Circulation

CASES AND TRACES

A Tale of 2 Blocks

ECG CHALLENGE Ajay Pillai , MD

A 63-year-old woman with a history of paroxysmal atrial fibrillation, severe aor- Kenneth A. Ellenbogen ,
tic stenosis, and ascending aortic aneurysm status after placement of a 23-mm MD
On-X mechanical prosthesis with replacement of the ascending aorta presented Santosh K. Padala, MD
with a 3-day history of palpitations and shortness of breath. Figure 1 shows the
12-lead ECG at the time of presentation. Over the ensuing 72 hours, the two 12-
lead ECGs shown in Figures 2 and 3 are obtained. What do the ECGs in Figures 1
and 3 demonstrate? What is the mechanism of the widened QRS complexes in
Figures 1 and 3?
Please turn the page to read the diagnosis.
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Figure 1. Presenting ECG demonstrates atrial fibrillation with a ventricular rate of 144 bpm and a QRS duration of 160 milliseconds with a typical
left bundle-branch block morphology (QS in V1, broad monophasic notched R wave in leads 1, V5, and V6).

© 2021 American Heart Association, Inc.

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 Pillai et al ECG Challenge

CASES AND TRACES

Figure 2. Twelve-lead ECG after 5 mg IV metoprolol administration shows normal sinus rhythm with a rate of 84 bpm, left atrial enlargement, and a
QRS duration of 100 milliseconds.

RESPONSE TO ECG CHALLENGE bpm) and a QRS duration of 100 milliseconds. Figure 3
demonstrates sinus bradycardia (48 bpm), blocked pre-
Figure 1 demonstrates atrial fibrillation with a ventricu-
mature atrial contractions (Figure 4) in bigeminy, and a
lar rate of 144 bpm and a QRS duration of 160 millisec-
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QRS duration of 160 milliseconds with an LBBB mor-

onds with a left bundle-branch block (LBBB) morphol-
phology. The development of LBBB at faster and slower
ogy. Figure  2 demonstrates normal sinus rhythm (84
heart rates is caused by aberrancy.

Figure 3. Twelve-lead ECG 72 hours after presentation showed sinus bradycardia at a rate of 48 bpm, left atrial enlargement, and blocked prema-
ture atrial contractions in bigeminy.

Circulation. 2021;143:1062–1065. DOI: 10.1161/CIRCULATIONAHA.120.052981 March 9, 2021 1063

 Pillai et al
CASES AND TRACES
Figure 4. Sinus bradycardia with arrows depicting blocked premature atrial contractions in bigeminy.
Aberrant conduction describes a state of transient
bundle-branch block and occurs as a result of supraven-
tricular impulse transmission during periods of physi-
ological refractoriness or depressed conductivity. The
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mechanisms of intermittent aberrancy include tachycar-
dia-dependent (phase 3) aberrancy, bradycardia/decel-
eration–dependent (phase 4) aberrancy, and concealed
transseptal conduction.1 All 3 mechanisms of aberrant
conduction are responsible for the wide QRS complexes
in this case.
Tachycardia-dependent aberration (Figure  1) repre-
sents rate-dependent block, a commonly appreciated
physiological phenomenon, caused by excitation dur-
ing phase 3 of the action potential (Figure 5B). Because
the accelerated impulse occurs at a less negative trans-
membrane potential, a portion of the Na+ channels
remain refractory and unavailable for depolarization.
Ashman phenomenon is a commonly encountered
example and typically results in right bundle-branch
block after a long-short RR interval because the refrac-
tory period of the right bundle branch is longer than
that of the left bundle branch. However, at tachycardic
rates, phase 3 aberration may manifest as LBBB (Fig-
ure 1) because the effective refractory period of the left
bundle branch prolongs to a greater degree than the
right bundle branch at faster rates.2 Perpetuation of
LBBB in the present case could additionally be caused
by concealed transseptal conduction retrogradely into
the left bundle branch.
1064 March 9, 2021
ECG Challenge
Deceleration-dependent aberrancy is uncommon
and occurs when impulse conduction fails to propagate
in tissue after the usual refractory period. In Figure 3,
the widening of the QRS complexes at slower heart
rates is caused by phase 4 block. The premature atrial
contraction likely blocks in the atrioventricular node, re-
sulting in a long cycle length in the His-Purkinje system
(H-H interval) of ≈1200 milliseconds and phase 4 block
in the left bundle branch.
Phase 4 block is believed to reflect pathological His
bundle conduction. The magnitude of the phase 0
depolarization depends on the resting membrane po-
tential during diastole or phase 4. Normal His-Purkinje
physiology maintains a phase 4 resting potential of ap-
proximately −90 mV.
As His-Purkinje fibers become diseased, Purkinje cells
exhibit spontaneous diastolic depolarization, a property
characteristic of pacemaker cells and not typically ap-
preciated in normal His-Purkinje fibers at >40 bpm.3
Phase 4 aberration is deceleration-dependent because
the increase of time in diastole results in continued
spontaneous diastolic depolarization with a rise in the
phase 4 resting membrane potential (less negative than
−90 mV). This results in a decrease in the amplitude of
phase 0 depolarization and inactivation of Na+ channels
and may consequentially result in block (Figure 5C).
The patient’s burden of atrial arrhythmias improved
after therapeutic thoracentesis. There was no indication
for permanent pacemaker implantation.
Circulation. 2021;143:1062–1065. DOI: 10.1161/CIRCULATIONAHA.120.052981
 Pillai et al ECG Challenge

CASES AND TRACES

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Figure 5. Mechanisms of transient aberrant conduction.

A, Action potentials in a normal conduction system with propagation of the action potential down the right (RBB) and left (LBB) bundle branches. B, Effects of a
stimulus that arrives early during phase 3 of the action potential before completion of myocardial repolarization. Because fewer Na+ channels (and hence conduc-
tion tissue) are available during this period, the resulting depolarization results in block (*). This occurs preferentially in the LBB, resulting in aberrant conduction.
C, In the diseased conduction system, Purkinje cells exhibit spontaneous diastolic depolarization during phase 4 of the action potential cycle. Excitation from a less
negative resting state results in a decreased amplitude of phase 0 depolarization and may result in block and subsequent aberrant conduction (*). AVN indicates
atrioventricular node.

ARTICLE INFORMATION REFERENCES

Correspondence 1. Issa Z, Miller JM, Zipes DP. Intraventricular conduction abnormalities. In:
Ajay Pillai, MD, Division of Cardiac Electrophysiology, Virginia Commonwealth Clinical Arrhythmology and Electrophysiology: Third Edition. Elsevier;
University, Gateway Bldg, 3rd Floor, 3-216, 1200 E Marshall St, Richmond, VA 2018:286–304.
23298. Email ajay.pillai@vcuhealth.org 2. Shenasa M, Josephson ME, Wit AL. Paroxysmal atrioventricu-
lar block: electrophysiological mechanism of phase 4 conduction
Affiliations block in the His-Purkinje system: a comparison with phase 3 block.
Division of Cardiac Electrophysiology, Pauley Heart Center, Virginia Common- Pacing Clin Electrophysiol. 2017;40:1234–1241. doi: 10.1111/
wealth University, Richmond. pace.13187
3. Lee S, Wellens HJJ, Josephson ME. Paroxysmal atrioventricular
Disclosures block. Heart Rhythm. 2009;6:1229–1234. doi:10.1016/j.hrthm.
None. 2009.04.001

Circulation. 2021;143:1062–1065. DOI: 10.1161/CIRCULATIONAHA.120.052981 March 9, 2021 1065