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SUPERVENTRICULAR TACHYCARDIA
105
50 mm/sec), which artifi cially slows the recording of
the cardiac cycle on the paper so that the underlying
cardiac rhythm may be easier to detect.
16
Beyond the standard 12-lead EKG and monitoring,
additional testing may not be necessary, depending
on the clinical presentation of the patient with SVT.
For example, in otherwise healthy patients with prior
episodes of AVNRT following a given trigger and no
other history of cardiac disease, additional laboratory
and radiology testing has a low yield.
Alternatively, if the patient’s history and presentation
suggest another underlying etiology for the SVT, such as
thyroid disease or structural heart disease, further testing
is warranted. Additional testing can include serum elec-
trolytes (particularly potassium levels), thyroid function
tests, digoxin level, chest radiograph, echocardiogram,
and event monitor as indicated. Some of these tests,
such as the echocardiogram and event monitor, can be
obtained as an outpatient after treatment in the ED.
Treatment and disposition
The initial treatment should focus on acute resusci-
tative measures as needed if the patient is in a state
of cardiovascular collapse. If the patient is otherwise
stable, the approach to the patient is to terminate the
SVT as safely and expeditiously as possible, using
either vagal maneuvers, pharmacologic intervention,
or electrical cardioversion. Vagal maneuvers and the
pharmacologic interventions generally increase AV
block, and in doing so, terminate AV node-dependent
SVTs including AVRNT and AVRT. In some cases,
AV node-independent atrial tachycardias may also
respond to these measures as well, either by slowing
of the ventricular response rate or actual termination
of the dysrhythmia itself. Because of the potential for
rapid deterioration into a life-threatening dysrhyth-
mia, resuscitative equipment, including a defi brillator,
should be close at hand.
Vagal maneuvers include carotid massage, Valsalva,
and facial immersion in cold water. These measures
increase vagal tone and prolong the AV nodal refrac-
toriness, leading to AV block and termination of AV
node-dependent SVTs. Carotid massage in the elderly
should be undertaken with caution, and only after aus-
cultation to determine the absence of a carotid bruit.
Pressure is applied at the level of the cricoid cartilage
for approximately fi ve seconds in a fi rm circular move-
ment, and repeated on the other side if needed.
premature atrial beat, and terminates with a P wave,
unlike atrial tachycardias.
The appearance of AVRT on the 12-lead EKG is
dependent on whether conduction is orthodromic or
antidromic. Orthodromic AVRT presents as a narrow
complex tachycardia (unless aberrant or bundle branch
block conduction is present) as ventricular activation
occurs down the normal conduction system. Most
patients have visible retrograde P waves best seen in
V1 and the inferior leads.
13
AVRT is typically a short-
RP tachycardia, but if retrograde conduction is sig-
nifi cantly delayed, the RP interval can be prolonged.
Other electrocardiographic fi ndings more commonly
seen with orthodromic AVRT include QRS alternans
(alternating QRS complex amplitude) and ST-segment
depression more than 2 mm in several leads.
14
Antidromic AVRT, where ventricular activation
occurs through the accessory pathway, results in a
wide complex tachycardia. Retrograde P waves are
frequently seen, often in a 1:1 ventriculoatrial rela-
tionship.
12
The P wave and PR interval are variable,
depending on the retrograde conduction through the
AV node for atrial depolarization.
With AVRT, evidence of the accessory pathway or
ventricular preexcitation may be seen as a shortening of
the PR interval and an initial slurring of the QRS com-
plex upstroke on the baseline 12-lead EKG. These so-
called delta waves have been reported to be present on
EKGs in up to 0.15–0.25% of the general population.
4
Most accessory pathways are capable of bidirectional
conduction (anterograde and retrograde). However, a
small subset only allow retrograde conduction, and are
referred to as “concealed.”
5
These accessory pathways
do not produce preexcitation or delta waves on the
EKG and can only result in orthodromic AVRT. Wolff-
Parkinson-White (WPW) syndrome refers to patients
who have both preexcitation and tachydysrhythmias.
