ECG differential diagnosis of narrow QRS complex ... - Semes

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acreditada 

REVIEW ARTICLE 

ECG differential diagnosis of narrow QRS complex 

tachycardia in the emergency department: A review 

of common rhythms and distinguishing features 

MATTHEW P. BORLOZ 1 , DUSTIN G. MARK 2 ,JESSE M. PINES 3,4,5 , WILLIAM J. BRADY 6 

1 

Departamento de Emergencias. Universidad de Georgetown/Hospital Center Washington, Washington, 

EE.UU. 2 Departamento de Cuidados Intensivos. Universidad Health System de Pennsylvania. Filadelfia, EE.UU. 

3 

Departamento de Emergencias. Universidad Health System de Pennsylvania. Filadelfia, EE.UU. 4 Centro de 

Epidemiología Clínica y Bioestadística, Facultad de Medicina, Universidad de Pennsylvania. Filadelfia, EE.UU. 

5 

Instituto Leonard Davis. Universidad de Pennsylvania. Filadelfia, EE.UU. 6 Departamento de Emergencias. 

Universidad de Virginia, Charlottesville, EE.UU. 

CORRESPONDENCE: 

William Brady 

Department of Emergency 

Medicine 

University of Virginia Health 

System 

Charlottesville, VA. EE.UU. 

E-mail: wb4z@virginia.edu 

RECEIVED: 

5-2-2010 

ACCEPTED: 

7-4-2010 

CONFLICT OF INTERES: 

None 

The differentiation of narrow complex tachycardias (NCT) is a commonly encountered 

diagnostic dilemma in the adult emergency department. Some NCTs (e.g., sinus 

tachycardia) are secondary to the presenting complaint (e.g., fever, anxiety, pain) and will 

respond to appropriate treatment of the inciting pathologic insult. Alternatively, other 

NCTs (e.g., atrial fibrillation, AV nodal reentrant tachycardia) may indeed be the cause of 

the chief complaint (e.g., palpitations, lightheadedness from poor perfusion) and must be 

positively identified and primarily managed. An appreciation of the similarities and 

differences among these NCTs is necessary for appropriate recognition. This article 

delineates which demographic, historical, and electrocardiographic characteristics are 

helpful in identifying the following rhythms: sinus tachycardia, sinus node reentrant 

tachycardia, unifocal atrial tachycardias, multifocal atrial tachycardia, atrial fibrillation, 

atrial flutter, atrioventricular nodal reentrant tachycardia, and atrioventricular reentrant 

tachycardia. In addition, a discussion of various diagnostic maneuvers, such as adenosine 

administration, is included. [Emergencias 2010;22:369-380] 

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

Introduction 

The clinical manifestations resulting from narrow 

complex tachycardias (NCT) are a not uncommon 

reason for presentation to the emergency 

department (ED) 1 . NCTs are defined as 

rhythms with a rate greater than 100 beats per 

minute (bpm) and a QRS complex duration less 

than 120 milliseconds (msec) in the adult patient. 

NCTs are most often supraventricular in origin, 

arising from the sinus node, the atria, or the atrioventricular 

(AV) junction. While narrow complex 

ventricular tachycardia has been reported 2 , the 

latter is very rare and, thus, will not be discussed 

further in this paper. 

Because NCTs are numerous and their differences 

subtle, it is important for the emergency 

physician to understand the differences among 

these rhythms in order to render a correct diagnosis 

and appropriate management. While we do 

not discuss specific treatment of these rhythms, 

we do address diagnostic maneuvers, such as 

adenosine administration, and acknowledge that 

these may be both diagnostic and therapeutic. In 

no circumstance should the diagnostic process 

limit timely management of an unstable patient. 

Electrocardiographic Differential Diagnosis 

Sinus tachycardia (ST) 

Physiologic sinus tachycardia refers to a NCT 

that originates from the SA node and is due to increased 

automaticity, rather than a reentrant 

mechanism. The atrial rate is greater than 100 

Emergencias 2010; 22: 369-380 369

M. P. Borloz et al. 

bpm and is largely regular with slight variations 

over time 3,4 . The P wave morphology is identical 

to that seen in sinus rhythm and appears positive 

in leads I, II, III, and aVF 5-7 and biphasic 7,8 or negative 

5 in lead V 1 (Figures 1A and B). The onset of 

ST is gradual, exhibiting a “warm up” period, and 

is not initiated by atrial or ventricular premature 

beats 4,7,9,10 . Perhaps the most telling feature of ST 

is that it occurs in the setting of underlying physiologic 

stress or pharmacologic influence, namely 

fever, infection, anxiety, stimulant drug use, or hypotension, 

among many others 4,7,9 . When frequent 

premature atrial contractions (PACs) accompany 

ST, it may be difficult to differentiate from multifocal 

atrial tachycardia (MAT, discussed below) 3 . 

