Studies
in P Wave
Synchronization*
PHILIP SAMET, M.D., F.A.c.c., CESAR CASTILLO, M.D. and ~YILLIAM H. BERNSTEIN, M.D., F.A.C.C. Miami
Beach,
msec.
N THE course of studies on the physiologic bases of electronic cardiac pacing, an investigation of P wave synchronization was undertaken. P wave synchronization is defined as the application of a ventricular endocardial stimulus at a preset interval after a P wave, simulating the electrophysiology of the WolffParkinson-White syndrome, at least when the preset atrioventricular delay is less than the control Pi-R interval. The purpose of this paper is to report the electrocardiographic changes that occur after application of a right ventrictllar endocardial stimulus applied at varving in ter\rals after a sinus P wave.
In a few patients, right ventricular pacing was employed to determine whether retrograde P waves could be detected by the standard or right atria1 leads.
I
~~ETH~DS
AND
Florida
RESULTS
&fed of Increasing P-Right
LTuztric.ulor Stimulus
wave synchronization 60 msec. after the P wa\re (control P--R interval 190 msec.) is shown in Figure 1. Lead II and the right atria1 electrocardiogram are shown together with the right altd left atria1 pressure curves and the femoral arterial pressure pulse. The first two electrocardiographic colupleses are control normal beats. The last four tvere recorded after the onset of P wave s\-nchronization at a P--R of 0.06 sec. The pa&n is similar to that seen in the \Volff-Parkinson-White syndrome. The P wave is not altered during synchronization, whereas the QRS complex undergoes radical change due to aberrant depolarization. ST refers to the stirmrlus applied to the right ventricular electrode-cathctel during P wave synchronization. ‘l% l’-ST interval is increased to 150 and 180 IIISPC. in Figure 2. These intervals are sufIicientl\- long so that the normal pathway of \-cntric(llar depolarization is utilized (note the normal QRS complex in the intra-atria1 electrocardiogram), despite distortion of the limb lead QRS COIIIplex by the stimulus itself. Increase of the P-ST interval to 410 msec. (Fig. 3) throws the ventricular stimulus into the T \vave, into the absolute refractory period. Further increase to 430 msec. (Fig. 4) results in the patterns of interpolated premature beats since the stilnulus is followed by an aberrant QRS complex without a succeeding retrograde P wave. Further increase of the P-ST interval to 440 to 450 (Fig. 5) results in a complete change in the electrocardiographic patterns in lead II and the atria1 (P-ST)
MATERIALS
‘l‘hirtk-one patients (aged 18-63 yr.) with normal sinus rhythm \~ere studied. Five patients were free of hpart disease : 15 had rheumatic heart disease and Il. pulmonary emphysema with or without car pulmonale. L4 .3..5 or 5F bipolar electrode-catheter (U. S. Cathcrer Co.) \vas passed into the right ventricular outflo\\- tract and a second bipolar electrode-catheter into the right atrium. .4 third No. 6F, 100 cm. long Lehman catheter \vas passed into the pulmonary artery. In some subjects the left atrium was entered by percutaneous femoral vein cannulation and transsrptal left atria1 puncture. A Cournand needle \vas employed to can&ate a systemic artery. Indicator-dilution cardiac outputs were recorded with indocyanine grcrn employing Gilford densitometers and Harvard constant infusion-withdrawal units. ,411 data wcrc recorded on an eight channel Electronics for Medicine recorder. R&lit atria1 electrocardiqrums were recorded simultaneously \vith a limb lead, usually lead II. The right atria1 P wave was also passed to the low level input of a Medtronic coupled pulse-generator, model 5837; the P wave was amplified and triggered a stimulus delivered to the right ventricular electrode-catheter at fixed, preset intervals varying from 60 to 800 msec. after the P wave, in steps of 10
Interval:
P
* Frown the Section of Cardiology, Department of Medicine, Mt. Sinai Hospital, Miami Beach, and the University of Miami School of Medicine, Coral Gables, Fla. This work was supported by grants from the National Heart Institute.