AVRT is the most common dysrhythmia seen in these
patients, accounting for 9% of reentry tachycardias in
patients with accessory pathways.
4
Detecting underlying atrial rhythms can be diffi -
cult on a standard 12-lead EKG in the setting of SVT
because of the rapid ventricular activity. Recording
continuous electrocardiographic activity during peri-
ods of enhanced AV blockade (thus decreasing the
ventricular activity as with vagal maneuvers) can be
important in determining the underlying atrial rhythm.
In addition, diagnosis can be enhanced by doubling
the EKG machine paper speed (from 25 mm/sec to
CHAPTER 7
106
as an event monitor), and the utility of further treat-
ment including pharmacologic prophylaxis or catheter
ablation, can be determined at that time.
Section IV: Decision making
Accurate diagnosis is the major challenge, as other •
potentially life-threatening tachydysrhythmias and
etiologies must be considered and evaluated.
The EKG should be assessed for the regularity •
of the rhythm, QRS width and morphology, and
P-wave activity (Table 7-1).
Treatment options include vagal maneuvers, •
pharmacologic interventions, and electrical
cardioversion.
If these measures are unsuccessful, pharmacologic
intervention should be considered. Adenosine induces
a transient, but intense, AV blockade that is highly
effective in terminating the majority of SVTs. A 6 mg
dose has been shown to terminate 62.3% of cases, and
the larger 12 mg dose, 91.4% of AV node-dependent
SVTs.
17
While the half-life of the medication is quite
short, patients should be warned that the medication
will cause intense, but transient, chest tightness, nau-
sea, and fl ushing sensations. The medication should
also be used cautiously in the setting of asthma or
COPD, as it can cause acute bronchospasm. Adenosine
blocks the action of theophylline, and can be potenti-
ated by dipyridamole.
Other pharmacologic agents that may be useful in
SVT include calcium channel blocking agents (vera-
pamil, diltiazem) and beta-blocking agents (esmolol,
metoprolol). These medications increase AV block,
and can be useful in treating AVNRT and AVRT.
However, these agents should be used cautiously in
the setting of hypotension, history of heart block, or
congestive heart failure because of their potential to
exacerbate the patient’s cardiovascular status.
In addition, these agents should not be used in
the setting of WPW or an accessory pathway, where
blockade of the AV node can actually increase trans-
mission of impulses down the accessory pathway,
leading to potentially lethal ventricular tachydys-
rhythmias or even ventricular fi brillation. Other anti-
dysrhythmic agents that can be used for SVT, and in
particular in the setting of WPW, include procain-
amide, propafenone, or fl ecainide.
5
If these measures
fail, or if the patient deteriorates and becomes hemo-
dynamically unstable, electrical cardioversion should
be performed expeditiously.
If treatment is successful, most patients can be
safely discharged home from the ED. Patients should
be admitted for further evaluation if they are hemo-
dynamically unstable; have evidence of cardiac injury,
ischemia, or compromise such as acute heart failure; or
have another underlying condition requiring inpatient
care. If discharged, most patients can follow up with
their regular provider for further evaluation and test-
ing. Conditions warranting referral to an electrophysi-
ologist include wide complex tachycardias or evidence
of a preexcitation syndrome, signifi cant presenting
symptoms such as syncope, or recurrent episodes
that are having a signifi cant detrimental effect on the
patient’s life. Subsequent need for further testing (such
Table 7-1. Differential diagnosis for tachydysrhythmia.
Regular
Rate
Narrow
QRS
Complex
Sinus Tachycardia
Sinus Node Reentry Tachycardia
Atrial Tachycardia
Atrial Flutter
AVNRT
AVRT—orthodromic
Focal Junctional Tachycardia
Nonparoxysmal Junctional
Tachycardia
Wide
QRS
Complex
Regular tachycardias with aber-
rancy or BBB or preexcitation
Paced Tachycardia
AVRT—antidromic
Ventricular Flutter
Ventricular Tachycardia
Hyperkalemia
Drug Toxicity (tricyclics, cocaine)
Irregular
Rate
Narrow
QRS
Complex
Atrial Fibrillation
Atrial Flutter with variable block
Atrial Tachycardias with variable
block
Tachycardia with PACs, PVCs, PJCs
Digitalis toxicity
Multifocal Atrial Tachycardia
Wide
QRS
Complex
Irregular tachycardias with aber-
rancy or BBB or preexcitation
Polymorphic VT (torsades de
pointes)
SUPERVENTRICULAR TACHYCARDIA
107
Delacretaz E. Supraventricular tachycardia. 5 New Engl J
Med. 2006;354:1039–1051.
