07-ElectroCardEMPrint

Bradycardias and Heart Blocks

Figures

Figure 3-10.
Second-degree AV block with 2:1 conduction. The 12-lead ECG shows 2:1 AV conduction. Two other findings
are the QS complexes in II, III, and aVF, indicating a nonacute inferior MI, and the prolonged PR interval for the
conducted P waves. This ECG can easily be mistaken for sinus bradycardia, since the second P wave can be
overlooked as a biphasic T wave.

41

Electrocardiography in Emergency Medicine

Figures

Figure 3-11.
High-grade second-degree AV block. This 12-lead ECG shows an AV conduction ratio of 3:1, indicating that
only every third P wave is conducted, resulting in pronounced bradycardia (32 beats/min). The QRS complexes
are wider than normal, indicating the block is located in the bundle branches or the His-Purkinje system. There
is a right bundle-branch block configuration (rSR' in V1 and rS in I). There are deeply inverted T waves in leads
I, aVL, and V2 through V4. High-grade AV blocks advance to third-degree block without warning. Artificial
pacing should be instituted without delay.

42

Bradycardias and Heart Blocks

Figures

Figure 3-12.
Third-degree (complete) AV heart block. Complete AV dissociation is shown in all three tracings. P waves
march through the QRS complexes. The ventricular complexes occur at slow rates and are generated by an
idioventricular pacemaker. The QRS complexes in tracings A and B have wide and distorted shapes. In tracing
C, the QRS complexes are narrow and occur at a faster rate than in the prior tracings, confirming the junctional
escape origin. Tracing C reveals an acute injury pattern.

A

B

C

43

Electrocardiography in Emergency Medicine

Figures

Figure 3-13.
Sinus arrest. This tracing shows simultaneous records of leads II and V1. The first two beats have P waves
before the wide QRS complexes, at a rate of 40/min. The pause lasts for almost 6 seconds, causing syncope.
The failure of back-up pacemakers in the AV junction or His-Purkinje system indicates widespread pacemaker
dysfunction. A transcutaneous pacemaker resulted in 1:1 capture until a permanent pacemaker could be
inserted.

Figure 3-14.
Sinus arrest. Two periods of sinus arrest occurred following the fourth and fifth P-QRS-T complexes and lasted
more than 2.5 seconds. The remaining sinus beats are otherwise normal.

A
B

44

C h apter f o u r

Narrow Complex Tachycardias

Theresa M. Schwab, MD, and Christopher H. Ross, MD

Narrow complex tachycardias are defined as understanding (or misunderstanding) of
dysrhythmias with a rate faster than 100 beats/ presentation or mechanism. Supraventricular
min and a QRS duration of 120 msec or less. The tachycardia means any tachyarrhythmia
normal QRS duration indicates normal activation originating from the atria or AV junction
of both ventricles through the atrioventricular and therefore encompasses all narrow
(AV) junction, the bundle of His, the bundle complex tachycardias. However, paroxysmal
branches, and the terminal Purkinje conduction supraventricular tachycardia commonly refers to
system. This synchronous activation of the regular, nonventricular tachycardias other than
ventricles requires activation proximal to the multifocal atrial tachycardia, atrial fibrillation,
ventricular tissue using the atrial and/or AV or atrial flutter. Atrial tachycardia means any
junctional tissue for its origin and maintenance.1 tachycardia originating in the atrium, although
Narrow complex tachycardias comprise a variety it commonly refers to tachycardia arising from
of rhythms (Table 4-1). An understanding of the an ectopic atrial area of enhanced automaticity
interpretation and classification of these entities or occasionally reentry. Junctional tachycardia
can direct clinicians to the appropriate diagnoses means any tachycardia that involves the AV
and treatments. Correct identification of these node and thus includes atrioventricular node
entities can be challenging, however, because reentrant tachycardia (AVNRT), atrioventricular
“distinguishing” ECG findings are often absent. reentrant tachycardia via an accessory pathway
(AVRT), and accelerated junctional tachycardias
The terminology used in clinical practice usually arising from discreet foci of increased
for narrow complex tachycardias is often automaticity in the AV node or bundle of His
imprecise and confusing.2 Terminology is (variously termed focal junctional, paroxysmal
based both on clinical behavior (paroxysmal, junctional, nonparoxysmal junctional, automatic
nonparoxysmal, persistent, permanent, junctional, accelerated AV junctional, or
sustained, or nonsustained) and on mechanism junctional ectopic tachycardia). We have chosen
(automatic, accelerated, focal, ectopic, reentrant, to use terminology defined in the 2003 ACC/
or reciprocating). This leads to several terms AHA/ESC guidelines for the management of
that are imprecise based on antiquated
45

Electrocardiography in Emergency Medicine

patients with supraventricular arrhythmias,2 characteristics of reentrant circuits: the
although many of the same inconsistencies exist. dysrhythmias are often precipitated by a
premature contraction, immediately begin
The basic mechanisms of all tachyarrhythmias at their maximal rate, are fixed (no beat-
fall into three categories: reentrant, to-beat variability), and cease completely
automatic, and triggered3 (Table 4-2): (no slow down of the dysrhythmia). The
response of these rhythms to medications
1. Reentry (or circus movement) is the most and electrical interventions depends on
common mechanism, involving conduction the location of the circuit. If the AV node
down an anterograde path and back up a is involved, the reentrant circuit can be
retrograde path. It occurs either within a terminated by interventions that slow AV
single locus (such as within the sinus node, nodal conduction, such as vagal maneuvers
the atria, or the AV node) or across multiple and adenosine. If the AV node is not
sites, as with AVRT (anterograde through involved, as with atrial flutter, the rhythm
the AV node and His-Purkinje system to will not change when AV nodal conduction
the ventricles and then retrograde over is blocked, although ventricular rate will
an accessory atrioventricular pathway to transiently slow.
the atrium). It is typically associated with
rhythms arising from the AV node and the 2. Enhanced automaticity occurs when
immediately surrounding tissues. dysrhythmias arise from diseased tissue
(abnormal automaticity) or from fibers
For a reentrant circuit to occur, two that have pacemaker capability but do not
pathways must exist with different rates normally function in this manner (enhanced
of conduction and recovery. The initial
electrical impulse, often a premature Table 4-2.
complex, depolarizes one limb of the Mechanisms of tachyarrhythmias and their
circuit while the other is refractory after the characteristics
previous depolarization. When the impulse
completes its transit down the first limb Reentry
(anterograde), which is now refractory, it • often precipitated by premature contraction
travels back up the now recovered second • begin at their maximal rate, no warm-up period
limb (retrograde) to the initiation point. • fixed rate (no beat-to-beat variability)
The cycle continues until this balance • cease abruptly, no slow-down period
of depolarization and refractoriness • examples: atrial flutter, AV reentrant tachycardia,
is altered by a change in conduction AV nodal reentrant tachycardia, sinuatrial nodal
properties. This pattern establishes the reentry

Table 4-1. Enhanced automaticity
Narrow complex tachycardias • often precipitated by adrenergic stimulation or
medications such as digoxin
Sinus tachycardia • exhibit warm-up and slow-down periods
Sinuatrial nodal reentrant tachycardia • beat-to-beat variability
Inappropriate sinus tachycardia • examples: sinus tachycardia, multifocal atrial
Atrial fibrillation tachycardia, focal atrial tachycardia, focal and
Multifocal atrial tachycardia nonparoxysmal junctional tachycardia
Atrial flutter
Focal atrial tachycardia Triggered (early or late after-depolarization)
Focal and nonparoxysmal junctional tachycardia • often caused by conditions that increase the QT
AV nodal reentrant tachycardia interval
AV reentrant tachycardia • more likely to occur when sinus rate is slow
• often associated with digoxin
46 • examples: focal atrial tachycardia, torsade de
pointes

Narrow Complex tachycardias

automaticity). Rhythms associated with sinus heart rate is 220 beats/min minus years
enhanced automaticity are often precipitated of age. Sinus tachycardia can be challenging to
by adrenergic stimulation, tend to accelerate diagnose at rates of 150 or greater when the P
to their maximal rate, and are not initiated wave is “buried” in the terminal portion of the
by premature contractions. They have beat- T wave. A diligent search for the buried P wave
to-beat variability and decelerate gradually. often reveals the definitive diagnosis (Figure 4-2).
They often do not respond predictably to Small decreases in rate, such as occur with fluid
pharmacologic or electrical interventions resuscitation or carotid massage, can sometimes
but may respond to overdrive pacing. “uncover” the buried P wave. Inappropriate sinus
Examples of narrow complex tachycardias tachycardia (sometimes called nonparoxysmal
caused by both abnormal and enhanced sinus tachycardia) is a condition without apparent
automaticity are focal atrial tachycardia and heart disease or other causes of sinus tachycardia
nonparoxysmal junctional tachycardia. (such as hyperthyroidism or fever). The cause of
inappropriate sinus tachycardia is unknown, but
3. Triggered dysrhythmias are caused by early abnormal autonomic control is inherent to this
or late after-depolarizations, depending disease. Sinuatrial nodal reentrant tachycardia is
on when they arise in the action potential. quite uncommon and accounts for fewer than 5%
Ventricular arrhythmias associated with QT of patients referred for electrophysiologic studies.
prolongation, such as torsade de pointes, are
commonly caused by this mechanism, as are Focal Atrial Tachycardia
tachyarrhythmias associated with digoxin
toxicity. Focal atrial tachycardia is one of the less
common causes of regular narrow complex
These mechanisms for various narrow complex tachycardias. It is most often caused by enhanced
tachycardias are illustrated in Figure 4-1. automaticity but is occasionally the result of
reentry or triggering.4 In atrial tachycardia,
Sinus Tachycardia a single atrial focus takes over pacing from
the sinuatrial node, typically at a rate of 150
Sinus tachycardia is a regular narrow complex to 250 beats/min (Figure 4-3). As with other
tachycardia characterized by 1) normal AV dysrhythmias caused by enhanced automaticity,
conduction, represented by a P wave before every
QRS complex with a fixed PR interval, and 2) Table 4-4.
an impulse that originates from the sinus node, Causes of atrial fibrillation
represented by uniform P-wave morphology that
is upright in leads I, II, and aVF and inverted Alcohol intake
in aVR. The rate may vary and often shows a Autonomic dysfunction
gradual variation over time and in response Cardiac or thoracic surgery
to therapy. A general guideline for maximum Cardiomyopathy of any cause
Congenital heart disease
Table 4-3. Heart failure
ECG characteristics of focal atrial tachycardia Hypertension
caused by enhanced automaticity Hyperthyroidism
Myocardial infarction/ischemia
100 to 250 beats/min Pericarditis
Warm-up at onset and slow-down at offset (if captured Pulmonary disease
on monitoring) Rheumatic heart disease
Lack of sawtooth flutter waves Sick sinus syndrome
AV nodal blockade does not terminate tachycardia Supraventricular arrhythmias
Classic rhythm of digoxin toxicity, especially with AV Valvular heart disease
nodal block
Occasionally caused by reentry

