Introduction

The clinical manifestations resulting from nar-row complex tachycardias (NCT) are a not un-common reason for presentation to the emer-gency department (ED)1. NCTs are defined asrhythms with a rate greater than 100 beats perminute (bpm) and a QRS complex duration lessthan 120 milliseconds (msec) in the adult patient.NCTs are most often supraventricular in origin,arising from the sinus node, the atria, or the atri-oventricular (AV) junction. While narrow complexventricular tachycardia has been reported2, thelatter is very rare and, thus, will not be discussedfurther in this paper.

Because NCTs are numerous and their differ-ences subtle, it is important for the emergencyphysician to understand the differences among

these rhythms in order to render a correct diag-nosis and appropriate management. While we donot discuss specific treatment of these rhythms,we do address diagnostic maneuvers, such asadenosine administration, and acknowledge thatthese may be both diagnostic and therapeutic. Inno circumstance should the diagnostic processlimit timely management of an unstable patient.

Electrocardiographic Differential Diagnosis

Sinus tachycardia (ST)

Physiologic sinus tachycardia refers to a NCTthat originates from the SA node and is due to in-creased automaticity, rather than a reentrantmechanism. The atrial rate is greater than 100

Emergencias 2010; 22: 369-380 369

REVIEW ARTICLE

ECG differential diagnosis of narrow QRS complextachycardia in the emergency department: A reviewof common rhythms and distinguishing features

MATTHEW P. BORLOZ1, DUSTIN G. MARK2, JESSE M. PINES3,4,5, WILLIAM J. BRADY6

1Departamento de Emergencias. Universidad de Georgetown/Hospital Center Washington, Washington,EE.UU. 2Departamento de Cuidados Intensivos. Universidad Health System de Pennsylvania. Filadelfia, EE.UU.3Departamento de Emergencias. Universidad Health System de Pennsylvania. Filadelfia, EE.UU. 4Centro deEpidemiología Clínica y Bioestadística, Facultad de Medicina, Universidad de Pennsylvania. Filadelfia, EE.UU.5Instituto Leonard Davis. Universidad de Pennsylvania. Filadelfia, EE.UU. 6Departamento de Emergencias.Universidad de Virginia, Charlottesville, EE.UU.

The differentiation of narrow complex tachycardias (NCT) is a commonly encountereddiagnostic dilemma in the adult emergency department. Some NCTs (e.g., sinustachycardia) are secondary to the presenting complaint (e.g., fever, anxiety, pain) and willrespond to appropriate treatment of the inciting pathologic insult. Alternatively, otherNCTs (e.g., atrial fibrillation, AV nodal reentrant tachycardia) may indeed be the cause ofthe chief complaint (e.g., palpitations, lightheadedness from poor perfusion) and must bepositively identified and primarily managed. An appreciation of the similarities anddifferences among these NCTs is necessary for appropriate recognition. This articledelineates which demographic, historical, and electrocardiographic characteristics arehelpful in identifying the following rhythms: sinus tachycardia, sinus node reentranttachycardia, unifocal atrial tachycardias, multifocal atrial tachycardia, atrial fibrillation,atrial flutter, atrioventricular nodal reentrant tachycardia, and atrioventricular reentranttachycardia. In addition, a discussion of various diagnostic maneuvers, such as adenosineadministration, is included. [Emergencias 2010;22:369-380]

Key words: QRS complex tachycardia. Emergency department. Common rhythms.

CORRESPONDENCE:William BradyDepartment of EmergencyMedicineUniversity of Virginia HealthSystemCharlottesville, VA. EE.UU.E-mail: wb4z@virginia.edu

RECEIVED:5-2-2010

ACCEPTED:7-4-2010

CONFLICT OF INTERES:None

Formaciónacreditada

bpm and is largely regular with slight variationsover time3,4. The P wave morphology is identicalto that seen in sinus rhythm and appears positivein leads I, II, III, and aVF5-7 and biphasic7,8 or nega-tive5 in lead V1 (Figures 1A and B). The onset ofST is gradual, exhibiting a “warm up” period, andis not initiated by atrial or ventricular prematurebeats4,7,9,10. Perhaps the most telling feature of STis that it occurs in the setting of underlying physi-ologic stress or pharmacologic influence, namelyfever, infection, anxiety, stimulant drug use, or hy-potension, among many others4,7,9. When frequentpremature atrial contractions (PACs) accompanyST, it may be difficult to differentiate from multi-focal atrial tachycardia (MAT, discussed below)3.