Brembilla-Perrot B, Marcon F, Bosser G, et al. 6
Paroxysmal tachycardia in children and teenagers with
normal sinus rhythm and without heart disease. Pacing
Clin Electrophysiol. 2001;24:41–45.
Tikkanen I, Metsarinne K, Fyhrquist F. Atrial natriuretic 7
peptide in paroxysmal supraventricular tachycardia.
Lancet. 1985;2:40–41.
Leitch J, Klein G, Tee R, Murdock C, Teo WS. Neurally 8
mediated syncope and atrial fi brillation (letter). N Engl J
Med. 1991;324:495–496.
Gursoy S, Steuer G, Brugada J, Andreis E, Brugada P. 9
The hemodyamic mechanism of pounding in the neck in
atrioventricular nodal reentrant tachycardia. N Engl J
Med. 1992;327:772–774.
Kazzi AA, Wong H: Other supraventricular tachy-10
dysrhythmias. In: Chan TC, Brady WJ, Harrigan RA,
Ornato JP, Rosen P, eds. ECG in Emergency Medicine
and Acute Care. Philadelphia: Elsevier; 2005.
Kalbfl eisch SJ, el-Atassi R, Calkins H, Langberg JJ, 11
Morady F. Differentiation of paroxysmal narrow QRS
complex tachycardias using the 12-lead electrocardio-
gram. J Am Coll Cardiol. 1993;21:85–89.
Kumar UN, Rao RK, Scheinman MM. The 12-lead elec-12
trocardiogram in supraventricular tachycardia. Cardiol
Clin. 2006;24:427–437.
Chen SA, Tai CT, Chiang CE, et al. Electrophysiologic 13
characteristics, electropharmacologic responses and
radiofrequency ablation in patients with decremen-
tal accessory pathway. J Am Coll Cardiol. 1996;28:
723–727.
Jaeggi ET, Gilljam T, Bauersfeld U, et al. 14
Electrocardiographic differentiation of typical atrio-
ventricular node reentrant tachycardia from atrio-
ventricular reciprocating tachycardia mediated by
concealed accessory pathway in children. Am J Cardiol.
2003;91:1084–1090.
Zhong YM, Guo JH, Hou AJ, et al. A modifi ed elec-15
trocardiographic algorithm for differentiating typi-
cal and atrioventricular node re-entrant tachycardia
from atrioventricular reciprocating tachycardia medi-
ated by concealed accessory pathway. Int J Clin Pract.
2006;11:1371–1377.
Accardi AJ, Holmes JF. Enhanced diagnosis of narrow 16
complex tachycardias with increased electrocardiograph
speed. J Emerg Med. 2002;22:123–127.
DiMarco JP, Miles W, Akhtar M, et al. Adenosine for 17
paroxysmal supraventricular tachycardia: dose rang-
ing and comparison with verapamil: assessment in
placebo-controlled, multicenter trials. Ann Intern Med.
1990;113:104–110.
Avoid drugs like digoxin that increase conduction •
via the accessory pathway, given the risk of
precipitating very rapid ventricular rates or
ventricular fi brillation (Table 7-2).
Most patients treated in the ED for SVT can be •
discharged to home safely, assuming hemodynamic
stability and no co-morbid conditions.
References
Lim SH, Anantharaman V, Teo WS, Goh PP, Tan ATH. 1
Comparison of treatment of supraventricular tachycar-
dia by valsalva maneuver and carotid sinus massage.
Ann Emerg Med. 1998;31:30–35.
