Clinical Review & Education
Challenges in Clinical Electrocardiography
Recurrent Syncope in the Emergency Department
A Lethal Cause Not for the Faint Hearted
Derek S. Chew, MD; Saman Rezazadeh, MD, PhD; Robert J. Miller, MD
A woman in her 50s with a history of hypertension and alcohol
abuse presented to the emergency department with 4 episodes of
syncope in the preceding 24 hours. She denied prodromal symp-
toms of chest pain, dyspnea, palpitations or presyncope. Her medi-
cations included perindopril, metoprolol, and a magnesium supple-
ment. On examination, her blood pressure was 121/79 mm Hg, heart
rate was 65 bpm, and her respiratory rate was 24 breaths/min.
She was afebrile and had normal oxygen saturations on room air.
A 12-lead electrocardiogram (ECG) was obtained (Figure 1).
Questions: What is the likely etiology of her syncope, and what
should you do next?
ECG Interpretation
The ECG revealed sinus rhythm at approximately 60 bpm, with
diffuse nonspecific ST-segment changes, giant U waves, and slur-
ring of the T waves into the U waves. It is challenging to assess the
precise corrected QT(U) interval in the context of R-R interval
variability and the presence of giant U waves; however, the QT(U)
Figure 1. Initial 12-Lead Electrocardiogram
I aVR
II aVL
III aVF
II
The electrocardiogram revealed sinus rhythm at approximately 60 bpm, with
diffuse nonspecific ST-segment changes, giant U waves, and slurring of the
T waves into the U waves. The QT(U) interval is markedly prolonged and
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interval is markedly prolonged and likely approximates 732 milli-
seconds. A couplet of premature ventricular contractions (PVCs)
with different morphologies initiate on the T wave of the preced-
ing beat.
Clinical Course
While awaiting assessment in the emergency department, she suf-
fered a cardiac arrest secondary to polymorphic ventricular tachy-
cardia (VT) requiring cardiopulmonary resuscitation for several min-
utes with spontaneously recovery of sinus rhythm (Figure 2). During
her cardiac arrest, she received intravenous magnesium 5 mg but
did not require defibrillation. She was also given intravenous
amiodarone 300 mg and began an infusion of 1 mg/min. Her heart
rate decreased to 50 bpm, and she continued to have brief epi-
sodes (<30 second) of polymorphic VT. Her initial blood tests re-
vealed a serum potassium value of 1.9 mmol/L (to convert to mEq/L,
divide by 1.0) and serum magnesium of 1.07 mmol/L (to convert to
mEq/L, divide by 0.5). She was admitted to the hospital, and a tem-
V1 V4
V2 V5
V3 V6
approximates 732 milliseconds. A couplet of premature ventricular contractions
with different morphologies initiate on the T wave of the preceding beat.
(Reprinted) JAMA Internal Medicine Published online April 10, 2017 E1
 Clinical Review & Education Challenges in Clinical Electrocardiography

Figure 2. Telemetry Monitoring in the Emergency Department Showing Torsades de pointes

The telemetry monitor revealed frequent premature ventricular contractions with "R on T" phenomenon that trigger runs of Torsades de pointes. The first episode
of Torsades de pointes was self-terminating. The second episode of Torsades de pointes required defibrillation.