47

Electrocardiography in Emergency Medicine

this rhythm tends to accelerate at initiation The differential diagnosis for an irregular
to its maximal rate and is not initiated by a narrow complex tachycardia includes multifocal
premature contraction. It has beat-to-beat atrial tachycardia and any regular tachycardia
variability and decelerates gradually. This rhythm arising from the atrium that is associated
generally does not respond to vagal maneuvers. with variable AV block or frequent premature
Of the group of dysrythmias commonly ventricular beats. The hallmark features of
referred to as paroxysmal supraventricular atrial fibrillation are the marked irregularity
tachycardia, atrial tachycardia accounts for and lack of clear atrial activity (Table 4-5).
approximately 10% of cases5 (Table 4-3).
Multifocal Atrial Tachycardia
Atrial Fibrillation
Multifocal atrial tachycardia classically occurs
Atrial fibrillation is the most common as a complication of pulmonary disease, but
sustained dysrhythmia in clinical practice and it can also be seen in patients with congestive
is increasing in frequency.6 It is characterized heart failure, sepsis, myocardial infarction,
by a lack of organized electrical activity in the hypokalemia, and methylxanthine toxicity. In
atria. The atria are stimulated and depolarized multifocal atrial tachycardia, multiple atrial
at rates ranging from 400 to 700 beats/min, foci occur as a result of abnormal automaticity,
resulting in fibrillatory activity. This activity causing an irregular rhythm. The criteria for
produces characteristic fibrillatory waves that multifocal atrial tachycardia include at least
can be coarse or fine. There are no discrete P three different P-wave morphologies on a
waves, and the fibrillatory pattern is evident in rhythm strip, with variable PR intervals (Figure
the ECG baseline (Figure 4-4). The AV junction 4-5, Table 4-6). The rate varies between 100
is stimulated in a random fashion, resulting in and 200 beats/min. The QRS complexes do
an irregular ventricular rate that varies from 100 not vary in morphology.7 Treatment centers
to 200 beats/min, usually around 140 beats/min. on correcting the underlying disease that is
The ventricular rate during atrial fibrillation creating the rhythm disturbance. Rarely is this
can be quite variable, depending on autonomic rhythm responsible for a patient’s symptoms.
tone, the electrophysiologic properties of the AV
node, and the effects of medications that act on Atrial Flutter
the AV conduction system. Untreated ventricular
responses of less than 100 beats/min suggest the Atrial flutter is characterized by rapid,
presence of AV node disease. The QRS complex regular atrial activation with an atrial rate
is narrow unless there is a preexisting or rate- usually above 240 beats/min (unless slowed
related bundle-branch block or conduction by disease or medication). Atrial flutter
down an accessory pathway. Atrial fibrillation typically occurs by a reentrant mechanism
can occur in persons without intrinsic cardiac that runs from the right atrium to the left in a
or systemic disease as well as in association counterclockwise direction. Other mechanisms
with various clinical states (Table 4-4). of atrial flutter such as reentry in the left
atrium and reentry around surgical incisions
Table 4-5. in the atria are seen less commonly. As in atrial
ECG characteristics of atrial fibrillation
Table 4-6.
Rapid and irregular atrial fibrillatory activity with an atrial ECG characteristics of multifocal atrial tachycardia
rate typically faster than 300 beats/min
Irregularly irregular ventricular response, with rate of 90 Irregularly irregular rhythm, usually with rate faster than
to 200 beats/min 100 beats/min
No detectable P waves At least three different P-wave morphologies
Varying PP, RP, and PR intervals
48

Narrow Complex tachycardias

fibrillation, the ventricular response depends ischemia, infarction, cardiomyopathy, or digoxin
on the status of atrioventricular function. toxicity.10 This is also referred to as accelerated
AV junctional tachycardia (Table 4-8). ECG
On ECG, atrial flutter waves are seen as findings include rates ranging from 70 to 130.10
sawtooth atrial complexes and are best seen in Retrograde activation of the atria results in a
leads II, III, aVF and V1 (Figure 4-6). Flutter retrograde P wave that is often obscured by
waves appear as atrial complexes of constant the QRS complex, but it may be seen following
morphology, polarity, and cycle length, with a or, rarely, preceding the QRS.5 As with other
rate typically at 300 and ranging from 240 to automatic rhythms, there are usually warm-up
340 beats/min. The sawtooth pattern of flutter and cool-down phases. AV dissociation might
waves is pathognomonic and is characterized by be seen as a result of a functional AV node
a positive P-wave deflection alternating with a that is made refractory to sinus impulses by
negative P-wave deflection. These appear because continuing partial or complete depolarizations
of rotation of the circuit along the base of the from the competing junctional pacemaker.
atrium. This pattern can distort the ST segment, This is identified by noting a difference in the
which can provide a clue to this diagnosis. sinus and ventricular rates without a clear
Inability to identify the isoelectric point in lead association between the P waves and the QRS
II is highly suggestive of atrial flutter since the complexes. This dysrhythmia generally does not
circuit is almost never perpendicular to lead terminate with vagal stimulation or adenosine.
II. There is often a block associated with this Focal junctional tachycardia (also known as
rhythm, since the AV node cannot conduct at the paroxysmal junctional, junctional ectopic,
fast rates (>200 bpm) it receives. The resultant or automatic junctional) primarily occurs
ventricular rate is therefore often at 150 (2:1 in children, occurs at rates up to 250 beats/
block) or 100 (3:1 block) beats/min (Table 4-7). min, and can show periods of irregularity.

Transient blockage of the AV node with vagal Atrioventricular Node Reentry
maneuvers or adenosine will slow the ventricular Tachycardia
rate and allow the flutter waves to be visualized
more clearly (Figure 4-6B). Because the AV node With AVNRT, the reentrant circuit is confined
is not part of the reentrant circuit, administration to the AV node. The rate is regular, usually
of adenosine will not terminate this rhythm.8,9 140 to 220 beats/min (Table 4-9), and the QRS
complex is narrow, unless there is a preexisting
Nonparoxysmal Junctional
Tachycardia Table 4-8.
ECG characteristics of nonparoxysmal junctional
Nonparoxysmal junctional tachycardia refers tachycardia
to focal sites of enhanced automaticity/triggered
activity in the AV node or the bundle of His.2 Also known as accelerated AV junctional tachycardia
These sites are uncommon in adults; when they Rates of 70 to 130 beats/min
do occur, they are commonly associated with Uncommon in adults
Retrograde activation of the atria may be seen with P
Table 4-7. waves inverted in lead II, upright in aVR
ECG characteristics of atrial flutter May see AV dissociation
Most often caused by enhanced automaticity
250 to 350 beats/min Can occur in association with digitalis toxicity,
Usually abrupt onset and offset (if captured on monitor) postcardiac surgery, electrolyte abnormalities,
Flutter waves visualized as sawtooth pattern, best seen myocarditis, or myocardial ischemia
in leads II, III, aVF, and V1 Focal junctional tachycardia (also known as paroxysmal
ST-segment distortion such that no isoelectric point is junctional, junctional ectopic, or automatic junctional)
clearly identified in lead II occurs primarily in children, occurs at rates up to 250
beats/min, and can be erratic.

49

Electrocardiography in Emergency Medicine

or rate-related bundle-branch block. Following with AVRT than with AVNRT because of greater
an initiating premature complex, subsequent differences in time to depolarization of the
atrial depolarizations are retrograde. The P wave ventricle and retrograde depolarization of the
is either partially or completely obscured within atria (Table 4-10). Here, the PR interval is longer
the QRS in 90% to 95% of cases (Figure 4-7). than the RP interval, compared with normal
If it is visualized, it will appear retrograde. atrial impulse conduction through the AV node
to the ventricle, in which the PR interval is
AVNRT displays the typical characteristics shorter than the RP interval (Figure 4-7). Due to
of reentrant dysrhythmias. Of the group retrograde activation, the P waves in AVNRT are
of dysrythmias referred to as paroxysmal inverted in the inferior leads and upright in aVR.
supraventricular tachycardia, AVNRT accounts QRS alternans can be seen, which is alternating
for approximately 60% of cases.11 AVNRT will amplitude of the QRS complex, although this
terminate on AV nodal blocking with vagal has been seen in all atrial tachycardias and
stimulation, adenosine, or other agents. could simply be related to faster rates.12

Atrioventricular Reentry When AVRT is suspected, an accessory
Tachycardia via an Accessory pathway may be visible or concealed on the
Pathway normal sinus rhythm ECG. Visible conduction
through the accessory pathway manifests as a
AVRT is a reentrant circuit involving the AV short PR interval and a delta wave (slurring of the
node as well as an accessory pathway, a short initial portion of the R wave) and is termed Wolff-
muscle bundle that directly connects the atria Parkinson-White syndrome (see Chapter 12,
and ventricles. In the narrow complex form Preexcitation and Accessory Pathway Syndromes).
(orthodromic reciprocating tachycardia), the In approximately 30% of patients with accessory
impulse travels down the AV node, through pathways, however, there is no evidence of
the His-Purkinje system, up the accessory conduction on the baseline ECG in sinus rhythm.
pathway, and back to the AV node. Within the This “concealed bypass tract” often conducts
group of dysrhythmias commonly referred to in a retrograde fashion, allowing generation of
as paroxysmal supraventricular tachycardia, an orthodromic, reentrant tachyarrhythmia.
AVRT comprises approximately 30% of cases.11
Approach to Evaluation and
AVRT is often seen in younger patients, Diagnosis
compared with AVNRT. It is similar to AVNRT
in that it is a reentrant loop tachycardia initiated The initial step in the evaluation of any
by a premature contraction. A retrograde P patient with a narrow QRS tachycardia is to
wave is more commonly visible on the ECG determine whether there are symptoms or signs
of inadequate organ perfusion attributable to the
Table 4-9. rapid heart rate. If these are present and severe
ECG characteristics of atrioventricular nodal reentry (and the rhythm is not sinus tachycardia), then
tachycardia (AVNRT)
Table 4-10.
Fast, regular, narrow, without variation in ventricular rate ECG characteristics of atrioventricular reentry
Rates often between 140 and 250 beats/min, usually tachycardia via accessory pathway (AVRT)
180 to 200 beats/min
P waves are often concealed within in the QRS; the RP Fast, regular, narrow, without variation in ventricular rate
is usually <70 msec Retrograde P waves are more delayed and therefore
Concealed P waves can cause a pseudo S wave in more often distinct from the QRS than with AVNRT. The
inferior leads and pseudo R' wave in V1; recognized only RP interval is usually >70 msec
in comparison with the QRS complex in normal sinus Rates of 140 to 280 beats/min; usually 200 beats/min
rhythm
Atypical form with P wave preceding QRS is uncommon
(<5%)

50

Narrow Complex tachycardias

immediate cardioversion is recommended. If other tachycardias that originate in or near the
these are present but mild, a brief trial of fluid sinus node will have the same appearance (for
resuscitation/medication may be acceptable. example, sinuatrial nodal reentrant tachycardia
or atrial tachycardia). Sinus P waves can be
In the absence of instability, assessment of partially concealed by the preceding T wave at
the narrow complex tachycardia should begin rapid rates, and a brief trial of treatment of the
with determination of the ventricular rate and underlying cause, such as a fluid bolus, delivery
regularity (Table 4-11). An irregularly irregular of oxygen, or antipyrectic therapy, might slow
rhythm is usually atrial fibrillation, although the rate enough to clearly reveal sinus rhythm.
occasionally multifocal atrial tachycardia, atrial
flutter with variable block, or frequent premature If sinus rhythm is not suspected, the
complexes can be mistaken for atrial fibrillation. evaluation should proceed with assessment of
At fast rates, the irregularity of atrial fibrillation atrial activity for rate, P-wave morphology, the
could be missed; therefore, care should be taken relationship between atrial and ventricular rates,
to assess the regularity of the R-R interval. and the position of the P wave in relation to the
preceding and following QRS complexes.13 This
Once the clinician has determined that the will help localize the origin of the dysrhythmia
rhythm is a regular narrow complex tachycardia, to either the sinus node (sinus tachycardia), the
the evaluation should proceed with a search atria (atrial flutter or atrial tachycardia), or an
for sinus tachycardia. Sinus tachycardia is AV nodal source (AVRT, AVNRT, or accelerated
identified by a P wave that is upright in lead II junctional tachycardia). With fast rates, atrial
and inverted in aVR and precedes the QRS; rarely, activity can be difficult to discern. Maneuvers
to slow the rate or ventricular response are
Table 4-11. often diagnostic and can be therapeutic.
Diagnostic approach to narrow complex
tachycardias A search should be made for P waves that are
obscured by the QRS and/or T waves. Increasing
1. Determine if QRS complex is narrow (<0.12 msec) the paper speed during ECG recording might
2. Determine if ventricular response is irregularly improve identification of P waves.14 Limb lead
irregular II and precordial lead V1 are often optimal
for identification of the P wave. If the P-wave
• atrial fibrillation morphology is not characteristic of sinus
• multifocal atrial tachycardia rhythm, an ectopic atrial focus, a retrograde
• any atrial tachycardia with variable block or conducted P wave, or limb lead misplacement
should be considered. A sawtooth pattern, best
premature ventricular beats seen in lead II, is characteristic of atrial flutter.
• focal junctional tachycardia (rarely) A regular narrow complex tachycardia with a
3. Determine if the regular narrow complex tachycardia P wave preceding the QRS that demonstrates
is sinus tachycardia abnormal morphology is usually caused by atrial
• uniform P wave before every QRS complex tachycardia, especially if the presence of flutter
• P-wave morphology upright in lead II, inverted in waves can be excluded. A retrograde P wave
arising from the AV node can be identified if
aVR it follows the QRS complex (described as a PR
• fixed PR interval interval that is longer than the RP interval) and
• rate is not fixed shows reversal of P-wave morphology, being
4. Determine if the regular narrow complex tachycardia inverted in lead II and upright in aVR. Retrograde
terminates with AV nodal blocking P waves indicate that the rhythm arises from the
• AVNRT AV node and is most likely AVRT (or AVNRT),
• AVRT which will convert to sinus rhythm when the
5. Determine if the ventricular response of the regular AV node is blocked. It is rare but possible for
narrow complex tachycardia slows with AV nodal
blocking but fails to terminate 51
• sinus tachycardia
• atrial flutter
• focal atrial tachycardia
• focal and nonparoxysmal junctional tachycardia

