ECG IMAGE OF THE MONTH
Julia H. Indik, MD, PhD, Section Editor
From Bradycardia to Tachycardia:
Complete Heart Block
Kathleen Kearney, MD, Sonja Ellingson, MD, Karen Stout, MD, Kristen K. Patton, MD
Division of Cardiology, Department of Medicine, University of Washington, Seattle.
PRESENTATION
Syncope in the setting of heart block is usually, but not
invariably, due to bradycardia. This point was underscored
when a patients telemetry data proved surprising. The pa-
tient, a 74-year-old man with no history of cardiac disease,
initially presented to an urgent care facility after noting an
elevated reading on his home blood pressure monitor. He
described a 4-week history of dyspnea on exertion and poor
exercise tolerance but denied dizziness, syncope, chest pain,
orthopnea, lower-extremity edema, or other symptoms. His
medical history included obstructive sleep apnea, prostate
cancer in remission, and gastroesophageal reux disease, for
which his only medication was ranitidine. He denied any use
of tobacco or illicit drugs. His brother died of sudden car-
diac death before the age of 50 years. The patient was a
resident of the Pacic Northwest, and he had recently
travelled to South America.
Upon arrival to the clinic, his blood pressure was
200/100 mmHg with a pulse of 37 beats per minute. His
physical examination was otherwise unremarkable. A
12-lead electrocardiogram (ECG) showed complete heart
block with a ventricular escape rhythm (Figure 1).
Laboratory data revealed normal serum chemistry except
for a creatinine level of 1.3 mg/dL. The complete blood
count, iron studies, serum protein electrophoresis, and
coagulation prole all returned normal results. A chest
radiograph demonstrated an enlarged cardiac silhouette
with evidence of mild pulmonary edema but no hilar
lymphadenopathy.
Funding: None.
Conict of Interest: None of the authors have any conicts of interest
to report in association with this topic.
Authorship: All authors had access the data and a role in writing the
manuscript.
The corresponding author is Kathleen Kearney, MD, 1959 NE Pacic
St, Box 356422, Seattle, WA 98195.
E-mail address: KaKearney@cardiology.washington.edu
0002-9343/$ -see front matter 2015 Elsevier Inc. All rights reserved.
http://dx.doi.org/10.1016/j.amjmed.2015.04.013
Subsequently, the patient was admitted to the cardiac
intensive care unit with continuous telemetry and external
pacing pads in place. A few hours after admission, he had a
brief episode of witnessed syncope corresponding to a
wide complex rhythm on telemetry, and this was followed
by several shorter occurrences of the arrhythmia
(Figures 2 and 3). The subsequent rhythm abnormalities
were associated with light-headedness but not syncope.
ASSESSMENT
A 12-lead ECG was in progress when the syncopal event
occurred. This demonstrated pause-dependent polymorphic
ventricular tachycardia (Figure 4). Because the rhythm self-
terminated, the patient did not need external debrillation.
However, he underwent urgent transvenous pacer placement
and coronary angiography, which demonstrated only non-
obstructive coronary disease. Transthoracic echocardiogra-
phy conrmed normal left ventricular systolic function
without regional wall motion abnormalities and mild dia-
stolic dysfunction. No further episodes of polymorphic
ventricular tachycardia were observed after initiating ven-
tricular pacing at 80 beats per minute.
DIAGNOSIS
Complete heart block is characterized by complete disso-
ciation of atrial and ventricular electrical conduction, such
that no signals generated above the atrioventricular node,
including those emanating from the sinus node, are con-
ducted to the ventricles. Typical junctional or ventricular
escape rhythms result in pulse rates from 30-50 beats per
minute. Patients often present with dizziness, syncope, or
presyncope, as well as fatigue, poor exercise tolerance, and
dyspnea on exertion. The differential diagnosis of acquired
complete heart block includes myocardial ischemia,
especially in the right coronary artery distribution, medi-
cations that impair atrioventricular nodal conduction,
inltrative disease (particularly sarcoidosis), infection
Kearney et al Complete Heart Block with Polymorphic Ventricular Tachycardia 703

Figure 1 The baseline electrocardiogram (ECG) showed complete heart block with a sinus rate of 105 beats per minute, a wide
complex regular ventricular escape rhythm of 38 beats per minute, and a QTc of approximately 440 ms.

