An Irregular Escape Rhythm: What is the ... - Wiley Online Library

1 downloads 0 Views 180KB Size Report
mechanism leading to irregularity of an AV junctional es- cape rhythm is the occurrence of capture beats due to sinus impulses that depolarize the ventricles in ...
1056

JOURNAL

ARRHYTHMIA

OF THE

OF

Reprinted with permission from CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 13, No. 10, October 2002 Copyright ©2002 by Blackwell Futura Publishing, Inc.

MONTH

Section Editor: Fred Morady, M.D.

An Irregular Escape Rhythm: What is the Mechanism? GAETANO SATULLO, M.D.,* VINCENZO CARBONE, M.D., ` , M.D., and GIUSEPPE ORETO, M.D. MARIA PIA CALABRO From the Departments of Cardiology and Pediatrics, University of Messina, Messina; and *Department of Cardiology, Papardo Hospital, Messina, Italy

Case Presentation The tracing in Figure 1, recorded from an asymptomatic 64-year-old woman, shows sinus rhythm with complete AV block and narrow QRS complex escape rhythm. The R-R intervals are irregular, ranging from 0.96 to 1.16 seconds. What is the reason for the escape cycle variability? Commentary In the presence of advanced AV block, the most common mechanism leading to irregularity of an AV junctional escape rhythm is the occurrence of capture beats due to sinus impulses that depolarize the ventricles in advance, with respect to the ectopic pacemaker, resulting in shortening of the R-R interval. In the present case, however, capture phenomena do not explain the behavior of ventricular cycles, because at times R-R intervals undergo a shortening in the absence of potentially conducted sinus impulses. This is evident from the top strip, where the Ž rst four R-R cycles range from 1.16 to 1.13 seconds while the Ž fth and sixth cycles measure 1.08 seconds. Such a shortening cannot be due to a capture because in the two latter cycles the sinus P wave occurs so early that conduction of the sinus impulse to the ventricles appears almost impossible. Analysis of the tracing reveals that variability of the escape cycle is not random, but a deŽ nite relationship exists between timing of sinus impulses and duration of the escape intervals. This is suggested by the following Ž ndings: 1. Whenever no sinus P wave occurs between two consecutive escape beats, the escape cycle measures 1.08 secJ Cardiovasc Electrophysiol, Vol. 13, pp. 1056-1057, October 2002. Address for correspondence: Giuseppe Oreto, M.D., Via Terranova, 9, 98122 Messina, Italy. Fax: 39-090-675067; E-mail [email protected]

onds (for example, the last R-R interval in the bottom strip). 2. When a P wave occurs with an R-P interval that is either very short (,0.36 sec) or very long (.1.0 sec), the escape cycle length is once more 1.08 second (for example, the Ž rst two cycles in the third strip). 3. If a sinus P wave falls with an R-P interval ranging from 0.36 to 0.48 second, the escape cycle is longer than 1.08 second. The prolongation is minimal for R-P intervals slightly longer than 0.36 second (for example, the penultimate R-R interval in the top strip measures 1.11 seconds and the associated R-P interval is 0.38 sec), whereas in the presence of R-P intervals $0.40 second the prolongation of the escape cycle is more evident (for example, the Ž rst R-R interval in the top strip measures 1.16 seconds and the corresponding R-P interval is 0.42 sec). 4. Whenever the R-P intervals range from 0.49 to 1.0 second, the escape cycle is shortened. Such a shortening is maximal for R-P intervals ranging form 0.49 to 0.75 second and becomes progressively less with increasing R-P intervals. For example, the fourth escape cycle in the bottom strip measures 0.96 second and the R-P interval is 0.51 second, whereas the sixth cycle in the same strip measures 1.04 seconds and the corresponding R-P interval is 0.86 second. The relationship between R-P interval and escape cycle length is shown in Figure 2. It is evident that sinus impulses occurring relatively early after an escape complex delay the delivery of the ensuing ectopic impulse, leading to prolongation of the escape cycle, while relatively late sinus impulses accelerate the next discharge of the A-V junctional focus. The basic or “undisturbed” automatic cycle measures 1.08 second and is not affected by sinus impulses occurring either very early (,0.36 sec) or very late (.1.0 sec).

Figure 1. Recording of lead V1 (the three upper strips are continuous). Numbers below the tracing correspond to R-R intervals. Numbers above the tracing indicate R-P intervals, measured from the beginning of the QRS complex to the positive peak of the P wave. All time intervals are in seconds.

Satullo et al. Arrhythmia of the Month

Figure 2. Relationship between R-P intervals (horizontal axis) and R-R intervals (vertical axis). All time intervals are in seconds. See text for explanation.

1057

Transition between prolongation and the shortening phase is abrupt and occurs at a point called the “reversal point,” which in experimental and clinical examples of modulated parasystole occurs at about half of the parasystolic cycle length. In the curve shown in Figure 2, the reversal point occurs at 0.49 second, that is, at 45% of the escape cycle. The A-V junctional focus cannot be deŽ ned as truly parasystolic because (1) we do not have proof that impulses arising from sites distal to the block (e.g., ventricular extrasystoles) cannot reset the focus; and (2) the A-V junctional pacemaker is not “protected,” but sinus impulses are unable to discharge it as a consequence of complete A-V block. The unexpected “modulation” of this escape rhythm from the sinus node suggests that the A-V junctional pacemaker is immediately distal to the site of block so that sinus impulses are able to exert an electrotonic in uence upon the escape pacemaker. References

The biphasic phase-response curve shown in Figure 2 is very similar to those observed in modulated parasystole. In this situation, sinus or dominant impulses do not discharge or reset a “protected” focus but rather in uence it electrotonically. Early impulses result in prolongation, and late impulses result in shortening of the parasystolic cycle.1 ,2

1. Jalife J, Moe GK: Effects of electrotonic potentials on pacemaker activity of canine Purkinje Ž bers in relation to parasystole. Circ Res 1976;39:801-808. 2. Oreto G, Satullo G, Luzza F, Donato A, Maugeri Sacca` C, Arrigo F, Consolo F, Schamroth L: “Irregular” ventricular parasystole: The in uence of sinus rhythm on a parasystolic focus. Am Heart J 1988; 115:121-133.