REVIEW ARTICLE

Formacin
acreditada

ECG differential diagnosis of narrow QRS complex

tachycardia in the emergency department: A review
of common rhythms and distinguishing features
MATTHEW P. BORLOZ1, DUSTIN G. MARK2, JESSE M. PINES3,4,5, WILLIAM J. BRADY6
Departamento de Emergencias. Universidad de Georgetown/Hospital Center Washington, Washington,
EE.UU. 2Departamento de Cuidados Intensivos. Universidad Health System de Pennsylvania. Filadelfia, EE.UU.
3
Departamento de Emergencias. Universidad Health System de Pennsylvania. Filadelfia, EE.UU. 4Centro de
Epidemiologa Clnica y Bioestadstica, Facultad de Medicina, Universidad de Pennsylvania. Filadelfia, EE.UU.
5
Instituto Leonard Davis. Universidad de Pennsylvania. Filadelfia, EE.UU. 6Departamento de Emergencias.
Universidad de Virginia, Charlottesville, EE.UU.
1

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
Emergencias 2010; 22: 369-380

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
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M. P. Borloz et al.

bpm and is largely regular with slight variations

over time3,4. The P wave morphology is identical
to that seen in sinus rhythm and appears positive
in leads I, II, III, and aVF5-7 and biphasic7,8 or negative5 in lead V1 (Figures 1A and B). The onset of
ST is gradual, exhibiting a warm up period, and
is not initiated by atrial or ventricular premature
beats4,7,9,10. 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 others4,7,9. 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 latter4,5,7,9,11,12. The rate is
usually 100-150 bpm, and the rhythm is regular4,7.
In contrast to ST, the onset of SNRT is abrupt and
often initiated by a premature atrial impulse4-7,9-12.
Termination is similarly abrupt and may be effected with vagal maneuvers or adenosine administration5,9. This rhythm is often an incidental finding
seen on Holter monitoring, is typically non-sustained, and rarely causes clinically significant
symptomatology13. Sanders et al14 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
arise6,15. They are a relatively uncommon cause of

Figure 1. It shows a sinus tachycardia on ECG.

370

Figure 2. It shows a sinus node reentrant tachycardia on

ECG.

clinically significant NCT, as they comprise less

than 10% of documented cases4.
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
tissue7,13. 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 impulses3,16,17. 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
bpm4,11, and the presence or absence of AV block
does not rule the diagnosis in or out9,6,12,13.

Multifocal atrial tachycardia (MAT)

Multifocal atrial tachycardia is an irregular NCT
with a frequency of 0.08-0.36% among hospitalized patients18,19. 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
hypokalemia20. Triggered activity21 and enhanced
automaticity17 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
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ECG DIFFERENTIAL DIAGNOSIS OF NARROW QRS COMPLEX TACHYCARDIA IN THE EMERGENCY DEPARTMENT

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

Figure 4. It shows an atrial fibrillation 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
bpm24.

largement 3,34. Untreated ventricular rates range

from 100-200 bpm3,5 compromising diastolic ventricular filling, and often producing palpitations,
chest pain, and symptoms of congestive heart failure35.

Atrial fibrillation
Atrial fibrillation remains the most prevalent
form of narrow complex tachycardia 25. In the
United States, 2.3 million individuals carry this diagnosis26, and 0.2% of ED visits were attributed to
atrial fibrillation during 1993-200427. 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
hypomagnesemia25, or following excessive ethanol
intoxication, the so-called holiday heart syndrome28. The mechanism of atrial fibrillation appears to be multiple micro-reentrant wavelets in
the atria3,13. Paroxysms of atrial fibrillation may be
triggered by preceding alterations in autonomic
tone29 and/or ectopic foci frequently located in or
around the pulmonary veins30. 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 rhythm5,33. The
baseline may be isoelectric or may exhibit fibrillatory waves of varying morphology at a rate of
400-700 bpm3,5,25. 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 enEmergencias 2010; 22: 369-380

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 fibrillation13,36. Indeed, it may often be confused with
coarse atrial fibrillation37. 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 appearance5,36. Flutter waves are also frequently visualized in lead V1 and must be of uniform rate, amplitude, and morphology to be
so-called37. The atrial rate is regular and ranges
between 250 and 350 bpm, often close to or exactly 300 bpm5,33. 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 possible38. 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
response5.
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.
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M. P. Borloz et al.

