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THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
115
Clinical presentation
Historical features
Features of the past medical history that can help iden-
tify VT as the etiology of a WCT include older patient
age (over age 35 years), history of myocardial infarc-
tion or congestive heart failure, and recent angina.
Even though older age is associated with VT, geriatric
patients can still frequently present with sinus tachy-
cardia or atrial fi brillation with bundle branch block
as the cause of WCT. Thus, increasing patient age,
while associated with VT, cannot be relied upon as a
primary diagnostic feature.
Medical history of abnormal left ventricular func-
tion, such as from a past myocardial infarction or
congestive heart failure, is of signifi cant value and can
support a diagnosis of VT; as with age, however, these
features do not “guarantee” VT and their absence
does not support SVT with aberration.
Past dysrhythmia with prior EKG, if available, is
a critical piece of history. Other potentially impor-
tant history that can guide the diagnostic evalua-
tion includes automatic internal defi brillator, renal
insuffi ciency (hyperkalemia), the use of cardioactive
medications, or overdose. A history of coronary revas-
cularization (either coronary artery bypass grafting or
interventional coronary procedure), is not helpful in
the diagnosis of WCT unless there has been associated
infarction or scarring of the myocardium that would
make VT a more likely diagnosis. Gender and valvu-
lar or congenital heart disease are also not helpful in
distinguishing SVT from VT.
3
Physical examination
The physical examination does not provide useful
information in the distinction of SVT from VT. The
physical examination, however, is of considerable
importance in the identifi cation of hemodynamic sta-
bility, which will then guide therapy. The presence of
systemic hypoperfusion, ischemic chest discomfort,
response to therapeutic maneuvers, are of little value
in this diagnostic determination.
If one considers all patients encountered with WCT
from the perspective of the cardiologist, approximately
80% will be diagnosed with VT; this preponderance
of VT, however, probably refl ects the bias of diffi cult
cases referred to electrophysiology centers.
2,4,10,11
The
emergency physician, however, likely encounters a
much broader range of causes of the WCT presenta-
tion: VT as well as numerous other causes of the WCT.
A review of WCT encountered in the ED demonstrates
the exact opposite distribution of rhythm etiologies:
80% supraventricular tachycardia with aberrant con-
duction and 20% ventricular tachycardia; sinus tachy-
cardia and atrial fi brillation, both with bundle branch
block morphology, are the most frequent forms of
WCT seen in the greater ED population.
12
Many clinical decision rules have been suggested as
guides to the determination of the cause of the wide
complex tachycardia.
6,9,10,13
Certain aspects of these
guides and decision tools can be valuable; however,
some of the rules have used aberrantly conducted
SVT as the default diagnosis. Such an approach
is potentially problematic, as it defaults to the less
severe diagnosis of SVT. Utilizing therapies aimed at
SVT when VT is occurring can result in cardiovascu-
lar collapse and death.
13,14
Also, these decision rules
are somewhat cumbersome to apply, and are associ-
ated with poor rates of interobserver reliability (dem-
onstrated in that different physicians use the same
decision tool in different fashion).
If VT is the likely diagnosis based upon an analysis
of the presentation (history and electrocardiogram),
then therapy can be tailored to this entity. In other
cases, if the rhythm distinction is not possible, whether
because of an unclear medical history or an unreveal-
ing EKG, the approach in the ED should focus on the
patient, not just the electrocardiogram. In many cases,
discovering the specifi c etiology of the WCT may not
be possible in the ED.
Figure 8.5 (a) Sinus tachycardia with bundle branch block.
(b) Sinus tachycardia with a giant R wave of an early
ST-segment elevation myocardial infarction. (c) Atrial
fi brillation with a bundle branch block. (d) Atrial fi brillation
with a bundle branch block. (e) Paroxysmal supraventricular
tachycardia with a rate-related bundle branch block.
(f) Paroxysmal supraventricular tachycardia with a
preexisting bundle branch block. (g) Wolff-Parkinson-
White syndrome-related wide QRS complex (antidromic)
tachycardia. (h) Wolff-Parkinson-White syndrome-related
atrial fi brillation. (i) Sodium channel toxicity with a wide
QRS complex sinus tachycardia. (j) A wide complex
tachycardia related to hyperkalemia.
CHAPTER 8
116
at such rapid heart rates; the use of an electrocardio-
graphic caliper or other measuring methods is useful
in these situations.