HE-0850343
and HE-09782-01.
\'O~u!vf~lb I').FEHRLTARY
1967
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Samet,
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and Bernstein
1. P wavesynchronyat a P-ST interval of 0.06 sec., simulating the Wolff - Parkinson - White syndrome. Control observations to the left (P - R = 0.19 sec.). Lead II and the right atria1 (I.A.)
FIG.
electrocardiogram are shown together with the right (R.A.) and left (L.A.) atria1 curves and the femoral arterial (F.A.) pulse curve. The sinus P waves are clear in the right atria1 electrocardiogram.
2. Same patient as in Figure The P-ST interval has been increased to 0.75 and 0.18 sec. The FIG.
1.
right ventricular stimulus is ineffective, i.e., ventricular depolarization is by the normal pathway.
FIG. 3. Same patient. The P-ST interval is increased to 0.47 sec., but the right ventricular stimulus is still ineffective, as the stimulus falls in the absolute refractory period.
electrogram. A retrograde P wave, which follows each QRS complex, is detected by the Medtronic stimulator and is followed by a An effective stimulus and a QRS complex. The sinus re-entry mechanism is thus initiated. P-P interval (Fig. 1) is 0.72 sec.; the retrograde P-P interval is shorter, 0.67 sec. In addition,
the shape of the retrograde and sinus P waves differ. The ventricular rate becomes a function of the P-ST interval and is greater during the re-entry rhythm than during the control preceding sinus rhythm. The data in another patient (Fig. 6-8) provide further insight into the mechanism of the THE
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P Wave
Synchronization
209
FIG. 4. Same patient. The P-ST interval is increased to 0.43 sec. To the right, alternate stimuli are effective and produce aberrant ventricular beats. There are no retrograde P waves, and the sinus P wave rhythm is undisturbed.
FIG. 5. Same patient. The P-ST interval is increasedto 0.44 to 0.45 sec. A ventricular rhythm with retrograde P waves is present.
change in the QRS complex as the P-ST interval is lengthened. In Figure 6 the stimulus falls in the absolute refractory period and is ineffective. When the P-ST interval is increased to 0.57 sec., the same changes described in Figure 5 occur, and a ventricular rhythm with retrograde P waves is noted (Fig. 7). The mechanism of the rhythm in Figures 5 and 7 is probably as follows: The first effective idioventricular beat (produced by application of the stimulus ST to the right ventricular endocardial surface) is followed by a retrograde P wave. In turn, the latter is followed by another stimulus at a preset interval of 0.57 sec., providing another idioventricular beat and a retrograde VOLUME
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The rhythm is thus perpetuated by a P wave. re-entry mechanism involving an external pathThe way through the Medtronic stimulator. retrograde P-P cycle is shorter than the sinus P-P cycle length. In Figure 8 the electrocardiogram of right ventricular pacing is shown. Each QRS complex is followed by a retrograde P wave, as in Figure 7. The form of the retrograde P wave in Figures 7 and 8 is similar and differs from the sinus P wave in Figure 6. Re-entry Mechanisms: The electrocardiographic patterns in Figure 9 provide further insight into the mechanism of the re-entry capture of the cardiac rhythm as the P-ST interval Each of the is altered to more than 320 msec.
Samet,
210
Time I_-...-
liner:0.04
set
Castillo
and Bernstein
75mm Jsec
FIG. 6. Control data in a secondpatient. Lead II and the right atria1 electrocardiogram are shown. The stimulus falls in the absolute refractory period.