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 5069% 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, im-

pulses 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 circuit9,39-42. 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
impulse40.
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.

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

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 Grsoy 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 atri-

oventricular 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 impulse3,10,12,13,25,33. Rates typically range from 140-240
bpm25. 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 focus44. The presence of AV
block during tachycardia effectively excludes the
diagnosis of AVRT6,9,10,12,13,45-48. 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

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M. P. Borloz et al.

Aurcula
Nodo
sinusal

A
D

Va
accesoria

Ventrculos

Sistema
HISPurkinje

Figure 9. It shows a diagram of atrioventricular reentrant

tachycardias 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 tachycardia49. 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 mechanism50.
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 studies41,51,54. 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,

as compared to men, thus potentially facilitating

the mechanism of AVNRT53.
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 analysis41,52.
Another investigator proposes that the reason for
this is the presence of a longer AV conduction delay in males versus females53. 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 age41,51.

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 common3,33. Whatever the ventricular rate, the R-R interval should
show little or no beat-to-beat variation in the absence of medications or vagal maneuvers3,25.
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

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

significant differences in atrial or ventricular rates

among these same tachycardia types55,56. Despite a
higher mean rate in AVRT versus AVNRT, Kay et
al57 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 impulse3,11. MAT may be confused with atrial fibrillation9,23,58.
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 block59. 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 activity60.
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 irregular3,59.

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 activity3,5. A particular pattern of P wave,
Emergencias 2010; 22: 369-380

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
V13,5,6,33.
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 aVF5-7 and a biphasic7,8 or negative5 P wave in lead V1. 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
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M. P. Borloz et al.

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 1012,39,42,45,57,62,63
. Some investigators have attempted to
define a specific value for the RP interval in comparing common AVNRT and AVRT. Zhong et al64
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 al65, Arya et al66 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
376

and uncommon AVNRT, it is exceedingly rare and,

when present, typically appears at the initiation of
the rhythm and does not persist10,12,25,46,47.
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 period3,33. 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 V1. 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 results3.

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 AVRT45,55,67,some authors have suggested that this is solely a rate-related phenomenon and is independent of tachycardia mechanism5768,69. 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 NCTs44,64,70-72.
Ho et al71 found that ST segment elevation in lead
aVR was helpful in differentiating AVRT from AVNRT 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 abnormality64,71. 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
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ECG DIFFERENTIAL DIAGNOSIS OF NARROW QRS COMPLEX TACHYCARDIA IN THE EMERGENCY DEPARTMENT

during PSVT and that it provides no differential

diagnostic information regarding the mechanism
of the tachycardia71,73,74. In addition, it is not indicative of underlying coronary artery disease or
concurrent ischemia among patients with AVRT or
AVNRT73,74. Arya et al66 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 AVNRT6,25, AVRT
using a rapidly conducting bypass tract25, SNRT4-7,9,
and atrial reentrant tachycardias25.
The initiating stimulus is also helpful. Premature atrial impulses are typically responsible for
the onset of AVNRT3,4,6,9,10,12,13,25,33, AVRT with a rapidly conducting bypass tract3,10,12,13,25,33, and sinus
node5,12 and atrial reentrant12,25 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 AVNRT12,13 or AVRT10,12,25,
although this is less commonly the case. Neither
PACs nor PVCs are implicated in the initiation of
ST9, automatic atrial tachycardias3,12, or AVRT using
a slowly conducting bypass tract10, which all display a gradual acceleration in the atrial rate.
Emergencias 2010; 22: 369-380

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 V1 or a pseudo S
deflection in the inferior leads is highly specific for
AVNRT55,75. 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 MAT4,25. 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 alone25.
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 tachycardia9,12,25.
However, as the exception to the rule, sinus and
atrial reentrant tachycardias may terminate or
even show transient acceleration with vagal maneuvers6,7,12.
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 veloci377

M. P. Borloz et al.

ty) effects on the SA node and AV node, respectively25,76. The resultant effects on various NCTs are
similar to those seen with vagal maneuvers 3,57,9,15,25,77
. 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 time78. 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 al60 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.