Atrial fi brillation with a bundle branch block
commonly presents in the ED with tachycardia and
marked irregularity of the ventricular response.
12
In
situations with normal atrioventricular conduction
(i.e., no ventricular preexcitation), each QRS complex
is similar in morphology to its neighbors. In WPW-
related atrial fi brillation, the rate is extremely rapid
with some degree of beat-to-beat variation in QRS
complex morphology; furthermore, delta waves can
be seen. With polymorphic ventricular tachycardia,
there is both irregularity and differences in QRS com-
plex morphology. In this situation, the degree of beat-
to-beat variation is usually very prominent, more so
than seen in WPW with atrial fi brillation.
Once the rate and regularity have been reviewed,
certain features of the QRS complex may be of value.
Combinations of the QRS complex width and axis are
reportedly of signifi cant import, but yet, when evalu-
ated real-time in the ED, do not demonstrate signifi -
cant utility; these features are cumbersome to apply
and thus of lower diagnostic yield.
7,9,17
One feature of
the QRS complex, however, which is both valuable
and straightforward is QRS complex concordance.
Concordance is defi ned as the conformity of the QRS
complexes in an all-positive or an all-negative direc-
tion across the precordial leads (from leads V1-V6).
Positive (Figure 8-6) and negative (Figure 8-7) con-
cordance of the QRS complexes in the precordial
leads has been shown to usually be VT.
18,19
Three other features of the EKG, though rare, are
of value as their presence supports a VT diagnosis:
atrioventricular dissociation, fusion beats, and cap-
ture beats. Multiple studies have reported that the
presence of AV dissociation approaches 100% speci-
fi city for VT.
9,17
AV dissociation is identifi ed by the
presence of P waves distinct from the QRS complex,
but not in direct relationship to each QRS complex
(Figure 8-8). AV dissociation is reportedly uncom-
mon, occurring in only 10% of presentations; yet, it
is likely present more frequently if the EKG (rhythm
monitoring and 12-lead electrocardiogram) is scruti-
nized closely. Aktar et al. note that the presence of AV
dissociation on EKG correctly diagnoses VT in all of
their study patients in whom these features were pres-
ent on EKG.
4
Vereckei et al. also note that the pres-
ence of AV dissociation correctly diagnoses VT in all
pulmonary edema, or extremely rapid ventricular
response are potential indicators of hemodynamic
instability, and should be utilized in determining the
most appropriate treatment course at the bedside.
Physicians often associate hemodynamic instability
with VT and stability with SVT with aberrant conduc-
tion. However this association is incorrect. Patients
can present with WCT, ultimately be diagnosed with
VT, and tolerate the dysrhythmia clinically while con-
versely, SVT can cause marked hemodynamic instabil-
ity, requiring emergent electrical cardioversion.
11
One
study of patients presenting with VT fi nds that patients
are hemodynamically stable 77% of the time.
15
Electrocardiographic features
The EKG, whether as a single-lead rhythm analysis or
a complete 12-lead electrocardiogram, plays a pivotal
role in the evaluation of the patient with WCT; yet, it
still may not reveal the specifi c rhythm diagnosis. In
the patient in extremis, single-lead analysis is usually
adequate, but if possible, a 12-lead EKG may further
assist in this evaluation. In the stable patient, both
rhythm monitoring and 12-lead electrocardiography
is recommended. Prior EKG studies, if available in
timely fashion, can be very helpful.
Inspection of the EKG should begin with evalua-
tion of rate, regularity, evidence of AV dissociation,
and QRS complex morphology.
16
However, the utility
of ventricular rate in differentiating among the many
causes of WCT is unclear. In one such study, heart
rate in ventricular tachycardia is most often between
130–170 beats per minute, while patients with SVT
are more likely to have heart rates between 170–200
beats per minute.
7
This study also fi nds, however, that
both groups of patients have individuals with rates
above 200 beats per minute.
7
Therefore, in clinical
practice, both VT and SVT can result in a broad range
of heart rates; this signifi cant overlap of heart rates
and variability of various dysrhythmias’ rates mark-
edly reduces the value of this fi nding.
Signifi cant irregularity of the ventricular response
can suggest several different rhythm diagnoses: atrial
fi brillation with bundle branch block, WPW-related
atrial fi brillation, and polymorphic ventricular tachy-
cardia (Figures 8-4d–f, 8-5c, 8-5d, and 8-5h). Other
dysrhythmias to be considered are regular in terms of
the ventricular response. Determining the presence of
irregularity at extremely rapid heart rates is diffi cult,
as the “naked” eye often does not discern irregularity
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
117
Figure 8.6 Ventricular tachycardia with positive QRS
complex concordancy.