Sinus node reentrant tachycardia (SNRT) 

As the name implies, sinus node reentrant 

tachycardia is due to a reentrant mechanism within 

or adjacent to the sinus nodal tissue 4,7 . This 

rhythm is indistinguishable from sinus tachycardia 

on a simple 12-lead ECG (Figure 2), as the P wave 

position, axis, and morphology are essentially 

identical to those of the latter 4,5,7,9,11,12 . The rate is 

usually 100-150 bpm, and the rhythm is regular 4,7 . 

In contrast to ST, the onset of SNRT is abrupt and 

often initiated by a premature atrial impulse 4-7,9-12 . 

Termination is similarly abrupt and may be effected 

with vagal maneuvers or adenosine administration 

5,9 . This rhythm is often an incidental finding 

seen on Holter monitoring, is typically non-sustained, 

and rarely causes clinically significant 

symptomatology 13 . Sanders et al 14 report an incidence 

of 3% in their series of patients referred for 

electrophysiologic (EP) study. 

Refer to Figure 2 for an example of SNRT 

which, based solely on this rhythm segment, is 

impossible to separate from typical sinus tachycardia. 

Unifocal Atrial Tachycardias 

Unifocal atrial tachycardias are due to automatic, 

triggered, or reentrant mechanisms, depending 

on the clinical scenario in which they 

arise 6,15 . They are a relatively uncommon cause of 

Figure 1. It shows a sinus tachycardia on ECG. 

Figure 2. It shows a sinus node reentrant tachycardia on 

ECG. 

clinically significant NCT, as they comprise less 

than 10% of documented cases 4 . 

Reentrant atrial tachycardias depend on diseased 

atrial tissue to create adjacent areas of tissue 

with variant speeds of conduction and refractory 

periods. As such, they usually arise following 

atrial surgeries or within otherwise diseased atrial 

tissue 7,13 . When seen in a patient without underlying 

heart disease, enhanced automaticity is likely 

the mechanism. Onset and termination are typically 

gradual and occur without the influence of 

premature impulses 3,16,17 . Triggered activity is implicated 

in atrial tachycardia seen in the setting of 

digoxin toxicity (often accompanied by AV 

block) 7 . 

Unifocal atrial tachycardias, by definition, originate 

from a single area of the atrium (unlike 

MAT), the location of which governs the appearance 

of the P wave. For example, if the focus is 

near the SA node, the P wave will be similar in 

appearance to that during sinus rhythm. If, however, 

the atrial impulse is initiated low in the right 

atrium, the P wave may be negative in leads II, III, 

and aVF 6 . The atrial rate is typically 100-250 

bpm 4,11 , and the presence or absence of AV block 

does not rule the diagnosis in or out 9,6,12,13 . 

Multifocal atrial tachycardia (MAT) 

Multifocal atrial tachycardia is an irregular NCT 

with a frequency of 0.08-0.36% among hospitalized 

patients 18,19 . It typically occurs in the elderly 

in the setting of cardiopulmonary disease and is 

most commonly associated with chronic obstructive 

pulmonary disease (COPD). Associations also 

exist with pulmonary embolism, hypoxemia, and 

hypokalemia 20 . Triggered activity 21 and enhanced 

automaticity 17 have been proposed as likely mechanisms; 

however, consensus is lacking, and the 

precise mechanism remains elusive. 

Very specific electrocardiographic criteria define 

MAT; these include an atrial rate > 100 bpm, 

three or more distinct non-sinus P wave morphologies 

(in the same lead), an isoelectric baseline 

(i.e., no flutter or fibrillation waves), and irregularity 

of the PP, PR, and RR intervals (Figure 

3) 5,22,23 . Despite the clear diagnostic criteria, this 

370 Emergencias 2010; 22: 369-380

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

Figure 3. It shows a multifocal atrial achycardia on ECG. 

rhythm may be difficult to distinguish from sinus 

rhythm with frequent PACs or atrial fibrillation. 

Kastor et al 23 support the administration of a 

small dose of an intravenous beta-adrenergic or 

calcium-channel antagonist in order to slow the 

atrial rate and allow the clinician to search the 

baseline for distinct P waves supportive of MAT 

or fibrillatory waves consistent with atrial fibrillation. 

This diagnostic maneuver should be pursued 

with caution in the absence of clear data to 

support a normal left ventricular ejection fraction. 

While atrial rates typically range from 100-220 

bpm 5 , some authors propose lowering the rate 

threshold for diagnosis from 100 bpm to 90 

bpm 24 . 

Atrial fibrillation 

Figure 4. It shows an atrial fibrillation on ECG. 

