An unusual mechanism of arrhythmia production

J. ELECTROCARDIOLOGY, 9 (4) 1976 371-373

An Unusual Mechanism of Arrhythmia Production BY RICHARD A. CARLETON, M.D., F.A.C.C.*

SUMMARY

CASE REPORT

An u n u s u a l electrocardiogram (ECG) is presented which demonstrates two mechanisms of c o m m u n i c a t i o n between the atria and the ventricles. The first appears to reflect o r d i n a r y a t r i o - v e n t r i c u l a r i m p u l s e propagation. The second appears likely to represent stimulation of the ventricles by mechanical atrial systole.

A 52 year old man experienced oppressive retrosternal chest pain, associated with diaphoresis, nausea and vomiting, during the hour preceding presentation to the hospital. The patient was immediately placed in the Coronary Care Unit for electrocardiographic monitoring. Physical examination showed a diaphoretic man in moderate discomfort from precordial pain. The blood pressure was 110/70 mm Hg; the pulse was 78/min and regular. The cardiovascular examination revealed a 4th heart sound b u t was otherwise normal. The admission ECG i l l u s t r a t e d sinus rhythm, a P-R interval of 290 msec, with QRS deformities and ST-T changes indicative of an inferior wall myocardial infarction. Serial creatine phosphokinase determinations confirmed the presence of myocardial infarction. The patient convalesced uneventfully apart from a brief period of arrhythmia. The patient was placed on a continuous electrocardiographic display system using a right s u b c l a v i c u l a r - - 4th left i n t e r s p a c e p a r a s t e r n a l electrode placement. Approximately six hours after admission, the ECG illustrated in Fig. 1 was recorded. This represents two excerpts from a continuous strip obtained during one minute. The a r r h y t h m i a subsequently disappeared; the first degree atrio-ventricular block displayed in Fig. 1 disappeared over the succeeding 48 hours. The patient convalesced without further detected arrhythmias and was discharged from the hospital.

I n i t i a t i o n or m a i n t e n a n c e of c a r d i a c rhythms is a process generally considered to result from s p o n t a n e o u s depolarization of automatic cells or from disordered impulse p r o p a g a t i o n . 1 Those r h y t h m m e c h a n i s m s which probably reflect disorders of impulse propagation include parasystole and the process called reentry. 2 Yet it is clear that other mechanisms for r h y t h m generation exist. Oscillating membrane potentials following a preceding impulse m a y cause p r e m a t u r e beats. 3 Mechanical stimulation can also produce cardiac depolarization. This mechanism is commonly seen during cardiac catheterization. Other examples of this include the single precordial " t h u m p " a i m e d at r e v e r t i n g v e n t r i c u l a r tachycardia, 4 and rhythmic delivery of blows to the chest to generate a sustained r h y t h m in the presence of complete atrio-ventricular block. 5 These external "thumps" have been likened to electrical energy discharges of 1-10 Watt-seconds. This paper illustrates an unusual arrhythmia - - one which appears to d e m o n s t r a t e p r e m a t u r e v e n t r i c u l a r depolarizations related to the mechanical activity of the atria r a t h e r than to either a u t o m a t i c i t y or disordered impulse propagation.

DISCUSSION The recording demonstrates a number of phenomena. The P waves are variable. The P-P interval, as indicated in Table I, varies from 680 msec to 850 msec. The P wave morphology varies slightly, b u t is always bi-phasic. The P wave p r e c e d i n g QRS complex B a p p e a r s to be slightly different and is unusually premature. This may represent an ectopic atrial premature beat. Overall, the nature of the atrial arrhythmia is unclear and m a y reflect slight

From the Dartmouth Medical School, Hanover, New Hampshire. *Professor of Medicine Reprint requests to: Richard A. Carleton, M.D., Professor and Chairman, Department of Medicine, Dartmouth Medical School, Hanover, NH 03755. 371

372

CARLETON

TABLE I Intervals derived from Fig. 1 The P-P and R-R intervals are between designated P-QRST complexes;the P-R relationshipsare those immediately preceding each QRS complex. Complex

1

A

P-P

2

3

780

P-R

180

R-R

580

Complex

7

760

I

760

J

150

R-R

640

700

130

780

C

810

520

790

360

980

L 800

170

740

4

190

K

800

P-R

680

360 350

960

P-P

B

750

850

140

810

i!2

A

3

B

..........4

C

920

180

920

170

630

710

720

900

980

710

520

850

360

9

160

G

750

130

P

360

6

750

8 720

F

820

360

0 850

E

700

760

110

820

5

140

N

v a r i a t i o n in locale of p a c e m a k e r a c t i v i t y within the sinus node or within the atria or may represent a nonrespirophasic sinus arrhythmia. There are two types of QRS complexes. Each P wave is followed by one or another type of QRS complex. The first type follows P w a v e s after an i n t e r v a l of 350-360 msec. These QRS complexes have a duration of approximately 100 msec and have an R-S morphology. The second type of QRS complex has a duration of approximately 130 msec and has an r-S-R morphology. The two types of QRS complexes are d e s i g n a t e d n u m e r i c a l l y or alphabetically respectively. The n u m e r i c a l l y d e s i g n a t e d QRS complexes appear to bear a cause-effect relationship to the antecedent P waves and have a relatively fixed P-R relationship of 350-360 I

150

M

120

770

580

790

D

350

900

650

9

~

,'

~.! ,

~

I: .....