Electrocardiography in Emergency Medicine

a retrograde P wave to precede the QRS. 9. Glatter KA, Cheng J, Dorostkar P, et al. Electrophysiologic
effects of adenosine in patients with supraventricular
With regular narrow complex tachycardia, tachycardia. Circulation. 1999;99:1034-1040.

the diagnosis is often achieved with vagal 10. Surawicz B, Knilans TK, Chou T-C. Chou’s
Electrocardiography in Clinical Practice: Adult and
maneuvers or adenosine treatment to block Pediatric. Philadelphia, PA: Saunders; 2001:xiv,709.

the AV node (Table 4-11). Atrial or automatic 11. Wagner GS, Marriott HJL. Marriott’s Practical Electrocardiography.
Philadelphia, PA: Lippincott Williams & Wilkins; 2000.
tachycardias will persist despite slowed
12. Green M, Heddle B, Dassen W, et al. Value of QRS
ventricular conduction, whereas the reentry alteration in determining the site of origin of narrow QRS
supraventricular tachycardia. Circulation. 1983;68:368-373.
tachycardias—AVRT and AVNRT—will
13. Kalbfleisch SJ, el-Atassi R, Calkins H, et al. Differentiation
terminate. More prolonged AV nodal blockade of paroxysmal narrow QRS complex tachycardias using the
12-lead electrocardiogram. J Am Coll Cardiol. 1993;21:85-89.
can be achieved with calcium channel or β-
blocking agents for prolonged rate control. 14. Gaspar JL, Body R. Best evidence topic report. Differential
diagnosis of narrow complex tachycardias by increasing
References electrocardiograph speed. Emerg Med J. 2005;22:730-732.

1. Ganz LI, Friedman PL. Supraventricular
tachycardia. N Engl J Med. 1995;332:162-173.

2. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al.
ACC/AHA/ESC guidelines for the management of patients
with supraventricular arrhythmias—executive summary.
A report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines and
the European Society of Cardiology Committee for Practice
Guidelines (writing committee to develop guidelines
for the management of patients with supraventricular
arrhythmias) developed in collaboration with NASPE-Heart
Rhythm Society. J Am Coll Cardiol. 2003;42:1493-531.

3. Waldo AL, Wit AL. Mechanisms of cardiac
arrhythmias. Lancet. 1993;341:1189-1193.

4. Goodacre S, Irons R. ABC of clinical electrocardiography:
atrial arrhythmias. BMJ. 2002;324:594-597.

5. Wellens HJ. 25 years of insights into the
mechanisms of supraventricular arrhythmias.
Pacing Clin Electrophysiol. 2003;26:1916-1922.

6. Chugh SS, Blackshear JL, Shen WK, et al. Epidemiology
and natural history of atrial fibrillation: clinical
implications. J Am Coll Cardiol. 2001;37:371-378.

7. Kastor JA. Multifocal atrial tachycardia. N
Engl J Med. 1990;322:1713-1717.

8. DiMarco JP, Miles W, Akhtar M, et al. Adenosine for
paroxysmal supraventricular tachycardia: dose ranging
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controlled, multicenter trials. The Adenosine for PSVT
Study Group. Ann Intern Med. 1990;113:104-110.

Key Facts

• The initial assessment of patients with narrow complex tachycardia should determine whether
signs or symptoms of instability are present.

• Initial assessment of the ECG from a patient with narrow complex tachycardia should determine the
regularity of the ventricular response.

• The differential diagnosis for a regular narrow complex tachycardia can generally be categorized into
sinus, atrial (atrial tachycardia and atrial flutter), or AV nodal (AVRT and AVNRT) sources.

• A P wave originating from the sinus node will be upright in limb lead II and inverted in aVR.
• At fast ventricular response rates, increasing the paper speed during ECG recording could improve

detection of P waves.
• Atrial tachycardia with AV block is classically associated with digoxin toxicity.

52

Narrow Complex tachycardias

Figures

Figure 4-1.
Mechanisms of supraventricular tachycardias. A: In sinus rhythm, the impulse originates in the sinus node
and travels through the AV node and His-Purkinje system to the ventricle. This generates a P wave, which
is upright in II and inverted in aVR. B: In focal atrial tachycardia, an ectopic atrial focus provides source of
impulse formation. The P wave often appears ectopic but will appear sinus in origin if the focus is near the
sinus node. C: In nonparoxysmal junctional tachycardia, the ectopic focus originates in the AV node or His
bundle, generating a retrograde P wave, which is inverted in II and upright in aVR. D: In AVNRT, a reentrant
circuit in the AV node generates a retrograde P wave (inverted in II and upright in aVR) that is often obscured
within the QRS complex. E: In the narrow complex form of AVRT, the impulse travels anterograde through the
AV node and retrograde through the accessory pathway. F: In the wide complex form of AVRT, the impulse
travels anterograde through the accessory pathway and retrograde through the AV node. Images courtesy of
Jeffrey A. Tabas, MD.

AB

Normal sinus rhythm Focal atrial tachycardia

C D

Nonparoxysmal junctional tachycardia AV nodal reentry (AVNRT)

E F

Narrow complex AV nodal bypass reentry (AVRT) Wide complex AV nodal bypass reentry (AVRT)
(Orthodromic=anterograde through AV node (Antidromic=retrograde through AV node)

53

Electrocardiography in Emergency Medicine

Figures

Figure 4-2.
Sinus rhythm. A: This ECG reveals a rapid narrow complex tachycardia at a rate of 134 beats/min. An initial
search reveals P waves that are obscured by the T wave because of the rapid rate. Further inspection reveals
a P wave that is upright in lead II and inverted in aVR, highly suggestive of sinus tachycardia (arrows). B: After
fluid resuscitation and antipyretics, the sinus tachycardia resolved. Inspection reveals better resolution of the
P wave, which is separated from the T wave at the slower rate and is clearly of sinus origin. Images courtesy of
Jeffrey A. Tabas, MD.

A

B

54

narrow complEx tachycardias

Figures

Figure 4-3.
Atrial tachycardia with AV block. This ECG demonstrates a rapid, regular narrow complex tachycardia with
P waves that precede each QRS complex. The P-wave morphology is inverted in lead II and upright in lead
aVR, demonstrating an ectopic atrial focus. Atypical AVNRT and focal junctional tachycardia are part of
the differential diagnosis. From: Stahmer SA, Cowan R. Tachydysrhythmias. Emerg Med Clin North Am.
2006;24:11-40. Used with permission from Elsevier.

Figure 4-4.
Atrial fibrillation. This ECG demonstrates a rapid, narrow complex tachycardia at the rate of 204 beats/min.
On initial review, the rhythm appears to be regular. On closer review, however, some irregularity is noted. At
very rapid rates, atrial fibrillation can appear regular unless care is taken to assess the regularity of ventricular
response. Image courtesy of Jeffrey A. Tabas, MD.

55

Electrocardiography in Emergency Medicine

Figures

Figure 4-5.
Multifocal atrial tachycardia. This ECG reveals a narrow complex irregular tachycardia with three or more
P-wave morphologies (p) and varying PR intervals. From: Stahmer SA, Cowan R. Tachydysrhythmias. Emerg
Med Clin North Am. 2006;24:11-40. Used with permission from Elsevier.

56

Narrow Complex tachycardias

Figures

Figure 4-6.
Atrial flutter. A: Rapid, regular, narrow complex tachycardia at a rate of 154 beats/min. Flutter waves are
apparent in leads in II, III, aVF, and V1. B: After treatment with adenosine, AV conduction is transiently slowed
and flutter waves are more apparent when ventricular response is slower. Conduction transiently decreases
from 2:1 to 3:1 AV block (stars). Images courtesy of Jeffrey A. Tabas, MD.

A

B

** * * **

57

Electrocardiography in Emergency Medicine
Figure 4-7.
AVNRT. A: This ECG reveals a regular, narrow complex tachycardia at a rate of 191 beats/min. At this rate,
several causes, including AVNRT, AVRT, atrial flutter, and focal atrial tachycardia, must be considered. P
waves are not clearly visible, although there is a suggestion of an inverted P wave in limb lead III that occurs
roughly 120 msec after the R wave. This would suggest AVRT, although in the acute situation, this could not be
determined with certainty, and, in fact, electrophysiologic testing confirmed AVNRT. B: An ECG obtained after
treatment with 6 mg of adenosine and resolution of the tachycardia. The patient is now in sinus rhythm. There
is no evidence of accessory conduction in this resting tracing. Images courtesy of Jeffrey A. Tabas, MD.

A

B

58

C h apter f i ve

Wide Complex Tachycardias

Gus M. Garmel, MD

A widened QRS complex represents a delay or wise approaches and extensive examination
abnormality in normal ventricular depolarization, of criteria for interpretation have failed to
in which an electrical stimulus passes from provide acceptable agreement among physicians
the AV node down the ventricular conduction regarding ECG diagnosis.4,5 An understanding of
system, terminating in the ventricular myocardial the causes of wide complex tachycardia allows
cells, as seen on surface electrocardiography.1 appreciation of when recognition and accurate
The term wide complex tachycardias, also treatment selection are possible and when
known as broad complex or wide QRS complex empiric treatment is indicated because accurate
tachycardias, refers to rhythm disturbances diagnosis is not possible. This understanding
with a QRS complex duration (width) of 0.12 is essential to prevent mismanagement
second (120 msec) or more at a rate of more and reduce morbidity and mortality.6,7
than 100 beats/min. An understanding of wide
complex tachycardias involves consideration Approach to Wide Complex
of whether the rhythm and its associated Tachycardia
tachycardia originate from the ventricle itself
(ventricular tachycardia [VT]) or from above the As with all conditions in emergency medicine,
ventricle (supraventricular tachycardia [SVT]) in the initial consideration in the individual with
association with aberrant conduction, accessory wide complex tachycardia is whether there
conduction, or underlying QRS prolongation. is instability, represented by inadequate end-
organ perfusion attributable to the dysrhythmia.
Patients who present to the emergency Instability in a patient with wide complex
department with wide complex tachycardia tachycardia is determined by evidence of
often present diagnostic and therapeutic hypotension, pulmonary edema, confusion,
challenges.2,3 The goal of this chapter is to remove angina, or poor skin perfusion, not the rate or
the “complex” from wide complex tachycardia QRS complex width. An approach in which the
identification and management. Despite the clinician errs on the side of considering a patient
desire to accurately interpret the ECG with wide “unstable” is most prudent. An individual’s
complex tachycardia, the development of step- hemodynamic status does not help determine the