Figure 8.7 Ventricular tachycardia with negative QRS
complex concordancy.
Figure 8.8 A. Ventricular tachycardia
with atrioventricular dissociation
(note obviously dissociated P waves
[arrows]). B. Insert from the EKG
rhythm in “A” with irregularities
of the QRS complex (arrows)
likely representing “less obvious”
atrioventricular dissociation.
CHAPTER 8
118
of ventricular origin. The resulting QRS complex
is a fusion of the ventricular and supraventricular
beats; it is “more narrow” with a different mor-
phology than the underlying WCT tachycardia.
18
Capture beats (Figure 8-10) result from a complete-
ly-conducted supraventricular depolarization that
passes through the His-Purkinje system, electrically
activating the ventricular myocardium.
16,18
A cap-
ture beat has the morphology of the native narrow
sinus rhythm.
35 patients in whom the EKG fi ndings were present.
17
Brugada et al. include the presence of AV dissociation
in their criteria, although these same studies also con-
fi rm the rare occurrence of the fi ndings on EKG even
in the presence of a known VT.
9
Fusion and capture beats, also rare in the WCT
patient, strongly support a VT diagnosis. A fusion
beat (Figure 8-9) results from simultaneous ventricu-
lar activation from a normally-conducted supraven-
tricular beat through the AV node, along with beat
Figure 8.9 Ventricular tachycardia with fusion beats (arrows).
Figure 8.10 Ventricular tachycardia with capture beats (arrows).
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
119
At this point, the P wave further lessens in ampli-
tude, ultimately disappearing with continued serum
potassium elevation; the sine wave with loss of the P
wave characterizes the “sinoventricular” rhythm of
hyperkalemia.
Purposeful and accidental overdose of numerous
medications can affect the EKG. Sodium channel
blocking agents such as tricyclic antidepressants can
cause sinus tachycardia, widening of the QRS com-
plex, and an extreme right axis deviation of the ter-
minal QRS complex with a deep S wave in lead I and
prominent R` wave in lead aVr (Figure 8-12).
The Wolff-Parkinson-White (WPW) syndrome can
cause several different wide complex tachycardias,
Beyond the traditional electrocardiographic fi nd-
ings noted above, a variety of diseases can lead to
unique rhythm presentations. Patients in renal fail-
ure often develop hyperkalemia. Elevated serum
potassium can cause several different electrocar-
diographic abnormalities, including prominent T
waves, QRS complex widening, and a sinoventricu-
lar rhythm. Prominent T waves are considered the
fi rst signifi cant electrocardiographic manifestation
of hyperkalemia. At progressively higher serum lev-
els, the QRS complex widens (Figure 8-11), at times
resembling a bundle branch block; eventually, the
QRS complex blends with the T wave, forming a
“sine-wave,” or sinusoidal, structure on the EKG.
Figure 8.11 A widened QRS complex in a patient with hyperkalemia.
Figure 8.12 A 12-lead EKG in tricyclic antidepressant
ingestion, demonstrating a sinus tachycardia, a widened
QRS complex, and a rightward axis deviation of the
terminal portion of the QRS complex (deep S wave in lead I
and prominent R wave in lead aVr).
CHAPTER 8
120
metabolic or drug-induced cause of dysrhythmia should
be considered.
Even in hemodynamically stable patients with undif-
ferentiated WCT, the rhythm should be considered
VT until proven otherwise, unless sinus tachycardia
with bundle branch block pattern, sodium channel
blockade-related tachycardia, or hyperkalemia-asso-
ciated tachycardia is likely. Patients who are hemo-
dynamically stable on presentation can be managed
initially with medication. Should the clinical status
deteriorate, electrical cardioversion can be utilized as
secondary therapy.
In a stable patient with an undifferentiated WCT,
procainamide is very effective in terminating the dys-
rhythmia. Using a dose of 10 mg/kg, one study fi nds
that procainamide terminates approximately 80% of
stable WCT (in this case, monophorphic ventricular
tachycardia); in contrast, the same study fi nds that
lidocaine dosed at 1.5 mg/kg terminates only 20%
including AV reentry (antidromic) tachycardia
(Figure 8-13A) and preexcited atrial fi brillation (Figure
8-13B). In both cases, the rate will be extremely rapid
with a markedly widened QRS complex and delta
wave. In WPW with atrial fi brillation, the beat-to-beat
variation in the QRS complex morphology is clear.