Fox DJ, Tschenko A, Krahn D, et al. Supraventricular 2
tachycardia: diagnosis and management. Mayo Clin
Proc. 2008;83:1400–1411.
Orejarena LA, Vidaillet H Jr, DeStefano F, et al. 3
Paroxysmal supraventricular tachycardia in the general
population. J Am Coll Cardiol. 1998;31:150–157.
Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, 4
et al. ACC/AHA/ESC guidelines for the management of
patients with supraventricular arrhythmias—executive
summary. J Amer Coll Cardiol. 2003;42:1493–1531.
Table 7-2. Emergency department interventions for
patients in svt.
Vagal Maneuvers Valsalva
Carotid Sinus Massage
Facial Ice Water Immersion
Pharmacologic
Interventions
Adenosine
Calcium Channel Blocking Agents
– Diltiazem
– Verapamil
Beta-Blocking Agents
– Metoprolol
– Propranolol
– Esmolol
Pharmacologic
Interventions
in setting of:
Procainamide
Flecainide
Propafenone
Ibutilide
– Refractory SVT
– Atrial Fibrillation
with Preexcitation
Electrical
Cardioversion
108
Cardiovascular Problems in Emergency Medicine: A discussion-based review, First Edition.
Edited by Shamai A. Grossman and Peter Rosen.
© 2011 John Wiley & Sons, Ltd. Published 2011 by John Wiley & Sons, Ltd.
The differential diagnosis of wide
complex tachycardia—ED diagnostic
and management considerations
Nathan Charlton
1
& William J. Brady
2
1
Assistant Professor of Emergency Medicine, Department of Emergency Medicine,
Consultant in Toxicology, Division of Medical Toxicology, Department of Emergency
Medicine, Medical Director, Blueridge Poison Center, University of Virginia Health System,
Charlottesville, VA, USA
2
Vice Chair, Department of Emergency Medicine, Professor of Emergency Medicine and
Medicine, University of Virginia Health System, Charlottesville, VA, USA
8
Section I: Case presentation
A 54-year-old woman drove to the emergency depart-
ment (ED) with complaints of palpitations and weak-
ness. The patient noted the onset of these symptoms
approximately 1 hour prior. She also complained of
mild dyspnea. Her medical history was signifi cant for
a myocardial infarction with stent placement, conges-
tive heart failure, diabetes mellitus, and hypertension.
On examination, the emergency physician found an
alert, mildly distressed woman appearing her stated
age. The vitals signs were: blood pressure 115/
70 mmHg, pulse 180 beats/min, respirations 24 breaths/
min, and oxygen saturation of 95% on room air. The
cardiac examination revealed a rapid regular rate
without murmur or gallop; the lungs were clear to
auscultation with appropriate aeration. The cardiac
monitor demonstrated a wide complex tachycardia
(WCT), rapid and regular (Figure 8-1); the 12-lead
EKG showed similar fi ndings (Figure 8-2).
Based upon the patient’s age, medical history, and
electrocardiographic fi ndings with a WCT, the emer-
gency physician felt that the rhythm was likely ven-
tricular tachycardia (VT). The patient remained
hemodynamically stable, but with persistence of the
WCT. Intravenous amiodarone (150 mg) was given
over approximately 15 minutes, and then repeated.
No response was noted after the second dose of amio-
darone. Intravenous procainamide was prepared, but,
unfortunately, the patient’s respiratory status worsened
and the blood pressure dropped to 80 mmHg systolic.
Given continued tachycardia recalcitrant to medical
therapy and a worsening hemodynamic status, the
patient was electrically cardioverted with a return to
a sinus rhythm.
Section II: Case discussion
Dr Peter Rosen: I think the most interesting question
in the management of an acute tachycardia is, “What
do you do fi rst?” Is it necessary to get a 12-lead EKG?
How do you decide whether you are going to treat
the patient chemically versus giving a counter-shock?
What sedation, if any, would you use if you thought
the patient needed immediate counter-shock? How
much time would you be willing to spend trying to
sort out the kind of tachycardia your patient has prior
to initiating therapy?