Atrial fibrillation remains the most prevalent 

form of narrow complex tachycardia 25 . In the 

United States, 2.3 million individuals carry this diagnosis 

26 , and 0.2% of ED visits were attributed to 

atrial fibrillation during 1993-2004 27 . Patients may 

present to the ED with worsening of their chronic 

atrial fibrillation due to poorly controlled ventricular 

rates or with paroxysmal atrial fibrillation associated 

with hyperthyroidism 5,25 , hypokalemia or 

hypomagnesemia 25 , or following excessive ethanol 

intoxication, the so-called “holiday heart syndrome” 

28 . The mechanism of atrial fibrillation appears 

to be multiple micro-reentrant wavelets in 

the atria 3,13 . Paroxysms of atrial fibrillation may be 

triggered by preceding alterations in autonomic 

tone 29 and/or ectopic foci frequently located in or 

around the pulmonary veins 30 . Atrial fibrillation is 

also the second most common tachycardia experienced 

by patients with the Wolff-Parkinson-White 

syndrome, seen in 20-25% 31,32 . 

Electrocardiographically (Figure 4), the absence 

of P waves and the irregularly irregular ventricular 

response are the hallmarks of this rhythm 5,33 . The 

baseline may be isoelectric or may exhibit fibrillatory 

waves of varying morphology at a rate of 

400-700 bpm 3,5,25 . The amplitude of the fibrillatory 

waves is suggestive of the underlying pathology. 

Fine fibrillatory waves ( 0.5 mm amplitude) are 

associated with ischemic heart disease, while 

coarse waves (> 0.5 mm) signify left atrial enlargement 

3,34 . Untreated ventricular rates range 

from 100-200 bpm 3,5 compromising diastolic ventricular 

filling, and often producing palpitations, 

chest pain, and symptoms of congestive heart failure 

35 . 

Atrial flutter (AF) 

Atrial flutter is most commonly due to a 

macro-reentrant circuit within the right atrium 

and shares many etiologic features with atrial fibrillation 

13,36 . Indeed, it may often be confused with 

“coarse” atrial fibrillation 37 . Typical AF (type 1) involves 

either a counterclockwise (common) or 

clockwise (less common) reentrant circuit. Counterclockwise 

circuits produce downward deflections, 

called flutter waves, in the inferior leads; 

these are classically referred to as having a “sawtooth” 

appearance 5,36 . Flutter waves are also frequently 

visualized in lead V1 and must be of uniform 

rate, amplitude, and morphology to be 

so-called 37 . The atrial rate is regular and ranges 

between 250 and 350 bpm, often close to or exactly 

300 bpm 5,33 . A less common variant of AF, 

termed type II, produces faster atrial rates, typically 

in the range of 340-430 bpm. Because the AV 

node is usually incapable of conducting impulses 

to the ventricles at these rates, AV block is almost 

always present; although, 1:1 conduction is possible 

38 . Two-to-one AV block, which is most common, 

will produce a ventricular rate around 150 

bpm in type I AF, whereas 3:1 AV block will result 

in a ventricular rate of 100 bpm. While the degree 

of AV block is often fixed, it may also be 

variable, yielding an irregular ventricular 

response 5 . 

Refer to Figure 5A for examples of atrial flutter 

with a regular rate of 150 bpm (upper panel) and 

a rapid, irregular form of atrial flutter (atrial flutter 

with variable block, lower panel). Note Figure 5B, 

demonstrating sinus tachycardia initially misdiagnosed 

as atrial flutter due to the “classic” rate of 

150 bpm. Note the normal P wave polarity in the 

limb leads. This finding, along with significant 

rate variation observed over a very short period of 

time, ultimately contributed to the correct electrocardiographic 

diagnosis – very rapid sinus tachycardia. 

Emergencias 2010; 22: 369-380 371


Figure 5. It shows an atrial flutter with a regular rate of 150 

bpm (upper panel) and an atrial flutter, note the normal P wave 

polarity on a 12-lead ECG. 

Atrioventricular nodal reentrant tachycardia 

(AVNRT) 

AV nodal reentrant tachycardia accounts for 50- 

69% of all regular NCTs (excluding those associated 

with pre-excitation) 10,39 . AVNRT depends on socalled 

“dual AV node physiology,” which indicates 

that the AV node has two distinct tracts capable of 

conducting impulses, one of which conducts slowly 

but has a short refractory period, and the other 

of which conducts rapidly but has a relatively 

longer refractory period. During sinus rhythm, impulses 

are typically carried by the “fast” (also 

known as “beta”) pathway, and the “slow” (also 

known as “alpha”) pathway is unused. Common 

AVNRT is initiated when a premature atrial impulse 

finds the fast pathway refractory and instead uses 

the slow pathway to conduct to the His-Purkinje 

system. By the time the impulse reaches the ventricles, 

the fast pathway has repolarized, and the 

impulse is carried by this tract in a retrograde fashion. 

