ECG of the Month

Satoko Nishimura 1Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Lance C. Visser 1Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Catherine T. Gunther-Harrington 1Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Yu Ueda 1Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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Joshua A. Stern 1Department of Medicine & Epidemiology, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616.

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A14-year-old 7.3-kg (16.1-lb) spayed female West Highland White Terrier was evaluated at a veterinary medical teaching hospital for possible pacemaker implantation to treat suspected sick sinus syndrome (SSS). Three days earlier, the dog had multiple collapse episodes; periods of sinus arrest were detected during an ECG examination. At that time, results of a CBC and serum biochemical analysis were within reference intervals. Transthoracic echocardiography revealed mild myxomatous mitral and tricuspid valve degeneration without cardiac chamber enlargement (American College of Veterinary Internal Medicine classification1 stage B1) as well as mild pulmonary hypertension. The dog's history included chronic cough (presumed breed-related pulmonary fibrosis) for which theophylline (unknown dosage) was prescribed. After a diagnosis of SSS was made, theophylline administration was discontinued and terbutaline sulfate was prescribed at a dosage of 0.34 mg/kg (0.15 mg/lb) orally every 12 hours. Despite terbutaline administration, the dog continued to have syncopal episodes and was referred for possible pacemaker implantation.

On physical examination at the veterinary medical teaching hospital, findings included dull mentation, a grade II/VI left apical systolic murmur, bradycardia (heart rate, 36 beats/min) with an irregular cardiac rhythm. Three-view thoracic radiographic findings included mild generalized cardiomegaly and a mild diffuse interstitial pulmonary pattern, which were considered likely age-related changes; there was no evidence of cardiac decompensation or clear suspicion of pulmonary fibrosis. A serum electrolyte panel revealed hyperlactatemia (7.6 mmol/L; reference interval, 0 to 2.5 mmol/L) with no other notable electrolyte disturbances. Six-lead ECG and an atropine response test were performed.

ECG Interpretation

The ECG recording at time of the evaluation revealed a highly irregular rhythm with a heart rate ranging from 20 to 200 beats/min (Figure 1). The rhythm had short periods of sinus tachycardia and frequent periods of sinus arrest lasting up to 6.5 seconds, followed by resumption of sinus tachycardia or occurrence of junctional escape complexes. The narrow, upright complex that terminated a prolonged sinus arrest was consistent with a junctional escape complex given its upright and narrow morphology, its occurrence following a pause, and the lack of a preceding P wave of sinus origin. The R-R interval immediately preceding the junctional escape complex measured 6,500 milliseconds, which is equivalent to an instantaneous rate of 9 depolarizations/min. This constellation of ECG findings (ie, short periods of sinus tachycardia, frequent periods of sinus arrest, and failure of the subsidiary pacemakers) when coupled with syncope is consistent with a diagnosis of SSS.2

Figure 1—
Figure 1—

Lead II ECG tracing (continuous strips) obtained from a 14-year-old dog with sick sinus syndrome during evaluation at a veterinary medical teaching hospital for possible pacemaker implantation. A period of sinus tachycardia was followed by sinus pauses lasting up to 6.5 seconds. The pauses were terminated by either a sinus complex or a junctional escape complex (asterisk). The junctional escape complex in this tracing occurs after an interval of 6,500 milliseconds, which is equivalent to an instantaneous rate of 9 depolarizations/min, indicative of failure of subsidiary pacemaker activity. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.60

The dog underwent an atropine response test in which an ECG examination was performed 30 minutes after SC administration of atropine sulfate at a dose of 0.04 mg/kg (0.018 mg/lb). After atropine administration, the ECG examination revealed sinus tachycardia at a rate of 220 beats/min with resolution of sinus arrest. This was considered a positive response to atropine administration; thus, medical management with propantheline bromide (4.3 mg/kg [1.95 mg/lb], PO, q 8 h) was initiated in addition to continued treatment with terbutaline.

The dog underwent continuous ECG monitoring in the intensive care unit. A 6-lead ECG examination was repeated the following day (Figure 2). This recording revealed a regular rhythm at a rate of 125 beats/min. Atrial depolarization (P') waves were seen as negative deflections in leads II, III, and aVF. The P’ waves were positive in all other evaluated leads. The duration of the PR interval (approx 60 milliseconds) was consistent and considered normal. The morphology of the QRS complexes was normal (upright and narrow), and each complex was associated with a P’ wave. Negative P’ waves can be observed when the atrial impulse originates in the lower (inferior) portions of the atria. Alternatively, negatively deflected P’ waves could represent retrograde conduction of P’ waves from a junctional rhythm or the combination of a junctional rhythm with type II isorhythmic atrioventricular dissociation. For the dog of the present report, the P’ waves were consistently associated with QRS complexes and had fixed, normal PR intervals; therefore, the possibility of a junctional rhythm with retrograde P’ wave conduction or with type II isorhythmic AV dissociation was considered less likely. The ECG findings were interpreted as consistent with a supraventricular rhythm with P’ waves that originated from the lower (inferior) portions of the atria and were responsible for generation of the associated QRS complexes. On the basis of the characteristic negative deflection of the P’ waves in leads II, III, and aVF, differential diagnoses for the origin of the atrial depolarizations included the coronary sinus (CS) or the inferior portion of the left atrium. Dextrocardia was another consideration but was ruled out by echocardiographic and thoracic radiographic findings, making coronary sinus rhythm (CSR) the probable diagnosis.

