A 9-year-old spayed female domestic shorthair cat was evaluated at a veterinary teaching hospital for right carpal arthrodesis following a traumatic hyperextension injury. At the time of the evaluation, the cat was receiving buprenorphine hydrochloride (0.06 mg) transmucosally twice daily and robenacoxib (6.0 mg) orally once daily for pain associated with the injury as prescribed by the referring veterinarian. The cat had idiopathic epilepsy, which had been diagnosed 3 years prior and controlled with twice-daily oral administration of levetiracetam (62.5 mg). A diagnosis of mild hypertrophic cardiomyopathy had also been made 5 years prior, but the cat was not receiving any cardiac medications. Findings of the pre-anesthesia physical examination were unremarkable aside from right carpal swelling and intercarpal joint instability (rectal temperature, 37.8°C [100.1°F]; pulse rate, 168 beats/min; and respiratory rate, 32 breaths/min). The cat weighed 7.1 kg (15.6 lb) but was markedly overconditioned, and medication doses were calculated on the basis of an approximate lean body weight of 5.5 kg (12.1 lb).
Prior to anesthesia, cardiology consultation was undertaken. Echocardiography revealed a moderate increase in left ventricular free wall thickness and normal chamber sizes consistent with the previous diagnosis of mild hypertrophic cardiomyopathy. The timing lead ECG during echocardiography revealed sinus rhythm with a heart rate of 180 beats/min and low-voltage R waves, which were considered to be a result of either the patient's obesity or an axis deviation; however, a 6-lead ECG examination was not performed because of the cat's fractious nature. The cat was deemed a suitable candidate for general anesthesia.
The cat was premedicated with midazolam hydrochloride (0.18 mg/kg [0.08 mg/lb]), methadone hydrochloride (0.27 mg/kg [0.12 mg/lb]), and alfaxalone (0.47 mg/kg [0.21 mg/lb]) IM, followed by additional doses of alfaxalone (0.5 mg/kg [0.23 mg/lb]) and methadone (0.2 mg/kg [0.09 mg/lb]) 20 minutes later, which resulted in adequate sedation. A 22-gauge IV cephalic catheter was placed, and an infusion of lactated Ringer solution (2 mL/kg/h [0.9 mL/lb/h]) was started and maintained throughout anesthesia. Anesthesia was induced with alfaxalone (1 mg/kg [0.45 mg/lb]) administered IV. The cat was intubated, and anesthesia was maintained via inhalation of isoflurane and oxygen. Preoperative radiography was performed. During this procedure, the cat was stable except for hypothermia (35° to 35.8°C [95° to 96.4°F]). A baseline rhythm strip was printed (Figure 1).
Rhythm strip obtained from a 9-year-old 7.1-kg (15.6-lb) domestic shorthair cat that had been anesthetized for right carpal arthrodesis. Notice the sinus bradycardia with a mean heart rate of 125 beats/min. The QRS complex morphology is triphasic with a notched R wave of low voltage (0.15 mV). There is also borderline ST-segment elevation (0.1 mV). Paper speed = 25 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 252, 10; 10.2460/javma.252.10.1214
ECG interpretation
The cat's initial ECG tracing indicated sinus bradycardia with a mean heart rate of 125 beats/min. The QRS complex morphology was triphasic with a notched R wave of low voltage (0.15 mV [reference range, ≤ 0.9 mV]1), similar to that observed in the echocardiographic timing lead ECG. There was also borderline ST-segment elevation (0.1 mV). Blockade of the radial and median nerves in the right forelimb was performed with a nerve stimulator and total volume of 1.33 mL of 0.5% bupivacaine. At this time, the cat was noted to be bradycardic with a heart rate of 90 beats/min and moderately hypotensive with a Doppler ultrasonography-measured systolic arterial pressure of 80 mm Hg. The cat's rectal temperature at this time remained low (33.4°C [92.2°F]) despite the use of a forced-air warming blanket. No ECG recording was printed at this point. The cat was administered glycopyrrolate (5 μg/kg [2.27 μg/lb]), and its heart rate increased to approximately 100 beats/min with minimal change in systolic arterial blood pressure. Five minutes later, ECG monitoring revealed a change in the QRS complex morphology, and a second ECG strip was printed (Figure 2). In this recording, there were 2 QRS complex morphologies with similar heart rates; the first appeared identical to that of the QRS complexes in the initial ECG strip, and the second was biphasic with a deep S wave and a high-normal QT interval (0.14 seconds; reference range, 0.07 to 0.20 seconds]1). These differing complex types occurred in alternating runs and occasionally in a bigeminal pattern. There was a persistent borderline ST-segment elevation (0.1 mV). At this time, systolic arterial blood pressure increased to 90 mm Hg, as measured by Doppler ultrasonography. A second warming blanket was placed, and the cat's rectal temperature reached 35°C (95°F) by the end of the surgical procedure. The cats’ respiratory rate, end-tidal carbon dioxide concentration, and pulse oximetry values did not change notably throughout the procedure. The cat recovered from anesthesia without incident and appeared comfortable after surgery.
