Wide and Narrow Qrs Complexes After Arthroscopy

Abstract

An obese (5 feet 5 inches, 224 pounds) 57-year-old woman with high blood pressure, diabetes mellitus, and arthritis underwent arthroscopy for a painful left knee. After the procedure, the electrocardiographic monitor in the recovery room showed alternately narrowing and widening QRS complexes, and a 12-lead electrocardiogram was obtained (Figure) Figure Twelve-lead electrocardiogram obtained in the recovery room. See text for explication. The first three QRS complexes are wide (0.17 seconds) and occur regularly (R-R interval = 1.09 seconds; rate = 55/minute), and no P waves are seen. The next three QRS complexes become progressively more narrow, and a P wave can be seen in front of each, with a steadily lengthening P-R interval. These QRSs are fusion beats. The next four complexes (7–10) are completely sinus-initiated with normal P waves, a P-R interval of 0.17 seconds, and a QRS duration of 0.09 seconds. The last four complexes show gradually shortening P-R intervals and widening QRSs that once again are fusion complexes. thus, at times sinus rhythm completely captures the ventricles and at other times shows isorhythmic atrioventricular dissociation from an idioventricular rhythm. During each transition in rhythm, there are numerous ventricular fusion beats. What allows the idioventricular rhythm to emerge and then disappear is sinus bradycardia with slight sinus arrhythmia. As P waves first appear on the left side of the tracing, the P-P intervals are as short as 1.00 seconds, whereas toward the right side of the tracing where the Ps disappear into the wide QRSs, The P-P intervals are as long as 1.10 seconds. The idioventricular rhythm is almost perfectly regular, with R-R intervals of 1.09 to 1.08 seconds (rates of 55–56/minute). The sinus arrhythmia may not only facilitate the intermittent isorhythmic atrioventricular dissociation, but may be a consequence of it. As the sinus rate slows and the P waves slip into the idioventricular QRSs, the absence of a preceding atrial contraction and the lack of synchronous ventricular systole cause a fall in stroke volume that activates the baroreceptors. This activation inhibits the parasympathetic stimulation and increases the sympathetic stimulation of the heart and thereby increases the sinus rate. As P waves come earlier and sinus rhythm returns, the appropriately timed atrial systole and the synchronous ventricular contraction resulting from normal depolarization produce an increase in stroke volume that causes the baroreceptors to increase parasympathetic tone and decrease sympathetic tone. thus, the sinus rate slows; the P waves slip into the idioventricular QRSs; and the cycle begins again (1, 2). Could the wide QRSs in this patient be junctional escape beats in someone with intermittent left bundle branch block? Two findings refute that possibility. The first is the morphology of the QRS. Both an R wave >0.04 seconds in lead V1 or V2 (here 0.05 seconds in both leads) and a duration from the beginning of the QRS to the nadir of the S wave of >0.07 seconds in lead V1 or V2 (here 0.10 to 0.12 seconds in both leads) strongly favor ventricular ectopy over left bundle branch block (3). Second, when left bundle branch block is intermittent, it usually occurs following short R-R intervals;that the wide QRSs in this patient follow the longer R-R intervals strongly suggests ventricular ectopy. The fact that the wide QRSs resemble left bundle branch block is a good indication that the automatic focus giving rise to the idioventricular rhythm is in the right ventricle. Idioventricular rhythm usually occurs in patients with heart disease. For example, it often is seen in patients with acute myocardial infarction, and its occurrence there is associated with an increased incidence of ventricular tachycardia (4, 5). Although our patient has multiple risk factors for cardiac disease, she has never had any definite indication of it. Idioventricular rhythm is usually transient, most often does not cause symptoms, and rarely requires treatment (3, 6). Our patient was taking metoprolol for her high blood pressure. It is possible that a slowing of the sinus node by the beta-blocker and an increase in ventricular automaticity as a result of the increased sympathetic activity attending the operative procedure collaborated in producing this arrhythmia.