A 14-year-old castrated male domestic medium-hair cat was evaluated by the cardiology service of a veterinary teaching hospital because of episodes of collapse. The collapse episodes became evident to the owner 1 week prior to the evaluation and were reported to occur multiple times each day. The collapse episodes were variable in intensity from hind limb weakness to complete loss of consciousness and postural tone.
On physical examination, the cat was bright, alert, and responsive. It weighed 3.7 kg (8.14 lb) and had a body condition score of 2.5 (on a scale of 1 to 5). Rectal temperature was 38.1°C (100.6°F). Mucous membranes were pink and slightly tacky; capillary refill time was < 2 seconds. Thoracic auscultation revealed an irregular heart rhythm, and the heart rate was 225 beats/min. Femoral pulses were considered normal and synchronous with the heartbeat, and a normal left-sided precordium was palpated. A left parasternal, grade 2 to 3/6, systolic, ejection-type heart murmur was detected. Lung sounds were considered normal, and respiratory rate was 32 breaths/min. On palpation, peripheral lymph nodes appeared to be normal in size and shape. Abdominal palpation revealed no detectable masses, and no signs of pain were elicited. Eyes, ears, nose, and mouth were normal in appearance and clear of debris. The owner reported that the cat had no notable medical history and was not receiving any supplements or medications.
A blood sample was collected for a CBC, serum biochemical analysis, and assessment of serum thyroxine and cardiac troponin I concentrations. On the day of evaluation, hematologic abnormalities included lymphopenia (800 cells/μL; reference range, 1,800 to 7,000 cells/μL). Results of serum biochemical analyses were all within reference ranges. Serum total thyroxine concentration was within reference limits (1.52 ng/dL; reference range, 0.7 to 2.6 ng/dL). Thoracic radiographic findings (including hyperexpansion of the lungs and bronchial markings) were consistent with feline asthma. The size and shape of the heart were considered normal. Electrocardiography was performed (Figure 1), followed by an echocardiographic examination. Echocardiography revealed no evidence of structural cardiac disease. A mild dynamic right ventricular outflow tract obstruction was evident when the heart rate was elevated and was suspected to be the source of the noted heart murmur. Arterial systolic blood pressure was 136 mm Hg (determined via Doppler ultrasonographya), and serum cardiac troponin I concentration was within reference limits (0.19 ng/mL; reference range, < 0.2 ng/mL). Electrocardiography was repeated after the echocardiographic examination (approx 60 minutes after the first ECG assessment; Figure 2).
Six-lead ECG tracings obtained from a 14-year-old domestic medium-hair cat that was evaluated because of episodes of collapse multiple times each day during the preceding week. The intensity of the collapse episodes varied from hind limb weakness to complete loss of consciousness and postural tone. Sustained atrial tachycardia with a 2:1 conduction rate attributable to Mobitz type 2 second-degree atrioventricular block is evident. A ventricular premature complex of left bundle branch block morphology is present as the third complex. Paper speed = 50 mm/s; 1 mV = 20 mm.
Citation: Journal of the American Veterinary Medical Association 242, 7; 10.2460/javma.242.7.926
Six-lead ECG tracings obtained from the cat in Figure 1 approximately 60 minutes after completion of the first ECG assessment (an echocardiographic examination was performed during the elapsed interval). Sustained atrial tachycardia is observed with ventricular bigeminy (ventricular premature complexes of left bundle branch block morphology). Ventricular bigeminy ceases and for the last 6 beats of the tracings, the rhythm converts to that observed initially in Figure 1. Paper speed = 50 mm/s; 1 mV = 20 mm.
Citation: Journal of the American Veterinary Medical Association 242, 7; 10.2460/javma.242.7.926
ECG Interpretation
With the cat in right lateral recumbency, a 6-lead ECG examination was performed prior to the echocardiographic examination (Figure 1). The initial ECG tracings revealed atrial tachycardia with a 2:1 conduction rate. The atrial rate was 480 beats/min (P-P interval, 0.125 seconds) with a ventricular response of 240 beats/min (R-R interval, 0.25 seconds). A wider and taller complex consistent with a ventricular premature beat was also evident; the P wave that appeared before this QRS complex was too close to initiate a sinus complex, and the preceding R-R interval was shortened (0.20 seconds). A compensatory pause was observed. The amplitude and duration of the QRS complexes were considered normal (approx 0.6 mV and 40 milliseconds, respectively).
Another 6-lead ECG examination was performed following the echocardiographic examination (approx 60 minutes after the first ECG assessment; Figure 2). The atrial tachycardia continued at an atrial rate of 480 beats/min. A bigeminal pattern was evident with tall and wide QRS complexes (similar to the pattern observed in the initial tracings [Figure 1]) and regular compensatory pauses. During the period of ventricular bigeminy, the R-R interval of the premature beats was shorter (0.15 seconds) than that of the ventricular premature beat in the initial tracings (0.20 seconds); this resulted in a shorter compensatory pause (3 P-P intervals instead of 4 P-P intervals). At the end of the tracing, the 2:1 conduction rate returned with a stable ventricular response rate of 240 beats/min. The mean ventricular response rate during the bigeminal period was 340 beats/min, and the bigeminal period corresponded to periods of observed weakness in the cat. A vagal maneuver was performed by manual ocular pressure, but the heart rhythm and rate did not change. The effects of injectable drugs were not investigated at the hospital because of financial constraints of the owner.
