The Journal of Emergency Medicine, Vol. 45, No. 1, pp. 65–69, 2013Copyright � 2013 Elsevier Inc.

Printed in the USA. All rights reserved0736-4679/$ - see front matter

http://dx.doi.org/10.1016/j.jemermed.2012.11.068

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Selected Topics:Critical Care

ATRIAL TACHYCARDIA MIMICKING ATRIOVENTRICULAR NODALREENTRY TACHYCARDIA

Wesley P. Eilbert, MD and Neal Patel, MD

Department of Emergency Medicine, University of Illinois Hospital and University of Illinois College of Medicine, Chicago, IllinoisReprint Address: Wesley P. Eilbert, MD, Department of Emergency Medicine, University of Illinois Hospital,

1740 W. Taylor Street, Chicago, IL 60612

, Abstract—Background: The term supraventriculartachycardia (SVT) is used to describe tachydysrhythmiasthat require atrial or atrioventricular nodal tissue for theirinitiation and maintenance. SVT can be used to describeatrioventricular nodal reentry tachycardia, atrioventricularreentry tachycardia, and atrial tachycardia (AT). AT is theleast common of these SVT subtypes, accounting for only10% of cases. Although the suggested initial management ofeach SVT subtype is different, they all can present with sim-ilar symptoms and electrocardiographic findings. Objective:Discuss the pathophysiology, diagnosis, and treatment of ATas compared with other types of SVT. Case Report: Wereport a 56-year-old woman with symptoms and electrocar-diographic findings consistent with SVT. Although standardtreatment with intravenous adenosine failed to convert theSVT, it revealed AT as the cause of the tachydysrhythmia.The AT was successfully terminated with beta-blockadeand the patient eventually underwent successful radioabla-tion of three separate AT foci. Conclusions: AT frequentlymimics other more common forms of SVT. AT might be rec-ognized only when standard treatment of SVT has failed.Identification of AT in this setting is crucial to allow formore definitive therapy. � 2013 Elsevier Inc.

, Keywords—atrial tachycardia; supraventricular tachy-cardia; SVT; adenosine; focal atrial tachycardia

INTRODUCTION

The term supraventricular tachycardia (SVT) is used todescribe tachydysrhythmias that require atrial or atrio-

ne 2012; FINAL SUBMISSION RECEIVED: 28 Octobovember 2012

65

ventricular nodal tissue for their initiation and mainte-nance (1). SVT can be used to describe atrioventricularnodal reentry tachycardia (AVNRT), atrioventricularreentry tachycardia (AVRT), and atrial tachycardia (AT)(2). Of these SVT subtypes, AVNRT is most common,accounting for 60% of cases. Approximately 30% ofSVT cases are due to AVRT, and 10 % are due toAT (1). Although the suggested initial management ofeach of these SVT subtypes is often different, they canpresent with similar symptoms and electrocardiographicfindings. We report a case of AT in a patient presentingas, and initially treated for, AVNRT.

CASE REPORT

A 56-year-old woman presented to the EmergencyDepartment complaining of three separate episodes ofpalpitations with chest pressure, each lasting approxi-mately 2 h, occurring during the previous day. Each epi-sode was of sudden onset and resolution, without anyidentified exacerbating or relieving factors. The patientcame to the Emergency Department for evaluation, asher most recent episode seemed more severe and was as-sociated with dyspnea and lightheadedness. The patient’smedical history was significant for rheumatic heart dis-ease with tricuspid regurgitation, and mechanical aorticand mitral valve replacements, for which she took warfa-rin. She was also being treated for diabetes mellitus,hypertension, and hyperlipidemia. She had no previous

er 2012;

Figure 1. The patient’s initial electrocardiogram.

66 W. P. Eilbert and N. Patel

history of dysrhythmia or ischemic heart disease. Shereported no recent fevers or illnesses, and denied alcohol,tobacco, and illicit drug use. There was no family historyof heart disease or dysrhythmia.