Sinus node reentrant tachycardia (SNRT)

As the name implies, sinus node reentranttachycardia is due to a reentrant mechanism with-in or adjacent to the sinus nodal tissue4,7. Thisrhythm is indistinguishable from sinus tachycardiaon a simple 12-lead ECG (Figure 2), as the P waveposition, axis, and morphology are essentiallyidentical to those of the latter4,5,7,9,11,12. The rate isusually 100-150 bpm, and the rhythm is regular4,7.In contrast to ST, the onset of SNRT is abrupt andoften initiated by a premature atrial impulse4-7,9-12.Termination is similarly abrupt and may be effect-ed with vagal maneuvers or adenosine administra-tion5,9. This rhythm is often an incidental findingseen on Holter monitoring, is typically non-sus-tained, and rarely causes clinically significantsymptomatology13. Sanders et al14 report an inci-dence of 3% in their series of patients referred forelectrophysiologic (EP) study.

Refer to Figure 2 for an example of SNRTwhich, based solely on this rhythm segment, isimpossible to separate from typical sinus tachycar-dia.

Unifocal Atrial Tachycardias

Unifocal atrial tachycardias are due to auto-matic, triggered, or reentrant mechanisms, de-pending on the clinical scenario in which theyarise6,15. They are a relatively uncommon cause of

clinically significant NCT, as they comprise lessthan 10% of documented cases4.

Reentrant atrial tachycardias depend on dis-eased atrial tissue to create adjacent areas of tis-sue with variant speeds of conduction and refrac-tory periods. As such, they usually arise followingatrial surgeries or within otherwise diseased atrialtissue7,13. When seen in a patient without underly-ing heart disease, enhanced automaticity is likelythe mechanism. Onset and termination are typi-cally gradual and occur without the influence ofpremature impulses3,16,17. Triggered activity is impli-cated in atrial tachycardia seen in the setting ofdigoxin toxicity (often accompanied by AVblock)7.

Unifocal atrial tachycardias, by definition, origi-nate from a single area of the atrium (unlikeMAT), the location of which governs the appear-ance of the P wave. For example, if the focus isnear the SA node, the P wave will be similar inappearance to that during sinus rhythm. If, how-ever, the atrial impulse is initiated low in the rightatrium, the P wave may be negative in leads II, III,and aVF6. The atrial rate is typically 100-250bpm4,11, and the presence or absence of AV blockdoes not rule the diagnosis in or out9,6,12,13.

Multifocal atrial tachycardia (MAT)

Multifocal atrial tachycardia is an irregular NCTwith a frequency of 0.08-0.36% among hospital-ized patients18,19. It typically occurs in the elderlyin the setting of cardiopulmonary disease and ismost commonly associated with chronic obstruc-tive pulmonary disease (COPD). Associations alsoexist with pulmonary embolism, hypoxemia, andhypokalemia20. Triggered activity21 and enhancedautomaticity17 have been proposed as likely mech-anisms; however, consensus is lacking, and theprecise mechanism remains elusive.

Very specific electrocardiographic criteria de-fine MAT; these include an atrial rate > 100 bpm,three or more distinct non-sinus P wave mor-phologies (in the same lead), an isoelectric base-line (i.e., no flutter or fibrillation waves), and ir-regularity of the PP, PR, and RR intervals (Figure3)5,22,23. Despite the clear diagnostic criteria, this

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370 Emergencias 2010; 22: 369-380

Figure 1. It shows a sinus tachycardia on ECG.

Figure 2. It shows a sinus node reentrant tachycardia onECG.

rhythm may be difficult to distinguish from sinusrhythm with frequent PACs or atrial fibrillation.Kastor et al23 support the administration of asmall dose of an intravenous beta-adrenergic orcalcium-channel antagonist in order to slow theatrial rate and allow the clinician to search thebaseline for distinct P waves supportive of MATor fibrillatory waves consistent with atrial fibrilla-tion. This diagnostic maneuver should be pur-sued with caution in the absence of clear data tosupport a normal left ventricular ejection fraction.While atrial rates typically range from 100-220bpm5, some authors propose lowering the ratethreshold for diagnosis from 100 bpm to 90bpm24.