Management
Patients presenting with a WCT and signifi cant hemody-
namic compromise should be prepared for an immediate
electrical cardioversion. This approach is appropriate
for VT and most forms of SVT with aberrant conduc-
tion. Patients with sinus tachycardia complicated by
bundle branch block, sodium channel blockade-related
tachycardia, or hyperkalemia-associated tachycardia
should not undergo electrical cardioversion, but instead
should receive therapy targeted at these various condi-
tions. In patients refractory to standard WCT therapy, a
Figure 8.13 A wide QRS complex tachycardia in the Wolff-Parkinson-White syndrome. A. An atrioventricular reentry
(antidromic) tachycardia. B. Atrial fi brillation.
THE DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA—ED DIAGNOSTIC AND MANAGEMENT CONSIDERATIONS
121
fi brillation may be dependent upon the rapid rate to
maintain cardiac output in the face of pronounced
hypovolemia or inadequate vascular tone; attempts
at rate control in this setting, rather than manage-
ment of the underlying process, can lead to patient
deterioration.
The QRS complex widening from both sodium
channel blockade and hyperkalemia must be
approached in a different fashion from traditional
WCTs. The QRS complex widening with tachycardia
in the setting of poisoning with a sodium channel-
blocking agent should be treated with intravenous
sodium bicarbonate. An initial bolus of 1–2 mEq/kg
should be followed by a repeat EKG to evaluate for
narrowing of the QRS complex. Repeat sodium bicar-
bonate boluses, continuous infusion, or both can be
used to improve conduction and increase contractil-
ity. The QRS complex duration can be monitored to
determine the response to therapy.
The primary goals in treating a WCT due to hyper-
kalemia are to stabilize the myocardium and lower the
serum potassium concentration. Intravenous calcium
chloride or calcium gluconate will assist in stabilization
of the myocyte. Several different agents can transiently
lower the serum potassium. Beta-adrenergic agonists
push potassium into cells through activation of a mem-
brane potassium pump; albuterol is the most com-
monly used beta-agonist in this setting. Insulin works
to activate the sodium potassium ATPase, thereby shift-
ing potassium into cells; 10 units of regular insulin are
administered intravenously initially along with 25 grams
of dextrose to avoid hypoglycemia. Sodium bicarbon-
ate both shifts potassium into cells and increases renal
excretion of potassium; the initial recommended dose
is 1 mEq/kg intravenously. Magnesium sulfate, given
at a dose of 8 mEq intravenously, will also cause inter-
nal shifting of potassium. As these measures primarily
serve to temporarily decrease serum potassium concen-
trations, defi nitive measures must be taken to decrease
overall potassium body burden (i.e., hemodialysis or
sodium polystyrene, Kayexalate). Furthermore, repeat
therapy may be necessary if the time to defi nitive man-
agement is prolonged.
Section IV: Decision making
For a WCT with hemodynamic compromise, •
electrical cardioversion is the fi rst line treatment.
of stable WCT.
20
Procainamde has the added benefi t
of being a relatively safe agent for use in preexcita-
tion syndrome-related tachycardia (atrial fi brillation
and AV reentry tachycardia). A common adverse
effect and signifi cant limitation of procainamide is
hypotension, which is usually an infusion-related
problem. For this reason, procainamide is not sug-
gested for use in patients with signifi cantly impaired
left ventricular function or acute pulmonary edema.
Standard procainamide dosing is as follows: a maxi-
mum of 17 mg/kg infused at a rate of 20 mg/min;
alternatively, 100–200 mg increments of procain-
amide can be infused in slow intravenous “push”
fashion over 2–5 minutes, thus allowing for a full
loading dose in more rapid fashion. The method of
administration is dependent upon both the patient’s
situation and the clinician’s resources. Therapeutic
endpoints for procainamide include full loading
dose achieved, development of clinically signifi cant
hypotension, or dysrhythmia termination.
Amiodarone should be considered the second line
agent for treatment of an undifferentiated WCT in
which procainamide has failed to produce a cardiover-
sion. It can be considered a fi rst line agent in patients
with pronounced left ventricular dysfunction. A recent
study fi nds that 150 mg/kg of amiodarone terminates
only 29% of stable ventricular tachycardias.