This pattern continues in order to produce 

“common” AVNRT (also known as typical AVNRT 

or slow-fast AVNRT). A premature ventricular impulse 

may also initiate this rhythm if the impulse is 

blocked in the retrograde direction by the slow 

pathway and follows the fast pathway. The impulse 

then proceeds via the slow pathway in the 

antegrade direction and back up the fast pathway 

for retrograde transmission. 

In 3-10% of cases, the fast pathway may have 

a shorter refractory period than the slow pathway, 

allowing for reversal of the circuit 9,39-42 . “Uncommon” 

AVNRT (also known as atypical AVNRT or 

fast-slow AVNRT) occurs when antegrade conduction 

follows the fast pathway and retrograde conduction 

is carried by the slow pathway. It is generally 

initiated by a premature ventricular 

impulse 40 . 

Because of the rapid retrograde transmission of 

the impulse in common AVNRT, the P wave is 

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. 

372 Emergencias 2010; 22: 369-380


Figure 7. It shows an atrioventricular nodal reentrant tachycardia 

on ECG. Note the P wave is hidden by the QRS complex. 

hidden by the QRS complex in 69% of cases (Figure 

6A) 39 . In the remainder of cases, the P wave 

immediately follows the QRS complex (Figure 6B), 

at times obscuring the terminal portion of the 

complex and resulting in “pseudo deflections” 

(discussed below). In contrast, because retrograde 

conduction in uncommon AVNRT occurs via a 

slow pathway, the ventricles are activated long 

before the atria, so the P wave appears closer to 

the subsequent QRS complex than to that which 

precedes it. 

Patients with common AVNRT may report a 

sensation of pounding in the neck, which correlates 

with concomitant atrial and ventricular contraction, 

elevated right atrial pressures, and flow 

reversal from the right atrium to the systemic venous 

system. In a study by Gürsoy et al 43 , this 

finding was reported by 50 of 54 (93%) of patients 

with this rhythm and by none of the 190 

patients with other NCTs. 

Atrioventricular reentrant tachycardia (AVRT) 

Atrioventricular reentrant tachycardia mechanistically 

occurs via a reentrant circuit that involves 

both the AV node and an accessory atrioventricular 

pathway. AVRT may be divided into 

two principal categories designated by the direction 

of travel through the AV node and the accessory 

pathway: orthodromic and antidromic. Orthodromic 

AVRT indicates that antegrade 

conduction occurs through the AV node with retrograde 

conduction via the accessory pathway 

(Figure 7A), resulting in a narrow QRS complex 

tachycardia. Conversely, antidromic AVRT occurs 

with antegrade conduction down the accessory 

pathway and retrograde conduction through the 

AV node, producing a wide QRS complex tachycardia. 

Onset of AVRT is abrupt and is typically initiated 

by a premature atrial or ventricular impulse 

3,10,12,13,25,33 . Rates typically range from 140-240 

bpm 25 . ST segment elevation is seen in lead aVR, 

due to retrograde atrial activation; this finding can 

be helpful in differentiating AVRT from AVNRT or 

AT with a right atrial focus 44 . The presence of AV 

block during tachycardia effectively excludes the 

diagnosis of AVRT 6,9,10,12,13,45-48 . Refer to Figure 7B for 

an example of orthodromic AVRT. 

Evaluation of Available Demographic 

and Electrocardiographic Features 

Demographics (Age and Gender) 

Investigators have attempted to identify age 

and gender differences among patients with 

supraventricular tachycardias in an effort to define 

specific characteristics that aid in determining the 

most likely mechanism 41,49-54 . While younger patients 

are more likely to experience paroxysmal 

supraventricular tachycardia (PSVT) in the absence 

of known cardiovascular disease and females are 

Figure 8. It shows an atrioventricular nodal reentrant tachycardia on a 12-lead ECG. Note he P wave 

immediately follows the QRS coomplex “pseudo deflections”. 

Emergencias 2010; 22: 369-380 373


Aurícula 

Nodo 

sinusal 

Vía 

accesoria 

Ventrículos 

Sistema 

HIS- 

Purkinje 

Figure 9. It shows a diagram of atrioventricular reentrant 

tachycardia’s mechanism. 

more than twice as likely as males to be diagnosed 

with PSVT (70%), no definitive conclusions 

can be made regarding the influence of age or 

gender on the mechanism of the tachycardia 49 . In 

a population of 485 patients with NCT without 

overt electrocardiographic evidence of pre-excitation, 

investigators determined that AVNRT was 

the most common mechanism of supraventricular 

tachycardia in all age groups, from teenage to 

elderly, and that age was not a reliable predictor 

of tachycardia mechanism 50 . 