Atrial fibrillation

Atrial fibrillation remains the most prevalentform of narrow complex tachycardia25. In theUnited States, 2.3 million individuals carry this di-agnosis26, and 0.2% of ED visits were attributed toatrial fibrillation during 1993-200427. Patients maypresent to the ED with worsening of their chronicatrial fibrillation due to poorly controlled ventricu-lar rates or with paroxysmal atrial fibrillation asso-ciated with hyperthyroidism5,25, hypokalemia orhypomagnesemia25, or following excessive ethanolintoxication, the so-called “holiday heart syn-drome”28. The mechanism of atrial fibrillation ap-pears to be multiple micro-reentrant wavelets inthe atria3,13. Paroxysms of atrial fibrillation may betriggered by preceding alterations in autonomictone29 and/or ectopic foci frequently located in oraround the pulmonary veins30. Atrial fibrillation isalso the second most common tachycardia experi-enced by patients with the Wolff-Parkinson-Whitesyndrome, seen in 20-25%31,32.

Electrocardiographically (Figure 4), the absenceof P waves and the irregularly irregular ventricularresponse are the hallmarks of this rhythm5,33. Thebaseline may be isoelectric or may exhibit fibrilla-tory waves of varying morphology at a rate of400-700 bpm3,5,25. The amplitude of the fibrillatorywaves is suggestive of the underlying pathology.Fine fibrillatory waves (� 0.5 mm amplitude) areassociated with ischemic heart disease, whilecoarse waves (> 0.5 mm) signify left atrial en-

largement3,34. Untreated ventricular rates rangefrom 100-200 bpm3,5 compromising diastolic ven-tricular filling, and often producing palpitations,chest pain, and symptoms of congestive heart fail-ure35.

Atrial flutter (AF)

Atrial f lutter is most commonly due to amacro-reentrant circuit within the right atriumand shares many etiologic features with atrial fib-rillation13,36. Indeed, it may often be confused with“coarse” atrial fibrillation37. Typical AF (type 1) in-volves either a counterclockwise (common) orclockwise (less common) reentrant circuit. Coun-terclockwise circuits produce downward deflec-tions, called flutter waves, in the inferior leads;these are classically referred to as having a “saw-tooth” appearance5,36. Flutter waves are also fre-quently visualized in lead V1 and must be of uni-form rate, amplitude, and morphology to beso-called37. The atrial rate is regular and rangesbetween 250 and 350 bpm, often close to or ex-actly 300 bpm5,33. A less common variant of AF,termed type II, produces faster atrial rates, typical-ly in the range of 340-430 bpm. Because the AVnode is usually incapable of conducting impulsesto the ventricles at these rates, AV block is almostalways present; although, 1:1 conduction is possi-ble38. Two-to-one AV block, which is most com-mon, will produce a ventricular rate around 150bpm in type I AF, whereas 3:1 AV block will resultin a ventricular rate of 100 bpm. While the de-gree of AV block is often fixed, it may also bevariable, yielding an irregular ventricularresponse5.

Refer to Figure 5A for examples of atrial flutterwith a regular rate of 150 bpm (upper panel) anda rapid, irregular form of atrial flutter (atrial flutterwith variable block, lower panel). Note Figure 5B,demonstrating sinus tachycardia initially misdiag-nosed as atrial flutter due to the “classic” rate of150 bpm. Note the normal P wave polarity in thelimb leads. This finding, along with significantrate variation observed over a very short period oftime, ultimately contributed to the correct electro-cardiographic diagnosis – very rapid sinus tachy-cardia.

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Figure 3. It shows a multifocal atrial achycardia on ECG. Figure 4. It shows an atrial fibrillation on ECG.

Atrioventricular nodal reentrant tachycardia(AVNRT)

AV nodal reentrant tachycardia accounts for 50-69% of all regular NCTs (excluding those associat-ed with pre-excitation)10,39. AVNRT depends on so-called “dual AV node physiology,” which indicatesthat the AV node has two distinct tracts capable ofconducting impulses, one of which conducts slow-ly but has a short refractory period, and the otherof which conducts rapidly but has a relativelylonger refractory period. During sinus rhythm, im-

pulses are typically carried by the “fast” (alsoknown as “beta”) pathway, and the “slow” (alsoknown as “alpha”) pathway is unused. CommonAVNRT is initiated when a premature atrial impulsefinds the fast pathway refractory and instead usesthe slow pathway to conduct to the His-Purkinjesystem. By the time the impulse reaches the ven-tricles, the fast pathway has repolarized, and theimpulse is carried by this tract in a retrograde fash-ion. This pattern continues in order to produce“common” AVNRT (also known as typical AVNRTor slow-fast AVNRT). A premature ventricular im-pulse may also initiate this rhythm if the impulse isblocked in the retrograde direction by the slowpathway and follows the fast pathway. The im-pulse then proceeds via the slow pathway in theantegrade direction and back up the fast pathwayfor retrograde transmission.