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Electrocardiography in Emergency Medicine

cause of the wide complex tachycardia (although patients with accessory pathways results
this was a common misconception in the past).2 in a widened QRS complex. Impulse
conduction can travel through the AV
Wide Complex Tachycardia of node alone, resulting in narrow complexes
Supraventricular Origin (unless there is conduction delay); through
both the AV node and the accessory
Any supraventricular dysrhythmia can pathway simultaneously, resulting in
be a source of wide complex tachycardia. In fusion complexes of variable duration (a
general, supraventricular rhythm disturbances QRS complex with a delta wave is one
can be seen as irregularly irregular, as in atrial example); or through the accessory pathway
fibrillation and multifocal atrial tachycardia, intermittently or exclusively, resulting in a
or generally regular, as in sinus tachycardia, prolonged QRS duration (Figure 5-2). With
atrial flutter, focal atrial tachycardia, and reentrant circuits involving an accessory
reentrant circuits through the atrioventricular pathway and the AV node, terminology
(AV) node (see Chapter 4, Narrow Complex is based on the direction of conduction
Tachycardias). Three basic mechanisms for through the AV node. Conduction
QRS widening should be considered in a anterograde through the AV node and
patient with wide complex tachycardia from retrograde through the accessory pathway is
a supraventricular origin (Table 5-1): termed orthodromic and results in a narrow
QRS complex (see Figure 4-1E). Conduction
1) Preexisting widening can be caused retrograde through the AV node and
by preexisting bundle-branch block or anterograde through the accessory pathway
intraventricular conduction delay. This may is termed antidromic and results in a wide
be suspected when the same QRS pattern is QRS complex (see Figure 4-1F).
evident on a baseline ECG (if available). Other causes of QRS complex widening
include medication toxicity (see Chapter 17,
2) Widening may be caused by aberrant ECG Manifestations of Drug Overdose) and
ventricular conduction, which is the metabolic abnormalities (see Chapter 15,
temporary, abnormal intraventicular Metabolic Abnormalities: Effects of Electrolyte
conduction of supraventricular impulses, Imbalances and Thyroid Disorders on the ECG).
usually due to a change in cycle length.8 Rapid identification should direct the initiation
This is also known as rate-related bundle- of life-saving therapeutic interventions.
branch block or Ashman phenomenon.
Right bundle-branch block (RBBB) is most Table 5-1.
common, representing 80% to 85% of all Supraventricular tachycardia: causes of wide QRS
aberrant conduction (Figure 5-1). complex

3) Widening can be caused by conduction Preexisting bundle-branch block or interventricular
through an accessory pathway, in which the conduction delay
normal electrical impulses originating from Rate-related bundle-branch block (Ashman aberrancy or
the atria reach ventricular tissue earlier Ashman phenomenon)
than expected. Conduction through an Conduction through an accessory pathway
accessory pathway causes widening due to Other causes
premature activation of the ventricle. This hyperkalemia
differs from bundle-branch block, which medications/intoxications
causes widening due to delayed activation
of the ventricle. Conduction down the
accessory pathway usually occurs at faster
rates than through the AV node and can
cause extremely rapid ventricular response
with risk of degeneration into ventricular
dysrhythmias. Not all conduction in

60

wide complex tachycardias

Wide Complex Tachycardia with a may be ineffective in patients with torsade de
Ventricular Origin pointes. Treatment with magnesium infusion is
recommended; if that is unsuccessful, therapies
Sustained VT is defined as successive to increase the heart rate such as agents with
rapid ventricular complexes that last more β-adrenergic or dopaminergic effect should
than 30 seconds or require intervention be started or a pacemaker should be placed.
for termination. Nonsustained VT involves Torsade de pointes can be refractory to or
more than three successive rapid ventricular recurrent following electrical cardioversion.
complexes lasting less than 30 seconds. VT can
be classified as monomorphic or polymorphic Multifocal VT refers to VT with two or more
(Table 5-2); this distinction has important ventricular morphologies in a patient without
implications for identifying the underlying QT-interval prolongation. It is less common
cause and for making therapeutic choices. than torsade de pointe and occurs primarily in
patients with previous myocardial infarction
In monomorphic VT, complexes of a single and abnormal left ventricular function.
morphology occur at a rate between 120 and 200
beats/min (Figure 5-3). Classic features include a Bidirectional VT, consisting of alternating
regular rate, the presence of AV dissociation, the QRS complexes with opposite directions,
presence of capture and fusion beats, concordance is one type of multifocal VT. It is typically
of the QRS complexes across the precordium, associated with digoxin toxicity (Figure
and a left bundle-branch pattern (see below). 5-5).12–14 This wide complex tachycardia
Unfortunately, diagnostic algorithms based on generally has a RBBB pattern, with the QRS
the presence or absence of these features lack complexes alternating between right and
sufficient accuracy for use in the clinical setting. left axis deviation in the limb leads.

Polymorphic VT includes torsade de pointes, One additional consideration for wide
multifocal VT, and bidirectional VT. Torsade complex tachycardia with a ventricular origin
de pointes is characterized by ventricular is tachycardia caused by paced rhythms.
complexes that vary in a sinusoidal pattern at (See Chapter 14, Pacemakers and Pacemaker
a rate usually between 200 and 250 beats/min Dysfunction, for a discussion of this.)
(Figure 5-4). It is associated with underlying QT
prolongation and is more likely to occur during Differentiation Between VT
episodes of bradycardia, when the QT interval is and SVT
prolonged.9 It has been associated with congenital
prolonged QT syndrome, multiple electrolyte Although it is generally accepted that the 12-
abnormalities, many antiarrhythmic agents lead ECG is inadequate for definitive diagnosis
(ibutilide, sotalol, and the Class Ia agents, for of wide complex tachycardia in the emergency
example), and other medications (phenothiazines, department, an understanding of essential ECG
tricyclic antidepressants, and pentamidine).10,11 characteristics of various causes can direct
Identification is essential because treatments treatment. For example, antiarrhythmic therapy
that are appropriate for monomorphic VT for monomorphic VT might be inappropriate in
the patient with torsade de pointes, because it
Table 5-2. could contribute to QT lengthening. Similarly,
Ventricular causes of wide complex tachycardia the optimal treatment choice differs for atrial
fibrillation with conduction through an
Monomorphic VT accessory pathway and for monomorphic VT.15
Polymorphic VT Ultimately, however, no clinical characteristics
torsade de pointes or ECG approach has been shown to have
multifocal VT acceptable precision in determining the cause
bidirectional VT of wide complex tachycardia.16 In many cases,
Paced rhythms the “final” determination of the cause is not of
utmost importance, even for a stable patient in

61

Electrocardiography in Emergency Medicine

the emergency department. It may be perfectly The R-R interval in VT is constant in more than
acceptable for an emergency physician to 90% of cases.19 The clinician must recognize,
provide a final interpretation of the abnormal however, that VT can manifest some irregularity
ECG with wide complex tachycardia as “wide because of changes in cycle length, fusion or
complex tachycardia of uncertain (undetermined) capture beats, multifocal ventricular complexes,
etiology.” In fact, this could result in better patient or intermittent episodes of the dysrhythmia.
care, allowing the focus of care to be directed
toward the patient and patient management, The Confusion with Fusion/Capture Beats
not the correct interpretation of the ECG.
Fusion beats are hybrid QRS complexes
Clinical Features resulting from simultaneous supranodal and
infranodal (ventricular) activation of ventricular
Eighty percent of all patients who present tissue. They are therefore intermediate in
with wide complex tachycardia will ultimately morphology and width from either a capture or
be diagnosed with VT,17 although this reported ventricular beat (Figure 5-7). Capture beats are
figure may be higher than the actual percentage supraventricular impulses that travel through
seen in the emergency department because the normal conducting system, resulting in
of referral bias and the citation of older QRS complexes that are similar (or identical)
literature.18 Individuals with previous myocardial to the “normal” QRS complex18 (Figure 5-7).
infarction, coronary artery disease, or known Fusion and capture beats are diagnostic for
structural heart disease are significantly VT. However, similar complexes can appear
more likely to present with a ventricular in atrial fibrillation with conduction down an
rather than supraventricular cause of wide accessory pathway. With atrial fibrillation and
complex tachycardia. The likelihood of VT also an accessory pathway, an apparent capture
increases with advanced age. An individual’s complex represents exclusive conduction of an
hemodynamic status does not help determine atrial impulse through the AV node, while an
the cause of the wide complex tachycardia. It apparent fusion complex represents coincident
is incorrect to consider that only VT can be conduction of the impulse through the AV node
unstable or that SVT of any etiology does not and the accessory pathway. The two can be
cause hemodynamic compromise. Clues that distinguished by timing—fusion and capture
support the diagnosis of SVT include a QRS beats occur prematurely in VT but occur either
complex pattern that is identical to previously prematurely or after delay in atrial fibrillation
identified bundle-branch block, aberrant with an accessory pathway (Figure 5-8).
conduction, or SVT with an accessory pathway.
Brief attempts to transiently block the AV node in Precordial Concordance
stable patients with regular rates and suspicion
for SVT can reveal the underlying rhythm or Precordial concordance means that the main
even terminate the dysrhythmia. However, direction of the QRS complexes is the same in
this surprisingly is not definitive for SVT. all precordial leads. Positive precordial QRS
concordance can occur during VT or during
Regularity SVT using a left posterior accessory pathway
for AV conduction. Therefore, precordial
The cause of regular wide complex tachycardia concordance does not discriminate between
can rarely be determined with certainty in VT or SVT with aberrant conduction. Negative
clinical practice; therefore, this presentation precordial concordance is nearly always VT,
should be treated as ventricular tachycardia. but the “rule” is not 100%20,21 (Figure 5-9).
An irregular wide complex tachycardia can
suggest a supraventricular source, such as atrial AV Dissociation
fibrillation with an accessory pathway, especially
in a young person with a fast rate (Figure 5-6). The presence of AV dissociation (ie, atrial
activity independent of ventricular activity)
62

supports the diagnosis of VT. However, wide complex tachycardias
AV dissociation might rarely be seen in AV
junctional tachycardias. AV dissociation VT,23 Brugada’s four-step approach to regular
is identified by detection of separate rates tachycardias,24 and morphologic criteria based
for p waves and QRS complexes. on bundle-branch pattern (positive and negative
deflections). These algorithms can be complex,
The presence of ventricular-to-atrial (VA) and they lack acceptable interobserver agreement.
conduction, evident from a retrograde p wave in Each algorithm has inherent limitations that
the QRS complex, also supports the diagnosis of can lead to ECG misidentifications.25–29 Because
VT. The use of sensitive recording devices such none of these approaches is recommended for
as esophageal leads has demonstrated that VA emergency physicians, they are only mentioned
conduction occurs in up to half of patients with here, with appropriate references provided.
VT.19 It is more common with slower rates (<200
beats/min). The RP interval of the retrograde Other Approaches to Diagnosis
atrial beat is generally 0.11 second (almost three Transesophageal atrial “pill” electrodes
small boxes) or longer.19 Both AV dissociation
and VA conduction can be challenging to can be used to record atrial activity, which
identify, because the p wave is often obscured by may help identify AV dissociation or 1:1
the QRS complex and components of the QRS VA conduction (both representative of VT).
complex may resemble p waves (Figure 5-10). This approach is unlikely to have a place in
emergency practice because of its cost, lack
QRS Complex Axis and Duration of availability, and difficulty of use; there are
safety concerns, and emergency physician
In some cases, the QRS axis or QRS duration experience with this technology is limited.
can provide additional support for VT as These pills are not indicated for patients
the cause of the wide complex tachycardia experiencing hemodynamic compromise.
pattern. An axis more negative than –90° or
more positive than +180° suggests VT. A QRS The role of transesophageal
complex with right bundle-branch pattern electrocardiography in the diagnosis of wide
and duration of more than 0.14 second or complex tachycardia has received much
left bundle-branch pattern and duration attention as a method to search for disparity
of more than 0.16 second supports VT. between the atrial and ventricular rates, thereby
identifying VT, although emergency medicine
QRS Morphology literature on this approach is limited.30–33

