fixed positions with respect to each other.⁸ The P-P and R-R intervals are similar in rate, which results in only slight variations in the PQ intervals. The cat of the present report had type I IAVD.

Transient IAVD in 2 cats has been reported previously.^3,4 Both of those affected cats were severely hypothermic when the rhythm was detected, whereas the cat of the present report here had a normal rectal temperature during anesthesia. It is postulated that hypothermia can predispose humans to develop IAVD because hypothermia decreases spontaneous depolarization of pacemaker cells and slows impulse conduction.⁹ Isorhythmic atrioventricular dissociation in humans undergoing anesthesia is fairly commonly reported.^10,11,12 In people, IAVD has been associated with the use of nitrous oxide,¹³ epinephrine,¹⁴ opioids,¹² and halogenated anesthetics.¹² The cat of the present report received hydromorphone and an inhalation anesthetic; this is a commonly used protocol in general practice, but anesthesia may have been a contributing cause of the transient IAVD in this cat. The cat underwent echocardiography, the findings of which were unremarkable. Therefore, the cause of the transient IAVD in this cat remained speculative. One hypothesis for the development of type I IAVD is related to the cyclic variations in blood pressure. As the P waves move toward the QRS complexes in ECG tracings, eventually the 2 components overlap. The manifests as a decreased contribution of atrial contraction to ventricular filling, which causes a small decrease in blood pressure. Such a blood pressure decrease stimulates the arterial baroreceptors, thereby activating the sympathetic nervous system, shortening the subsequent P-P intervals, and increasing the sinus node discharge rate. Once the PQ intervals return to normal, the sinus node discharge rate should slow. At this point, the P waves can begin to migrate toward the QRS complexes again in ECG tracings.¹¹ For the cat of the present report, blood pressure was reportedly normal during anesthesia, although direct arterial blood pressure monitoring was not performed.

The diagnosis of anesthesia-associated IAVD can be difficult, as little if any change occurs in the rate or morphology of QRS complexes on the ECG tracings.¹³ However, a study¹⁴ of humans who developed transient IAVD during anesthesia revealed a substantial reduction in mean arterial pressure and cardiac output, compared with findings when those people were in sinus rhythm. In healthy anesthetized humans who develop IAVD, these decreases can be mild; in the previous study,¹⁴ the decrease in systolic arterial blood pressure was 17%. Typically, the hemodynamic effects of AV dissociation are negligible, although the effects may be more pronounced when a patient has hypovolemia or congestive heart failure.¹⁵ In people with poor heart function, the loss of the normal atrial contribution to left ventricular filling can affect cardiac output. At rest, atrial contraction contributes only a small amount of left ventricular filling; however, in states of tachycardia, this contribution increases because there is less time for passive ventricular filling. Therefore, treatment for transient IAVD is sometimes required. In people, administration of atropine,¹³ ephedrine,¹⁴ succinylcholine,¹⁵ or β-adrenoceptor antagonists¹⁰ can result in resolution of IAVD and is sometimes required when there is evidence of hemodynamic compromise. The choice of drug depends on whether the arrhythmia causes slowing of the sinus node discharge rate (for which treatment with atropine is appropriate) or whether a faster subsidiary pacemaker emerges (for which treatment with a β-adrenoceptor antagonist is appropriate). Another option for treatment of IAVD induced during anesthesia includes decreasing the inhalation anesthesia agent concentration, which may promote conversion of the patient back to a sinus rhythm.¹⁶ For the cat of the present report, anesthesia was discontinued, and IAVD appeared to resolve (as determined on the subsequent surface ECG recording). As such, it remained unclear whether any of the aforementioned medical treatments would have been effective for this cat. If this rhythm occurs, persons monitoring patients during anesthesia should be alert for signs of hemodynamic compromise and intervene if required. It is not known whether an animal that develops IAVD during anesthesia would develop the arrhythmia again during subsequent anesthetic episodes; however, if repeated anesthetic episodes are required, certain precautions, including use of total IV anesthesia instead of inhalation anesthesia and ready access to atropine or β-adrenoceptor antagonists, would be recommended.