In 3-10% of cases, the fast pathway may havea shorter refractory period than the slow pathway,allowing for reversal of the circuit9,39-42. “Uncom-mon” AVNRT (also known as atypical AVNRT orfast-slow AVNRT) occurs when antegrade conduc-tion follows the fast pathway and retrograde con-duction is carried by the slow pathway. It is gen-erally initiated by a premature ventricularimpulse40.

Because of the rapid retrograde transmission ofthe impulse in common AVNRT, the P wave is

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372 Emergencias 2010; 22: 369-380

Figure 6. It shows a sinus tachycardia with a ventricular rate of 150 bpm. In conrast to atrial flutter,note the normal P wave polarity on a 12-lead ECG.

Figure 5. It shows an atrial flutter with a regular rate of 150bpm (upper panel) and an atrial flutter, note the normal P wavepolarity on a 12-lead ECG.

hidden by the QRS complex in 69% of cases (Fig-ure 6A)39. In the remainder of cases, the P waveimmediately follows the QRS complex (Figure 6B),at times obscuring the terminal portion of thecomplex and resulting in “pseudo deflections”(discussed below). In contrast, because retrogradeconduction in uncommon AVNRT occurs via aslow pathway, the ventricles are activated longbefore the atria, so the P wave appears closer tothe subsequent QRS complex than to that whichprecedes it.

Patients with common AVNRT may report asensation of pounding in the neck, which corre-lates with concomitant atrial and ventricular con-traction, elevated right atrial pressures, and flowreversal from the right atrium to the systemic ve-nous system. In a study by Gürsoy et al43, thisfinding was reported by 50 of 54 (93%) of pa-tients with this rhythm and by none of the 190patients with other NCTs.

Atrioventricular reentrant tachycardia (AVRT)

Atrioventricular reentrant tachycardia mecha-nistically occurs via a reentrant circuit that in-volves both the AV node and an accessory atri-

oventricular pathway. AVRT may be divided intotwo principal categories designated by the direc-tion of travel through the AV node and the acces-sory pathway: orthodromic and antidromic. Or-thodromic AVRT indicates that antegradeconduction occurs through the AV node with ret-rograde conduction via the accessory pathway(Figure 7A), resulting in a narrow QRS complextachycardia. Conversely, antidromic AVRT occurswith antegrade conduction down the accessorypathway and retrograde conduction through theAV node, producing a wide QRS complex tachy-cardia.

Onset of AVRT is abrupt and is typically initiat-ed by a premature atrial or ventricular im-pulse3,10,12,13,25,33. Rates typically range from 140-240bpm25. ST segment elevation is seen in lead aVR,due to retrograde atrial activation; this finding canbe helpful in differentiating AVRT from AVNRT orAT with a right atrial focus44. The presence of AVblock during tachycardia effectively excludes thediagnosis of AVRT6,9,10,12,13,45-48. Refer to Figure 7B foran example of orthodromic AVRT.

Evaluation of Available Demographicand Electrocardiographic Features

Demographics (Age and Gender)

Investigators have attempted to identify ageand gender differences among patients withsupraventricular tachycardias in an effort to definespecific characteristics that aid in determining themost likely mechanism41,49-54. While younger pa-tients are more likely to experience paroxysmalsupraventricular tachycardia (PSVT) in the absenceof known cardiovascular disease and females are

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Figure 7. It shows an atrioventricular nodal reentrant tachy-cardia on ECG. Note the P wave is hidden by the QRS com-plex.

Figure 8. It shows an atrioventricular nodal reentrant tachycardia on a 12-lead ECG. Note he P wa-ve immediately follows the QRS coomplex “pseudo deflections”.

more than twice as likely as males to be diag-nosed with PSVT (70%), no definitive conclusionscan be made regarding the influence of age orgender on the mechanism of the tachycardia49. Ina population of 485 patients with NCT withoutovert electrocardiographic evidence of pre-excita-tion, investigators determined that AVNRT wasthe most common mechanism of supraventriculartachycardia in all age groups, from teenage toelderly, and that age was not a reliable predictorof tachycardia mechanism50.

With regard to gender, overall PSVT incidenceis relatively evenly distributed between men andwomen; however, in the specific case of AVNRT,there appears to be a higher prevalence of diseaseamong female patients, ranging from 68-76% asobserved in three separate studies41,51,54. While thereason for this unbalanced gender distribution isunclear, one study has demonstrated that womentend to have a shorter AV nodal block cyclelength and enhanced ventriculoatrial conduction,

as compared to men, thus potentially facilitatingthe mechanism of AVNRT53.

