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The Mechanism of Synchronization Isorhythmic A-V Dissociation II. in Clinical Studies By MATrHEW N. LEVY, M.D., AND JOSEF EDFLSTEIN, M.D. Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 SUMMARY The electrocardiographic patterns recorded from seven patients with isorhythmic A-V dissociation fall into two distinct groups. In pattern I, the P wave fluctuates cyclically back and forth across the QRS complex. The mechanism responsible for this type of A-V synchronization represents a typical biologic feedback control system. The P-R interval is a determinant of stroke volume, which in turn influences the arterial blood pressure. The blood pressure has an inverse effect on the discharge frequency of the S-A node through the baroreceptor reflex. The S-A nodal frequency then affects the P-R interval, to close the feedback loop. In pattem II, the P wave is in a fairly constant position relative to the QRS complex. It is usually coincident with the QRS complex or appears on the ST segment or first half of the T wave. The mechanism producing synchronization in pattern II type of isorhythmic dissociation has not been established conclusively. Additional Indexing Words: Arteriosclerotic heart disease Arrhythmia Complete heart block Atrial contraction Myocarditis Junctional rhythm Electrocardiogram recently been noted in dogs with experimentally produced complete heart block.8 In these animals, synchronization was critically dependent upon the accompanying rhythmic fluctuations in arterial blood pressure; when such pressure variations were precluded, synchronization ceased. A feedback control loop was shown to be operative, in which a change in P-R interval affects the blood pressure, the change in blood pressure alters the S-A nodal frequency, and the consequent change in cardiac cycle duration alters the P-R interval, to complete the loop. In the study described herein, observations have been made on a group of patients with various forms of isorhythmic dissociation to determine whether such a correlation between P-R interval and arterial blood pressure also prevails in the clinical arrhythmia. IT HAS been recognized for many years that in complete heart block, there is a distinct tendency toward synchronization of atria and ventricles.'- 3 In the absence of ventricular pacing, the ventricular contraction frequency is ordinarily much less than the atrial contraction frequency. In such cases, synchronization is manifested as an integral ratio of atrial to ventricular contractions (such as 2:1, 3:1, and 3:2). Patients with severely impaired A-V conduction but without complete block have a pronounced tendency toward A-V synchronization when the ventricles are paced at a frequency close to the spontaneous sinoatrial (S-A) nodal rate.7 A similar manifestation has From the Departments of Investigative Medicine and Cardiology, Mt. Sinai Hospital, Cleveland, Ohio. This work was supported by Grant HE-10951-03 from the U. S. Public Health Service. Received May 26, 1970; revision accepted for publication July 14, 1970. Circulation, Volume XLII, October 1970 Artificial pacemaker Digitalis toxicity P-R interval Methods Observations were made on seven patients with various forms of A-V dissociation. In three of 689 LEVY, EDELSTEIN 690 Figure 1 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Continuous strip (lead II) from a patient (case 1) with complete heart block; right yentricular pacing. Innt 150- 0 Figure 2 Correlation between the electrocardiogram and the arterial blood pressure (mm Hg) in case 1. Right ventricle was paced at 67 stimuli/min. these patients, isorhythmic dissociation had developed spontaneously. One of these patients had chronic myocarditis, and the other two had arteriosclerotic heart disease with digitalis toxicity. In the remaining four patients, three with third-degree A-V block and one with seconddegree (2:1) block, temporary transvenous pacemakers had been inserted into the right ventricular cavity. In the course of studies preparatory to the insertion of permanent pacemakers, the tendency for A-V synchrohization was determined by gradually varying the ventricular pacemaker frequency. An indwelling needle was inserted into the brachial or radial artery, and the arterial pressure and the electrocardiogram were registered simultaneously on an Electronics for Medicine recorder. Results Case 1: Complete A-V Block with Ventricular Pacing The electrocardiogram shown in figure 1 was recorded from an 84-year-old man with complete heart block. When the pacemaker frequency was adjusted to 65 stimuli/min, which was close to the spontaneous atrial frequency, a stable, persistent synchronization of atria and ventricles ensued. The two strips displayed in the figure are continuous, and they reveal the characteristic pattern of the oscillation of the P wave about the QRS. At the beginning of the top strip, the P-R interval was 0.23 sec, which was the maximum positive value. The P wave marched