Dr Amal Mattu: I would begin by looking for signs of
hemodynamic instability. If the patient is in an unsta-
ble tachycardia, then I would consider rapid electrical
cardioversion. Hemodynamic instability in the pres-
ence of a tachycardia can by defi ned by four param-
eters: the presence of hypotension, the presence of a
decreased level of consciousness, the presence of acute
congestive heart failure, and the presence of ischemic
chest pain. Any one of these four parameters would
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
109
ventricular or supraventricular. Of course, the treating
physician is the most appropriate person to determine
the initial therapeutic strategy.
Dr Shamai Grossman: I would do a 12-lead EKG sim-
ply to verify that this is a wide complex rhythm, and
that you are not dealing with something artifactual,
which is more common than we like to think. This
would be particularly appropriate in the hemodynami-
cally stable patient.
PR: What about sedation in this patient?
AM: If the patient can tolerate waiting several minutes
for sedation, then ideally I would like to administer
etomidate, propofol, or ketamine. If those agents are
potentially defi ne an unstable tachycardia. If a patient
has an unstable tachycardia, then that patient would
likely need electrical cardioversion. A possible excep-
tion would be if the patient has minimal symptoms or
instability, and the wide complex rhythm is most likely
a supraventricular tachycardia; then, in that case, I
might try adenosine fi rst if it’s readily available.
Regardless of whether I have a 12-lead EKG or not,
I can make a decision to cardiovert simply by observ-
ing the monitor. The two primary exceptions that I
would make are the two tachycardias that one does
not cardiovert: sinus tachycardia (ST) and multifo-
cal atrial tachycardia (MAT). Any other tachycardia,
narrow or wide, in an unstable patient ought to be
cardioverted without worrying about whether it is
Figure 8.1 Wide complex tachycardia in lead II.
Figure 8.2 Wide complex tachycardia. The rate is approximately 170 bpm with a regular rhythm. Evidence of
atrioventricular dissociation is seen in multiple leads.
CHAPTER 8
110
than amiodarone? For example, would you give her
procainamide on the grounds that perhaps she had a
Wolf-Parkinson-White (WPW) Syndrome?
AM: Assuming that the patient is hemodynamically
stable with a wide complex tachycardia, I would look
at the rhythm strip fi rst and then a full 12-lead EKG.
Of primary importance to me is whether the rhythm
is regular or irregularly irregular. If it is a wide regular
tachycardia, then I would feel comfortable using ami-
dodarone or procainamide. If it is irregularly irregular,
than there are really only two things in the differen-
tial: atrial fi brillation with a bundle branch block or
atrial fi brillation with WPW. To tell the difference
between these two, you must look at the morphology
of the QRS complex. If the QRS morphology remains
the same beat-to-beat, then the rhythm is likely atrial
fi brillation with a bundle branch block, and you can
use any agent you want. If the QRS complex has
changing morphologies in a beat-to-beat, then that
suggests atrial fi brillation with WPW. In caring for
this patient, one should avoid using amiodarone.
Instead, this patient should be treated chemically with
procainamide or cardioverted electrically.
Procainamide is an excellent choice because it is
appropriate for ventricular tachycardia, atrial fi bril-
lation with a bundle branch block, and atrial fi bril-
lation with WPW. Although procainamide seems to
have fallen out of favor, it is an excellent medication
to consider in the stable wide complex tachycardia
patient. Regarding other treatments, such as magne-
sium, I do not think empiric magnesium is very helpful
unless the patient has torsades de pointes, or has some
type of underlying condition that makes one consider
hypomagnesemia.
PR: It seems to me that every time I try to give pro-
cainamide, the blood pressure immediately falls. Is
that because I run it too fast, or is that just one of the
consequences of using that drug?
WB: Procainamide is a very effective medication. It
has the ability to treat dysrhythmias that are supraven-
tricular or ventricular in origin. The major drawback
to procainamide is it cannot be used rapidly because
patients will develop hypotension, and in certain cases
can develop worsening intraventricular conduction,
such as further widening of the QRS complex.