With respect to the Wolff-Parkinson-White(WPW) syndrome, there appears to be a malepreponderance, shown to be approximately two-fold in both a population study and a study of pa-tients referred for electrophysiologic analysis41,52.Another investigator proposes that the reason forthis is the presence of a longer AV conduction de-lay in males versus females53. This longer delay fa-vors pre-excitation via active accessory AV path-ways. Approximately 50% of patients withaccessory AV pathways will experience their firstepisode of tachycardia before age 20, as opposedto patients with AVNRT and atrial tachycardia,who are more likely to initially present after 20years of age41,51.

Rate

In general, the ventricular rate of the tachycar-dia is rarely helpful in differentiating one type ofNCT from another. One exception to this is in thecase of type I atrial flutter, which exhibits an atrialrate between 250-350 bpm and frequently con-ducts with 2:1 AV block, yielding a ventricularrate around 150 bpm. A 3:1 AV block with a ven-tricular rate of 100 bpm is also common3,33. What-ever the ventricular rate, the R-R interval shouldshow little or no beat-to-beat variation in the ab-sence of medications or vagal maneuvers3,25.

In an electrophysiologic study which included100 patients with either AVNRT or AVRT and 27patients with atrial “ectopic” tachycardia, themean atrial rate varied from 167-170 bpm. Sever-al other studies have also failed to demonstrate

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374 Emergencias 2010; 22: 369-380

Figure 9. It shows a diagram of atrioventricular reentranttachycardia’s mechanism.

Aurícula

A

BC

D

SistemaHIS-PurkinjeVentrículos

Víaaccesoria

Nodosinusal

Figure 10. It shows an atrioventricular reentrant tachycardia on a 12 lead-ECG.

significant differences in atrial or ventricular ratesamong these same tachycardia types55,56. Despite ahigher mean rate in AVRT versus AVNRT, Kay etal57 found that, after multivariate analysis, higherrates were not predictive of AVRT. In general, ratealone is not a reliable predictor of tachycardiamechanism.

Regularity

The regularity of the rhythm can be remark-ably helpful in differentiating the mechanisms ofvarious NCTs. Specifically, the finding of a clearlyirregular rhythm significantly narrows the list ofpotential diagnoses. Just as atrial fibrillation is “ir-regularly irregular,” atrial fibrillation with rapidventricular response may be similarly described.An irregularly irregular NCT with definite P wavesis likely multifocal atrial tachycardia (MAT). Notethat the diagnosis of MAT formally requiresdemonstration of three discrete P wave morpholo-gies. PR intervals differ from beat to beat due tothe variable location of the inciting atrial im-pulse3,11. MAT may be confused with atrial fibrilla-tion9,23,58.

The presence of regular periods of tachycardiapunctuated by apparent pauses, so called “groupbeatings,” indicates atrial flutter or ectopic atrialtachycardia with variable AV block59. Differentia-tion of these may be facilitated by searching for“flutter” waves in the former and discrete P waves(although non-sinus) in the latter, though this isoften difficult due to fast ventricular rates, whichmay obscure interpretation of atrial activity60.

The finding of a regular rhythm includes everyother mechanism of NCT, so the clinician is ad-vised to focus on alternative discriminating char-acteristics for further diagnosis. It should be men-tioned that although sinus tachycardia is typicallyconsidered a regular rhythm, it may be mildly ir-regular3,59.

P Wave (Presence, Axis, and Morphology)

The presence of discrete P waves may be diffi-cult to determine with fast atrial and ventricularrates. When present, however, the location of theP wave relative to the QRS complex is quite help-ful (refer to the discussion of P wave location).Conversely, the absence of P waves with an irreg-ularly irregular ventricular rate greater than 100bpm strongly suggests atrial fibrillation with rapidventricular response. Fibrillatory waves are seenon the baseline and represent disorganized atrialelectrical activity3,5. A particular pattern of P wave,

the “flutter wave,” is seen in place of typical Pwaves in patients with atrial flutter, most often atan atrial rate of 250-350 bpm. These flutterwaves, which give the baseline the classic “saw-tooth” appearance, are most easily identified inthe inferior leads (i.e., II, III, aVF) and in leadV1