porary transvenous pacemaker was placed for overdrive pacing at
a rate of 90 bpm while her electrolyte abnormalities were re-
versed. Amiodarone was also discontinued. Within 24 hours of her
hospital admission, she developed significant alcohol withdrawal that
required sedation and intubation. Upon review of her home situa-
tion, her family found many empty bottles of vodka and cough syrup
that contained dextromethorphan.
Discussion
Torsades de pointes (TdP) is a specific form of polymorphic VT that
occurs in the setting of congenital or acquired QT(U) interval pro-
longation, typically with rates of 200 to 250 bpm. The original de-
scription of TdP or twisting of the points was coined in 1966, be-
cause the QRS complexes of changing amplitudes appeared to twist
around the isoelectric line and reminded the authors of the TdP
movement in ballet.1
Importantly, TdP is not simply a description of the twisting
QRS morphology. Its definition also requires the presence of a
prolonged QT(U) interval, generally exceeding 500 milliseconds.
Other features of TdP include a short-long-short initiation pattern
for VT, which consists of a short-coupled PVC followed by a
compensatory pause and another PVC that falls close to the
peak of the T wave (the so-called R on T PVC). This is due to the
fact that the QT(U) interval is partially determined by the
length of the preceding R-R interval, with a longer R-R interval
generating a longer subsequent QT(U) interval. The resulting TU
wave changes (ie, further QT[U] prolongation and abnormal
morphology of the TU complex) following the postextrasystolic
pause is one of best predictors of TdP.2 In addition, TdP episodes
usually exhibit a warm-up phenomenon, with the first few beats
of exhibiting longer cycle lengths compared with subsequent
beats. Finally, TdP often terminates spontaneously, with the
last 2 to 3 beats showing slowing of the arrhythmia. However,
TdP can degenerate into ventricular fibrillation resulting in
sudden cardiac death.3
Accurate identification of TdP is critically important because
the etiology and management of TdP is distinct from other types
of polymorphic or monomorphic VT. The cornerstones of TdP
management include correction of underlying causes, use of
pharmacologic agents or temporary pacing to shorten the ven-
tricular refractory period, and avoidance of antiarrhythmic drugs
that may exacerbate TdP.4 Importantly, the use of class IA antiar-
rhythmics (such as procainamide) can prolong the QT(U) interval
further, perpetuating the arrhythmia. Amiodarone, which
also results in QT prolongation, is infrequently associated with
TdP in the absence of electrolyte disorders and concomitant
QT-prolonging agents.5
Intravenous magnesium should be given as a first-line agent re-
gardless of the serum magnesium level, as a normal serum level may
not reflect the intracellular stores which account for 99% of total
body magnesium. Magnesium can attenuate episodes of TdP by de-
creasing calcium influx, thus lowering the amplitude of early after-
depolarizations that lead to TdP. As previously mentioned, increas-
ing the heart rate with temporary pacing shortens the QT(U) interval
and prevents pauses that lead to initiation of TdP. Isoproterenol can
also be used to increase the heart rate until temporary pacing can
be initiated.6 However, its use requires caution in patients with
known coronary artery disease, older age, or other cardiac risk fac-
tors, because isoproterenol may increase myocardial oxygen de-
mand resulting in ischemia. Immediate defibrillation should be per-

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 Challenges in Clinical Electrocardiography Clinical Review & Education

formed for patients with TdP that does not terminate spontaneously
or that degenerates into ventricular fibrillation.
This patient presented with multiple episodes of syncope
likely due to episodes of TdP. Her initial ECG revealed a markedly
prolonged QT(U) interval of 732 milliseconds, resulting from
severe hypokalemia and potentially dextromethorphan
ingestion.7 Upon replacement of serum potassium and clearance
of her dextromethorphan, her QT(U) interval normalized to
440 milliseconds and her arrhythmias resolved.
Take-Home Points
Torsades de pointes is a specific form of polymorphic ventricular
tachycardia requiring the presence of a prolonged QT(U) interval
as part of its definition and is often preceded by a short-coupled
premature ventricular contractions (PVC) followed by a compen-
satory pause and another PVC that falls close to the peak of the
T wave (ie, short-long-short initiation pattern).
Torsades de pointes is usually self-terminating but can be associ-
ated with hemodynamic instability or degenerate into ventricular
fibrillation.
The recognition of TdP and its differentiation from other forms
of ventricular tachycardia are important for initiating specific
management strategies (ie, intravenous magnesium, overdrive
pacing).
The cornerstones of TdP management include: (1) the correction
of underlying causes; (2) use of pharmacologic agents or tempo-
rary pacing to shorten the ventricular refractory period; and
(3) avoidance of antiarrhythmic drugs that may exacerbate TdP.
Intravenous magnesium is a first-line agent regardless of the se-
rum magnesium level, because a normal serum level may not re-
flect the intracellular stores which account for 99% of total body
magnesium. Magnesium may attenuate episodes of TdP by de-
creasing calcium influx and lowering the amplitude of early after-
depolarizations that lead to TdP.

ARTICLE INFORMATION
Author Affiliations: Department of Cardiac
Sciences, Libin Cardiovascular Institute of Alberta,
University of Calgary, Calgary, Alberta, Canada.
Corresponding Author: Derek S. Chew, MD,
FRCP(C), Foothills Medical Center, 1403 29th St
NW, Calgary, AB T2N 1T9, Canada
(dchew@ucalgary.ca).
Section Editors: Zachary D. Goldberger, MD, MS;
Nora Goldschlager, MD; Elsayed Z. Soliman, MD,
MSc, MS.
Published Online: April 10, 2017.
doi:10.1001/jamainternmed.2017.0580
Conflict of Interest Disclosures: None reported.
Additional Contributions: We thank Sheila
Klassen, MD, for her helpful comments on an earlier
draft of this manuscript; she was not compensated
for her contributions.
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