Clinical Review & Education
Challenges in Clinical Electrocardiography
Alternating Ventricular Complexes After Overdose
From an Herbal Medication
Kathy T. Vo, MD; Jeffrey A. Tabas, MD; Craig G. Smollin, MD
A woman in her 50s with no medical problems presented to the
emergency department with complaints of chest burning, short-
ness of breath, diffuse paresthesias, and dizziness. She was in her
normal state of health until an hour after drinking a home-brewed
tea containing leaves and roots prescribed by a Chinese herbalist.
She had normal mental status and vital signs. Seventeen minutes
after arrival, the patient complained of feeling worse. An ECG was
obtained (Figure 1).
Question: What are the pertinent electrocardiogram (ECG)
findings, and what is the likely cause?
Interpretation
The ECG shows bidirectional ventricular tachycardia at a regular rate
of 158 bpm. There are 2 distinct QRS complexes that are alternat-
ing beat to beat. The QRS complex labeled 1 displays RBBB with left
anterior fascicular block (LAFB). There is an RR in lead V1, a slurred
S wave in lead V6, and left axis deviation, as evidenced by a nega-
tive QRS in aVF and a positive QRS in lead 1. The QRS complex la-
beled 2 displays right bundle branch block (RBBB) with left poste-
rior fascicular block (LPFB). There is an RR in lead V1, a slurred S wave
in lead V6, and extreme right axis deviation as evidenced by a posi-
tive QRS in aVL and a negative QRS in lead I. P waves are present
after each QRS. The R-P interval (start of QRS to start of P wave) is
0.16 milliseconds.
Clinical Course
Laboratory studies conducted 10 minutes after patient arrival were
only notable for a white blood cell count of 11 300/L (reference
Figure 1. Electrocardiogram at Presentation
I aVR V1
II aVL V2
III aVF V3
VI
II
V5
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range, 4000-11 000/L; to convert to 109/L, multiply by .001) and
a potassium level of 3.3 mEq/L (reference range, 3.5-5.0 mEq/L; to
convert to mmol/L, multiply by 1). Troponin was undetectable. The
patients condition rapidly deteriorated and she developed mul-
tiple different rhythms with widened QRS morphology and inter-
mittent pulselessness requiring cardiopulmonary resuscitation. She
was intubated and cardioversion was attempted. In consultation with
the cardiology and electrophysiology services, multiple interven-
tions were attempted without success, including adenosine, amio-
darone, lidocaine, diltiazem, and verapamil. After 3 hours of at-
tempted resuscitation, venoarterial extracorporeal membrane
oxygenation was instituted. After 12 hours, her cardiac rhythm con-
verted back to normal sinus. Her clinical course was complicated by
multiorgan failure resulting from the prolonged resuscitation. Labo-
ratory analyses of her initial serum and urine, and samples of the tea
she drank on the day of presentation, were positive for aconitine.
Discussion
Aconitine and other related alkaloids are highly potent cardiovas-
cular and neurological toxins and belong to the Aconitum plant spe-
cies. In Europe and the United States, toxic effects typically occur
after inadvertent ingestion of the wild, unprocessed plant.1 In tra-
ditional Chinese medicine, aconite roots are typically used after pro-
cessing, and are prescribed for the treatment of arthritis, general
pains, and other conditions.2 The plant processing involves soak-
ing and boiling to hydrolyze the aconite alkaloids into less toxic de-
rivatives. However, faulty processing after harvest or medicinal
preparation may result in higher-than-intended toxin concentration.3
V4
V5
V6
(Reprinted) JAMA Internal Medicine Published online June 5, 2017 E1
 Clinical Review & Education Challenges in Clinical Electrocardiography
Figure 2. Enlarged View of Electrocardiogram
A Enlarged view of V1
1
2
P P
P P
QRS QRS
V1 QRS QRS
B Enlarged view of aVR, aVL, aVF, and rhythm strip
P
aVR
aVL
P
aVF
P perkalemic or hypokalemic periodic paralysis.9
P waves are present after each QRS complex (arrowheads).