3,5,6,33.Examination of the P wave axis may yield ad-

ditional information regarding the etiology ofthe NCT, particularly in the case of unifocal atrialtachycardia. Determining the P wave axis in-volves identifying the polarity of the P wave aspositive, negative, or biphasic in particular leads.Rhythms that originate from the SA node, locat-ed in the superior right atrial myocardium (i.e.,sinus tachycardia [Figure 5B], sinus node reen-trant tachycardia), will show upright P waves inleads I, II, III, and aVF5-7 and a biphasic7,8 or nega-tive5 P wave in lead V1. Ectopic atrial tachycardiasoriginating from tissue adjacent to the SA nodeare difficult to distinguish from those arisingfrom the node itself using a standard 12-leadECG. Ectopic atrial tachycardias and atrial reen-trant tachycardias arising from sites distant fromSA nodal tissue, however, will have variable Pwave axes and morphologies12. Tang et al61

showed that leads aVL and V1 were most usefulin differentiating a right atrial focus from a leftatrial focus. A positive or biphasic P wave in leadaVL correlates with a right atrial focus (sensitivity88%, specificity 79%), while a positive P wave inlead V1 supports a left atrial focus (sensitivity93%, specificity 88%). In addition, negative Pwaves in the inferior leads (i.e., leads II, III, aVF)correlate with an inferior atrial focus, while posi-tive P waves in these leads indicate a superior fo-cus. Not all NCTs with negative P waves in theinferior leads originate from an inferior atrial fo-cus, however, as this P wave axis deviation canalso be due to retrograde atrial conduction froman AV junction focus, as may be seen in AVNRT.In summary, the primary strength of P wave axisdetermination lies in the diagnosis of both ec-topic left atrial foci and MAT, the former demon-strating positive P waves in lead V1, the latterexhibiting variable P wave axes and morpholo-gies in a single lead.

P Wave Location (RP Interval)

The RP interval describes the duration from theQRS complex to the subsequent P wave. This du-ration is compared to the PR interval of therhythm, and based on their relative values, arhythm may be called a “short RP” or “long RP”

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tachycardia. A short RP tachycardia is one inwhich the RP interval is shorter than the PR inter-val. One may think of this as the P wave followingthe QRS complex instead of preceding it. Exam-ples of short RP tachycardias are common AVNRT(Figure 6B) and orthodromic AVRT (Figure 7B)with a rapidly conducting accessory pathway. Ashort RP tachycardia may also be seen with atrialtachycardia in the presence of a long PR interval,usually at higher rates. Long RP tachycardias,which represent the “normal” P wave to QRScomplex relationship, include sinus tachycardia(ST), sinus node reentrant tachycardia (SNRT),atrial tachycardias, uncommon AVNRT, and ortho-dromic AVRT with a slowly conducting accessorypathway. This classification is often helpful in un-derstanding NCT mechanisms and diagnosingthese rhythms from the surface ECG.

In some cases, the P wave may be hiddenwithin the QRS complex, representing a subtypeof the short RP tachycardias. This finding almostexclusively occurs during common AVNRT, andhas been found to be the single most useful ob-servation on 12-lead ECG analysis that can distin-guish AVNRT from AVRT. Conversely, AVNRT canpresent as a short RP tachycardia in up to 30% ofcases, thus mimicking AVRT, making the absenceof QRS masking relatively non-specif ic10-

12,39,42,45,57,62,63. Some investigators have attempted todefine a specific value for the RP interval in com-paring common AVNRT and AVRT. Zhong et al64

demonstrated mean values of 89 ± 13 msec and134 ± 29 msec, respectively. In an attempt to vali-date an algorithm designed for pediatric patientsby Jaeggi et al65, Arya et al66 looked at a specificcutoff of 100 msec to discriminate AVRT fromcommon AVNRT in a population of adult patients.Sensitivity and specificity for this finding were73% and 88%, respectively. As might be expect-ed, with a decrease in the cutoff value to 80msec, the investigators noted increased sensitivity(85%) but decreased specificity (69%).

AV Block

The presence of AV block during an episode ofNCT greatly narrows the differential diagnosis. AVblock is not possible with a rhythm that employsthe normal atrioventricular conduction pathwayfor antegrade conduction and an accessory path-way for retrograde conduction because this tachy-cardia is dependent on a “patent” AV tract. As aresult, orthodromic AVRT may be eliminated fromthe differential if AV block is present6,9,10,12,13,45-48.While 2:1 AV block is possible with both common

and uncommon AVNRT, it is exceedingly rare and,when present, typically appears at the initiation ofthe rhythm and does not persist10,12,25,46,47.

AV block in NCT then indicates either sinustachycardia (ST) or reentrant and automatic atrialtachycardias (including MAT, atrial fibrillation, andatrial flutter)6,9,12,13. Some degree of AV block, typi-cally 2:1 or 3:1, is nearly always present with atri-al flutter, as the AV node is incapable of sustainingatrioventricular conduction at the typical atrialrate of 300 bpm, though 1:1 conduction may ex-ist for a short period3,33. Because of this, a consis-tent ventricular rate of 150 or 100 bpm shouldalert the clinician to look closer for flutter wavesin the inferior leads and lead V1. Atrial fibrillation,which exhibits atrial rates of over 400 bpm, simi-larly does not allow for 1:1 conduction throughthe AV node, but the degree of AV block is notpredictable, and an irregular rhythm results3.