Classically, a RBBB pattern is more likely to Therapy
be SVT. Exceptions are common enough that
this “rule” is not helpful for the emergency Pharmacologic treatment of stable patients
practitioner (Figure 5-11). The value of should follow the most updated American
descriptions of the QRS complex morphology Heart Association guidelines,34 with “expert
that characterize VT, such as a V1 lead with consultation” advised. For regular rhythms,
an R-wave duration of more than 30 msec, such as VT or any uncertain rhythm, current
notching of the S wave, or an S-wave duration recommendations are to treat for VT with
greater than 70 msec, is discussed below. recommended agents such as intravenous
amiodarone and prepare for elective synchronized
Algorithms to Determine the Origin of a cardioversion (as long as the patient remains
Wide Complex Tachycardia clinically stable). If, on the other hand, the
wide complex tachycardia is irregular, and
Many algorithms have been developed atrial fibrillation with an accessory pathway is
to determine the source of wide complex thought to be the cause, pharmacologic therapy
tachycardia. They include Wellens’ criteria,22 with procainamide or other recommended
Kindwall’s four electrophysiologic criteria for agents should be considered, and AV nodal
blocking agents (eg, adenosine, digoxin,

63

Electrocardiography in Emergency Medicine

diltiazem, verapamil) should be avoided. For for his efforts in obtaining and formatting
torsade de pointes, the clinician should search many of the ECGs used in this chapter.
and treat for medication toxicity or electrolyte
disturbance. An intravenous loading dose of References
magnesium followed by infusion is currently
recommended. If this is unsuccessful, agents 1. Dubin D. Rapid Interpretation of EKG’s. 3rd ed.
that increase chronotropy and therefore Tampa, FL: C.O.V.E.R. Publishing Co; 1970.
shorten the QT interval should be used.34 For
bidirectional VT, assessment of and treatment 2. Morady F, Baerman JM, DiCarlo LA, et al. A
for digoxin toxicity should be considered. prevalent misconception regarding wide complex
tachycardia. JAMA. 1985;254(19):2790-2792.
Acknowledgments
3. Mason JW, Stinson EB, Winkle RA, et al. Mechanisms
Dr. Garmel is grateful to the cardiology of ventricular tachycardia: wide, complex ignorance.
groups at Kaiser Santa Clara and Santa Teresa, Am Heart J. 1981;102(6):1083-1087.
who assisted with the selection of several
ECGs used in this chapter. Appreciation is 4. Herbert ME, Votey SR, Morgan MT, et al. Failure to agree
also extended to Doris Hayashikawa and her on the electrocardiographic diagnosis of ventricular
staff at the Health Sciences Library, Kaiser tachycardia. Ann Emerg Med. 1996;27(1):35-38.
Santa Clara, for their continuous support
of academic projects. Finally, Bill H. Bosse, 5. Isenhour JL, Craig S, Gibbs M, et al. Wide-complex
CBET (Northern California Regional Systems tachycardia: continued evaluation of the diagnostic
Administrator, Philips TraceMaster, Kaiser criteria. Acad Emerg Med. 2000;7(7):769-773.
Foundation Hospitals), is to be commended
6. McGovern B, Garan H, Ruskin JN. Precipitation of cardiac
arrest by verapamil in patients with Wolff-Parkinson-
White syndrome. Ann Intern Med. 1986;104:791-794.

7. Stewart RB, Bardy GH, Greene HL. Wide complex
tachycardia: misdiagnosis and outcome after emergent
therapy. Ann Intern Med. 1986;104:766-771.

8. Wagner GS, Marriott HJL. Marriott’s Practical Electrocardiography.
Philadelphia, PA: Lippincott Williams & Wilkins; 2000.

9. Vukmir RB. Torsade de pointes: a review. Am
J Emerg Med. 1991;9(3):250-255.

Key Facts

• Unstable patients require defibrillation or emergent cardioversion (with sedation considered).
• The treatment of patients presenting with wide complex tachycardia should be based on the clinical

or hemodynamic status of the individual, not on the ECG.
• The ECG in patients with wide complex tachycardia is not always helpful in determining the cause

of the rhythm disturbance and may not even have clinical relevance in the emergent setting.
• Algorithms and diagnostic criteria intended to help clinicians correctly interpret wide complex

tachycardia are not foolproof.
• It is perfectly acceptable to interpret an ECG demonstrating wide complex tachycardia as “wide

complex tachycardia of uncertain etiology.”
• In a patient with regular wide complex tachycardia of uncertain cause, assume the diagnosis to be

VT and treat as such, given the high pretest probability of VT and minimal negative consequences if
incorrect.
• Identify and treat torsade de pointes; its causes and treatments differ from those for monomorphic
VT.
• Characteristics diagnostic of VT, ie, capture and fusion beats, AV dissociation, and VA retrograde
conduction, can be difficult to interpret on the ECG.
• A trial of adenosine may be reasonable in a patient with regular wide complex tachycardia of
uncertain cause but should be avoided in irregular wide complex tachycardia because it could
contribute to more rapid conduction through an accessory pathway.
• Medications that block the AV node (other than adenosine) should be avoided in patients with wide
complex tachycardia unless recommended by expert consultation.

64

wide complex tachycardias

10. Keren A, Tzivoni T, Gavish D, et al. Etiology, warning 22. Wellens HJJ, Bar FWHM, Lie KI. The value of the
signs and therapy of torsade de pointes: a study of electrocardiogram in the differential diagnosis of a tachycardia
10 patients. Circulation. 1981;64(6):1167-1174. with a widened QRS complex. Am J Med. 1978;64:27-33.

11. Engrav MB, Coodley G, Magnusson AR. Torsade de pointes after 23. Kindwall KE, Brown J, Josephson ME. Electrocardiographic
inhaled pentamidine. Ann Emerg Med. 1992;21(11):1403-1405. criteria for ventricular tachycardia in wide complex
left bundle-branch block morphology tachycardias.
12. Kummer JL, Nair R, Krishnan SC. Images in cardiovascular Am J Cardiol. 1988;61:1279-1283.
medicine: bidirectional ventricular tachycardia caused by
digitalis toxicity. Circulation. 2006;113(7):e156-e157. 24. Brugada P, Brugada J, Mont L, et al. A new approach to
the differential diagnosis of a regular tachycardia with a
13. Piccini J, Zaas A. Cases from the Osler Medical Service at wide QRS complex. Circulation. 1991;83:1649-1659.
Johns Hopkins University: digitalis toxicity with bidirectional
ventricular tachycardia. Am J Med. 2003;115(1):70-71. 25. Littmann L, McCall MM. Ventricular tachycardia
may masquerade as supraventicular tachycardia
14. Ma G, Brady WJ, Pollack M, et al. in patients with preexisting bundle-branch
Electrocardiographic manifestations: digitalis block. Ann Emerg Med. 1995;26:98-101.
toxicity. J Emerg Med. 2001;20(2):145-152.
26. Olshansky B. Ventricular tachycardia masquerading
15. Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al. as supraventricular tachycardia: a wolf in sheep’s
ACC/AHA/ESC guidelines for the management of patients clothing. J Electrocardiol. 1988;21(4):377-384.
with supraventricular arrhythmias—executive summary.
A report of the American College of Cardiology/American 27. Gutierrez-Macias A, Sanz-Prieto JC, Aguirre-Herrero
Heart Association Task Force on Practice Guidelines and J, et al. Wide-complex tachycardia: diagnostic value
the European Society of Cardiology Committee for Practice of the Brugada algorithm in emergency medicine.
Guidelines (writing committee to develop guidelines Acad Emerg Med. 2001;8(3):300-301.
for the management of patients with supraventricular
arrhythmias) developed in collaboration with NASPE-Heart 28. Pollack A, Falk RH. New criteria for diagnosis of regular, wide-
Rhythm Society. J Am Coll Cardiol. 2003;42:1493-1531. complex tachycardias. Circulation. 1992;85(5):1955-1956.

16. Baerman JM, Morady F, DiCarlo LA, et al. Differentiation 29. Dassen WRM, Karthaus VLJ, Talmon JL, et al. Evaluation
of ventricular tachycardia from supraventricular of new self-learning techniques for the generation of
tachycardia with aberration: value of clinical criteria for differentiation of wide-QRS tachycardia
history. Ann Emerg Med. 1987;16(1):40-43. in supraventricular tachycardia and ventricular
tachycardia. Clin Cardiol. 1995;18:103-108.
17. Brady WJ, Skiles J. Wide QRS complex tachycardia: ECG
differential diagnosis. Am J Emerg Med. 1999;17(4):376-381. 30. Brembilla-Perrot B, Beurrier D, Houriez P, et al. Wide
QRS complex tachycardia: rapid method of prognostic
18. Akhtar M, Shenasa M, Jazayeri M, et al. Wide QRS evaluation. Int J Cardiol. 2004;97:83-88.
complex tachycardia: reappraisal of a common clinical
problem. Ann Intern Med. 1988;109:905-912. 31. Koscove E. Diagnosis of ventricular tachycardia
[letter]. Ann Emerg Med. 1996;28(2):244.
19. Surawicz B, Knilans TK, Chou T-C. Chou’s
Electrocardiography in Clinical Practice: Adult and 32. Jenkins J, Wu D, Arzebacher R. Computer diagnosis of
Pediatric. Philadelphia, PA: Saunders; 2001:xiv,709. supraventricular and ventricular arrhythmias: a new
esophageal technique. Circulation. 1979;60:977-987.
20. Volders PGA, Timmermans C, Rodriguez LZ, et
al. Wide QRS complex tachycardia with negative 33. Haley JH, Reeder GS. Wide-complex
precordial concordance: always a ventricular origin? tachycardia. Circulation. 2000;102:e52.
J Cardiovasc Electrophysiol. 2003;14(1):109-111.
34. 2005 American Heart Association guidelines for
21. Kappos KG, Andrikopoulos GK, Tzeis SE, et al. Wide- cardiopulmonary resuscitation and emergency cardiovascular
QRS-complex tachycardia with a negative concordance care: management of symptomatic bradycardia and
pattern in the precordial leads: are the ECG criteria always tachycardia. Circulation. 2005;112(24):67-77.
reliable? Pacing Clin Electrophysiol. 2006;29:63-66.

65

ElEctrocardiography in EmErgEncy mEdicinE

Figures

Figure 5-1.
Aberrant ventricular conduction. This ECG demonstrates an irregular, narrow complex tachycardia with
intermittent wide complexes. The arrows point to aberrantly conducted beats caused by a short coupling
(R-R) interval (x) following a long coupling interval (y). This is referred to as Ashman aberrancy or Ashman
phenomenon. From: Stahmer SA, Cowan R. Tachydysrhythmias. Emerg Med Clin North Am. 2006;24:11–40.
Used with permission.

Figure 5-2.
Conduction in atrial fibrillation with accessory pathway. In patients with atrial fibrillation and an accessory
pathway, atrial beats may be conducted through (A) the AV node exclusively, resulting in narrow complex
ventricular beats, (B) the AV node and accessory pathway coincidentally, resulting in fusion ventricular beats
of variable duration, or (C) the accessory pathway exclusively, resulting in a wide complex ventricular beat.
Images courtesy of Jeffrey A. Tabas, MD.

aBc

66

wide complex tachycardias

Figures

Figure 5-3.
Monomorphic ventricular tachycardia. A patient presented with a regular tachycardia at 225 beats/min and
a QRS complex duration of 160 msec with a left bundle-branch pattern. There is no upper limit of heart rate,
which excludes the diagnosis of VT, although SVT with aberrant conduction tends to be associated with a
higher heart rate than VT.

Figure 5-4.
Torsade de pointes. A patient presented with a wide complex tachycardia at a rate of 208 beats/min. The
amplitude of the QRS complexes appears to expand and compress in an accordion pattern, best seen in the
rhythm strip of lead II. Image courtesy of Jeffrey A. Tabas, MD.

67

Electrocardiography in Emergency Medicine

Figures

Figure 5-5.
Bidirectional ventricular tachycardia associated with digitalis toxicity. This rhythm strip shows ventricular
complexes with intermittent alternating orientations, resulting in some irregularity of the rhythm. From:
Piccini J, Zaas A. Images of Osler: cases from the Osler Medical Service at Johns Hopkins University. Am J
Med. 2003;115[1]:70-71. Used with permission from Excerpta Medica, Inc.

Figure 5-6.
Atrial fibrillation with accessory pathway. A 35-year-old man presented with palpitations that had lasted
several hours. His ECG shows a rate of 209, with marked irregularity, and a QRS width of 130 msec. Treatment
with procainamide slowed his ventricular response, and he eventually converted to sinus rhythm. There was
no evidence of preexcitation on his sinus rhythm ECG. Image courtesy of Jeffrey A. Tabas, MD.