This patient presented with multiple rhythms, including a pat-
tern of bidirectional ventricular tachycardia, a form of fascicular left
ventricular tachycardia which alternates conduction down the left
anterior and left posterior fascicle. With fascicular VT, the QRS can
be as narrow as 100 milliseconds, possibly owing to a junctional ori-
gin with spread of activation over the His-Purkinje system, al-
though typically it is wider.4 In addition, there was ventriculoatrial
(VA) retrograde conduction, illustrated in lead V1 (Figure 2A). To con-
firm the presence of a retrograde P wave rather than misinterpre-
tation of a portion of the QRS complex, examine the P wave in other
simultaneously recorded leads (Figure 2B). While a retrograde P wave
can also occur with AV junctional tachycardias, it may be present with
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ventricular tachycardia, and the longer R-P interval (0.16 millisec-
onds) is more suggestive of VA conduction. An R-P interval dura-
tion less than 0.10 milliseconds favors junctional tachycardia.
Other diagnoses to consider include bigeminy, which will have
a sinus P wave and conducted QRS, followed by a premature ven-
tricular complex (PVC). There will be a compensatory pause after the
PVC and before the next sinus P wave. Therefore, it is important to
look for paired beats with a P wave preceding 1 of the complexes.
Interpolated PVCs may be another mimic, an uncommon finding in
which PVCs are not followed by a compensatory pause but rather
occur early and can appear sandwiched between 2 normal beats. In
addition, the presence of electrical alternans may suggest pericar-
dial effusion, which typically presents with a low-voltage ECG in ad-
dition to varying amplitudes of the QRS. Alternating patterns of nor-
mal conduction with bundle branch block may also appear similarly.
Controversy exists in the medical literature with regard to the
site of origin of bidirectional VT. Electrophysiologic studies have dem-
onstrated that a ventricular origin is the most common, with many
bidirectional tachycardias showing a classic RBBB and alternating
fasicular block morphology. Tai et al5 favored automaticity or trig-
gered activity vs isolated reentry or reentry as the mechanism in aco-
nite poisoning.
Aconite alkaloids exert their toxic effect on the sodium chan-
nels in cardiac, nerve, and muscle tissue. The affinity for cardiac fast
sodium channels results in increased inotropy while delaying the fi-
nal repolarization phase of the action potential, thereby promoting
premature excitation.6 Refractory ventricular tachycardia and asys-
tole are the leading causes of death after aconite ingestion.3
Aconite can produce a variety of arrhythmias, including ventricu-
lar ectopy, ventricular tachycardia, ventricular fibrillation, and tor-
sades de pointes.7 Bidirectional VT, an unusual tachyarrhythmia that
typically occurs in the setting of severe structural heart disease, is also
caused by aconite toxicity. However, in toxicology, bidirectional VT is
more frequently associated with digitalis poisoning. In a review of 72
cases of bidirectional VT by Cohen et al,8 44% of cases had atrial fi-
brillation and digitalis was used in 82%. Bidirectional VT has also been
observed in other clinical settings in which patients have structurally
normal hearts, such as catecholaminergic polymorphic VT and hy-
Treatment of aconite poisoning is largely supportive. In one ret-
rospective review of the literature, Coulson et al10 found flecainide
or amiodarone to be associated with a greater return to sinus rhythm
than lidocaine or cardioversion. Prolonged cardiopulmonary resus-
citation and extracorporeal therapies may help support hemody-
namic status as the toxin is excreted.
Take-Home Points
Bidirectional ventricular tachycardia is a form of fascicular left ven-
tricular tachycardia, which alternates conduction down the left an-
terior and left posterior fascicle.
Fascicular ventricular tachycardia can present with narrow QRS
complexes.
Retrograde P waves may be present in ventricular tachycardias.
Bidirectional ventricular tachycardia suggests a toxic effect from
aconite or digoxin.
Aconite alkaloids have a high affinity for cardiac fast sodium chan-
nels, causing premature excitation of myocytes.
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ARTICLE INFORMATION
Author Affiliations: Department of Emergency
Medicine, University of California, San Francisco,
San Francisco (Vo, Tabas, Smollin); California Poison
Control System, San Francisco Division, San
Francisco (Vo, Smollin).
Corresponding Author: Kathy Vo, MD, University
of California, San Francisco, California Poison
Control System, San Francisco Division, 2789 25th
St, Suite 2202, San Francisco, CA 94110
(kathy.vo@ucsf.edu).
Section Editors: Zachary D. Goldberger, MD, MS;
Nora Goldschlager, MD; Elsayed Z. Soliman, MD,
MSc, MS.
Published Online: June 5, 2017.
doi:10.1001/jamainternmed.2017.1839
Conflict of Interest Disclosures: None reported.
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2017 American Medical Association. All rights reserved.
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Challenges in Clinical Electrocardiography Clinical Review & Education
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