Rhythm strip obtained from the cat in Figure 1 later during the surgical procedure. P waves are visible throughout the strip with a mean heart rate of 130 beats/min, and the PR intervals are consistent throughout the recording. The QRS complex morphology is different from that of the complexes in the rhythm strip obtained earlier. In this recording, complexes have an rS morphology, slurring of the ST segment, borderline ST-segment elevation (0.1 mV), and high-normal QRS complex duration (0.04 seconds) and QT interval (0.14 seconds). Paper speed = 25 mm/s; 2 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 252, 10; 10.2460/javma.252.10.1214
Discussion
For the cat of the present report, the most likely cause for the differing QRS complex morphologies observed during anesthesia and surgery was isorhythmic atrioventricular dissociation (IAVD). Atrioventricular dissociation can occur as a result of slowing of the normal pacemaker rate or acceleration of a junctional or ventricular focus.2 Given the sinus bradycardia in the cat of this report, a high ventricular escape focus was considered most likely. The cat's heart rate of 125 beats/min was consistent with previously reported ventricular escape rates in cats.3 The rhythm is described as isorhythmic because of the similar heart rates of the sinus complexes and escape complexes; the escape beats mimic true sinus complexes owing to the apparent maintenance of the PR intervals, although the P waves are just in fortuitous proximity. Specifically, this type of IAVD is designated type II because the relationship between P waves and QRS complexes is static during the observed recording.4 Conversely, type I IAVD is characterized by oscillations of the P waves through the QRS complexes and back, which are associated with variation in baroreceptor response because of variable contribution of atrial systole to ventricular filling.4
Alternatively, the rhythm may represent phase 3 or phase 4 aberrancy, which is a form of rate-dependent conduction abnormality. If an impulse arrives at the ventricles sooner than the preceding one, it may arrive during phase 3 of the action potential. If this occurs, the membrane potential is more positive, making fewer fast sodium channels available; the complex occurs during the relative refractory period and therefore may be conducted aberrantly.2 Phase 4 aberrancy occurs with slowing of the R-R interval such that latent pacemakers in the His-Purkinje system start to spontaneously depolarize toward threshold. This results in some fibers becoming unavailable to propagate the subsequent action potential; thus, aberrancy occurs with longer R-R intervals.2 Phase 3 and phase 4 aberrancies were both considered less likely occurrences than IAVD in the cat of the present report, because there was no measurable difference in R-R intervals at the time of transition in QRS complex morphologies.
Atrioventricular dissociation has been reported with the use of volatile inhalant anesthetics, and such an effect may have occurred in the cat of the present report. Inhalant anesthetic agents depress sinoatrial and AV nodal automaticity, whereas the distal conduction system may be spared, allowing an accelerated pacemaker to predominate.5 However, AV dissociation is not common in patients undergoing general anesthesia; therefore, hypothermia was suspected to be a major contributor to the arrhythmia in the cat of the present report. Hypothermia decreases spontaneous depolarization of pacemaker cells and slows impulse conduction.6 Hypothermia-induced IAVD is typically not responsive to atropine, which may explain the inadequate response to glycopyrrolate for the case described in the present report; despite administration of glycopyrrolate, the cat remained bradycardic for the duration of the procedure.6 Atrioventricular dissociation in an awake hypothermic, bradycardic cat has been previously reported.7 It was postulated that the hypothermia led to bradycardia, thereby predisposing the cat of that report to IAVD. Hypothermia may also increase the risk for supraventricular arrhythmias and potentially ventricular arrhythmias.6 Therefore, it is difficult to determine whether the ventricular complexes were truly escape beats due to sinus bradycardia or accelerated ectopic foci in the bradycardic cat of either the present or previous report.7
For the cat of the present report, the QRS complexes of the sinus beats were of normal duration, but the morphology suggested there may be aberrancy in conduction. A 6-lead ECG would have been required to characterize any axis deviation that might have been present. This may have been related to the cat's mild cardiomyopathy or may have been normal variation8 for this animal.
The high-normal QT interval was suspected to be a consequence of the cat's profound hypothermia, but may also have been attributable to bradycardia. Hypothermia prolongs the action potential duration and results in abnormal repolarization.6 For the cat of the present report, a 6-lead ECG could not be obtained prior to anesthesia because of the patient's fractious nature; thus, QT-interval duration for this animal under conditions of normal heart rate and body temperature was not available for comparison.
In the case described in the present report, the borderline ST-segment elevation was a questionable finding; assessment of a 6-lead ECG recording was recommended for better evaluation of the ST segment because evaluation of timing leads may be inaccurate. If ST-segment elevation was truly present, it could be indicative of myocardial ischemia attributable to either anesthesia-induced hypotension or perhaps the cat's underlying cardiomyopathy.8 Induced hypotension is desirable during surgical procedures with high expected blood loss to mitigate risk for severe hemorrhage and allow better surgical field visibility, and myocardial infarction is rare in surgical patients with induced hypotension.9 Because ischemia is dependent on both myocardial supply and demand, it is plausible that the decreased afterload caused by systemic hypotension offsets any decreased coronary perfusion. Osborne waves, defined as positive deflections in the terminal portion of the QRS complex and elevation of the J point, are classically associated with hypothermia6,10 but have a more rounded appearance than the flat ST-segment changes observed in the case described in the present report.
Acknowledgments
The authors declare that there were no conflicts of interest.
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