References
1 Orejarena LA, Vidaillet H, DeStefano F, Nordstrom DL, Vierkant RA,
Smith PN, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31:150-7.
2 Hayes JJ, Stewart RB, Greene L, Bardy GH. Narrow QRS ventricular
tachycardia. Ann Intern Med. 1991;114:460-3.
3 Stahmer SA, Cowan R. Tachydysrhythmias. Emerg Med Clin N Am.
2006;24:11-40.
4 Kazzi AA, Wong H. Other supraventricular tachydysrhythmias. In:
Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P, editors. ECG in
emergency medicine and acute care. 1st ed. Filadelfia: Elsevier;
2005. p. 104-11.
5 Carnell J, Singh A. An evidence-based approach to supraventricular
tachydysrhythmias. Emerg Med Pract. 2008;10:1-26.
6 Pieper SJ, Stanton MS. Narrow QRS complex tachycardias. Mayo
Clin Proc. 1995;70:371-5.
7 Wathen MS, Klein GJ, Yee R, Natale A. Classification and terminology
of supraventricular tachycardia. Diagnosis and management of the
atrial tachycardias. Cardiol Clin. 1993;11:109-20.
8 Chan TC. P wave. In: Chan TC, Brady WJ, Harrigan RA, Ornato JP,
Rosen P, editors. ECG in emergency medicine and acute care. 1st
ed. Filadelfia: Elsevier; 2005. p. 48-52.
9 Xie B, Thakur RK, Shah CP, Hoon VK. Clinical differentiation of narrow QRS complex tachycardias. Emerg Med Clin N Am.
1998;16:295-330.
10 Josephson ME, Wellens HJJ. Differential diagnosis of supraventricular
tachycardia. Cardiol Clin. 1990;8:411-42.
11 Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med.
1995;332:162-73.
12 Wu D. Supraventricular tachycardias. JAMA. 1983;249:3357-60.
13 Benditt DG, Goldstein MA, Reyes WJ, Milstein S. Supraventricular
tachycardias: mechanisms and therapies. Hosp Pract (Off Ed).
1988;23:161-73.
14 Sanders WE, Sorrentino RA, Greenfield RA, Shenasa H, Hamer ME,
Wharton JM. Catheter ablation of sinoatrial node reentrant tachycardia. J Am Coll Cardiol. 1994;23:926-34.
15 Kadish A, Passman R. Mechanisms and management of paroxysmal
supraventricular tachycardia. Cardiol Rev. 1999;7:254-64.
16 Wu D, Denes P. Mechanisms of paroxysmal supraventricular tachycardia. Arch Intern Med. 1975;135:437-43.
17 Kumar UN, Rao RK, Scheinman MM. The 12-lead electrocardiogram
in supraventricular tachycardia. Cardiol Clin. 2006;24:427-37.
18 Phillips J, Spano J, Burch G. Chaotic atrial mechanism. Am Heart J.
1969;78:171-9.
19 Scher DL, Arsura EL. Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment. Am Heart J. 1989;118:574-80.
20 McCord J, Borzak S. Multifocal atrial tachycardia. Chest. 1998;113:203-9.
21 Schwartz M, Rodman D, Lowenstein SR. Recognition and treatment
of multifocal atrial tachycardia: a critical review. J Emerg Med.