Figure 2—
Figure 2—

Six-lead ECG tracing obtained from the dog in Figure 1 after 1 day of hospitalization while it was receiving oral treatment with propantheline (4.3 mg/kg [1.9 mg/lb]) and terbutaline (0.34 mg/kg [0.155 mg/lb]). The rhythm is regular with a heart rate of 125 beats/min. All P’ waves and QRS complexes appear associated with each other, with a PR interval of fixed and normal duration (60 milliseconds). The P’ waves are negatively deflected in leads II, III, and aVF. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.60

Discussion

Coronary sinus rhythm is proposed to be secondary to the presence of pacemaker cells in the region of the upper portion of the atrioventricular node extending into the CS.3 Anatomically, the CS courses along the sulcus between the left atrium and the left ventricle, and its ostium empties into the right atrium. The CS is the largest cardiac vein that receives blood from the coronary veins, and it extends from the valve of the great cardiac vein to the ostium of the CS.4

Embryologically, the CS is a left atrial structure.3,5 In humans, a small bundle of muscle fibers has been identified entering the atrioventricular node from the area of the CS.3,6 These muscle fibers are considered remnants of the left-sided sinoatrial (SA) node and have a structure similar to those in the SA node and the auricular musculature.3,6,7 Additionally, the CS region is notable for its abundance of ganglion cells.6 Therefore, the CS area likely possesses a high level of automaticity and possible pacemaker activity.3,6 The large number of ganglion cells renders this region quite sensitive to autonomic impulses.6

The ECG criteria for diagnosis of CSR include inverted (negative) P’ waves in leads II, III, and aVF; upright (positive) P’ waves in lead aVR; and P'R intervals of normal or slightly reduced duration in all recorded leads.3,5-9 All of these ECG findings were identified in the case described in the present report. Although not evaluated in this dog, an inverted (negative) P’ wave in lead V6 may also be observed with CSR.5 The generation of negatively deflected P’ waves in lead II is illustrated (Figure 3). Because the CS ostium is located in the posteroseptal region of the right atrium, impulses generated in this region would create a wave front in the opposite direction to the ones associated with impulses generated from the SA node.

Figure 3—
Figure 3—

Schematic diagram of the coronary sinus (CS) and its ostium. The CS courses along the left atrium (LA) and empties into the right atrium (RA) at the posteroseptal aspect. The presumed location of the sinoatrial node (SAN) relative to the CS ostium is depicted on the same plane. Impulses originating from the CS ostium and along the CS (depicted here by stars) generate wave fronts (shown as gray arcs) in the opposite direction to a wave front from the SAN, thereby creating negatively deflected P’ waves in lead II. The general path of lead II is depicted.

Citation: Journal of the American Veterinary Medical Association 255, 1; 10.2460/javma.255.1.60

In humans, CSR can be experimentally reproduced by use of a pacing catheter to stimulate an impulse in the orifice of the CS.3,5,8 Lau et al5 also found that these P'-wave changes are consistently observed in both dogs and humans when the os of the CS is electrically stimulated. Interestingly, these ECG criteria are achieved even when various regions of the great cardiac vein of dogs are electrically stimulated.5 In the experiment by Lau et al,5 pacing of the inferior left atrium in close proximity to the CS produced P’ waves identical to and indistinguishable from those observed with CSR. This indicates that the negatively deflected P’ waves of the dog of this report could also have originated from the inferior left atrium or along the great cardiac vein. The reason for this resemblance may be attributed to the common site of impulse formation or a common intra-atrial conduction pathway.5

Coronary sinus rhythm is believed to result from depression of pacemaker activity of the SA node.3 Experiments by Chiba and Hashimoto3 revealed that CSR could be induced by catecholamine injection into the CS region when the SA node activity is simultaneously suppressed by bethanechol injected into the sinus node artery in dogs. Therefore, CSR may develop when SA pacemaker activity is strongly suppressed, especially by cholinergic mechanisms, and when the CS region is stimulated by an adrenergic mechanism. To our knowledge, naturally occurring CSR in dogs has not been reported. The dog of the present report had SSS with depressed SA node activity. In addition, this dog had decreased vagal stimulation and increased sympathetic stimulation as a result of oral administration of propantheline and terbutaline, respectively. Although not identical, the condition of the dog of the present report was similar to that of the dogs with experimentally induced CSR in the study by Chiba and Hashimoto.3 However, in the case described in the present report, rhythms originating from the inferior left atrium could not be ruled out, and an intracardiac electrophysiologic assessment would be required for a definitive diagnosis.

References

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  • 2. Ward JL, Defrancesco TC, Tou SP, et al. Outcome and survival in canine sick sinus syndrome and sinus node dysfunction: 93 cases (2002–2014). J Vet Cardiol 2016;18:199212.

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  • 5. Lau SH, Cohen SI, Stein E, et al. P waves and P loops in coronary sinus and left atrial rhythms. Am Heart J 1970;79:201214.

  • 6. Coronary sinus rhythms and auriculoventricular nodal rhythms. Acta Paediatr 1952;41:4157.

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  • 9. Moore EN, Jomain SL, Stuckey JH, et al. Studies on ectopic atrial rhythms in dogs. Am J Cardiol 1967;19:676685.

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