68

widE complEx tachycardias

Figures

Figure 5-7.
Capture and fusion beats in VT. Multilead rhythm strip demonstrating capture beats (solid arrows) and fusion
beats (open arrows), highly suggestive of VT. Note that these beats occur earlier than the next ventricular beat
would be expected. From: Brady WJ, Skiles J. Wide QRS complex tachycardia: ECG differential diagnosis. Am
J Emerg Med. 1999;17[4]:376-381. Used with permission from Elsevier.

Figure 5-8.
Apparent capture and fusion beats in a patient with atrial fibrillation and Wolff-Parkinson-White syndrome
with rapid ventricular conduction. Note the row of apparently regular, wide complex beats followed by a
delayed and slightly narrower beat with a different morphology (open arrow). This slightly narrower beat
could be a fusion caused by coincident beats conducted down the AV node and the accessory pathway. This is
unlike fusion seen with VT, which represents coincident beats conducted down the AV node and arising from
the ventricles and therefore occurs with a normal or shortened R-R interval. A narrow complex beat (solid
arrow) represents a “capture” beat, which can be seen with VT or atrial fibrillation. This is due to sporadic
activation of the ventricle by conduction through the AV node. However, the capture beat of VT also occurs
with a shortened R-R interval since it is conducted before the next regularly occurring ventricular complex.
Image courtesy of Jeffrey A. Tabas, MD.

69

Electrocardiography in Emergency Medicine

Figures

Figure 5-9.
Precordial concordance. This ECG demonstrates wide complex tachycardia with a rate just under 200
beats/min. It appears quite regular. The QRS duration is 155 msec, and its morphology is V1-positive (RBBB-
like). Although positive precordial concordance is present, an AV nodal reentry mechanism with aberrant
conduction was confirmed during subsequent testing.

70

wide complex tachycardias

Figures

Figure 5-10.
AV dissociation. This is a regular wide complex tachycardia at 115 beats/min with a right bundle-branch
morphology. Careful scrutiny reveals P waves (P) in the lead II rhythm strip at a regular rate of 107, which is
slightly slower than the ventricular rate. Pseudo-P waves in lead III (arrows) resemble retrograde P waves but
are identified as part of the QRS complex because they are synchronous with the terminal portion of the QRS
in other leads. Image courtesy of Amal Mattu, MD.

71

Electrocardiography in Emergency Medicine

Figures

Figure 5-11.
Atypical monomorphic VT. ECG tracing from a 76-year-old woman with wide complex tachycardia,
demonstrating a rate of 152, a right bundle-branch block pattern, and a left superior axis. She spontaneously
converted to normal sinus rhythm with a normal ECG. An electrophysiologic diagnosis of idiopathic left
ventricular tachycardia was confirmed, caused by a reentry loop in the LV apex. This VT often responds to
verapamil, although the use of calcium channel blockers in patients presenting to the emergency department
with wide complex tachycardia of uncertain etiology is not recommended. Image courtesy of
E.M. Koscove, MD.

72

C h apter s i x

Acute Coronary Ischemia and Infarction

Luis H. Haro, MD

Emergency physicians encounter patients on The Prehospital ECG
a daily basis with symptoms suggestive of ACS.
Among these symptoms, chest pain is by far The prehospital ECG is an underutilized
the most common. According to the National component in modern ACS care. Prehospital
Hospital Ambulatory Medical Care Survey, ECGs can be obtained by advanced EMS
conducted by the Centers for Disease Control personnel and transmitted while en route to a
and Prevention, an estimated 110 million visits hospital in advanced EMS systems in the United
were made to hospital emergency departments States. If transmission is a problem, the computer
in 2004; chest pain was the chief complaint read is highly accurate and can be called into the
for 5,637,000 (5.4%) of them.1 Not all patients receiving emergency department. This will allow
with chest pain have ACS. The American Heart emergency department personnel to be ready to
Association calculated that 879,000 people initiate fibrinolysis or alert cardiology for PPCI.
with ACS were discharged from hospitals in The use of prehospital ECGs reduces door-to-
2003 (considered a conservative estimate). This needle time for in-hospital fibrinolysis by a mean
number was derived by adding the number of of 10 minutes and, according to data from the
hospital discharges for myocardial infarction (MI) National Registry of Myocardial Infarction 2,
(767,000) and for unstable angina (112,000).2 reduces the door-to-balloon-time for PPCI by a
Given this patient volume, an understanding of mean of 23 minutes.3 The use of prehospital ECGs
the ECG changes indicative of ACS is paramount can also help EMS systems triage more efficiently.
to emergency physicians and extremely The patient with MI with ST-segment elevation
important for patients, as it allows immediate (STEMI) who is in cardiogenic shock benefits
risk stratification and therapeutic decisions (eg, from being transferred to a center with PPCI
administration of a -blocker, thrombolysis, capability and emergent revascularization.4 If an
or activation of a catheterization team for ECG is not obtained during prehospital transport
primary percutaneous intervention [PPCI]). or if the patient arrives by private vehicle, a
door-to-ECG time of 10 minutes is encouraged.5

73

Electrocardiography in Emergency Medicine

Normal and Nondiagnostic Patterns of Ischemia
ECGs In the presence of normal conduction, the

Patients with ACS include those whose T wave is usually upright in I, II, and V3 to V6;
clinical presentations cover the following range inverted in lead aVR; and variable in leads III,
of diagnoses: unstable angina, MI without ST- aVF, aVL, and V1, with rare normal inversion in
segment elevation (NSTEMI), and STEMI.5 The V2. In ischemia, T waves are inverted, symmetric,
standard 12-lead ECG and use of additional ECG and mostly transient (the aberrations occur
techniques, including right-sided leads (V3R while the patient is symptomatic) (Figure 6-1).
through V6R), posterior leads (V7, V8, and V9), Therefore, any T-wave inversions in V2 to V6 are
and continuous ST-segment monitoring, allow considered pathologic. In such a case and in the
detection of changes suggestive of ischemia. presence of chest pain or its equivalent, there
However, among patients who have chest pain is usually no myocardial damage, as measured
and are subsequently diagnosed with AMI by by CK-MB or troponin, and the diagnosis is
cardiac isoenzyme concentration (CK-MB), unstable angina (UA) (Figure 6-1). If the T-wave
6% to 8% have normal ECGs and 22% to 35% inversion is persistent, there is nearly always
have nonspecific ECGs.6 In fact, malpractice some minimal troponin elevation; this pattern
cases often focus on the performance and use frequently is termed non–Q wave MI. A more
of electrocardiography (Table 6-1).7,8 Patients contemporary term denotes no ST-segment
with AMI who are mistakenly discharged from elevation recorded, appropriately termed non-
the emergency department have short-term STEMI (NSTEMI). UA and NSTEMI result
mortality rates of about 25%, at least twice from a nonocclusive thrombus, small risk area,
what would be expected if they were admitted.9 brief occlusion (spontaneously reperfused),
The legal costs that can result from such cases or an occlusion that maintains good collateral
constitute the largest category of losses from circulation. In many such cases, ST-segment
emergency department malpractice litigation.10 elevation or other ST-segment or T-wave
abnormalities would have been noted if an ECG
ECG Changes of ACS had been recorded at the appropriate time.6

Abnormalities in the ST segment, QRS Patterns of Injury
complex, and T waves indicate the extent In the early stages of an evolving STEMI,
of ischemia, injury, and necrosis.
prominent T waves are termed hyperacute and
Table 6-1. are defined as larger than 6 mm in the limb leads
Most common causes of malpractice losses related and larger than 10 mm in the precordial leads.
to acute chest pain and patients at higher risk of Unfortunately, these prominent T waves are not
being discharged from the emergency department specific for ischemia. Table 6-2 describes the
with AMI7,8
Table 6-2.
Most common causes of malpractice losses related to Differential diagnosis of prominent T waves
chest pain:
AMI (usually bulky, wide waves associated with chest
• failure to obtain an ECG pain and other associated cardiovascular symptoms)
• misinterpretation of an ECG Normal variant (in mid precordial leads of young
• failure to record data from the clinical evaluation patients)
Characteristics of patients at risk of being discharged Hyperkalemia (usually not associated with chest pain)
from the emergency department with AMI: Intracranial hemorrhage (associated with prolonged QT
• women younger than 55 years of age and presence of U waves)
• nonwhite patients Left ventricular hypertrophy
• shortness of breath as chief symptom LBBB
• normal or nondiagnostic ECG

74

Acute Coronary Ischemia and Infarction

differential diagnosis of prominent T waves. Table preferred as the baseline. STEMI is defined as
6-3 describes the evolution of ischemic changes ST-segment elevation of at least 0.1 mV (1 mm)
in relation to the onset of patient symptoms. in two or more contiguous leads11 (Figures 6-3,
Bulky, wide T waves are highly suggestive of 6-4, and 6-5). Leads I and aVL are considered
early STEMI and might be seen within the first contiguous leads, reflecting the “high lateral”
30 minutes after the onset of symptoms. In fact, portion of the left ventricle, even though they
the height of these T waves generally correlates are not proximate to each other on the 12-lead
well with the acuteness of the injury. At this ECG. Measurement of ST deviation at other
early phase, there is no cellular death. With levels (60 or 80 msec after the J point) is not
prolonged and significant occlusion (90% of advised. Some studies have suggested that a
the coronary artery), the prominent T waves well-informed subjective interpretation of the
remain as ST deviation develops (Figures 6- appearance of the ST segment is more accurate
2 and 6-3). ST-segment elevation represents a than measured criteria.12,13 The morphology of
myocardial region at risk for (irreversible) MI the ST segment is equally important, because
and usually leads to at least some myocardial it evolves from a normal minimally upward
cell death (measured by troponin elevation). The concave to one that is straight and then convex.
ST-segment elevation seen with AMI is called (See discussion in Chapter 9, ACS Mimics:
a current of injury, indicating that damage has Non–AMI Causes of ST-Segment Elevation.)
occurred to the epicardial layer of the heart.
Normally, the ST segment is isoelectric because After prolonged, non-reperfused coronary
no net current flow is occurring at this time. MI occlusion, as regional ST segments resolve
alters the electrical charge on the myocardial toward the isoelectric level, T waves invert
cell membranes, resulting in abnormal current (resulting in a biphasic appearance) in the same
flow and, in turn, ST-segment deviations. region (Figure 6-6). The ST segment usually
stabilizes within 12 hours, with full ST-segment
Disagreement exists regarding whether the resolution over the ensuing 72 hours. ST-segment
ST-segment elevation or depression should be elevation completely resolves within 2 weeks
measured from the upper edge of the PR segment after 95% of inferior and 40% of anterior MIs;
or from the TP segment to the upper edge of the persistence for more than 2 weeks is associated
ST segment at the J point. It should be noted, with greater morbidity.14 T waves can normalize
however, that the PR segment can be altered by over days, weeks, or months (Figure 6-2).15 In
atrial infarction, abnormal atrial repolarization, the presence of previous T-wave inversion, re-
or pericarditis; thus, the TP segment is often
Table 6-4.
Table 6-3. Prognostic features of ST-segment elevation (in
Evolution of ischemic changes in relation to onset of decreasing order of importance) associated with
symptoms larger MI, higher mortality rate, and greater benefit
from reperfusion therapy*
T waves: Peak within 30 minutes but can last several
hours. T waves invert with reperfusion (spontaneous Anterior location, compared with inferior or lateral16-20
or therapeutic); frequently normalize in days, weeks, Presence of ST-segment elevation and ST-segment
or months; and, less commonly, persist inverted depression or total ST deviation (absolute sum of ST-
indefinitely. segment elevation and ST-segment depression)21-23
ST segment: Elevates within minutes to hours. Without ST score (the sum of all ST-segment elevations) greater
early therapeutic reperfusion, usually stabilizes within than 1.2 mV (12 mm)19
12 hours but might remain elevated for days. Usually Distortion of the terminal portion of the QRS (as
resolves within 2 or 3 weeks. Persistence after 3 or 4 evidenced by loss of S wave in leads with RS
weeks is highly suggestive of a ventricular aneurysm. configuration), or J point more than 50% of the height of
Pathologic Q waves: Evolve within hours. With early the R wave24
reperfusion, might disappear completely. Without early *Some patients without these features might also have
reperfusion, persist indefinitely in 70% of cases. a large AMI.