With regard to gender, overall PSVT incidence 

is relatively evenly distributed between men and 

women; however, in the specific case of AVNRT, 

there appears to be a higher prevalence of disease 

among female patients, ranging from 68-76% as 

observed in three separate studies 41,51,54 . While the 

reason for this unbalanced gender distribution is 

unclear, one study has demonstrated that women 

tend to have a shorter AV nodal block cycle 

length and enhanced ventriculoatrial conduction, 

C 

D 

A 

B 

as compared to men, thus potentially facilitating 

the mechanism of AVNRT 53 . 

With respect to the Wolff-Parkinson-White 

(WPW) syndrome, there appears to be a male 

preponderance, shown to be approximately twofold 

in both a population study and a study of patients 

referred for electrophysiologic analysis 41,52 . 

Another investigator proposes that the reason for 

this is the presence of a longer AV conduction delay 

in males versus females 53 . This longer delay favors 

pre-excitation via active accessory AV pathways. 

Approximately 50% of patients with 

accessory AV pathways will experience their first 

episode of tachycardia before age 20, as opposed 

to patients with AVNRT and atrial tachycardia, 

who are more likely to initially present after 20 

years of age 41,51 . 

Rate 

In general, the ventricular rate of the tachycardia 

is rarely helpful in differentiating one type of 

NCT from another. One exception to this is in the 

case of type I atrial flutter, which exhibits an atrial 

rate between 250-350 bpm and frequently conducts 

with 2:1 AV block, yielding a ventricular 

rate around 150 bpm. A 3:1 AV block with a ventricular 

rate of 100 bpm is also common 3,33 . Whatever 

the ventricular rate, the R-R interval should 

show little or no beat-to-beat variation in the absence 

of medications or vagal maneuvers 3,25 . 

In an electrophysiologic study which included 

100 patients with either AVNRT or AVRT and 27 

patients with atrial “ectopic” tachycardia, the 

mean atrial rate varied from 167-170 bpm. Several 

other studies have also failed to demonstrate 

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

374 Emergencias 2010; 22: 369-380


significant differences in atrial or ventricular rates 

among these same tachycardia types 55,56 . Despite a 

higher mean rate in AVRT versus AVNRT, Kay et 

al 57 found that, after multivariate analysis, higher 

rates were not predictive of AVRT. In general, rate 

alone is not a reliable predictor of tachycardia 

mechanism. 

Regularity 

The regularity of the rhythm can be remarkably 

helpful in differentiating the mechanisms of 

various NCTs. Specifically, the finding of a clearly 

irregular rhythm significantly narrows the list of 

potential diagnoses. Just as atrial fibrillation is “irregularly 

irregular,” atrial fibrillation with rapid 

ventricular response may be similarly described. 

An irregularly irregular NCT with definite P waves 

is likely multifocal atrial tachycardia (MAT). Note 

that the diagnosis of MAT formally requires 

demonstration of three discrete P wave morphologies. 

PR intervals differ from beat to beat due to 

the variable location of the inciting atrial impulse 

3,11 . MAT may be confused with atrial fibrillation 

9,23,58 . 

The presence of regular periods of tachycardia 

punctuated by apparent pauses, so called “group 

beatings,” indicates atrial flutter or ectopic atrial 

tachycardia with variable AV block 59 . Differentiation 

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 is 

often difficult due to fast ventricular rates, which 

may obscure interpretation of atrial activity 60 . 

The finding of a regular rhythm includes every 

other mechanism of NCT, so the clinician is advised 

to focus on alternative discriminating characteristics 

for further diagnosis. It should be mentioned 

that although sinus tachycardia is typically 

considered a regular rhythm, it may be mildly irregular 

3,59 . 

P Wave (Presence, Axis, and Morphology) 

The presence of discrete P waves may be difficult 

to determine with fast atrial and ventricular 

rates. When present, however, the location of the 

P wave relative to the QRS complex is quite helpful 

(refer to the discussion of P wave location). 

Conversely, the absence of P waves with an irregularly 

irregular ventricular rate greater than 100 

bpm strongly suggests atrial fibrillation with rapid 

ventricular response. Fibrillatory waves are seen 

on the baseline and represent disorganized atrial 

electrical activity 3,5 . A particular pattern of P wave, 

the “flutter wave,” is seen in place of typical P 

waves in patients with atrial flutter, most often at 

an atrial rate of 250-350 bpm. These flutter 

waves, which give the baseline the classic “sawtooth” 

appearance, are most easily identified in 

the inferior leads (i.e., II, III, aVF) and in lead 

3,5,6,33 

V 1 . 

Examination of the P wave axis may yield additional 

information regarding the etiology of 

the NCT, particularly in the case of unifocal atrial 

tachycardia. Determining the P wave axis involves 

identifying the polarity of the P wave as 

positive, negative, or biphasic in particular leads. 