378

1994;12:353-60.
22 Wrenn K. Wandering atrial pacemaker and multifocal atrial tachycardia. In:
Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P, editors. ECG in emergency medicine and acute care. 1st ed. Filadelfia: Elsevier; 2005. p. 101-3.
23 Kastor JA. Multifocal atrial tachycardia. N Engl J Med.
1990;322:1713-7.
24 Kothari SA, Apiyasawat S, Asad N, Spodick DH. Evidence supporting
a new rate threshold for multifocal atrial tachycardia. Clin Cardiol.
2005;28:561-3.
25 Sager PT, Bhandari AK. Narrow complex tachycardia. Differential
diagnosis and management. Cardiol Clin. 1991;9:619-40.
26 Kannel WB, Benjamin EJ. Status of the epidemiology of atrial fibrillation. Med Clin N Am. 2008;92:17-40.
27 McDonald AJ, Pelletier AJ, Ellinor PT, Camargo CA. Increasing US
emergency department visit rates and subsequent hospital admissions for atrial fibrillation from 1993 to 2004. Ann Emerg Med.
2008;51:58-65.
28 Crozier I, Melton I, Pearson S. Management of atrial fibrillation in
the emergency department. Int Med J. 2003;33:182-5.
29 Bettoni M, Zimmerman M. Autonomic tone variations before the
onset of paroxysmal atrial fibrillation. Circulation. 2002;105:2753-9.
30 Hassaguerre M, Jas P, Shah DC, Takahashi A, Hocini M, Quiniou G,
et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary veins. N Engl J Med. 1998;339:659-66.
31 Keating L, Morris FP, Brady WJ. Electrocardiographic features of
Wolff-Parkinson-White syndrome. Emerg Med J. 2003;20:491-3.
32 Rosner MH, Brady WJ, Kefer MP, Martin ML. Electrocardiography in
the patient with the Wolff-Parkinson-White syndrome: diagnostic
and initial therapeutic issues. Am J Emerg Med. 1999;17:705-14.
33 Lowenstein SR, Halperin BD, Reiter MJ. Paroxysmal supraventricular
tachycardias. J Emerg Med. 1996;14:39-51.
34 Thurmann M, Janney JG Jr. The diagnostic importance of fibrillatory
wave size. Circulation. 1962;25:991-4.
35 Michael JA, Stiell IG, Agarwal S, Mandavia DP. Cardioversion of paroxysmal atrial fibrillation in the emergency department. Ann Emerg
Med. 1999;33:379-87.
36 Wrenn K. Atrial fibrillation and atrial flutter. In: Chan TC, Brady WJ,
Harrigan RA, Ornato JP, Rosen P, editors. ECG in emergency medicine and acute care. 1st ed. Filadelfia: Elsevier; 2005. p. 96-101.
37 Weinberg KM, Denes P, Kadish AH, Goldberger JJ. Development and
validation of diagnostic criteria for atrial flutter on the surface electrocardiogram. Ann Noninvasive Electrocardiol. 2008;13:145-54.
38 Kawabata M, Hirao K, Higuchi K, Sasaki T, Furukawa T, Okada H, et
al. Clinical and electrophysiological characteristics of patients having
atrial flutter with 1:1 atrioventricular conduction. Europace.
2008;10:284-8.
39 Wu D, Denes P, Amat-Y-Leon F, Dhingra R, Wyndham CRC, Bauernfeind R, et al. Clinical, electrocardiographic and electrophysiological
observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol. 1978;41:1045-51.
40 Brugada P, Br FWHM, Vanagt EJ, Friedman PL, Wellens HJJ. Observations in patients showing A-V junctional echoes with a shorter P-R
than R-P interval. Am J Cardiol. 1981;48:611-22.
41 Rodriguez LM, de Chillou C, Schlpfer J, Metzger J, Baiyan X, van
den Dool A, et al. Age at onset and gender of patients with different
types of supraventricular tachycardias. Am J Cardiol. 1992;70:1213-5.
42 Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S, Dhala A. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations. Circulation. 1993;88:282-95.
43 Grsoy S, Steurer G, Brugada J, Andries E, Brugada P. Brief report:
the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia. N Engl J Med. 1992;327:772-4.
44 Gorgels APM, Engelen DJM, Wellens HJJ. Lead aVR, a mostly ignored
but very valuable lead in clinical electrocardiography. J Am Coll Cardiol. 2001;38:1355-6.
45 Br FW, Brugada P, Dassen WRM, Wellens HJJ. Differential diagnosis
of tachycardia with narrow QRS complex (shorter than 0.12 second). Am J Cardiol. 1984;54:555-60.
46 Vassallo JA, Cassidy DM, Josephson ME. Atrioventricular nodal supraventricular tachycardia. Am J Cardiol. 1985;56:193-5.
47 Wellens HJJ, Wesdorp JC, Dren DR, Lie KI. Second degree block during reciprocal atrioventricular nodal tachycardia. Circulation.
1976;53:595-9.
48 Ribas CS, Baranchuk A, Connolly SJ, Morillo CA. Narrow QRS tachycardia with long R-P. Int J Cardiol. 2008;127:57-60.
49 Orejarena LA, Vidaillet H, DeStefano F, Nordstrom DL, Vierkant RA,
Smith PN, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31:150-7.
50 Brembilla-Perrot B, Houriez P, Beurrier D, Claudon O, Burger G, Vanon AC, et al. Influence of age on the electrophysiological mechanism of paroxysmal supraventricular tachycardias. Int J Cardiol.
2001;78:293-8.