21
Few
studies, however, have investigated the effi cacy of
amiodarone in stable WCT. In the hemodynamically
stable patient, the initial dose of amiodarone is 150 mg
intravenously over 10 minutes, which may be repeated
every 10 minutes as necessary to a maximum daily dose
of 2.2 grams. It should not be used for wide complex
rhythms related to Wolff-Parkinson-White syndrome
because of its AV-node blocking abilities.
Two common WCTs include sinus tachycardia
and atrial fi brillation, both with bundle branch
block confi guration. Sinus tachycardia with a bundle
branch block should be approached with an investi-
gation of the underlying cause of the dysrhythmia.
As this rhythm is likely a reactive dysrhythmia, issues
such as hypovolemia, hypoxia, or fever should be
considered as possible causes, and therapies should
be aimed at the correction of the underlying disease
process. Atrial fi brillation, either with or without a
bundle branch block pattern, can be challenging to
manage as hemodynamic instability in atrial fi brilla-
tion may or may not be related to the rapidity of the
ventricular response. A patient with chronic atrial
CHAPTER 8
122
Wellens HJ, Bar FW, Lie KI. The value of the electrocar-7
diogram in the differential diagnosis of a tachycardia with
a widened QRS complex. Am J Med. 1978;64:27–33.
Steurer G, Gursoy S, Frey B, et al. The differential diag-8
nosis on the electrocardiogram between ventricular
tachycardia and preexcited tachycardia. Clin Cardiol.
1994;17:306–308.
Brugada P, Brugada J, Mont L, Smeets J, Andries EW. 9
A new approach to the differential diagnosis of a regu-
lar tachycardia with a wide QRS complex. Circulation.
1991;83:1649–1659.
Steinman RT, Herrera C, Schluger CD, et al. Wide 10
QRS tachycardia in the conscious adult: Ventricular
tachycardia is the most frequent cause. JAMA. 1989;
261:1013–1016.
Morady F, Baerman JM, DiCarlo LA, et al. A prevalent 11
misconception regarding wide complex tachycardias.
JAMA. 1985;254:2790–2792.
Brady W. Unpublished data. University of Virginia 2009, 12
Charlottesville, VA.
Herbert ME, Votey SR, Mortan MT, et al. Failure to 13
agree on the electrocardiographic diagnosis of ven-
tricular tachycardia. Ann Emerg Med. 1996;27:
35–38.
Stewart RB, Bardy GH, Greene HL. Wide complex 14
tachycardia: misdiagnosis and outcome after emergent
therapy. Ann Intern Med. 1986; 104:766–771.
Domanovits H, Paulis M, Nikfardjam M, et al. Sustained 15
ventricular tachycardia in the emergency department.
Resuscitation. 1999;42:19–25.
Brady WJ, Skiles J. Wide QRS complex tachycar-16
dia: ECG differential diagnosis. Am J Emerg Med.
1999;17:376–381.
Vereckei A, Duray G, Szénási G, et al. New algorithm 17
using only lead aVR for differential diagnosis of wide
QRS complex tachycardia. Heart Rhythm. 2008;5:
89–98.
Goldberger ZD, Rho RW, Page RL. Approach to the 18
diagnosis and initial management of the stable adult
patient with a wide complex tachycardia. Am J Cardiol.
2008;101:1456–1466.
Gupta AK, Thakur RK. Wide QRS complex tachycar-19
dias. Med Clin North Am. 2001;85:245–266.
Gorgels AP, van den Dool A, Hofs A, et al. Comparison 20
of procainamide and lidocaine in terminating sustained
monomorphic ventricular tachycardia. Am J Cardiol.
1996;78;43–46.
Marill KA, deSouza IS, Nishijima DK, et al. Amiodarone 21
is poorly effective for the acute termination of ventricu-
lar tachycardia. Ann Emerg Med. 2006;47:217–224.
In sinus tachycardia with a bundle branch block, •
sodium channel blockade-related tachycardia, or
hyperkalemia-associated tachycardia, target the
underlying condition.
In a hemodynamically-stable WCT, the rhythm •
should be considered VT until proven otherwise,
but can be managed initially with procainamide.
Amiodarone should be used as a second line agent •
for an undifferentiated WCT, except in patients
with signifi cantly impaired left ventricular function
or acute pulmonary edema.
A QRS complex widening sodium channel blockade •
(TCA overdose) should be treated with sodium
bicarbonate.
