A 9-month-old 23.6-kg (51.9-lb) sexually intact female Golden Retriever was evaluated because of a heart murmur and tachycardia. On physical examination, a grade 5/6 right apical, coarse, band-shaped, pansystolic murmur was ausculted. The heart rate was 190 beats/min, and the rhythm was irregular. Severe left forelimb lameness was evident.
Echocardiography revealed marked dilation and hypertrophy of the right ventricle. Severely thickened tricuspid valve leaflets were present, resulting in severe valvular regurgitation consistent with tricuspid valve dysplasia (TVD). Electrocardiography was performed to evaluate the tachycardia. On the basis of orthopedic radiographic findings, a diagnosis of panosteitis was diagnosed. Pain was suspected to be contributing to the tachycardia, and treatment with analgesics was recommended in addition to administration of digoxin (5 μg/kg [2.3 µg/lb], PO, q 12 h).
ECG Interpretation
As part of the initial evaluation of the dog, a 6-lead ECG examination was performed (Figure 1). The recording revealed atrial flutter (AFL) with an atrial rate of 429 beats/min and an irregular ventricular rate that ranged from 97 to 188 beats/min (mean rate, 160 beats/min). Flutter (P’ or F) waves are deflected negatively in leads II, III, and aVF, which was suggestive of counterclockwise rotation of a macrorentrant circuit around the tricuspid valve annulus.1–4 Ta waves (representing repolarization of the atria1) followed most of the flutter waves.
Electrocardiographic tracings (6 leads) obtained during evaluation of a dog with a heart murmur and tachycardia. Subsequently, diagnoses of tricuspid valve dysplasia and pain associated with panosteitis were made. Notice the sawtooth baseline characteristic of atrial flutter with notched, widened QRS complexes defined by deep S waves most notably in leads II, III, and aVF. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 248, 11; 10.2460/javma.248.11.1245
The presence of grouped beating (paired ventricular complexes) in a bigeminal rhythm suggested that Wenckebach conduction was occurring at the atrioventricular (AV) node.1,4–7 Two levels of block were present within the AV node; the distal portion of the AV node had characteristics of Wenckebach conduction, as demonstrated in a ladder diagram (Figure 2).
Lead II ECG tracing for the dog in Figure 1 with a corresponding ladder diagram. In the ladder diagram, the upper zone represents atrial activation (A), the green zone represents conduction in the proximal portion of the atrioventricular (AV) node, the red zone represents conduction in the distal portion of the AV node, and the lowest zone represents ventricular activation (V). In this schematic representation of the proposed conduction patterns, the presence of concealed Wenckebach conduction at the proximal and distal portions of the AV node is evident; there is 2:1 conduction in the proximal portion of the AV node and 3:2 conduction in the distal portion of the node, which results in grouped beating (paired ventricular complexes). Notice that Ta waves (arrows) follow each F wave. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 248, 11; 10.2460/javma.248.11.1245
Once conducted, the QRS complexes were widened (duration, 0.08 seconds) with a notched R wave morphology.8 The S waves were deep in leads I, II (amplitude, −0.7 mV), III, and aVF. There was a right-axis deviation in the frontal plane. The ECG diagnosis was typical AFL with evidence of right ventricular enlargement and characteristics of TVD.
The dog was returned 4 months later for evaluation and was found to have developed right-sided congestive heart failure and atrial fibrillation. Treatment with furosemide (0.9 mg/kg [0.41 mg/lb], PO, q 24 h), enalapril (0.4 mg/kg [0.18 mg/lb], PO, q 24 h), and pimobendan (0.21 mg/kg [0.1 mg/lb], PO, q 12 h) was initiated, and the dosage of digoxin was not adjusted (resting heart rate, 145 beats/min). Subsequently, the dog was lost to follow-up.
