Clinical Review & Education
Challenges in Clinical Electrocardiography
Wide Complex Ventricular Rhythm in a Patient
After Collapse
Anoop Muniyappa, MS; Nora Goldschlager, MD
A nonsmoker in her 80s with a history of hypertension, dyslipid-
emia, and asthma was brought to the emergency department after
she was found collapsed in her apartment 2 days following a pos-
sible syncopal episode. She denied prior cardiac history, seizures,
syncope, presyncope, or falls. She had no diabetes or family medi-
cal history of coronary artery disease. She took metoprolol, 25 mg,
twice daily for hypertension prior to her fall.
The patient was afebrile with a heart rate of 65 beats per min-
ute (bpm) and recorded blood pressure of 165/144 mm Hg. She had
normal findings on cardiac, pulmonary, and neurologic examina-
tions. Initial laboratory data were notable for white blood cell count
of 16.2 109/L, serum sodium of 148 mmol/L, blood urea nitrogen
of 24 mg/dL (to convert to mmol/L, multiply by 0.357), creatinine
of 1.04 mg/dL (to convert to mol/L, multiply by 76.25), creatine ki-
nase of 5962 U/L (reference range, <145 U/L; to convert to kat/L,
multiply by 0.0167), and troponin of 1.95 ng/mL (reference range,
<0.04 ng/mL; to convert to g/L, multiply by 1.0). Initial electrocar-
diogram (ECG) results showed normal sinus rhythm with no ische-
mic changes. Skeletal x-ray results were normal. Computed tomog-
raphy results of the brain and cervical spine were normal. She was
treated with intravenous fluids and admitted to a telemetry unit for
cardiac rhythm monitoring. Overnight, she had multiple 10- to
20-second runs of a wide-QRS complex rhythm with heart rate in
the 50s (Figure).
Question: What is the rhythm and how should it be treated?
Figure. Rhythm Strip From Telemetry
N N N N
II 1 mV
1120 ms 1190 ms 1190 ms
V 1 mV
1080 ms 1090 ms 1100 ms
V V V V
II 1 mV
V 1 mV
Rhythm strip showing simultaneously recorded leads II and V1. F1 and F2, the black arrowheads indicate fusion beats. The blue bars demarcate the P-P intervals, and
the green bars demarcate the R-R intervals.
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Interpretation
The upper rhythm strip in the Figure shows initial sinus bradycardia
slowing from approximately 54 to 50 bpm. The sixth QRS complex
has a longer duration with an intermediate morphology compared
with the normally conducted sinus-stimulated narrow QRS com-
plex and the longer-duration QRS complex rhythm, thus represent-
ing a fusion complex (F1) in which the ventricles are depolarized from
both the normal atrioventricular (AV) node-His-Purkinje system and
the ectopic pacemaker. The subsequent monomorphic wide QRS
complex rhythm begins at approximately 56 bpm and slows to 53
bpm. The P waves are not easily discernible during the initial wide
QRS complex rhythm, but they reappear clearly by the fifth com-
plex of the lower rhythm strip at 59 bpm, consistent with isorhyth-
mic AV dissociation. The seventh QRS complex in the lower rhythm
strip is another fusion complex (F2) that occurs as the sinus pace-
maker resumes control of ventricular depolarization over the nor-
mal AV node-His-Purkinje system. These features are consistent with
an accelerated ventricular rhythm (AVR).
Clinical Course
The patient remained asymptomatic and hemodynamically stable
during both sinus and ventricular rhythms. Subsequent 12-lead ECGs
did not capture the AVR and did not show any evidence of ischemia
or arrhythmia. Over the next day, the patients hematologic and elec-
trolyte abnormalities resolved, creatine kinase levels down-
1190 ms 1070 ms 1080 ms
N V V V
1190 ms 1190 ms
F1
1130 ms
V V N N N
1050 ms 1040 ms 1030 ms 1020 ms
F2
(Reprinted) JAMA Internal Medicine Published online April 3, 2017 E1
 Clinical Review & Education Challenges in Clinical Electrocardiography