There are two different methods of procainamide
administration that depend on the acuity of the
not readily available, then I would consider a small
dose of midazolam. If the patient is markedly unsta-
ble, then I would not wait for the sedation, but rather
would proceed directly to electrical cardioversion.
PR: Does the patient’s age make any difference in this
particular protocol? In other words, if you had a very
young patient, for example, less than a year old, or an
elderly patient, in his late eighties, would that make
you move toward cardioversion more quickly?
Dr William Brady: One really must look at the entire
patient. The patient’s age is another piece of data that
must be included along with the other clinical fi nd-
ings, including the patient’s complaints, the focused
examination, and the electrocardiogram. However, I
would not look at age as the primary determinant to
drive the decision to electrically cardiovert instead of
utilizing medical therapy. Certainly, an older person
may be less physiologically able to withstand a dys-
rhythmia for a long period of time. But, if the patient
did present in a stable fashion, and was tolerating
the dysrhythmia, I would likely proceed with chemi-
cal therapy. Nevertheless, I would be watching that
elderly patient even more closely than our patient
today, the 54 year old.
PR: Do you think that it’s necessary to raise the
patient’s blood pressure before you attempt to convert
chemically or electrically? We know that in paroxysmal
atrial tachycardia (PAT), sometimes just a mild raise
in blood pressure can cause a conversion. I have seen
patients with PAT converted by placing cardioversion
pads on them, and getting a 20 mmHg rise without
any other therapy whatsoever. Does that play any role
in the management of this type of tachycardia, where
you have not bothered to distinguish whether it is a
ventricular or a supraventricular tachycardia?
SG: No, I would generally not make any effort to
raise the blood pressure if the patient is truly hemo-
dynamically unstable. The dysrhythmia is more likely
the cause of the hemodynamic instability. I think that
the focus has to be on managing the dysrhythmia.
Focusing on dysrhythmia management should then
increase the blood pressure.
PR: If you had a history that this patient had prior
episodes of tachycardia, and that she said she had a
congenital condition but cannot remember what it
was, would you be inclined to start with a drug other
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
111
physical examination of the neck in terms of distin-
guishing the type of tachycardia? The second question
is: given the reality that this women almost certainly
has an ischemic coronary syndrome, would you place
her on antiplatelet therapy?
SG: To answer your fi rst question, I think that starting
to look at the neck when you have a patient who is
potentially unstable with a wide complex tachycardia
would be moving in the wrong direction. Here, I think
the focus needs to be on the wide complex tachycar-
dia, and not to be led astray by the question: “Is this
an SVT with aberrancy?” This rhythm needs to be
considered a ventricular dysrhythmia alone. I think
that especially in the extreme conditions of the ED, it
is an error to spend prolonged periods of time looking
at the physical examination or other adjuncts, with the
hope of diagnosing the rhythm disturbance, when you
have a potentially unstable patient in front of you.
As far as starting antiplatelet therapy, I think that
this depends on the patient’s history, and age. The case
we are discussing today is someone with known coro-
nary disease who comes in with symptoms that are
suggestive of ischemia. This patient most likely has a
ventricular tachycardia secondary to either myocar-
dial excitability from an acute ischemic process, or
from scarring from the previous infarction. So start-
ing this patient on antiplatelet therapy, especially if
she were not already on it, is clearly appropriate given
the likelihood that she is actually having an acute
ischemic event. If the patient is young with no history
of coronary artery disease, or clearly has another eti-
ology for the dysrhythmia, then, starting antiplatelet
therapy without a more thorough investigation is not
a good idea.
PR: If an EMS unit is en route to your ED with a wide
complex tachycardia patient, when would you ask
them to perform electrical cardioversion?
WB: I would use the same markers of stability in
and out of the hospital. If the patient is unstable or
the ETA to the ED is excessive, I would consider a
sedative-assisted electrical cardioversion prior to ED
arrival. It must be stressed, however, that each case
is individual and the management decisions are best
made by the treating clinicians.
PR: In summary, I like to remember that an important
management decision in any acute tachycardia focuses
on the stability of the patient. Further, the urge to
patient and the acuity and volume of rest of your ED.