Discussion
Atrial flutter, a rapid atrial tachycardia caused by a macroreentrant loop within the right atrium, is characterized by the presence of saw tooth flutter waves on surface ECG recordings.1–4,9,10 In typical (type I) AFL, the circuit is dependent on traveling through a cavotriscuspid isthmus with most wave fronts rotating counterclockwise around this circuit, resulting in flutter waves appearing as negative deflections in leads II, III, and aVF.1–4,11 This configuration of atrial fibrillation is most common in both dogs and humans.1–4,9 The ventricular rate is an index of AV conductivity and is dependent on autonomic tone and the refractoriness of the AV node, which is modulated by concealed conduction.1,3–7,10
Most dogs with AFL have variable degrees of AV block.1,4–7,10 For the dog of this report, the AV block detected at the initial evaluation followed Wenckebach periodicity (Figure 1); the FR intervals gradually increased until AV block occurred following an F wave.1,4–7 Flutter waves penetrate the AV node to different degrees through its 4 regions: the atrionodal, nodal, nodal-His, and junctional regions. As the previous flutter wave affects the effective refractory period, the degree of penetration through the node varies from atrial beat to beat.1,3–7,10 This variation in AV nodal penetrance results in concealed conduction such that 2:1 conduction occurs in the proximal portion of the node and 3:2 conduction occurs in the distal portion of the node (Figure 2). The block in the proximal portion of the node is postulated to be a protective property of the atrionodal tissue to reduce the number of impulses conveyed to the ventricles during atrial tachyarrhythmias.4,7,9 Thus, AV block with 2:1 conduction from the proximal to distal portion of the node represents a normal functional phenomenon associated with the rapid auricular rate.4 In the distal nodal region, the velocity of 2 conducted F waves gradually decreases until the third impulse encounters absolute refractory tissue and is blocked. The incomplete penetrance in the node shortens the tissue recovery time, allowing the subsequent F wave to conduct more rapidly through the AV node.1,3–7,10 This occurs when the atrial beats in the Wenckebach cycle are odd in number.
In the absence of electrophysiologic examination, the exact conduction mechanism in AFL cannot be confirmed. A change in vagal tone provides another explanation for the alternating nodal conduction.1,4,7,10 Heightened vagal tone can enhance or diminish concealed conduction. The effect of conductile vagal enhancement is minimal at long coupling intervals and pronounced at short coupling intervals.12 By prolonging the effective refractory period, increased vagal tone can create AV nodal block with alternating 2:1 to 4:1 conduction.1,4,7,10 Given the typical Wenckebach periodicity and grouped beating of the ventricular response complexes, this interpretation is less likely for the case described in the present report.1,3–7
In the dog of the present report, right atrial enlargement secondary to TVD created a substrate for a macroreentry loop.9–11,13 Tricuspid valve dysplasia is a malformation of the right AV valve apparatus that results in severe valvular regurgitation.10,13 As the right atrium enlarges, the possibility for reentry develops because the circuit time around the dilated tricuspid valve annulus becomes greater than the absolute refractory period.9
Splintered QRS complexes are detected in approximately two-thirds of dog and cats with TVD.14 The degree of splintering can vary such that a single R wave can be notched and cannot cross the baseline or can be formed by 2 R waves of varying amplitudes.8,14 The splintered morphology paired with a widened QRS complex and a right axis deviation further supported the diagnosis of TVD in the case described in the present report.
Unstable reentrant circuits have been shown to predispose animals to developing atrial fibrillation.8,11,13 In humans, 75% of patients with AFL will develop paroxysmal or sustained atrial fibrillation.11 The physiologically remodeled atria also have a shortened effective refractory period during AFL such that any atrial premature depolarization increases the risk of initiating atrial fibrillation.11
In dogs, AFL can be treated by atrial rate or rhythm control or cessation of the abnormal circuit via ablation. Given the severity of heart disease in the dog of the present report, rhythm control was unlikely to be maintained and rate control was attempted with digoxin and pain management. Additionally, electrical cardioversion has been shown to be ineffective for treatment of dogs with AFL.2 Ventricular rate control can be obtained by prolonging the refractory period of the AV node through administration of β-adrenoceptor blockers, calcium antagonists, digoxin, or digitoxin.3,9,10,15
References
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