The cat was discharged from the hospital, and the owner was instructed to administer atenolol (6.25 mg, PO, q 12 h) and aspirin (7 mg, PO, q 3 d). Telephone consultation revealed that the collapse episodes had not resolved after 3 days of treatment. Administration of atenolol was discontinued, aspirin administration was continued, and oral treatment with 30 mg of extended-release diltiazem hydrochloride every 12 hours was initiated. Six months after the initial evaluation, the cat was maintained on the prescribed drug regimen and was reportedly free from episodes of collapse or weakness. Financial limitations of the client did not permit further evaluation of the cat.
Discussion
Narrow complex tachycardia can be difficult to differentiate between ventricular, junctional, and supraventricular rhythms. The cat of this report had 2:1 atrioventricular (AV) conduction with narrow complex tachycardia, which is a hallmark of some supraventricular tachycardias.1 A vagal maneuver (corneal pressure) resulted in no change in the heart rate or rhythm in this cat. Although some supraventricular tachycardias may terminate or slow with vagal stimulation (application of digital pressure on the eyes or carotid massage), this test is not sensitive for rhythm determination.2–5 Administration of diltiazem or esmolol is also commonly undertaken to determine the originating rhythm's dependence on the AV node.
Regular supraventricular tachycardias originate from the sinus node or atrial tissue or use the atria or AV junction as a part of the tachycardia circuit. Mechanisms for supraventricular tachycardias include reentry (sinus, atrial, nodal, and accessory pathways), altered automaticity (atrial or junctional), and triggered activity (delayed afterdepolarization–associated atrial tachycardia). Supraventricular tachycardias can also be grouped as AV node independent (atrial tachycardia) or AV node dependent (AV nodal reentrant tachycardia and AV reciprocating tachycardia). Differentiation of mechanisms often includes evaluation of P-wave morphology, R-P′ interval, onset and termination characteristics, the presence or absence of AV block, and response to vagal stimulation. The cat of this report had no response to vagal stimulation and had AV block with a 2:1 conduction rate. Both of these findings suggest that the cat had an AV node-independent arrhythmia (atrial tachycardia).1–5 Most AV node-dependent supraventricular tachycardias are associated with 1:1 conduction; however, 2:1 conduction occasionally occurs in some forms of AV nodal-dependent supraventricular tachycardia.6 In this cat, the second-degree AV block (Mobitz type 2) was physiologic and negated transmission of the rapid impulses and development of extreme tachycardia.3
The hallmark of sustained atrial tachycardia is a regular atrial rhythm that can exceed 300 beats/min with apparently normal QRS complex morphology unless bundle branch block, aberrant ventricular conduction, or ventricular preexcitation is present.3,4 Paroxysmal atrial tachycardia can sometimes be differentiated by the presence of 2 or more P-wave morphologies. The cat of this report had sustained atrial tachycardia with only a single P′-wave morphology. In the initial ECG tracings, the atrial rate was 480 beats/min and of those atrial impulses, only half resulted in ventricular activation. In the subsequent ECG tracings, the atrial rate remained at 480 beats/min but ventricular bigeminy was detected in the first portion of the tracing. Once the bigeminal rhythm terminated, the 2:1 conduction rate returned. All QRS complexes were considered normal in appearance, voltage, and duration, with the exception of the single ventricular premature complexes apparent in the third beat of the initial tracings and during the bigeminal rhythm subsequently. The QRS complexes appeared to have prolonged duration because P′ waves were nested within them.
Another differential diagnosis for the ECG findings for the cat of this report was AV dissociation. However, the P-R intervals (of conducted P waves) were very regular (0.09 seconds), a phenomenon not expected in AV dissociation.7 At first glance, the alternating position of P′ waves gave an impression of AV dissociation, but this was ruled out once the intervals and conduction ratios were measured.
For the cat of this report, the cause of arrhythmia was not determined via diagnostic evaluation. Previously reported biochemical causes of supraventricular tachycardia were ruled out because the cat's serum biochemical variables and serum total thyroxine concentrations were within reference ranges.8,9 Structural cardiac disease was not observed via echocardiography, although that finding did not rule out histopathologic changes to the conduction system.10
The cat's episodes of collapse did not cease or decrease in frequency after 3 days of atenolol administration, and a decision to substitute diltiazem treatment was made. Diltiazem has been reported to be an excellent drug for management of many supraventricular tachycardias because of its ability to slow ventricular response to atrial tachycardias and terminate AV nodal-dependent tachyarrhythmias. Diltiazem achieves this effect through prolongation of AV nodal refractoriness and slowing of AV nodal conduction and has been reported to convert atrial tachycardia to a normal sinus rhythm in a small percentage of cases.2 For the cat of this report, treatment with diltiazem reportedly resolved the collapse episodes; however, recommended reevaluations of the patient were never undertaken.
Model 811-B Transcutaneous Doppler, Parks Medical Electronics, Aloha, Ore.
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