Sinur P-P: 100 **c. 75mm/rec
Time liner: 0.04 IBC
FE. 7. Same patient as in Figure 6. The P-ST interval is increased to 0.57 sec. A ventricular rhythm with retrograde P waves is shown.
first two idioventricular beats to the left is followed by a retrograde P wave perpetuating the ventricular mechanism. Block of the retrograde P wave develops at the indicated time; the sinus node therefore regains control of the heart. Note that the sinus P-P interval (0.62 sec.) is again longer than the retrograde P-P interval (0.51 sec.). Another interesting facet of the problem should be mentioned. In another subject, at a P-ST interval of 390 to 400 msec., the stimulus fell within the absolute refractory period, and the ventricular response was absent. At a P-ST interval of 400 msec. or more, idioventricular pacing was present with retrograde P wave conduction. The control sinus P-P interval was 0.84 sec. The retrograde P-P interval at a P-ST of 400 msec. was 0.68 sec. As the P-ST interval was lengthened to 0.49 and 0.60 sec., the retrograde P-P interval increased to 0.70 and 0.78 sec. respectively. As the P-ST interval was lengthened during the
idioventricular the retrograde be anticipated.
retrograde P re-entry mechanism, P-P interval increased, as might
DISCUSSION Electronic pacers have been employed to bridge atrioventricular block for several years. Kahn et al.’ reported an experimental unit in 1960; Nathan and co-workers2 adapted the same principle to practical Clinical utilization. The resulting electrocardiographic pattern is similar to that described in the Wolff-ParkinsonWhite syndrome.Y A comparable technic has been utilized in the present study, with two bipolar catheters, one in the atrium for detecting the P wave and one in the ventricle for ventricular stimulation by a Medtronic coupled pulsegenerator. When the preset interval between the P wave and the ventricular stimulus {P-ST interval) is well below the control P-R interval, a syndrome similar to that of Wolff-ParkinsonTHE
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P Wave
FIG. 8. Same patient. Right ventricular waves similar to those in Figure 7.
rhythm
FIG. 9. Mechanism of ventricular The P-ST interval is 0.32 sec.
and sinus rhythm
pacing
When the delay of the White results (Fig. 1). P-ST stimulus approximates the control P-R interval, the ventricular stimulus is ineffective (Fig. 2). When the P-ST interval is made even longer and the stimulus falls between the QRS and T waves (absolute refractory period), the stimulus remains ineffective (Fig. 3). Further prolongation of the P-ST interval renders the stimulus effecti\,e, resulting in a ventricular beat that produces a retrograde P wave which is picked up by the stimulator that then delivers a ventricular stimulus, after the preset delay. A ventricular feedback rhythm is thus established with a re-entry mechanism. The resulting retrograde P wave has a contour different from the sinus P and is generally premature and, of course, follows rather than preThe rate of the retrocedes the QRS complex. grade P wave is invariably faster than that of the sinus P \.2-a\‘eand has the same contour as the retrograde P wave obtained during right ventricVOLUME
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211
Synchronization
is present
with retrograde
in a third
P
patient.