QRS Alternans

QRS alternans describes a beat-to-beat varia-tion in the morphology of the QRS complex,most easily seen as a difference in amplitude fromone beat to the next. While this finding is mostoften associated with accessory pathway-mediatedNCTs, such as orthodromic AVRT45,55,67,some au-thors have suggested that this is solely a rate-re-lated phenomenon and is independent of tachy-cardia mechanism5768,69. In summary, its use as adiscriminating factor is limited.

Lead aVR

Often ignored in the evaluation of the 12-leadECG, lead aVR may indeed provide some useful diagnostic information in differentiating NCTs44,64,70-72.Ho et al71 found that ST segment elevation in leadaVR was helpful in differentiating AVRT from AVN-RT and AT with a right atrial origin. In otherwords, the presence of ST segment elevation inlead aVR is suggestive of AVRT (Figure 7B). The STsegment elevation in this lead is thought to bedue to deformation of the ST segment by retro-grade atrial activation rather than from a true re-polarization abnormality64,71. While additional de-tails about the specific location of the accessorypathway may be gleaned from this finding, theirrelevance to care in the ED is limited.

ST Segment – T Wave Abnormalities

Several investigators have shown that ST seg-ment depression is a rate-related phenomenon

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during PSVT and that it provides no differentialdiagnostic information regarding the mechanismof the tachycardia71,73,74. In addition, it is not in-dicative of underlying coronary artery disease orconcurrent ischemia among patients with AVRT orAVNRT73,74. Arya et al66 indicated that while ST-seg-ment depression alone is not helpful in determin-ing tachycardia type, in combination with an RPinterval < 100 msec or no visible P wave, the ab-sence of ST-segment depression effectively rulesout AVRT. In other words, this finding had a highnegative predictive value (NPV = 95%) for AVRT.Without the caveats of an absent P wave or RP in-terval < 100 msec, the NPV was only 56%. Basedon their data, the authors also posit that ST-seg-ment depression � 3 mm in five or more leads(including limb leads and precordial leads) strong-ly suggests AVRT as the tachycardia mechanism.In summary, while data are somewhat conflicting,ST-T abnormalities may be helpful when otherfactors fail to indicate a definitive diagnosis.

Tachycardia Onset

If the clinician is fortunate enough to witnessthe onset of the tachycardia, determining themechanism becomes somewhat easier. A gradual“ramping up” of the atrial rate is characteristic ofST4,7,9 and automatic atrial tachycardia3,25, whilethe sudden onset of tachycardia is indicative of areentrant mechanism, including AVNRT6,25, AVRT using a rapidly conducting bypass tract25, SNRT4-7,9,and atrial reentrant tachycardias25.

The initiating stimulus is also helpful. Prema-ture atrial impulses are typically responsible forthe onset of AVNRT3,4,6,9,10,12,13,25,33, AVRT with a rap-idly conducting bypass tract3,10,12,13,25,33, and sinusnode5,12 and atrial reentrant12,25 tachycardias. Withcommon AVNRT, which uses the slow pathway forantegrade conduction and the fast pathway forretrograde conduction, the initiating prematureimpulse will show a significantly lengthened PRinterval as antegrade conduction shifts from thefast pathway (during sinus rhythm) to the slowpathway in order to set up the reentrant circuit.While some initial PR prolongation may be seen inAVRT using a concealed bypass tract, this is not asmarked as with AVNRT10. Premature ventricularimpulses may also initiate AVNRT12,13 or AVRT10,12,25,although this is less commonly the case. NeitherPACs nor PVCs are implicated in the initiation ofST9, automatic atrial tachycardias3,12, or AVRT usinga slowly conducting bypass tract10, which all dis-play a gradual acceleration in the atrial rate.

Pseudo Deflections

When a retrograde P wave occurs at the termi-nal end of the QRS complex, a “pseudo” deflec-tion can be seen. When seen in lead V1, it iscalled a “pseudo r'” wave, and when seen in theinferior leads (as an inverted P wave), it is termeda “pseudo S” wave. The presence of either a“pseudo r'” deflection in lead V1 or a “pseudo S”deflection in the inferior leads is highly specific forAVNRT55,75. It should be noted that a rate-relatedright ventricular conduction delay can produce afalse positive pseudo r' wave, independent of theunderlying rhythm, as might be seen in incom-plete right bundle branch block.