Emergencias 2010; 22: 369-380

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

51 Goyal R, Zivin A, Souza J, Shaikh SA, Harvey M, Bogun F, et al. Comparison of the ages of tachycardia onset in patients with atrioventricular nodal reentrant tachycardia and accessory pathway-mediated
tachycardia. Am Heart J. 1996;132:765-7.
52 Munger TM, Packer DL, Hammill SC, Feldman BJ, Bailey KR, Ballard
DJ, et al. A population study of the natural history of the Wolff-Parkinson-White syndrome in Olmsted County, Minnesota, 1953-1989.
Circulation. 1993;87:866-73.
53 Liu S, Yuan S, Kongstad O, Olsson SB. Gender differences in the
electrophysiological characteristics of atrioventricular conduction
system and their clinical implications. Scand Cardiovasc J.
2001;35:313-7.
54 Jazayeri MR, Hempe SL, Sra JS, Dhala AA, Blanck Z, Deshpande SS,
et al. Selective transcatheter ablation of the fast and slow pathways
using radiofrequency energy in patients with atrioventricular nodal
reentrant tachycardia. Circulation. 1992;85:1318-28.
55 Kalbfleisch SJ, El-Atassi R, Calkins H, Langberg JJ, Morady F. Differentiation of paroxysmal narrow QRS complex tachycardias using the
12-lead electrocardiogram. J Am Coll Cardiol. 1993;21:85-9.
56 Riva SI, Della Bella P, Fassini G, Carbucicchio C, Tondo C. Value of
analysis of ST segment changes during tachycardia in determining
type of narrow QRS complex tachycardia. J Am Coll Cardiol.
1996;27:1480-5.
57 Kay GN, Pressley JC, Packer DL, Pritchett ELC, German LD, Gilbert
MR. Value of the 12-lead electrocardiogram in discriminating atrioventricular nodal reciprocating tachycardia from circus movement
atrioventricular tachycardia utilizing a retrograde accessory pathway.
Am J Cardiol. 1987;59:296-300.
58 Schwartz M, Rodman D, Lowenstein SR. Recognition and treatment
of multifocal atrial tachycardia: a critical review. J Emerg Med.
1994;12:353-60.
59 Richmond HCT, Taylor L, Monroe MH, Littmann L. A new algorithm
for the initial evaluation and management of supraventricular tachycardia. Am J Emerg Med. 2006;24:402-6.
60 Accardi AJ, Miller R, Holmes JF. Enhanced diagnosis of narrow complex tachycardias with increased electrocardiograph speed. J Emerg
Med. 2002;22:123-6.
61 Tang CW, Scheinman MM, Van Hare GF, Epstein LM, Fitzpatrick AP,
Lee RJ, et al. Use of P wave configuration during atrial tachycardia to
predict site of origin. J Am Coll Cardiol. 1995;26:1315-24.
62 Josephson ME. Paroxysmal supraventricular tachycardia: an electrophysiologic approach. Am J Cardiol. 1978;41:1123-6.
63 Delacrtaz E. Supraventricular tachycardia. N Engl J Med.
2006;354:1039-51.
64 Zhong YM, Guo JH, Hou AJ, Chen SJ, Wang Y, Zhang HC. A modified electrocardiographic algorithm for differentiating typical atrioventricular node re-entrant tachycardia from atrioventricular recipro-