Rhythms that originate from the SA node, located 

in the superior right atrial myocardium (i.e., 

sinus tachycardia [Figure 5B], sinus node reentrant 

tachycardia), will show upright P waves in 

leads I, II, III, and aVF 5-7 and a biphasic 7,8 or negative 

5 P wave in lead V 1. Ectopic atrial tachycardias 

originating from tissue adjacent to the SA node 

are difficult to distinguish from those arising 

from the node itself using a standard 12-lead 

ECG. Ectopic atrial tachycardias and atrial reentrant 

tachycardias arising from sites distant from 

SA nodal tissue, however, will have variable P 

wave axes and morphologies 12 . Tang et al 61 

showed that leads aVL and V1 were most useful 

in differentiating a right atrial focus from a left 

atrial focus. A positive or biphasic P wave in lead 

aVL correlates with a right atrial focus (sensitivity 

88%, specificity 79%), while a positive P wave in 

lead V 1 supports a left atrial focus (sensitivity 

93%, specificity 88%). In addition, negative P 

waves in the inferior leads (i.e., leads II, III, aVF) 

correlate with an inferior atrial focus, while positive 

P waves in these leads indicate a superior focus. 

Not all NCTs with negative P waves in the 

inferior leads originate from an inferior atrial focus, 

however, as this P wave axis deviation can 

also be due to retrograde atrial conduction from 

an AV junction focus, as may be seen in AVNRT. 

In summary, the primary strength of P wave axis 

determination lies in the diagnosis of both ectopic 

left atrial foci and MAT, the former demonstrating 

positive P waves in lead V1, the latter 

exhibiting variable P wave axes and morphologies 

in a single lead. 

P Wave Location (RP Interval) 

The RP interval describes the duration from the 

QRS complex to the subsequent P wave. This duration 

is compared to the PR interval of the 

rhythm, and based on their relative values, a 

rhythm may be called a “short RP” or “long RP” 

Emergencias 2010; 22: 369-380 375


tachycardia. A short RP tachycardia is one in 

which the RP interval is shorter than the PR interval. 

One may think of this as the P wave following 

the QRS complex instead of preceding it. Examples 

of short RP tachycardias are common AVNRT 

(Figure 6B) and orthodromic AVRT (Figure 7B) 

with a rapidly conducting accessory pathway. A 

short RP tachycardia may also be seen with atrial 

tachycardia in the presence of a long PR interval, 

usually at higher rates. Long RP tachycardias, 

which represent the “normal” P wave to QRS 

complex relationship, include sinus tachycardia 

(ST), sinus node reentrant tachycardia (SNRT), 

atrial tachycardias, uncommon AVNRT, and orthodromic 

AVRT with a slowly conducting accessory 

pathway. This classification is often helpful in understanding 

NCT mechanisms and diagnosing 

these rhythms from the surface ECG. 

In some cases, the P wave may be hidden 

within the QRS complex, representing a subtype 

of the short RP tachycardias. This finding almost 

exclusively occurs during common AVNRT, and 

has been found to be the single most useful observation 

on 12-lead ECG analysis that can distinguish 

AVNRT from AVRT. Conversely, AVNRT can 

present as a short RP tachycardia in up to 30% of 

cases, thus mimicking AVRT, making the absence 

of QRS masking relatively non-specific 10- 

12,39,42,45,57,62,63 

. Some investigators have attempted to 

define a specific value for the RP interval in comparing 

common AVNRT and AVRT. Zhong et al 64 

demonstrated mean values of 89 ± 13 msec and 

134 ± 29 msec, respectively. In an attempt to validate 

an algorithm designed for pediatric patients 

by Jaeggi et al 65 , Arya et al 66 looked at a specific 

cutoff of 100 msec to discriminate AVRT from 

common AVNRT in a population of adult patients. 

Sensitivity and specificity for this finding were 

73% and 88%, respectively. As might be expected, 

with a decrease in the cutoff value to 80 

msec, the investigators noted increased sensitivity 

(85%) but decreased specificity (69%). 

AV Block 

The presence of AV block during an episode of 

NCT greatly narrows the differential diagnosis. AV 

block is not possible with a rhythm that employs 

the normal atrioventricular conduction pathway 

for antegrade conduction and an accessory pathway 

for retrograde conduction because this tachycardia 

is dependent on a “patent” AV tract. As a 

result, orthodromic AVRT may be eliminated from 

the differential if AV block is present 6,9,10,12,13,45-48 . 

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 of 

the rhythm and does not persist 10,12,25,46,47 . 