(endocarditis with valvular abscess or Lyme carditis), in-
ammatory disorders, genetic conduction abnormalities,
and idiopathic brosis and calcication of the conduction
system.1
Our patient was presumed to have age-associated
brosis of the conduction system, given the normal re-
sults on his coronary angiography and transthoracic
echocardiogram. Ruling out structural heart disease was
particularly important with his family history of sudden
death. He took no culprit medications and had no history of
cardiac surgery. His history indicated that he was at low
risk for Lyme or Chagas disease, and the normal laboratory
evaluation made cardiac amyloidosis and hemochromato-
sis unlikely. A chest radiograph showed that he did not
have hilar lymphadenopathy or other ndings to suggest
sarcoidosis, a commonly overlooked cause of complete
heart block in patients presenting prior to the sixth or
seventh decade of life.2
When a patient presents with complete heart block and
syncope, physicians should think beyond symptomatic
bradycardia or prolonged ventricular asystole and also
consider bradycardia-mediated polymorphic ventricular
tachycardia or torsades de pointes as a possible cause.3
Polymorphic ventricular tachycardia is identied by its
frequently changing QRS morphology and axis. Torsades
de pointes, translated as twisting of the points, is a
specic type of polymorphic ventricular tachycardia. First
described in the setting of complete heart block, it is
characterized by a rotating axis above and below the
electric baseline and by a prolonged QT interval.3
QT interval prolongation in patients with heart block can
be due to medications or acquired repolarization abnormal-
ities.4,5 In patients with concurrent torsades de points and
heart block, the ECG usually shows exaggerated length-
ening of the QT interval.6 Importantly, the QT interval is
dynamic and may only be extended just prior to the initiation
of torsades de pointes. QT prolongations, and thus torsades
de pointes, are often seen after a pause in electrical activity,
such as occurs after a premature ventricular complex. Our
patients initial corrected QT interval, at 440 ms, indicated
borderline prolongation (Figure 1), but it could be seen to
lengthen before the initiation of polymorphic ventricular
tachycardia (Figures 2-4). However, the variability of the
wide complex escape morphology made it especially dif-
cult to determine the true QTc interval.
Data suggest that there is a genetic predisposition to
reduced repolarization reserve; patients who have torsades
de pointes in the setting of atrioventricular block are more
likely to have polymorphisms in sodium or potassium
channel genes.7 Interestingly, patients with a genetic variant
are also more likely to have a family history of sudden
death, as in our patients case. The ECG captured during his
704
Figure 2 Telemetry showed normal sinus rhythm and complete heart block with a ventricular escape rhythm, followed by ventricular
ectopy and the onset of polymorphic ventricular tachycardia.
syncopal event (Figure 4) demonstrated complete heart
block with an unreliable ventricular escape rhythm and
multiform ventricular ectopy, occurring during the T wave
of a prolonged QT interval. This is known as an R on T
phenomenon, which triggers torsades de pointes during a
period of repolarization vulnerability.
MANAGEMENT
Patients who have complete heart block with an unstable
rhythm should receive urgent overdrive pacing. This was
The American Journal of Medicine, Vol 128, No 7, July 2015
accomplished in our patient by immediate placement of a
temporary transvenous pacing wire programmed at 80
beats per minute, which completely abolished his ven-
tricular arrhythmias. Medications to increase native heart
rate, such as isoproterenol, can be a bridge to pacing in
some instances but would be ineffective in those with
complete heart block. Antiarrhythmic medications are
contraindicated, especially potassium-channel blockers
such as amiodarone.1 These medications can slow the
ventricular escape rate and lengthen QT intervals, actually
increasing the risk of recurrent ventricular tachycardia.
Kearney et al Complete Heart Block with Polymorphic Ventricular Tachycardia 705

Figure 3 Telemetry demonstrated sinus rhythm and complete heart block with ventricular ectopy and nonsustained ventricular
tachycardia.

Permanent dual chamber pacemaker implantation
resolved our patients ventricular arrhythmias and exercise
intolerance. An implantable cardioverter-debrillator was
not indicated because pacing effectively prevented further
incidents of ventricular tachycardia. Class I indications for
pacemaker placement in patients with complete heart block
include symptomatic bradycardia or ventricular arrhythmias
presumed to be due to AV block.8
Polymophic ventricular tachycardia or tosades de pointes
is an infrequent, but life-threatening complication of com-
plete heart block, and requires immediate pacing therapy to
prevent sudden cardiac death. This case highlights this often
overlooked cause of syncope in the patient presenting with
complete heart block. Complete heart block and poly-
morphic ventricular tachycardia or torsades de pointes
should be managed with immediate pacing therapy to pre-
vent syncope and sudden cardiac death from a prolonged
episode of this life-threatening arrhythmia.
ACKNOWLEDGMENT
We thank Dr. Eric Krieger, MD, who helped obtain the
gures for this article.
706
Figure 4 An ECG obtained during the patients syncopal event disclosed complete heart block and polymorphic ventricular
tachycardia. ECG disclosed complete heart block and polymorphic ventricular tachycardia.
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