Diagnostic Maneuvers

Classification of NCTs into AV node-dependentand AV node-independent is helpful when consid-ering various diagnostic measures, both pharma-cologic and non-pharmacologic. The AV node-de-pendent NCTs include AVNRT and AVRT, whereasthe AV node-independent NCTs are ST, SNRT,reentrant and automatic atrial tachycardias, atrialfibrillation and flutter, and MAT4,25. Vagal maneu-vers, most commonly carotid sinus massage(CSM), increase vagal tone to decrease sinus auto-maticity and slow or block conduction throughthe AV node25,63. If vagal maneuvers cause AVblock without termination of the tachycardia,both AVNRT and AVRT may be eliminated fromthe differential. Indeed, up to 30% of reentrantAV node-dependent tachycardias are terminatedwith vagal maneuvers alone25.

In contrast, effective vagal maneuvers in AVnode-independent NCTs will produce AV block,but typically do not cause termination of the dys-rhythmia. In the case of atrial flutter, increasingthe degree of AV block clearly reveals the “saw-tooth” morphology of the flutter waves. Slowing,but not termination, of the tachycardia is seenwith ST, atrial fibrillation, and both unifocal (non-reentrant) and multifocal atrial tachycardia9,12,25.However, as the exception to the rule, sinus andatrial reentrant tachycardias may terminate oreven show transient acceleration with vagal ma-neuvers6,7,12.

Adenosine is often advocated as the pharma-cologic diagnostic agent of choice in the settingof undifferentiated NCT. Intravenous administra-tion of adenosine causes inhibition of adenylyl cy-clase in the myocardium, resulting in negativechronotropic and dromotropic (conduction veloci-

ECG DIFFERENTIAL DIAGNOSIS OF NARROW QRS COMPLEX TACHYCARDIA IN THE EMERGENCY DEPARTMENT

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ty) effects on the SA node and AV node, respec-tively25,76. The resultant effects on various NCTs aresimilar to those seen with vagal maneuvers3,5-

7,9,15,25,77. A 12 mg dose of adenosine, administeredintravenously in rapid fashion, terminates thenodal-dependent NCTs (i.e., AVRT and AVNRT)over 90% of the time78. Higher doses of adenosinemay be needed for refractory cases.

An additional diagnostic maneuver that hasbeen shown to be of benefit by Accardi et al60 isto double the speed of the ECG to 50 mm/sec inorder to increase the distance between adjacentcomponents of the tracing, allowing for easier vi-sualization. These investigators demonstrated asignificant increase in diagnostic accuracy from63% to 71% among emergency physicians evalu-ating NCT ECGs. As this technique poses no riskof harm to the patient, it would be difficult toreason against its use in challenging cases.

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Diagnóstico diferencial electrocardiográfico de la taquicardia de complejo QRS estrechoen el servicio de urgencias: una revisión de ritmos frecuentes y sus características distintivas

Borloz MP, Mark DG, Pines JM, Brady WJ

El diagnóstico diferencial de las taquicardias de complejo QRS estrecho (TQRSE) es un dilema común en los pacientesadultos que acuden a los servicios de urgencias. Algunas TQRSE (ej.: taquicardia sinusal) son secundarias a los motivosque propiciaron su consulta (ej.: fiebre, ansiedad, dolor) y responderán al tratamiento apropiado de la patología sub-yacente. Por otro lado, otras TQRSE (ej.: fibrilación auricular, taquicardia de reentrada nodal AV) pueden ser verdadera-mente el origen de la sintomatología principal (ej.: palpitaciones, mareo secundario a la hipoperfusión) y deben serpositivamente identificadas y tratadas. Para un correcto diagnóstico es necesario conocer las semejanzas y diferenciasentre las distintas TQRSE. Este artículo comenta cuáles son las características demográficas, clínicas y electrocardiográfi-cas que son de ayuda para identificar los siguientes ritmos: taquicardia sinusal, taquicardia de reentrada del nodo sinu-sal, taquicardia auricular unifocal, taquicardia auricular multifocal, fibrilación auricular, flutter auricular, taquicardia dereentrada del nodo auriculoventricular y taquicardia de reentrada auriculoventricular. Además, se realiza un comentariosobre las distintas maniobras diagnósticas, que vincluye la administración de adenosina. [Emergencias 2010;22:369-380]

Palabras clave: Taquicardia de complejo QRS. Servicio de urgencias. Ritmos frecuentes.