ular pacing. The interval between the QRS complex and the retrograde P wave is generally fixed. The longer the P-ST interval used to induce the re-entry rhythm, the greater is the retrograde P-P interval. Fusion P waves, as described by Kistin and Landowne,4 were not recognized in the present study. Retrograde P Waves Following I’entricular Premature Beats: The entire subject of retrograde ventriculoatrial conduction after ventricular premature beats in man has been reviewed by Kistin and Landowne.4 These observers found evidence of such conduction in 15 of 33 people studied with esophageal leads. The limited ability of these authors to detect retrograde conduction on surface leads was stressed, accounting for the belief held until Kistin’s work that such conduction is uncommon in man. The present authors are unaware of the previous use of intracardiac electrocardiography to detect retrograde P waves after induced
212
Samet,
Castillo
ventricular rhythms. In the present study we have detected retrograde P waves in fully 29 of 31 cases studied. This is a considerably higher percentage than noted by Kistin et a1.4 The reason for the difference is probably related to the fact that some of the ventricular premature beats in Kistin’s study occurred at the time of a sinus P wave, thereby rendering the atrium or atrioventricular node transiently refractory to retrograde conduction. Such a mechanism could not of course be operative in the present investigation. It is of further interest that we have recorded retrograde P waves in 4 of 6 patients with complete heart block and slow ventricular rates (less than 45) studied during right ventricular bipolar catheter pacing. These data will be reported elsewhere.5 Kistin and Landowne4 raised another problem in the interpretation of retrograde P waves following ventricular premature beats. The possibility that the aberrant QRS complexes recorded in the esophageal electrocardiogram may have been nodal with aberrant conduction could not be completely ruled out. The data in the present study, with ventricular complexes arising via a bipolar right ventricular catheter, prove that retrograde conduction may occur across the atrioventricular node after ventricular beats. Reciprocal Rhythm and Re-entry Mechanisms: KistinGJ has more recently analyzed the problem of reciprocal rhythm initiated by ventricular premature systoles, employing esophageal and standard leads. In 1 patient ventricular premature systoles with retrograde P waves and ventriculoatrial conduction times of 0.16 to 0.24 sec. were not associated with reciprocal rhythm. Ventricular premature systoles with ventriculoatrial conduction times of 0.39 to 0.49 sec. were frequently associated with reciprocal rhythm. Similar observations were made in a large number of other subjects. In the observations reported by us, the reincluded the Medtronic ciprocal pathway pacer unit. In three recent studies*-lo the problem of ectopic ventricular rhythms has been discussed in terms of the Wedensky effect (lowering of the excitability threshold by a strong stimulus) or in terms of a re-entry mechanism. Our data illustrate the feasibility of
and
Bernstein
the latter mechanism, at least under the experimental conditions employed. It is worthy to note that no episodes of ventricular fibrillation were produced in the present study, despite the fact that the stimuli were delivered throughout the entire cardiac cycle, including the vulnerable period. SUMMARY
The results of P wave synchronization in man employing a bipolar atria1 and a bipolar ventricular catheter have been presented. As the P-ventricular stimulus interval is increased, a ventricular rhythm with retrograde P waves and a re-entry mechanism was found. The characteristics of the rhythm are discussed together with the possible significance thereof. REFERENCES 1. KAHN, M., SENDEROFF, E., SHAPIRO, J., BLEIFER, S. B. and GRISHMAN, A. Bridging of interrupted A-V conduction in experimental chronic complete heart block by electronic means. Asn. Heart J., 59: 548, 1960. 2. NATHAN, D. A., SAMET, P., CENTER, S. and WV, C. Y. Long-term correction of complete heart block. Clinical and physiologic studies of a new type of implantable synchronous pacer. Prog. Cardiovas. Dis., 6: 538, 1964. 3. WOLFF, L., PARKINSON,J. and WHITE, P. D. Bundle branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia.
Am. Heart J., 5: 685, 1930. 4. KISTIN, A. D. and LANDOWNE, M.
Retrograde conduction from premature ventricular contractions, a common occurrence in the human heart. Circulation, 3: 738, 1951. 5. CASTILLO, C., SAMET, P. and BERNSTEIN, W. I-I. Retrograde P wave conduction in complete heart block. Brit. Heart J., in press. 6. KISTIN, A. D. Mechanism determining reciprocal rhythm initiated by ventricular premature systales. Multiple pathways of conduction. Am. J. Cardiol., 3: 365, 1959. 7. KISTIN, A. D. Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular premature systoles. Am. Heart J., 65: 162, 1963. Genesis and evolution of ectopic ventricular rhythm. Brit. Heart J., 28: 244, 1966. 9. CASTELLANOS, A., JR., LEMBERG, L., JOHNSON, D. and BERKOVITS, D. V. The Wedensky effect in the human heart. Brit. Heart J., 28: 276, 1966. 10. MOE, G. K. and MENDEZ, C. The physiologic basis Prog. Cardiovas. Dis., 8: of reciprocal rhythm.
8. SCHAMROTH, L.
461, 1966.
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