On presentation, the patient’s vital signs were notablefor a pulse of 172 beats/min with a regular rhythm, bloodpressure was 122/82 mm Hg, respiratory rate was 18breaths/min, and oral temperature was 37.4�C (99.2�F).Physical examination revealed a well-nourished womanin no distress. Her lungs were clear to auscultation andher heart was tachycardic with a mechanical click heardover the precordium. She did not have jugular venous dis-tension. Her initial electrocardiogram (ECG) (Figure 1)was interpreted as SVT, likely of the AVNRT subtypedue to the lack of visible P waves, with a right bundlebranch block. The right bundle branch block was old,as confirmed by comparison with an ECG from 3 yearsearlier (Figure 2).

The patient was given a 6-mg intravenous bolus ofadenosine with no response. After a 12-mg intravenousbolus of adenosine, a brief ventricular asystole ensued,which revealed apparent P waves at an approximate

Figure 2. The patient’s previous electrocardiogram from 3 years e

rate of 170 beats/min, most apparent in lead II ofa 12-lead rhythm strip (Figure 3). An esmolol drip wasthen started and titrated to achieve ventricular rate con-trol for presumed AT. After approximately 90 min on theesmolol drip, the patient converted to a sinus rhythm(Figure 4). The patient was admitted to the coronarycare unit for further monitoring.

On hospital day 1, the patient underwent transthoracicechocardiography, which revealed a moderately enlargedright ventricle and a moderately to severely dilated rightatrium with severe tricuspid valve regurgitation. The leftventricular function was normal. A nuclear medicinestress test showed no reversible ischemic changes. Thepatient was weaned off the esmolol drip and started onoral metoprolol. The metoprolol was eventually discon-tinued, however, due to symptomatic bradycardia. Onhospital day 6, the patient was taken for electrophysiol-ogy study and had successful ablation of three separateAT foci. The AT foci were believed to be the result ofa large surgical scar of the right atrium and a dilated rightatrium. The patient remained free of any tachydysrhyth-mias throughout the remainder of her hospitalization.

arlier.

Figure 3. Rhythm strip after a 12-mg intravenous bolus of adenosine was given, revealing P waves most visible in lead II.

Atrial Tachycardia 67

DISCUSSION

Ectopic ATwas first described by Gallavardin in 1922 (3).It is a rare dysrhythmia, occurring in only 0.46% of allpatients reporting symptoms of dysrhythmia (4). Theonset of symptoms can occur at any age, with the majorityof patients having their first dysrhythmic event betweenthe ages of 10 and 39 years (5). Most cases of AT occurin patients with structurally normal hearts, although therehas been a reported occurrence with abnormal myocar-dium caused by atrial scarring, as with our patient, aswell as myocyte hypertrophy, inflammatory infiltration,and fatty substitution (6,7). Patients can experiencea range of symptoms with AT, including palpitations,chest pain, dizziness, dyspnea, and syncope, withparoxysmal episodes lasting from seconds to hours.Feeding problems, vomiting, and tachypnea can occurin young children. A significant percentage of patientswill remain asymptomatic during episodes of AT (4).The atrial rate during AT usually ranges between 130and 250 beats/min, with younger patients tending to

Figure 4. The electrocardiogram after conversion to a sinus rhyth

have faster rates (8). The prognosis for patients with ATis generally benign, although tachycardia-induced car-diomyopathy can occur in those patients with incessantforms (9). Incessant forms of AT occur in 10%–15% ofpatients and result in symptoms >50% of the day (10).Spontaneous remission of AT has been reported in24%–63% of patients, with children and young adultsmore likely to have remission than older patients (4,7,11).

Although our patient was ultimately diagnosed withAT, some clarification should be made. ATs are dividedinto two subtypes, focal and macroreentrant (Figure 5).Focal AT is defined as atrial activation starting rhythmi-cally in a small area (<2 cm), from which it spreads outcentrifugally. In contrast, macroreentrant AT, more com-monly referred to as atrial flutter, is defined as atrial ac-tivation involving a reentrant circuit >2 cm in diameter(12). Focal AT, as with our patient, has three distinctelectrophysiologic mechanisms: triggered activity, en-hanced automaticity, and microreentry (10). Triggeredactivity is probably responsible for the majority offocal ATs and refers to tachycardia as a consequence

m.