Assuming the patient is stable, if you have the luxury
of having a quiet ED and a fair amount of staff to
help, you can infuse the drug at a load of 17 mg/kg
over about 45 minutes while carefully monitoring
the blood pressure and the clinical situation. If the
patient is more ill or you must administer the medica-
tion more rapidly, one can follow a different protocol
by giving the drug in 100–200 mg increments over
approximately 2–3 minutes, and repeating that every
5–10 minutes up to a total loading dose. Utilizing this
protocol, a full load can be infused much more rap-
idly. Nevertheless, with both administration strate-
gies, you can develop hypotension. In this case, it may
be diffi cult to determine if the hypotension is related
to the tachycardia, or related to your intervention.
I would err on the side of caution; if the patient devel-
ops hypotension, I would likely call that tachycardia
unstable, and consider electrical therapy.
PR: If the patient gave you a history of being on
digitalis but came in unstable, would that make you
reluctant to use cardioversion?
SG: I think that if that patient is unstable, the ther-
apy of choice, regardless of the patient’s past medi-
cal or medication history, needs to be electrical
cardioversion.
PR: Once the patient is stabilized from a rhythm stand-
point, laboratory testing can be pursued. If the fi rst
troponin should be slightly elevated, or if the second
troponin is slightly elevated, would you then deem it
necessary to arrange for immediate angiography on
this patient?
WB: The abnormal troponin value must be interpreted
within the context of the clinical situation. Thus, if
the patient’s presentation suggests an acute coronary
syndome (ACS) event, then I would pursue therapy
as appropriate for ACS, considering the postconver-
sion 12-lead EKG—such, of course, was the case with
our presentation in this chapter. If the situation does
not suggest ACS, however, then I would likely moni-
tor the patient’s situation closely with repeat troponin
testing. It must be remembered that a dysrhythmia
with or without stability can cause an elevation of the
serum troponin.
PR: Two questions: fi rst, going back to the original
assessment of this patient, is there any help in the
CHAPTER 8
112
that in a situation like this, we always have to keep
in mind the rest of what is going on in the ED. If you
have a patient who is borderline stable, but have an
ED that is very chaotic, then you have another very
legitimate reason to move forward, give the patient a
sedative agent, and perform electrical cardioversion.
Case resolution
The patient was admitted to the hospital without fur-
ther WCT. Serial cardiac biomarkers were elevated
with a typical rise-and-fall pattern characteristic of an
acute myocardial infarction. Cardiac catheterization
revealed occlusion of the right coronary artery; this
occlusion was stented. The patient was discharged
on hospital day three with non-ST-segment eleva-
tion myocardial infarction complicated by ventricular
tachycardia.
Section III: Concepts
The patient with a wide complex tachycardia (WCT)
can present both a diagnostic and a therapeutic chal-
lenge to the emergency physician (EP). WCT results
from a number of etiologies and produces a variety of
patient presentations. The term wide complex tachy-
cardia describes the rhythm scenario characterized
by a broad, or widened, QRS complex (greater than
0.12 seconds) and a ventricular rate over 120 beats
per minute in the adult patient (Figures 8-1 and 8-2).
In children, heart rates and QRS complex widths vary
with age. Consequently, children may present with
WCT, including ventricular tachycardia, with a QRS
duration of less than 120 ms; age-related values of
the QRS complex duration and ventricular rate defi ne
WCT in younger children (Figure 8-3).
1
The electrocardiographic differential diagnosis
of WCT classically includes VT and supraventricu-
lar tachycardia (SVT) with aberrant intraventricu-
lar conduction (Table 8-1 and Figures 8-4 and 8-5).
Electrocardiographically, VT can be described as
either monomorphic (one primary QRS complex type)
or polymorphic (greater than one QRS complex type)
ventricular tachycardia (Figure 8-4). Supraventricular
tachycardia with aberrant conduction includes any
supraventricular tachycardia (sinus tachycardia, atrial
fi brillation, atrial fl utter, or paroxysmal supraventricu-
lar tachycardia) occurring with abnormal conduction
over-interpret EKGs must be avoided—recall that the
ultimate rhythm diagnosis may not be possible even
with the performance and review of a 12-lead EKG.