trended, and troponin levels peaked at 2.18 ng/mL and down-
trended. The initial elevation in troponin was attributed to demand
ischemia in the setting of the patients fall and subsequent poor fluid
intake causing hypovolemia, consistent with the resolving acute kid-
ney injury and downtrending creatine kinase levels. A myocardial in-
farction (MI) was considered unlikely given the lack of ischemic symp-
toms or ECG changes indicative of MI. Owing to the sinus rates of
50 to 60 bpm, her metoprolol was discontinued and amlodipine was
prescribed. She continued to have infrequent runs of AVR over-
night, which were noted and not treated.
Discussion
Accelerated ventricular rhythm refers to an ectopic wide QRS complex
rhythm with at least 3 consecutive ventricular complexes at a typical
rate of 40 to 120 bpm, depending on the prevailing sinus rate.1 Accel-
erated ventricular rhythm is faster than the intrinsic ventricular rate
(<40 bpm) but slower than ventricular tachycardia (>100 bpm); the
onset and termination are gradual, usually accompanied by fusion
complexes.1 These characteristics differentiate AVR from similar-
appearing rhythms, such as ventricular tachycardia, AV block, supra-
ventricular tachycardia with intraventricular aberrancy, and antidromic
AV reentry tachycardia (AVRT). Lewis originally published examples of
AVRwithoutexplicitlyidentifyingitin1910,Harrisdescribedtherhythm
in the setting of experimental coronary occlusion in an animal model
in 1950, and Marriott and Menendez introduced the term accelerated
idioventricular rhythm (AIVR) to describe the arrhythmia in 1966.2
In our experience, AVR is commonly an incidental finding, and
it has been reported in the absence of structural heart disease.3 It
has been associated with reperfusion after acute MI.4,5 In addition,
AVR has been reported in the setting of acute MI, drug intoxication
(eg, halothane, aconitine, desflurane, cocaine, and digoxin), elec-
trolyte imbalance, postresuscitation after cardiac arrest, dilated car-
diomyopathy, hypertrophic cardiomyopathy, arrhythmogenic ven-
tricular cardiomyopathy, rheumatic heart disease, acute myocarditis,
and congenital heart disease in newborns.1,6
A widely accepted mechanism for AVR in acute MI is enhanced
automaticity of the His-Purkinje fibers, which results in a ventricu-
lar rhythm with a rate greater than that of the sinus pacemaker.7
Accelerated ventricular rhythm after percutaneous coronary
intervention (PCI) has been associated with increased vagal tone and
decreased sympathetic tone, which can decrease the sinus rate and
enable emergence of AVR.8
Most cases of AVR are hemodynamically stable, self-limited, and
require no treatment.1 In patients with impaired cardiac function,
poor ventricular filling may result from loss of AV synchrony, and
atropine can be used to increase sinus rate, improve AV conduc-
tion, and resolve hypotension.9
Acceleratedventricularrhythmhasbeenshowntohavenoimpact
on prognosis in patients with acute MI, patients with idiopathic dilated
cardiomyopathy,andchildrenwithcongenitalheartdisease.6 Inasmall
retrospective observational study,10 AVR was associated with lower
7-day survival in out-of-hospital cardiac arrest patients postresucita-
tion. There are no compelling data demonstrating increased risk of sus-
tainedventriculartachycardiaorventricularfibrillationafterAVR.Inpa-
tients with acute MI treated with thrombolytics, AVR is a moderately
good predictor of successful reperfusion when combined with other
noninvasive markers, such as ST-segment resolution.5 However, in pa-
tients with acute MI treated with PCI, AVR is a nonspecific marker of
reperfusion and has limited clinical significance.5
Take Home Points
Accelerated ventricular rhythm is a wide-QRS complex rhythm with
at least 3 consecutive ventricular complexes and a rate of 40 to
120 bpm, which is faster than a typical ventricular escape rhythm
but slower than ventricular tachycardia.
Accelerated ventricular rhythm is characterized by gradual onset
and termination and is often accompanied by fusion beats.
Accelerated ventricular rhythm is commonly an incidental finding
and can occur in patients without heart disease, but it has been
associated with reperfusion after MI and reported in a number of
other conditions.
Most cases of AVR are hemodynamically stable, self-limited, and
require no treatment.
Although AVR may be predictive of successful reperfusion when
combined with other markers like ST-segment resolution in
patients with acute MI treated with thrombolytics, it is of limited
clinical significance in patients with acute MI treated with PCI.

ARTICLE INFORMATION
Author Affiliations: School of Medicine, University of
California San Francisco, San Francisco (Muniyappa);
Division of Cardiology, Department of Medicine,
University of California San Francisco, San Francisco
(Goldschlager); Division of Cardiology, Department
of Medicine, San Francisco General Hospital,
San Francisco, California (Goldschlager).
Corresponding Author: Anoop Muniyappa, MS,
School of Medicine, University of California
San Francisco, 513 Parnassus Ave, Rm S-245,
San Francisco, CA 94143-0454
(anoop.muniyappa@ucsf.edu).
Section Editors: Zachary D. Goldberger, MD, MS; Nora
Goldschlager, MD; Elsayed Z. Soliman, MD, MSc, MS.
Published Online: April 3, 2017.
doi:10.1001/jamainternmed.2017.0467
not involved in the editorial review or the decision
to accept the manuscript for publication.
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3. Massumi RA, Ali N. Accelerated isorhythmic
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4. Goldberg S, Greenspon AJ, Urban PL, et al.
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6. Riera ARP, Barros RB, de Sousa FD, Baranchuk A.
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8. Bonnemeier H, Ortak J, Wiegand UK, et al.
Accelerated idioventricular rhythm in the
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Conflict of Interest Disclosures: None reported. 5. Osmancik PP, Stros P, Herman D. In-hospital 10. Tsai MS, Huang CH, Chen HR, et al.
arrhythmias in patients with acute myocardial Postresuscitation accelerated idioventricular
Disclaimer: Dr Goldschlager is Section Editor, rhythm. Intensive Care Med. 2007;33(9):1628-1632.
Challenges in Clinical Electrocardiography, but was infarction. Acute Card Care. 2008;10(1):15-25.

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