A 4-year-old 18-kg (39.6-lb) sexually intact male Labrador Retriever–Poodle mix was evaluated because of a 10-day history of anorexia and marked lethargy progressing to obtundation. The dog had previously been treated by the referring veterinarian with dexamethasone, oxytetracycline, and amoxicillin-clavulanate without noticeable improvement. On initial examination, the dog was weak but alert and responsive. Mucous membranes were pink with a normal capillary refill time (< 2 seconds). Heart rate was 80 beats/min with a regular rhythm and unremarkable thoracic auscultation, and the femoral pulses were strong and synchronous with the heartbeat. Abdominal palpation revealed no abnormalities. Rectal temperature was considered normal. Findings of a neurologic examination were unremarkable other than the dog's dull demeanor.
During the period when the clinical investigations were performed, bradycardia was detected with a heart rate of approximately 40 beats/min. Electrocardiography was performed.
ECG Interpretation
The initial ECG recording (Figure 1) revealed an irregular supraventricular rhythm with a mean rate of 44 beats/min. The P-wave amplitude and duration were 0.3 mV and 40 milliseconds, respectively. The PR interval was 140 milliseconds, and the QRS duration was 40 milliseconds; the R-wave amplitude in lead II was 3.6 mV. The QT interval was 260 milliseconds, and no elevation or depression of the ST segment was observed. The mean electrical axis was 110°. The rhythm was classified as marked sinus arrhythmia with first-degree atrioventricular (AV) block.
Initial 6-lead ECG recording obtained during evaluation of a 4-year-old sexually intact male Labrador Retriever–Poodle mix that had a 10-day history of anorexia and marked lethargy progressing to obtundation. There is an irregular supraventricular rhythm with a mean rate of 44 beats/min. Paper speed = 25 mm/s; 5 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 11; 10.2460/javma.253.11.1413
To determine whether the bradycardia was vagally mediated and whether it would respond to anticholinergic drugs during a potential anesthetic episode for further investigations, an atropine response test was performed with 0.04 mg of atropine sulfate/kg (0.018 mg/lb) administered SC. The ECG recording was continued after the injection because of the dog's marked lethargy and unwillingness to move.
Ten minutes after the atropine injection, the ECG revealed frequent nonconducted P waves, with an atrial rate of 190 beats/min (Figure 2). The QRS complexes were observed at a rate of 34 beats/min; they had a narrow, normal morphology identical to complexes on the previous ECG recording and were preceded by P waves with a PR interval of 140 milliseconds. The rhythm was classified as high-grade, second-degree AV block and first-degree AV block.
Lead II ECG tracings recorded at intervals after the dog received an SC injection of atropine sulfate (0.04 mg/kg [0.018 mg/lb]). A—At 10 minutes after the atropine injection, notice the frequently nonconducted P waves. Atrial rate is 190 beats/min, and ventricular rate is 34 beats/min. B—At 16 minutes after the atropine injection, 2:1 atrioventricular block is evident. Atrial rate is 240 beats/min, and ventricular rate is 120 beats/min. C—At 26 minutes after the atropine injection, notice the 1:1 atrioventricular conduction with a heart rate of 220 beats/min. For all traces, paper speed = 25 mm/s; 5 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 253, 11; 10.2460/javma.253.11.1413
Sixteen minutes after the atropine injection, the second-degree AV block was still present, although the AV conduction increased to 2:1. Increases in the atrial rate to 240 beats/min and in the ventricular rate to 120 beats/min were noted. The PR interval was still slightly prolonged at 140 milliseconds (Figure 2).
A final ECG trace was obtained 26 minutes after the atropine injection. The AV block had completely resolved, and the heart rate was 220 beats/min. The rhythm was classified as sinus tachycardia (Figure 2).
When the dog's heart rate finally increased to > 150 beats/min, the atropine response test was considered positive. Therefore, the initial bradycardia was classified as vagally mediated.
Discussion
Atropine sulfate is an anticholinergic agent that competitively inhibits acetylcholine at postganglionic parasympathetic neuroeffector sites.1 It is commonly used in the veterinary field for purposes of diagnosis and treatment of patients with bradyarrhythmias. An atropine response test can be performed to differentiate vagally mediated bradyarrhythmias from nonvagally mediated arrhythmias, and different protocols are described. In dogs, the test result is considered positive when the sinus node rate is > 150 beats/min at 30 minutes after an SC injection of atropine (0.04 mg/kg) or at 5 to 10 minutes after IV administration of a similar dose.2
For the case described in the present report, the continuous ECG recording allowed detection of various changes after atropine administration, including an initial increase in atrial rate, followed by AV block, and finally a complete positive response with increased sinus rate and 1:1 AV conduction. An asynchronous effect of atropine on the sinoatrial and AV nodes was evident in this dog. Such a paradoxical initial response has been described previously in reports of studies in which atropine was administered IV, SC, or IM to bradycardic dogs3; administered IV to healthy dogs4; or administered IV or SC to dogs undergoing general anesthesia.5 In bradycardic dogs, the IV route of administration induces AV block more consistently, but the block resolves more rapidly. As for the case described in the present report, the presence of AV block seemed to be mostly attributable to an increase in the sinus node rate prior to a change in ventricular rate rather than a decrease in ventricular rate.3
In humans, atropine facilitates AV nodal conduction and decreases both effective and functional refractory periods. However, it has also been reported as causing AV block or worsening a preexisting conduction abnormality such as conduction defects below the AV node.6
For the dog of the present report, had a typical protocol of obtaining an ECG recording before and 30 minutes after the SC injection of atropine been performed, the final response would have been considered positive and unremarkable.
It is debatable whether the changes described for the dog of the present report should be considered clinically important. However, given the potential adverse effects of atropine, some clinicians discourage its indiscriminate use (eg, prior to anesthesia).5 The authors of the present report would like to emphasize that the use of atropine in any patient needs to be carefully considered in light of the underlying heart rate and rhythm as well as the overall clinical situation.
In the case described in the present report, the response to atropine indicated that the dog's bradycardia was vagally mediated. Further investigations, including MRI, identified a brain tumor, although there were no indications of increased intracranial pressure. In view of this diagnosis, the dog was euthanized. The described ECG changes should alert clinicians to the potential paradoxical changes observed occasionally after the administration of atropine in dogs.
References
1. Plumb DC. Atropine sulfate. In: Plumb DC, ed. Plumb's veterinary drug handbook. 8th ed. Wiley Blackwell, 2015;126–131.
2. Kittleson MD. Drugs used in treatment of cardiac arrhythmias: drugs used to treat bradyarrhythmias. In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. Available at: www.vin.com/Members/Proceedings/Proceedings.plx?CID=SACARDIO&PID=11412&O=VIN. Accessed Nov 17, 2017.
3. Rishniw M, Tobias AH, Slinker BK. Characterization of chronotropic and dysrhythmogenic effects of atropine in dogs with bradycardia. Am J Vet Res 1996;57:337–341.
4. Rishniw M, Kittleson MD, Jaffe RS, et al. Characterization of parasympatholytic chronotropic responses following intravenous administration of atropine to clinically normal dogs. Am J Vet Res 1999;60:1000–1003.
5. Muir WW. Effects of atropine on cardiac rate and rhythm in dogs. J Am Vet Med Assoc 1978;172:917–921.
6. Schweitzer P, Mark H. The effect of atropine on cardiac arrhythmias and conduction. Part 1. Am Heart J 1980;100:119–127.