75

Electrocardiography in Emergency Medicine

occlusion of the coronary artery manifests as ST-segment depression of more than 2 mm in
ST-segment re-elevation and normalization of three or more leads carries a high probability that
terminal T-wave inversion, called T-wave pseudo- cardiac enzymes will be elevated. If PPCI is not
normalization because the T wave flips upright. performed, the 30-day mortality rate is 35%.27
With upright T waves, pseudo-normalization
should not be assumed if the previous ECG Reciprocal ST-segment depression improves
showing T-wave inversion was recorded the likelihood of STEMI. It represents the
more than 1 month earlier. Table 6-4 lists the electrical mirroring phenomenon observed on
prognostic features of ST-segment elevation. the ventricular wall opposite the transmural
injury and therefore does not reflect ischemia in
ST-Segment Depression the territory of the ST-segment depression. Table
Primary ST-segment depression, if not caused 6-5 describes the reciprocal changes associated
with anterior, inferior, and posterior STEMI.
by posterior STEMI or reciprocal changes
to ST-segment elevation, is an ECG sign of Patterns of Necrosis
subendocardial ischemia (Figure 6-7). In the When necrosis occurs, the electrical voltages
context of ACS, it indicates UA/NSTEMI. ST-
segment depression of even 0.5 mm from produced by this portion of the myocardium
baseline is associated with increased mortality, disappear. Instead of positive (R) waves over
but it is particularly significant when it is more the infarcted area, Q waves are recorded (either
than 1 mm (0.1 mV) in two or more contiguous a QR or QS complex). Q-wave formation begins
leads.25 This adverse prognostic association is within 1 hour and can be completed in 8 to
independent of an elevated troponin level.26 12 hours. Before the reperfusion era, MI was
Although ST-segment depression, especially classified based on its clinical pathology either
up-sloping ST-segment depression, might be as Q-wave or non–Q-wave MI, or as transmural
baseline and stable, the depression associated versus subendocardial MI. These terms were later
with UA/NSTEMI is transient and dynamic discovered to be clinically and pathologically
with a morphology that is usually flat or down- unrelated. Q waves were considered markers
sloping. Even 1 mm of ST-segment depression of irreversible infarction. Today it is well
following an R of more than 20 mm is very known that Q waves eventually disappear in
specific for ischemia; R less than 10 mm is up to 30% of patients with AMI who receive
sensitive but not specific (Figures 6-7 and 6-8). no reperfusion therapy and that, with early
reperfusion therapy, the Q waves disappear
Table 6-5. earlier (within a few days to weeks). Hence,
Reciprocal ST-segment depression: changes AMI is now classified as STEMI or NSTEMI.
according to area of infarction The Q-wave/non–Q-wave distinction remains
somewhat useful, because Q waves are associated
Anterior STEMI: Reciprocal ST-segment depression in at with a lower ejection fraction and a larger MI.
least one of leads II, III, and aVF in 40%-70% of cases
(Figures 6-3 and 6-10) suggestive of a proximal LAD Normal septal q waves must be differentiated
artery occlusion. from the pathologic Q waves of infarction.
Inferior STEMI: Reciprocal ST-segment depression
usually is present in leads I and aVL, and often in the Table 6-6.
precordial leads, especially V1 through V3 in 56% of Q-wave equivalents in the precordial leads
cases (Figure 6-9).
Posterior STEMI: Reciprocal ST-segment depression in R-wave diminution or poor R-wave progression
V1 through V4, with or without ST-segment elevation in Reverse R-wave progression, in which R waves increase
leads V5 and V6 or leads II, III, and aVF (truly reciprocal to then decrease in amplitude across the precordial leads
what would be ST-segment elevation on posterior leads) (although this must be distinguished from precordial
(Figure 6-15). Upright T waves and posterior lead ST- electrode misconnection)
segment elevation help to differentiate this entity from Tall R waves in leads V1 and V2, representing “Q waves”
inferior STEMI reciprocal ST-segment depression. of posterior infarction

76

Acute Coronary Ischemia and Infarction

Normal septal q waves are characteristically after presentation or very soon after therapy is
narrow and of low amplitude (as a rule, <0.04 associated with a good prognosis (Figure 6-6).
sec in duration). A Q wave is abnormal if its
duration is 0.04 second or more in lead I, all three Wellens Syndrome
inferior leads (II, III, aVF), or leads V3 through
V6 (Figure 6-10). A large QS complex can be a Wellens syndrome (Figure 6-11) refers to
normal variant in leads aVL, V1, and, rarely, in angina with T-wave inversion or biphasic T-
V2, making it difficult to distinguish from an old waves in the left anterior descending (LAD)
anterior septal MI. Q waves in V3 will hint toward artery distribution, particularly V2 through
infarct. In general, in the acute setting, pathologic V4, in the presence of persistent R waves and
ischemic Q waves (whether in V1 to V2 or aVL) critical stenosis of the LAD artery.29–31 ST-segment
without ST changes are relevant only from a elevation or depression is not a necessary
patient’s historical perspective. Risk stratification component of this syndrome. The ECG pattern
and decision to treat are based primarily on is also present in a pain-free state. Wellens’
clinical presentation, risk factors, and ST- and T- group noted that patients who were managed
wave abnormalities. There are Q-wave equivalents medically without angioplasty fared poorly; 75%
suggestive of ischemia (Table 6-6) and Q waves developed an anterior wall AMI, usually within
that are pathologic but nonischemic (Table 6-7). a matter of days. Identical T-wave morphology is
recorded in approximately 60% of patients who
Reperfusion have undergone successful reperfusion therapy
for anterior STEMI,32,33 suggesting that Wellens
A combination of angiographic evidence syndrome is a clinical condition created by
of microvascular perfusion and resolution of spontaneous reperfusion of a previously occluded
ST-segment elevation are the best predictors critical stenosis. Similar patterns occur in other
of outcome from STEMI.19 In fact, coronary coronary distributions, but the syndrome was
occlusion can be transient or dynamic with cyclic described originally in the LAD artery. Wellens
reperfusion and reocclusion and is represented syndrome is distinguished from benign T-wave
as transient ST-segment elevation (occurs in up inversion by 1) longer QT interval (>425 msec
to 20% of STEMI).28 On continuous ST-segment as opposed to 400 to 425 msec) and 2) location
monitoring after reperfusion therapy, recovery of V2 through V4 (as opposed to V3 through V5).
the ST segment to less than 50% of its maximal
height by 60 minutes is associated strongly with Area of Infarction
Thrombolysis in Myocardial Infarction category
3 (TIMI-3) reperfusion and even more strongly The cardiac blood supply is delivered by the
associated with good microvascular perfusion. three main coronary arteries (Figure 6-12).
A less sensitive but highly specific predictor of The ECG changes seen in patients with ACS
reperfusion is terminal T-wave inversion identical can also be described in terms of the location
to Wellens T waves. In patients who have STEMI, of the infarct. The anatomic location of the
the presence of negative T waves very early infarct determines the leads in which the typical
patterns appear. For example, with an acute

Table 6-7. Table 6-8.
Differential diagnosis of pathologic Q waves Indications to obtain a 15-lead ECG

Ischemic Q waves ST-segment depression in leads V1 through V3
LBBB Borderline ST-segment elevation in leads V5 and V6 or
Left ventricular hypertrophy borderline ST-segment elevation in leads II, III, and aVF
Chronic lung disease All ST-segment elevation, inferior wall AMIs (ST-
Hypertrophic cardiomyopathy segment elevation in leads II, III, and aVF)
Dilated cardiomyopathy Isolated ST-segment elevation in lead V1 or ST-segment
elevation in leads V1 and V2

77

Electrocardiography in Emergency Medicine

anterior wall MI, ST-segment elevations and occlusion of either the left circumflex or
tall hyperacute T waves appear in one or more the right coronary artery. Isolated posterior
of the anterior leads (chest leads V1 through V6 infarction is uncommon (occurring in 3% to
and extremity leads I and aVL) (Figures 6-3, 8% of all AMIs). STEMI in this distribution is
6-4, 6-13, and 6-14). With an inferior wall MI, difficult to diagnose, as it does not appear as
the ST-segment elevations and tall hyperacute ST-segment elevation in the conventional 12-
T waves are seen in inferior leads II, III, and lead ECG. Fortunately, pure posterior STEMI
aVF (Figure 6-9). Table 6-9 describes the is uncommon and most cases extend either to
relationship between the area of occlusion and the lateral wall, with changes in V6, or to the
the distribution of the ST-segment elevation. inferior wall, with changes in II, III, and aVF .

Several distinct observations regarding In pure posterior AMI, V1 through V3 offer
anatomic distribution patterns will enhance the several diagnostic clues39 (Figure 6-15). The
understanding of the ECG findings of ACS. The sensitivity and positive predictive value for the
characteristic feature of an anterior wall infarct diagnosis of posterior STEMI increase with
is the loss of normal R-wave progression in the the addition of posterior leads V7, V8, and V9.
chest leads. Normally, the height of the R wave
increases progressively from lead V1 to lead V6. Rapid recognition of acute posterior MI is of
An anterior infarct interrupts this progression; clinical importance for several reasons. First,
the result is pathologic Q waves in one or more patients with acute inferior or lateral wall
of the chest leads. Anteroseptal refers to these MI who also have posterior involvement are
changes in V1 and V2. Changes in V3 and V4 experiencing a large infarct. With increasing
are present in isolated anterior infarcts and V5 infarct size, the risk of dysrhythmia, left
and V6 for anteroapical infarcts (Figure 6-13). ventricular dysfunction, and death increases
Because distribution patterns often overlap, proportionally. Second, approximately 5% of
a simplified approach describes leads I, aVL, patients initially diagnosed with ST-segment
and V1 to V6 as anterior and then specifies the depression representing subendocardial ischemia
leads that show Q waves and ST/T changes. in the septal leads actually have experienced
posterior STEMI, with a subsequent unfortunate
Posterior Infarctions delay in reperfusion therapy. The easiest way to
distinguish between subendocardial ischemia
Posterior infarctions occur on the posterior of the LAD artery represented as ST-segment
surface of the left ventricle as a result of depression and reciprocal ST-segment depression

Table 6-9.
ST-segment elevation, location of STEMI, and corresponding coronary artery

