Bigeminal Rhythm X - JOURNAL of the Louisiana State Medical

ECG of the Month
Bigeminal Rhythm X
D. Luke Glancy, MD; Robert H. Drennan, MD
During evaluation for intermittent atypical chest pain of two weeks duration, a 59-year-old woman had an
electrocardiogram performed. (Figure).
What is your diagnosis?
Explication is on pg. 218
J La State Med Soc VOL 164 July/August 2012
223
Journal of the Louisiana State Medical Society
ECG of the Month
Presentation is on pg. 217
DIAGNOSIS: Sinus rhythm with monomorphic ventricular
bigeminy and ventriculophasic sinus arrhythmia. Otherwise, the
ECG is normal.
Ventricular premature complexes occurring after each
sinus-initiated QRS complex is the commonest form of bigeminal rhythm. In this instance, the premature complexes
resemble a left bundle branch block pattern, indicating that
they arise from the right ventricle.
Alternate sinus P waves are fused with the terminal
portion of each ventricular premature complex and reach the
atrioventricular conduction system in its absolute refractory
period. This prevents their conduction to the ventricles and
causes a compensatory pause before the next sinus P wave.
The sinus rhythm is slightly irregular. Because the
beginning of alternate P waves is buried in a ventricular
premature complex, the P-P intervals are best measured
from the end of one P wave to the end of the next P wave.
Such measurement reveals that the P-P intervals containing
two QRS complexes (sinus initiated and premature ventricular) consistently are shorter (0.67s) than P-P intervals
containing no QRS complex (0.72s). This ventriculophasic
sinus arrhythmia often is most clearly seen in electrocardiograms showing sinus rhythm with 2:1 atrioventricular
block but may be seen in any situation in which some sinus
P-P intervals contain QRS complexes, while others do not.
Two mechanisms have been postulated for ventriculophasic sinus arrhythmia. In one, the pressure of ejected
blood on the sinus node is thought to cause a momentary
increase in its rate, and thus, the P-P interval containing the
QRS complex is shorter than the P-P interval without a QRS.1
The second proposed mechanism states that the increase in
carotid sinus pressure with ventricular systole causes reflex
slowing of the sinus node some 200-500 ms after the peak
of mechanical systole, which, of course, is well after the
QRS. Thus, the slowing of the sinus rate occurs after the P-P
interval containing the QRS.1,2 The second explanation has
always made more sense to us. Furthermore, Prystowsky
and Klein have produced sinus node slowing in a patient
using neck-collar suction, and the timing of the slowing fits
with the second explanation, not the first.2
Our patient had no history of heart disease and in the
course of her workup for chest pain had a normal atropinedobutamine stress echocardiogram. She subsequently has
been treated more vigorously for her acid-reflux disease.
REFERENCES
1.
2.
Fisch C, Knoebel SB. Electrocardiography of Clinical Arrhythmias.
Armonk, NY: Futura;2000:6-10.
Prystowsky EN, Klein GJ. Cardiac Arrhythmias: An Integrated
Approach for the Clinician. New York: McGraw-Hill;1994:18-20.
224 J La State Med Soc VOL 164 July/August 2012
Dr. Glancy is a Professor and Dr. Drennan is a fellow in the Sections of
Cardiology, Departments of Medicine, Louisiana State University Health
Sciences Center and the Interim LSU Public Hospital, New Orleans.