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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- Interpretation

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

Figure. Rhythm Strip From Telemetry

1190 ms 1070 ms 1080 ms


II 1 mV

1120 ms 1190 ms 1190 ms 1190 ms 1190 ms

V 1 mV

1080 ms 1090 ms 1100 ms 1130 ms

II 1 mV

1050 ms 1040 ms 1030 ms 1020 ms

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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Clinical Review & Education Challenges in Clinical Electrocardiography

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

ARTICLE INFORMATION not involved in the editorial review or the decision 6. Riera ARP, Barros RB, de Sousa FD, Baranchuk A.
Author Affiliations: School of Medicine, University of to accept the manuscript for publication. Accelerated idioventricular rhythm. Indian Pacing
California San Francisco, San Francisco (Muniyappa); Electrophysiol J. 2010;10(1):40-48.
Division of Cardiology, Department of Medicine, REFERENCES 7. Castellanos A Jr, Lemberg L, Arcebal AG.
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Corresponding Author: Anoop Muniyappa, MS, tachycardia. Cardiac Electrophysiology: From Cell to Accelerated idioventricular rhythm in the
School of Medicine, University of California Bedside, 700704. Elsevier Saunders. Philadelphia, post-thrombolytic era: incidence, prognostic
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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
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Challenges in Clinical Electrocardiography, but was infarction. Acute Card Care. 2008;10(1):15-25.

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