! ! A

II

I

J

K

L

820

360

840

msec. It is presumed that these complexes represent transmission of impulses through the A-V junction and down the His bundle. The first degree A-V block is assumed to be that commonly associated with inferior infarction. The QRS complexes which are alphabetically designated have initial deflections similar to those presumed to result from normal impulse propagation. The QRS abnormality, manifest mainly as a large secondary R wave, occurs independently of the preceding cycle length and without variable degrees of aberrancy. This suggests that these are impulses of ventricular origin rather than supraventricular impulses subjected to intraventricular aberrancy. With the particular lead used for recording, such beats might well have originated in the left ventricle. The R-R inD

5

E

!It!

.

F

6

.

.

.

.

.

.

.

.

G

dT

:7,

H

:~ v : -

.

'l:

,iJ: :! ,l: ! 7

720

840

!r m : ~i~

I![!:-!:::: i:: :1 :Kt:t

150

11

360

860

730

160

10 850

H

M

N

!, O

]: t l! I 8

!'i 2i P

9

I0

II

Fig. 1. Two excerpts from an electrocardiographic recording. Two types of QRS complexes are evident. One type is designated numerically and the other alphabetically. Peaks and nadirs of QRS complexes have been retouched. J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

MECHANICALLY INDUCED ARRHYTHMIA?

terval b e t w e e n t h e s e complexes is widely variable and has neither a common denominator interval of parasystole nor the features of intermittent parasystole. 6 The short P-R relationships for the alphabetically designated beats, combined with the prolonged QRS complex, raises the possibility of accelerated conduction through a parajunctional pathway. The variation of the P-R relationship between 110 and 180 msec suggests, however, that these impulses are not conducted through any uniform path from the atria to the ventricles. Yet, there is a sufficiently p r e d i c t a b l e relationship b e t w e e n preceding P - w a v e s and the a l p h a b e t i c a l l y d e s i g n a t e d QRS c o m p l e x e s to i n d i c a t e a cause-effect relationship. Conversely, the coupling interval of alphabetically designated QRS complexes to an antecedent QRS complex is totally unpredictable, For example, the coupling interval between alphabetically designated beats and the preceding QRS complex ranges from 520 msec (3-B) to 650 msec (6-G) for sporadic beats, and to as great as 920 msec (N-O) for periods of sustained abnormal rhythm. This appears to preclude re-entrant mechanisms of generation of this rhythm. The consistent P-QRS sequence for every cardiac cycle, despite the irregular rhythm, indicates that atrial activity is reliably communicated to the ventricles. Yet, as shown in Fig. 1 and in Table I, this patient exhibited two routes of communication. The first seems likely to represent communication through the atrio-ventricular junctional-His bundle route. The second mode of communication of the atria with the ventricles has variable timing, b u t has sufficient predictability to induce e i t h e r early (complexes A,B,C,E,G,I,P) or r a t h e r late (complexes D,F,H.J - - O) ventricular depolarizations. The alphabetically designated ventricular depolarizations have variations in rate between 65 and 85/min, largely paralleling variations in atrial rate. This appears to indicate t h a t isorhythmic atrio-ventricular dissociation is not present. The variable P-R relationship of alphabetically designated beats appears to preclude impulse propagation through a pathway composed of excitable tissue.

J. ELECTROCARDIOLOGY, VOL. 9, NO. 4, 1976

373

An alternative hypothesis is that the atria are initiating v e n t r i c u l a r responses via a mechanical route. In turn, the variably timed, b u t always antecedent P waves, would suggest that ventricular depolarizations are initiated by the mechanical activity of the atria. The normal atrial electromechanical delay i n t e r v a l of a p p r o x i m a t e l y 100 msec, after which atrial mechanical systole propels blood into the ventricles, is consonant with this hypothesis. It seems likely that the arrhythmia demonstrated has occurred as a sequel to mechanical stimulation of the ventricles by a t r i a l systole. It is u n c l e a r w h e t h e r this mechanical stimulation was transmitted to the ventricles across the A-V groove, by blood entering and distending the ventricles, or by contact between a part of the A-V valve complexes and the ventricular wall. The electrocardiogram presented seems to show the induction of ventricular p r e m a t u r e beats and of ~slow" ventricular tachycardia by mechanical stimulation related to atrial systole. Perhaps recently infarcted ventricular muscle is particularly vulnerable to such stimulation. Perhaps careful search will reveal other instances of similar arrhythmias.

REFERENCES 1. HOFFMAN, B F AND CRANEFIELD, P F: Electrophysiology of the Heart. New York, McGraw-Hill, 1960 2. MOE, G K ANDMENDEZ,C: Physiologic basis of premature beats and sustained tachycardias. N Engl J Med 288:250, 1973 3. CRANEFIELD,P F, WIT,A L ANDHOFFMAN,B F: Genesis of cardiac arrhythmias. Circulation 47:190, 1973 4. PENNINGTON, J E, TAYLOR, J AND LOWN, B: Chest thump for reverting ventricular tachycardia. N Engl J Med 283:1192, 1970 5. WILD, J B AND GROVER, J D: The fist as an external cardiac pacemaker. Lancet 2:436, 1970 6. LANGENDORF,R AND PICK, A: Mechanisms of intermittent ventricular bigeminy. II. Parasystole, and parasystole or re-entry with conduction disturbance. Circulation 11:431, 1955