AMI location ST-segment elevation

Inferior II, III, and aVF

Inferior and right ventricular II, III, and aVF plus V1

Right-sided ECG: V4R

Inferior and posterior II, III, and aVF plus ST-segment depression V1 through V4

Inferior and lateral II, III, and aVF plus I, aVL, and/or V5 and V6

Anterior V2 through V4

Lateral I, aVL, V5, and/or V6

Right ventricular V1 through V3

Also, V1R through V6R, especially V4R

Anteroseptal V1 through V4

Posterior ST-segment depression in V1 through V4

ST-segment elevation in posterior leads V7, V8, and V9

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Acute Coronary Ischemia and Infarction

from a posterior STEMI is to obtain a 15-lead Ventricular Aneurysm
ECG that includes posterior leads (Table 6-8).
After a large anterior MI (less commonly
Body surface mapping, an ECG technique after an inferior MI), a ventricular aneurysm
that uses numerous leads on a patient’s anterior might develop. It is critical to distinguish ST-
and posterior chest, allows more complete segment elevation from an aneurysm and ST-
visualization of cardiac electrical activity. It is segment elevation from an MI. The persistence
an extension of an additional-lead ECG. Output of ST-segment elevation for 4 weeks or more
from body surface mapping is displayed in a suggests a ventricular aneurysm. When no
12-lead ECG format, an 80-lead ECG format, previous ECG is available, the presence of a
and on color contour maps. Posterior AMI QS wave in the setting of ST-segment elevation
is the most common AMI detected by body without T-wave inversion is highly suggestive
surface mapping not detected by 12-lead ECG.40 of a left ventricular aneurysm (Figure 6-17).
Body surface mapping is discussed in greater If left ventricular aneurysm is suspected,
detail in Chapter 8, New ECG Technologies for echocardiography should be performed to
Detection of Acute Myocardial Ischemia and rule out the diagnosis prior to administration
Infarction in the Emergency Department. of a thrombolytic. If echocardiography is not
possible and the suspicion is high, the patient
Right Ventricular Infarctions should be referred for a diagnostic angiogram
with possible PPCI where a ventriculogram
Right ventricular infarction is present in can also be performed. Ventricular aneurysms
25% (range, 20%–60%) of patients with inferior can lead to congestive heart failure and
infarction.41 The ECG demonstrates ST-segment ventricular arrhythmias, and a thrombus could
elevation of greatest magnitude in lead III form in an aneurysm and break off, causing
(inferior/right ventricular infarction compared a stroke or other embolic complication.
with leads II and aVF) and ST-segment elevation
in the right chest leads (V1R through V6R); in Right Bundle-Branch Block with
addition, it is important not to miss the subtle Myocardial Infarction
ST-segment elevation in lead V1 (Figure 6-
16). Clinically, the presentation of a patient MI can be diagnosed relatively easily in the
with chest pain, distended jugular veins, and presence of right bundle-branch block (RBBB).
hypotension should prompt an immediate MI affects the initial phase of ventricular
ECG with the addition of right-sided leads, depolarization, producing abnormal Q waves.
as a large right ventricular infarction might When RBBB and an infarct occur together,
cause cardiogenic shock. Patients with inferior a combination of patterns is seen: the QRS
wall STEMI with right ventricular infarction complex is abnormally wide (0.12 sec or more)
have a markedly worse prognosis (both acute as a result of the bundle-branch block, lead
cardiovascular complications and death) than V1 shows a terminal positive deflection, and
do patients with isolated inferior wall STEMI. lead V6 shows a wide S wave (Figure 6-18).

Table 6-10.
Sgarbossa criteria and index score for diagnosis of AMI* in the setting of LBBB42

Criterion Sensitivity and Specificity Points
5
ST-segment elevation of 1 mm or more in the 73% 92% 3
same direction as the QRS complex 2

ST-segment depression of 1 mm or more in lead V1, V2, or V3 25% 96% 79

ST-segment elevation greater than 5 mm opposite 31% 92%
the direction of the QRS complex

*An accurate diagnosis requires a minimum total score of 3.

Electrocardiography in Emergency Medicine

Left Bundle-Branch Block with Myocardial in 26,003 patients; in this study population,
Infarction 131 (0.5%) patients with AMI had LBBB. Table
6-10 lists the three ECG criteria with highest
Currently, no single or combination diagnostic specificity (90%) for diagnosing AMI in this
approach will reliably reveal AMI in a timely setting. Figure 6-19 demonstrates an ECG
fashion in the presence of left bundle-branch with an uncomplicated LBBB as well as an
block (LBBB). The best strategy for detection of evolving AMI in the presence of the LBBB.
AMI encompasses a sound understanding of the
anticipated ST-segment changes resulting from Other groups have applied the Sgarbossa
LBBB, identification of predefined abnormal criteria to patients with chest pain and LBBB in
findings suggestive of ischemia, a comparison the emergency department and found much less
with old ECGs, and an examination of serial promising results—very low sensitivity coupled
ECGs. As a general rule, LBBB typically shows with poor interobserver reliability. Gula et al43
poor R-wave progression in the septal leads. published the results of a community-based
Consequently, in LBBB, the normal septal R cohort study in which the Sgarbossa algorithm
waves are lost, simulating the pattern seen with had been applied, followed by a decision analysis
an anterior wall infarct. LBBB also interrupts regarding thrombolysis made with or without
the late phases of ventricular stimulation and use of the algorithm in an emergency department
therefore produces secondary ST/T changes. between 1994 and 1997. The ECG algorithm
indicated positive findings in only 3% of
During the past 5 decades, several ECG signs presentations and had a sensitivity of 10% (95%
have been proposed to aid in the diagnosis confidence interval, 2%–26%). Despite the low
of infarction, but, because of methodologic prevalence and poor sensitivity of the Sgarbossa
and applicability limitations, none has gained criteria for AMI in the setting of LBBB, the high
widespread acceptance. The best validated specificity of these criteria is reason for acute
criteria are those of Sgarbossa and colleagues,42 care physicians to know and understand them.
who developed and validated a clinical
prediction rule based on 10 ECG criteria tested The ECG diagnosis of MI and myocardial

Key Facts

• STEMI is defined as at least 1 mm of ST-segment elevation in two or more contiguous leads.
• During STEMI, the morphology of the initial portion of the ST segment evolves from a normal

minimally upward concave shape to one that is large and straight (“hyperacute”) and then convex.
• A persistent concave ST morphology is more common in nonischemic pathologic states.
• T-wave pseudo-normalization should not be assumed if the previous ECG showing T-wave inversion

was recorded more than 1 month earlier.
• ST-segment depression is associated with an adverse prognosis in the ACS patient, regardless of

troponin elevation.
• Reciprocal ST-segment depression strongly favors STEMI over other causes of ST-segment

elevation on the ECG (eg, pericarditis, benign early repolarization) and portends a worse prognosis
than for patients with STEMI without reciprocal changes.
• Wellens syndrome is associated with a high risk of anterior MI if medical therapy alone is employed.
Invasive therapy (angioplasty, stent placement, or revascularization) is associated with much better
outcomes.
• Sgarbossa’s criteria for AMI in the setting of LBBB have very high specificity, although poor
sensitivity. Their presence, therefore, warrants aggressive anti-ischemia therapy, but their absence
does not rule out ACS.

80

Acute Coronary Ischemia and Infarction

ischemia in patients with a paced rhythm is 5. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA
challenging. However, the diagnosis of AMI guidelines for the management of patients with ST-elevation
in the setting of a paced rhythm can be made myocardial infarction—executive summary. A report of the
in a limited number of cases. Sgarbossa and American College of Cardiology/American Heart Association
colleagues44,45 recently applied their criteria (see Task Force on Practice Guidelines (Writing Committee to revise
section on diagnosis of AMI in the setting of the 1999 guidelines for the management of patients with acute
LBBB) and reported the value of ST-segment myocardial infarction). J Am Coll Cardiol.
abnormalities in the diagnosis of AMI during 2004;44(3):671-719. (Erratum in J Am
ventricular pacing. ST-segment elevation of Coll Cardiol. 2005;45:1376.)
5 mm or more in predominantly negative QRS
complexes is the best marker, with a sensitivity 6. Smith SW, Withwam W. Acute coronary syndromes.
of 53% and specificity of 88%, and was the Emerg Med Clin North Am. 2006;24:53-89.
only criterion of statistical significance (Figure
6-20). The other criteria were not statistically 7. Lee TH, Goldman L. Evaluation of the patient with acute
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Figures

Figure 6-1.
T waves from ischemia are inverted and symmetric, mostly transient, and present while the patient is
symptomatic. T-wave inversions in V2 through V6 are always considered pathologic.

Figure 6-2.
Evolution of anterior STEMI, lead V2. A: Arrival at emergency department after 30 minutes of chest pain. B: 45
minutes after onset of symptoms, with hyperacute T waves. C: 70 minutes after onset of symptoms, with ST-
segment elevation, referred for emergent PPCI with stent to proximal LAD (symptoms-to-balloon time of 105
minutes). D: 3 hours post procedure, Q is present, suggesting transmural infarct. ST segments have decreased
and T waves have inverted (markers of reperfusion). E: 5 days after PPCI. ST segment is back to baseline. T-
wave inversion is near baseline and eventually might normalize.

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ElEctrocardiography in EmErgEncy mEdicinE

Figures

Figure 6-3.
In the early stages of evolving ischemia, a pattern of injury presents as hyperacute T waves (bulky and wide
T waves). This ECG has peaked T waves in V3 through V6. (Note that the J point is at baseline.) ST-segment
elevations are present in V6, I, and aVL. A bifascicular block and ST-segment depression represent reciprocal
changes in II, III, and aVF.

Figure 6-4.
ST-segment elevation in the anterior leads, as evidenced by J-point elevation in V1 through V3. ST morphology
is straight with elevation greater than 1 mm.

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acutE coronary ischEmia and infarction

Figures

Figure 6-5.
ST-segment elevation in the anterior and lateral leads, as evidenced by a J-point elevation in V1 through V5, I,
and aVL. There is loss of R-wave progression and early Q formation in V1 through V4.

Figure 6-6.
After prolonged, nonreperfused coronary occlusion, as regional ST segments resolve toward the isoelectric
level, T waves invert up to 3 mm in the same region.

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ElEctrocardiography in EmErgEncy mEdicinE

Figures

Figure 6-7.
Primary ST-segment depression not caused by posterior STEMI or reciprocal changes to ST-segment
elevation is a sign of subendocardial ischemia and, in the context of ACS, indicates UA/NSTEMI. ST-segment
depression of even 0.5 mm from baseline is associated with increased mortality, but it is particularly
significant when it is more than 1 mm (0.1 mV) in two or more contiguous leads. This ECG demonstrates
the ST-segment depression best in the inferior leads (I, II and aVF). There is also a lateral component. One
millimeter of ST-segment depression following an R of more than 20 mm is very specific for ischemia; R less
than 10 mm is sensitive but not specific.

Figure 6-8.
The ST-segment depression associated with UA/NSTEMI is transient and dynamic. ST-segment depression
morphology is usually flat or downsloping. This ECG demonstrates the ST-segment depression in the
anteroseptal leads V1 through V4. Posterior leads were normal.

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acutE coronary ischEmia and infarction

Figures

Figure 6-9.
Acute phase of an inferior wall STEMI. Note the reciprocal ST-segment depression in leads V1 through V3, I,
and aVL. Posterior leads (not shown) were normal.

Figure 6-10.
Acute phase of an anterolateral STEMI. As a rule, normal septal Q waves are less than 0.04 sec in duration.
A Q wave is abnormal if its duration is 0.04 sec or more in lead I, all three inferior leads (II, III, aVF), or leads
V3 through V6. In this ECG, Q waves are present in V1 through V3 of 0.08-sec duration as well as ST-segment
elevation. Notice the ST-segment elevation in I and aVL and reciprocal ST/T changes in the inferior leads II, III,
and aVF.

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Electrocardiography in Emergency Medicine

Figures

Figure 6-11.
Wellens syndrome refers to angina with T-wave inversion in the LAD distribution, particularly V2 through V4. In
this case, the patient was symptom free at arrival. Based on the T-wave changes on V2 through V4 and a history
of chest pain, he was taken for an emergent angiogram, which revealed 100% occlusion of the middle LAD
artery.

Figure 6-12.
Myocardial blood supply. The right coronary artery supplies both the inferior (diaphragmatic) portion of the
heart and the right ventricle. The left anterior descending coronary artery generally supplies the ventricular
septum and a large part of the left ventricular free wall. The left circumflex coronary artery supplies the lateral
wall of the left ventricle. This circulation pattern can be variable. Sometimes, for example, the left circumflex
artery also supplies the inferior portion of the left ventricle. Occlusion of the left circumflex or first diagonal
artery (a branch of the left circumflex) can present with minimal or no ST-segment elevation despite a large
myocardial risk area, because the lateral wall is more electrocardiographically silent.34-38

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acutE coronary ischEmia and infarction

Figures

Figure 6-13.
Anterolateral STEMI. Note the loss of R-wave progression, replaced with pathologic Q waves in leads V1
through V4. Early biphasic T-wave inversion suggests that some spontaneous reperfusion has taken place.

Figure 6-14.
Lateral STEMI. Ischemic changes in I and aVL with reciprocal changes in inferior leads II, III, and aVF.

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Figures

Figure 6-15.
Posterior infarction. The tall R waves and ST-segment depressions are reciprocal to the Q waves and ST-
segment elevations that would be recorded at the back of the heart. The positive taller and wider T-wave
changes represent the T-wave inversion that would be recorded in the back of the heart. The R:S wave ratio
is more than 1 in lead V2. These findings are representative of a posterior infarction. This patient also had an
inferior STEMI (leads II, III, aVF).

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