Treatment for a WCT due to hyperkalemia requires •
stabilizing the myocardium and lowering the serum
potassium, using calcium, beta-agonists, insulin,
sodium bicarbonate, magnesium, and ultimately
hemodialysis or sodium polystyrene, Kayexalate.
References
Meldon SW, Brady WJ, Berger S, Mannenbach M. 1
Pediatric ventricular tachycardia: a review with
three illustrative cases. Pediatr Emerg Care. 1994;
10:294–300.
Tchou P, Young P, Mahmud R, et al. Useful clinical cri-2
teria for the diagnosis of ventricular tachycardia. Am J
Med. 1988;84:53–56.
Baerman JM, Morady F, DiCario LA, de Buitleir M. 3
Differentiation of ventricular tachycardia from supraven-
tricular tachycardia with aberration: Value of the clinical
history. Ann Emerg Med. 1987;16:40–43.
Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou 4
PJ. Wide QRS complex tachycardia. Reappraisal of a
common clinical problem. Ann Int Med. 1988;109:
905–912.
Levitt MA. Supraventricular tachycardia with aberrant 5
conduction versus ventricular tachycardia: Differentiation
and diagnosis. Am J Emerg Med. 1988;6:273–277.
Antunes E, Brugada J, Steurer G, et al. The differential 6
diagnosis of a regular tachycardia with a wide QRS
complex on the 12-lead ECG: Ventricular tachycardia,
supraventricular tachycardia with aberrant intraven-
tricular conduction, and supraventricular tachycardia
with anterograde conduction over an accessory pathway.
PACE. 1994;17:1515–1524.
9
123
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.
Cardiac arrest
Benjamin J. Lawner
1
& Amal Mattu
2
1
Clinical Assistant Professor, Department of Emergency Medicine, University of Maryland
School of Medicine, Deputy EMS Medical Director, Baltimore City Fire Department
Baltimore, Maryland, USA
2
Professor and Residency Director, Department of Emergency Medicine, University of
Maryland School of Medicine, Baltimore, Maryland, USA
9
Section I: Case presentation
A 56-year-old woman was brought to the emergency
department (ED) by EMS personnel for evaluation
of a “possible cardiac arrest.” The patient had been
sitting with family members watching TV when she
began to complain about substernal chest pressure
and dyspnea. She became diaphoretic, and then
collapsed to the fl oor. The family members, who
were untrained in CPR, immediately began chest
compressions without checking for a pulse. After
approximately a minute, the patient began moving
spontaneously, though she remained unconscious.
Someone dialed 911.
The paramedics found the patient unconscious, but
breathing; she was spontaneously moving and local-
izing pain, but not following commands. The vital
signs were: blood pressure 80/60 mmHg, pulse 110
beats/min, respirations 22 breaths/min, pulse oximetry
97%. A fi nger stick glucose was 140 mg/dl. The EKG
showed sinus tachycardia, 2 mm ST-segment elevation
in leads II, III, and aVF, and 1 mm ST-segment depres-
sion in leads V1-V3. The paramedics placed the patient
on a cardiac monitor, applied 100% oxygen via non-
rebreather facemask, initiated a normal saline bolus,
and transported the patient, a trip of ten minutes, to
the ED.
The vital signs did not change during transport. The
past medical history included a history of renal failure,
with the patient receiving hemodialysis 3 times per
week; the last time was 2 days prior to the current
event. The patient also had insulin-dependent dia-
betes mellitus and hypertension. She had been doing
well until the arrest.
Shortly after arrival in the ED, the patient became
limp. The cardiac monitor showed a rhythm change
to a wide complex regular tachycardia with a rate of
160 beats/min. She had no palpable pulse and agonal
respirations.
Section II: Case discussion
Dr Peter Rosen: This case illustrates a number of my
prejudices about cardiac arrest. It’s a problem that
probably drove the origin of emergency medicine, but
I think it’s the wrong end of the disease to be treat-
ing. I don’t really think we’ve made great progress
in the management of cardiac arrest since we fi rst
started doing emergency medicine about 30 years
ago. There’s been a lot of controversy about the value
of citizen CPR, touted mostly by the Seattle system.
Nevertheless, when you talk to the people in Seattle,
they tell you some odd things, such as CPR doesn’t
work in asystole, and when they study the quality of
citizen CPR, there isn’t any difference between pro-
viders. It doesn’t seem to matter what citizens do, so
long as they do something; they haven’t been able to
CHAPTER 9
124
per minute, yet I think that to actually get someone
to do 100 compressions per minute and have good
compressions is really diffi cult. This limits the value of
ongoing animal experiments.