AV block in NCT then indicates either sinus 

tachycardia (ST) or reentrant and automatic atrial 

tachycardias (including MAT, atrial fibrillation, and 

atrial flutter) 6,9,12,13 . Some degree of AV block, typically 

2:1 or 3:1, is nearly always present with atrial 

flutter, as the AV node is incapable of sustaining 

atrioventricular conduction at the typical atrial 

rate of 300 bpm, though 1:1 conduction may exist 

for a short period 3,33 . Because of this, a consistent 

ventricular rate of 150 or 100 bpm should 

alert the clinician to look closer for flutter waves 

in the inferior leads and lead V 1 . Atrial fibrillation, 

which exhibits atrial rates of over 400 bpm, similarly 

does not allow for 1:1 conduction through 

the AV node, but the degree of AV block is not 

predictable, and an irregular rhythm results 3 . 

QRS Alternans 

QRS alternans describes a beat-to-beat variation 

in the morphology of the QRS complex, 

most easily seen as a difference in amplitude from 

one beat to the next. While this finding is most 

often associated with accessory pathway-mediated 

NCTs, such as orthodromic AVRT 45,55,67 ,some authors 

have suggested that this is solely a rate-related 

phenomenon and is independent of tachycardia 

mechanism 5768,69 . In summary, its use as a 

discriminating factor is limited. 

Lead aVR 

Often ignored in the evaluation of the 12-lead 

ECG, lead aVR may indeed provide some useful 

diagnostic information in differentiating NCTs 44,64,70-72 . 

Ho et al 71 found that ST segment elevation in lead 

aVR was helpful in differentiating AVRT from AVN- 

RT and AT with a right atrial origin. In other 

words, the presence of ST segment elevation in 

lead aVR is suggestive of AVRT (Figure 7B). The ST 

segment elevation in this lead is thought to be 

due to deformation of the ST segment by retrograde 

atrial activation rather than from a true repolarization 

abnormality 64,71 . While additional details 

about the specific location of the accessory 

pathway may be gleaned from this finding, their 

relevance to care in the ED is limited. 

ST Segment – T Wave Abnormalities 

Several investigators have shown that ST segment 

depression is a rate-related phenomenon 

376 Emergencias 2010; 22: 369-380


during PSVT and that it provides no differential 

diagnostic information regarding the mechanism 

of the tachycardia 71,73,74 . In addition, it is not indicative 

of underlying coronary artery disease or 

concurrent ischemia among patients with AVRT or 

AVNRT 73,74 . Arya et al 66 indicated that while ST-segment 

depression alone is not helpful in determining 

tachycardia type, in combination with an RP 

interval < 100 msec or no visible P wave, the absence 

of ST-segment depression effectively rules 

out AVRT. In other words, this finding had a high 

negative predictive value (NPV = 95%) for AVRT. 

Without the caveats of an absent P wave or RP interval 

< 100 msec, the NPV was only 56%. Based 

on their data, the authors also posit that ST-segment 

depression 3 mm in five or more leads 

(including limb leads and precordial leads) strongly 

suggests AVRT as the tachycardia mechanism. 

In summary, while data are somewhat conflicting, 

ST-T abnormalities may be helpful when other 

factors fail to indicate a definitive diagnosis. 

Tachycardia Onset 

If the clinician is fortunate enough to witness 

the onset of the tachycardia, determining the 

mechanism becomes somewhat easier. A gradual 

“ramping up” of the atrial rate is characteristic of 

ST 4,7,9 and automatic atrial tachycardia 3,25 , while 

the sudden onset of tachycardia is indicative of a 

reentrant mechanism, including AVNRT 6,25 , AVRT 

using a rapidly conducting bypass tract 25 , SNRT 4-7,9 , 

and atrial reentrant tachycardias 25 . 

The initiating stimulus is also helpful. Premature 

atrial impulses are typically responsible for 

the onset of AVNRT 3,4,6,9,10,12,13,25,33 , AVRT with a rapidly 

conducting bypass tract 3,10,12,13,25,33 , and sinus 

node 5,12 and atrial reentrant 12,25 tachycardias. With 

common AVNRT, which uses the slow pathway for 

antegrade conduction and the fast pathway for 

retrograde conduction, the initiating premature 

impulse will show a significantly lengthened PR 

interval as antegrade conduction shifts from the 

fast pathway (during sinus rhythm) to the slow 

pathway in order to set up the reentrant circuit. 

While some initial PR prolongation may be seen in 

AVRT using a concealed bypass tract, this is not as 

marked as with AVNRT 10 . Premature ventricular 

impulses may also initiate AVNRT 12,13 or AVRT 10,12,25 , 

although this is less commonly the case. Neither 

PACs nor PVCs are implicated in the initiation of 

ST 9 , automatic atrial tachycardias 3,12 , or AVRT using 

a slowly conducting bypass tract 10 , which all display 

a gradual acceleration in the atrial rate. 