In most instances, it does not matter if the dysrhyth-
mia is ventricular or supraventricular in origin if the
patient is unstable: electrical cardioversion is required
for both kinds of unstable tachycardia.
WB: I must reiterate the last point, do not focus
entirely on the EKG, but interpret it within the con-
text of the clinical presentation. Do not consider the
situation a diagnostic failure if you are unable to con-
fi rm the rhythm diagnosis in the initial presentation.
To review, many people fi nd themselves in the situ-
ation where they feel they must determine the cause
of the tachycardia before they can treat it. In this case
you have a patient who comes in who does have a
wide complex tachycardia. She has several historical
features, including her age and her cardiovascular his-
tory, which suggest that VT is the likely origin. Certain
electrocardiographic features can suggest VT, yet they
are uncommon; these are discussed within the chapter.
Regardless of the specifi cs of the presentation, what
one must initially determine is the need for emergent
electrical cardioversion.
The clinician must also consider the other forms of
wide complex tachycardia in this differential, includ-
ing sinus tachycardia with a bundle branch block,
sodium channel blocker poisoning as seen with a tricy-
clic antidepressant drug overdose, or the unusual case
of a hyperkalemia with a very rapid, wide complex
rhythm. These scenarios would be rhythm presenta-
tions that you would not want to treat electrically.
The clinician should be able to sort out these rhythms
based on historical clues, with the exception of the
sinus tachycardia with a bundle branch block, and
this occurrence is quite rare.
When you are left with an SVT with aberrant con-
duction versus VT, the key is to treat the patient. If
the patient presents in an unstable fashion, electrical
cardioversion is the therapy of choice. If the patient is
stable, observe closely while therapy is initiated. If you
are not worried about a Wolf-Parkinson-White-type
rhythm disturbance, then amiodarone is a reasonable
choice. If you have concern about WPW, then procain-
amide is a great choice. Realize that the patient can
become unstable at any time, if your medications do
not work, and that you may need to move rapidly and
use electrical therapy to address the problem. I think
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
113
within the ventricle (Figure 8-5). This abnormal intra-
ventricular impulse transmission can occur via bundle
branch block (fi xed and rate-related), ventricular pre-
excitation, and toxic-metabolic adverse effect on the
conduction system.
Numerous strategies aimed at assisting the clini-
cian with the proper diagnosis of WCT have been
proposed, emphasizing various data including patient
age, medical history, and the electrocardiogram.
2–9
Other factors, such as the physical examination or
Table 8-1. Electrocardiographic rhythm diagnoses in wide QRS complex tachycardia.
Ventricular Tachycardia
Supraventricular Tachycardia with Aberrant
Intraventricular Conduction
Monomorphic ventricular tachycardia
Polymorphic ventricular tachycardia
Torsade de pointes*
Sinus tachycardia**
Atrial fi brillation**
Atrial fl utter**
Paroxysmal supraventricular tachycardia**
Multifocal atrial tachycardia**
Atrial tachycardias**
WPW-related atrial fi brillation/atrial fl utter
WPW-related AV reentry (antidromic) tachycardia
Hyperkalemia-related tachycardia
Sodium-channel blockade toxicity-related tachycardia
* Note that torsade de pointes is a subtype of polymorphic ventricular tachycardia associated with abnormal
ventricular repolarization (prolonged QT interval).
** Occurring with associated bundle branch block.
Figure 8.3 Ventricular tachycardia in the pediatric patient (four-month-old male). The QRS complex duration is 0.10 msec
and the ventricular rate is 225 bpm.
CHAPTER 8
114
Figure 8.4 (a) Monomorphic ventricular tachycardia.
(b) Monomorphic ventricular tachycardia. (c) Monomorphic
ventricular tachycardia. (d) Polymorphic ventricular
tachycardia. (e) Polymorphic ventricular tachycardia.
(f) Polymorphic ventricular tachycardia (torsade de pointes).