The one advance in out-of-hospital care that is
likely benefi cial, which paramedics can do and rou-
tinely do now in Massachusetts, is to call ahead to the
ED with a 12-lead EKG. If the patient is restored to a
regular rhythm, and if the 12-lead EKG demonstrates
an ST elevation myocardial infarction (STEMI), we
can send them directly to the cardiac catheteriza-
tion laboratory, bypassing other hospitals that do
not have this availability. There are data that sug-
gest that the best option for this patient is immediate
revascularization.
1–3
If that’s true, then when you call
ahead and let the ED know you have an ST eleva-
tion MI in a patient who is in cardiac arrest, they can
potentially have the cardiac catheterization labora-
tory available more quickly, and you may signifi cantly
improve this person’s mortality.
PR: Since this case sounds to me like a dysrhythmic
event with probable VT and loss of consciousness, as
opposed to VF or asystole, what is the outcome of VT
arrest? I have not been impressed that VT arrest fares
much better than VF. I have seen a couple of patients
with VT who developed the rhythm in the ED instead
of in the fi eld, but when they were returned to a sinus
rhythm, they still never woke up nor regained mean-
ingful cardiac function.
Dr Edward Ullman: I think your real best chance is
to arrest in the ED. An article reports that in-hospital
cardiac arrests have an equal to or worse door-to-
defi brillation time compared to out-of-hospital car-
diac arrests. Clearly this is going to signifi cantly affect
outcome.
4
One advance that may help is to initiate
cooling of patients who suffer out-of-hospital cardiac
arrest, even while in the prehospital arena and during
transport.
5
In Boston, EMS is now starting to com-
mence hypothermia treatment.
DB: There is a prognostic difference between an isch-
emic-related VT or VF versus a patient who is dying of
sepsis who has a hypotensive cardiac arrest. But if we
lump together every outcome of in-hospital cardiac
arrest, it’s hard to interpret that data. In particular,
I would make the distinction that most of the car-
diac arrests associated with acute MIs are VF and not
VT, and usually respond to immediate defi brillation.
defi ne whether citizen CPR is having an effect on the
patient directly, or whether the benefi ts involve an
earlier call to the 911 system.
There does seem to be an advantage to defi brillators
in public buildings and airports, and it would seem,
over time, that our best success with cardiac arrest
is when it probably isn’t a cardiac arrest, in terms of
asystole or a ventricular fi brillation (VF), but probably
ventricular tachycardia (VT) or perhaps a seizure that’s
assumed to be a cardiac arrest, and the patient gets
shocked. These patients do very well; they come back
with great cerebral function. However, in terms of true
cardiac arrest, I think the outcome is still dismal, and it
would appear that all of our efforts to improve citizen
CPR have failed because we are treating the wrong end
of the disease. Currently or in 2009 (Since the guide-
lines have since been published), the best treatment for
cardiac arrest is immediate defi brillation, and if that
can’t be achieved, these patients don’t fare well.
Dr David Brown: I largely agree: survivors of out-of-
hospital cardiac arrest are most likely to be those who
can be successfully defi brillated in the fi eld. There are
a few subsets of patients who have a chance; this case
likely, VT arrest. These kinds of arrest are more likely
to be successfully defi brillated than some other kinds
of out-of-hospital cardiac arrest, such as asystole or
primary respiratory arrest leading to cardiac arrest.
Dr Amal Mattu: I would add that good compressions
may help, but the best chance for recovery is when the
patient has a rhythm that can respond to defi brilla-
tion. Otherwise, just focus on basic life support (BLS),
and transport as quickly as possible. Today, there is
a lot less emphasis on ventilation, instead focusing
on good compressions en route and hoping that the
patients may have a rhythm that can respond to defi -
brillation, but not much else can be done in the fi eld.
PR: Do you think the dog experiments or other animal
experiments on arrest, with the different positioning
of the thumpers and the different rates of compres-
sion, have any clinical relevance in humans?
Dr Shamai Grossman: The American Heart Association
(AHA) goes back and forth as to the appropriate rate
of compressions; however, I think that rescuers aren’t
very good at compressions to start with, and aren’t very
compliant with the continuous compressions either.
Currently, the AHA recommends 100 compressions