Pseudo Deflections 

When a retrograde P wave occurs at the terminal 

end of the QRS complex, a “pseudo” deflection 

can be seen. When seen in lead V 1 , it is 

called a “pseudo r'” wave, and when seen in the 

inferior leads (as an inverted P wave), it is termed 

a “pseudo S” wave. The presence of either a 

“pseudo r'” deflection in lead V 1 or a “pseudo S” 

deflection in the inferior leads is highly specific for 

AVNRT 55,75 . It should be noted that a rate-related 

right ventricular conduction delay can produce a 

false positive pseudo r' wave, independent of the 

underlying rhythm, as might be seen in incomplete 

right bundle branch block. 

Diagnostic Maneuvers 

Classification of NCTs into AV node-dependent 

and AV node-independent is helpful when considering 

various diagnostic measures, both pharmacologic 

and non-pharmacologic. The AV node-dependent 

NCTs include AVNRT and AVRT, whereas 

the AV node-independent NCTs are ST, SNRT, 

reentrant and automatic atrial tachycardias, atrial 

fibrillation and flutter, and MAT 4,25 . Vagal maneuvers, 

most commonly carotid sinus massage 

(CSM), increase vagal tone to decrease sinus automaticity 

and slow or block conduction through 

the AV node 25,63 . If vagal maneuvers cause AV 

block without termination of the tachycardia, 

both AVNRT and AVRT may be eliminated from 

the differential. Indeed, up to 30% of reentrant 

AV node-dependent tachycardias are terminated 

with vagal maneuvers alone 25 . 

In contrast, effective vagal maneuvers in AV 

node-independent NCTs will produce AV block, 

but typically do not cause termination of the dysrhythmia. 

In the case of atrial flutter, increasing 

the degree of AV block clearly reveals the “sawtooth” 

morphology of the flutter waves. Slowing, 

but not termination, of the tachycardia is seen 

with ST, atrial fibrillation, and both unifocal (nonreentrant) 

and multifocal atrial tachycardia 9,12,25 . 

However, as the exception to the rule, sinus and 

atrial reentrant tachycardias may terminate or 

even show transient acceleration with vagal maneuvers 

6,7,12 . 

Adenosine is often advocated as the pharmacologic 

diagnostic agent of choice in the setting 

of undifferentiated NCT. Intravenous administration 

of adenosine causes inhibition of adenylyl cyclase 

in the myocardium, resulting in negative 

chronotropic and dromotropic (conduction veloci- 

Emergencias 2010; 22: 369-380 377


ty) effects on the SA node and AV node, respectively 

25,76 . The resultant effects on various NCTs are 

similar to those seen with vagal maneuvers 3,5- 

7,9,15,25,77 

. A 12 mg dose of adenosine, administered 

intravenously in rapid fashion, terminates the 

nodal-dependent NCTs (i.e., AVRT and AVNRT) 

over 90% of the time 78 . Higher doses of adenosine 

may be needed for refractory cases. 

An additional diagnostic maneuver that has 

been shown to be of benefit by Accardi et al 60 is 

to double the speed of the ECG to 50 mm/sec in 

order to increase the distance between adjacent 

components of the tracing, allowing for easier visualization. 

These investigators demonstrated a 

significant increase in diagnostic accuracy from 

63% to 71% among emergency physicians evaluating 

NCT ECGs. As this technique poses no risk 

of harm to the patient, it would be difficult to 

reason against its use in challenging cases. 

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Emergencias 2010; 22: 369-380 379


Diagnóstico diferencial electrocardiográfico de la taquicardia de complejo QRS estrecho 

en 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 pacientes 

adultos que acuden a los servicios de urgencias. Algunas TQRSE (ej.: taquicardia sinusal) son secundarias a los motivos 

que propiciaron su consulta (ej.: fiebre, ansiedad, dolor) y responderán al tratamiento apropiado de la patología subyacente. 

Por otro lado, otras TQRSE (ej.: fibrilación auricular, taquicardia de reentrada nodal AV) pueden ser verdaderamente 

el origen de la sintomatología principal (ej.: palpitaciones, mareo secundario a la hipoperfusión) y deben ser 

positivamente identificadas y tratadas. Para un correcto diagnóstico es necesario conocer las semejanzas y diferencias 

entre las distintas TQRSE. Este artículo comenta cuáles son las características demográficas, clínicas y electrocardiográficas 

que son de ayuda para identificar los siguientes ritmos: taquicardia sinusal, taquicardia de reentrada del nodo sinusal, 

taquicardia auricular unifocal, taquicardia auricular multifocal, fibrilación auricular, flutter auricular, taquicardia de 

reentrada del nodo auriculoventricular y taquicardia de reentrada auriculoventricular. Además, se realiza un comentario 

sobre 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. 

380 Emergencias 2010; 22: 369-380

ECG differential diagnosis of narrow QRS complex ... - Semes

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