Emergencias 2010; 22: 369-380

cating tachycardia mediated by concealed accessory pathway. Int J

Clin Pract. 2006;60:1371-7.
65 Jaeggi ET, Gilljam T, Bauersfeld U, Chiu C, Gow R. Electrocardiographic differentiation of typical atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by
concealed accessory pathway in children. Am J Cardiol.
2003;91:1084-9.
66 Arya A, Kottkamp H, Piorkowski C, Schirdewahn P, Tanner H, Kobza R, et
al. Differentiating atrioventricular nodal reentrant tachycardia from tachycardia via concealed accessory pathway. Am J Cardiol. 2005;95:875-8.
67 Green M, Heddle B, Dassen W, Wehr M, Abdollah H, Brugada P, et al.
Value of QRS alternation in determining the site of origin of narrow
QRS supraventricular tachycardia. Circulation. 1983;68:368-73.
68 Morady F, DiCarlo LA, Baerman JM, de Buitleir, Kou WH. Determinants of QRS alternans during narrow QRS tachycardia. J Am Coll
Cardiol. 1987;9:489-99.
69 Morady F. Significance of QRS alternans during narrow QRS tachycardias. Pacing Clin Electrophysiol. 1991;14:2193-8.
70 Pahlm US, Pahlm O, Wager GS. The standard 11-lead ECG. J Electrocardiol. 1996;29 Suppl:270-4.
71 Ho YL, Lin LY, Lin JL, Chen MF, Chen WJ, Lee YT. Usefulness of ST-segment
elevation in lead aVR during tachycardia for determining the mechanism
of narrow QRS complex tachycardia. Am J Cardiol. 2003;92:1424-8.
72 Williamson K, Mattu A, Plautz CU, Binder A, Brady WJ. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006;24:864-74.
73 Nelson SD, Kou WH, Annesley T, de Buitleir M, Morady F. Significance of ST segment depression during paroxysmal supraventricular
tachycardia. J Am Coll Cardiol. 1988;12:383-7.
74 Kim YN, Sousa J, El-Atassi R, Calkins H, Langberg JJ, Morady F. Magnitude of ST segment depression during paroxysmal supraventricular
tachycardia. Am Heart J. 1991;122:1486-7.
75 Tai CT, Chen SA, Chiang CE, Lee SH, Wen ZC, Chiou CW, et al. A
new electrocardiographic algorithm using retrograde P waves for differentiating atrioventricular node reentrant tachycardia from atrioventricular reciprocating tachycardia mediated by concealed accessory pathway. J Am Coll Cardiol. 1997;29:394-402.
76 DiMarco JP, Sellers TD, Lerman BB, Greenberg ML, Berne RM, Belardinelli L. Diagnostic and therapeutic use of adenosine in patients
with supraventricular tachyarrhythmias. J Am Coll Cardiol.
1985;6:417-25.
77 Glatter KA, Cheng JC, Dorostkar P, Modin G, Talwar S, Al-Nimri M,
et al. Electrophysiologic effects of adenosine in patients with supraventricular tachycardia. Circulation. 1999;99:1034-40.
78 DiMarco JP, Miles W, Akhtar M, Milstein S, Sharma AD, Platia E, et
al. The Adenosine for PSVT Study Group. Adenosine for paroxysmal
supraventricular tachycardia: dose ranging and comparison with verapamil. Ann Intern Med. 1990;113:104-10.

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M. P. Borloz et al.

Diagnstico diferencial electrocardiogrfico de la taquicardia de complejo QRS estrecho

en el servicio de urgencias: una revisin de ritmos frecuentes y sus caractersticas distintivas
Borloz MP, Mark DG, Pines JM, Brady WJ
El diagnstico diferencial de las taquicardias de complejo QRS estrecho (TQRSE) es un dilema comn 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 respondern al tratamiento apropiado de la patologa subyacente. Por otro lado, otras TQRSE (ej.: fibrilacin auricular, taquicardia de reentrada nodal AV) pueden ser verdaderamente el origen de la sintomatologa principal (ej.: palpitaciones, mareo secundario a la hipoperfusin) y deben ser
positivamente identificadas y tratadas. Para un correcto diagnstico es necesario conocer las semejanzas y diferencias
entre las distintas TQRSE. Este artculo comenta cules son las caractersticas demogrficas, clnicas y electrocardiogrficas que son de ayuda para identificar los siguientes ritmos: taquicardia sinusal, taquicardia de reentrada del nodo sinusal, taquicardia auricular unifocal, taquicardia auricular multifocal, fibrilacin auricular, flutter auricular, taquicardia de
reentrada del nodo auriculoventricular y taquicardia de reentrada auriculoventricular. Adems, se realiza un comentario
sobre las distintas maniobras diagnsticas, que vincluye la administracin de adenosina. [Emergencias 2010;22:369380]
Palabras clave: Taquicardia de complejo QRS. Servicio de urgencias. Ritmos frecuentes.

380

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