Figure 5. Classification of supraventricular tachycardias.

68 W. P. Eilbert and N. Patel

of afterdepolarization, which results in new triggeredaction potentials. Enhanced automaticity is a result ofcells with enhanced diastolic phase-four depolarizationresulting in an increased firing rate. Microreentry refersto a small reentrant loop, smaller than that which can bemapped by an electrophysiology study.

Although all subtypes of SVT can present with similarsymptoms and an ECG showing a regular tachycardiawithout visible P waves, AVNRT is more likely thanAT or AVRT to not have discernible P waves present(13). Temporary atrioventricular (AV) nodal conductionblockage with vagal maneuvers or adenosine can be

Figure 6. Conduction through the atrioventricular (AV) node in supbegins in theatriaand isconducted through theAVnode. (B)AVnodain the AV node. (C, D) AV reentry tachycardia. The impulse travels incessory pathway between the atria and ventricles. Conduction thro

both therapeutic and diagnostic when treating SVT. Tounderstand the effects of AV nodal conduction blockageon the different SVT subtypes, knowledge of the electro-physiology of each subtype is necessary (Figure 6). Be-cause conduction through the AV node is required forcontinuation of the SVT with AVNRT and AVRT, termi-nation of the SVT with adequate AV nodal blockage isvirtually assured with these subtypes (2). AT forms ofSVT, both focal and macroreentrant, often have ‘‘un-masking’’ of their P waves and flutter waves, respectively,with AV nodal blockage, and the SVT resumes after theblockage ends, as with our patient.

Once diagnosed, AT should initially be treated ina fashion similar to the other SVT subtypes. Direct cur-rent cardioversion should be considered first-line therapyin patients with AT resulting in hemodynamic instability(10). Although direct current cardioversion is typicallyeffective for focal AT due to microreentry and triggeredactivity, it is usually ineffective for focal AT caused byenhanced automaticity (2,10,14). Termination of ATwith vagal maneuvers may be attempted, but is rarelysuccessful (2,7,14). Some forms of focal AT may beterminated with adenosine, specifically those caused bytriggered activity and microreentry (15,16). For acutemanagement of hemodynamically stable AT, mostauthorities recommend intravenous beta-blockers orcalcium-channel blockers (i.e., diltiazem or verapamil)

raventricular tachycardia. (A) Atrial tachycardia. The impulsel reentry tachycardia. The impulse travels ina reentrantcircuita reentrant circuit between the AV node and an abnormal ac-ugh the AV node is orthodromic (C) or antidromic (D).

Atrial Tachycardia 69

as initial therapy (2,6,7,10,14). Both of these drug classesare useful to control the ventricular rate because of theirAV nodal blocking properties. Furthermore, calcium-channel blockers and beta-blockers can terminate focalAT caused by enhanced automaticity, and beta-blockersmay be effective if the mechanism is triggered activity(2,7,14). Class IA and class IC anti-dysrhythmic agentsmay be effective in terminating AT, although they haveminimal or no AV nodal blocking properties to controlthe ventricular rate (10). Class III agents, most notablyamiodrone, are also effective at terminating AT and areespecially useful in patients with poor ventricular func-tion (2,10). Long-term treatment of AT has shiftedaway from pharmacologic therapy during the past 20years, with radiofrequency ablation now the preferredtreatment for cure (2,6,7,10,14).

CONCLUSIONS

AT is a relatively rare form of SVT that typically presentswith paroxysmal episodes of symptoms similar to theother subtypes of SVT. Likewise, the ECG findingswith AT may mimic the other more common formsof SVT. Erroneously treating AT as one of these otherSVT subtypes is probably a common occurrence, al-though it is frequently successful. AT may be recognizedonly when the standard acute treatment of SVT has failed.Identification of AT in this setting is crucial to allow formore definitive therapy.

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