progressively to the right with respect to the QRS and passed into and then through the QRS. The maximum Circulation, Volume XLII, October 1970 ISORHYTUMIC DISSOCIATION 691 A 3 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 0 Figure 3 Continuotus strip from a patient (case 2) with right ventricular pacing for treatment of secondclegree A-V block (2:1). R-P interval of 0.12 sec was reached at the end of the top strip. The P then moved to the left relative to the QRS, so that by the end of the bottom strip, the P was 0.21 sec before the QRS. This oscillation of the P about the QRS was repeated continuously, with a period of about 20 sec. The correlation of the arterial blood pressure and the electrocardiogram in this patient is shown in figure 2. At the left end of the record, the P was just visible at the end of the R wave, and the arterial blood pressure was 115/60 mm Hg. The P frequenicy at this point in time was slightly greater than the R frequency, so that by the seventh beat, the P appeared slightly in front of the QRS, and the blood pressure started to rise. As the P continued to move to the left of the QRS, the blood pressure rose progressively. At the end of the tracing, the P wave was well in front of the QRS, and the arterial pressure had increased to 160/85 mm Hg. The fluctuations in arterial pressure were periodic, witlh the pressure peaks correspondinig to the positive P-R intervals Circulation, Volume XLII, October 1970 and the pressure troughs coincidinig with the negative P-R (or R-P) intervals. Case 2: Second Degree A-V Block with Ventricular Pacing The four consecutive electrocardiographic strips shown in figure 3 were recorded from a 75year-old man who h-ad a pacing catheter inserted for the treatment of a 2:1 A-V block. The venitricular pacing frequency was gradually increased to 100 stimuli/min, which was close to the prevailing rate of the S-A node. This resulted in atrioventricular synchronization, which was manifested by a slow oscillation of the P xvave about the QRS complex. In strip A, the P shifted slowly from just in front of the QRS simitil it coincided with the QRS, and finallv reappeared in the ST segment or orn the iniitial portionl of the T wave (strip B). The frequency of the P xave then increased, and the P begani to marel to the left relative to the QRS, uintil it mioved to a maximum interval of 0.20 sec befor-e the QRS 692 LEVY, EDELSTEIN 100 75 50 25 0 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Figure 4 Correlation between the electrocardiogram (aVe) and the arterial blood pressure (mm Hg) in case 2. Right ventricle was paced at 100 stimuli/min. B C 0 Figure 5 Conlitnuiouis strip (lead V) from a patient rcith chronic myocarditis (case 3). (strips C and D). Thereafter, the P-wave frequency diminished, and the P again moved to the right and disappeared in the QRS complex (end of strip D). The correlation between the P-R interval anid the arterial blood pressure in this patient is displayed in figure 4. When the P wave and QRS complex were coincident, the blood pressure was 90/35 mm Hg. When the onset of the P wave preceded the QRS, then the arterial blood pressure increased to a maximum valuLe of 115/40 mm Hg. Case 3: Chronic Myocarditis with Spontaneous Isorhythmic Dissociation The four continuous strips of electrocardiogram shown-i in figure 5 were recorded from a 44-yearold man with chronic myocarditis. At the Circulation, Volume XLII, October 1970 ISORHYTHMIC DISSOCIATION 100o- 2-- 7510 693 - 0 0 0 ^): 0 ; k t ; 25 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Figure 6 Correlation between electrocardiogram (lead aVF) and arterial blood pressure (mm Hg) in a patient with complete heart block (case 4). Right ventricle paced at 84 stimuli/min. Note premature P waves before sixth and tenth QRS complexes and the consequent reductions in arterial blood pressure. beginning of strip A, the P wave was buried in the QRS complex. It gradually moved in front of the QRS, to reach a maximum P-R interval of 0.14 sec near the middle of strip A. Thereafter, the P wave gradually shifted back toward the QRS, to become lost in it again near the beginning of strip B. The P remained masked by the QRS for about 21 sec, and then reappeared in front of the QRS near the beginning of strip D. A maximum P-R interval of 0.14 sec was again attained, after which the P wave again moved to the right to disappear within the QRS complex once more. Intra-arterial blood pressure recordings in this patient revealed that when the P wave was located in front of the QRS, the blood pressure averaged 120/75 mm Hg. When the P wave coincided with the QRS complex, the blood pressure decreased to 105/70 mm Hg. Case 4: Complete Heart Block with Ventricular Pacing A pacemaker catheter was inserted in this 79year-old man for the treatment of complete heart block. Adjustment of the frequency of the pacemaker to that near the prevailing S-A nodal rate resulted in A-V synchronization, with the P wave oscillating slowly about the QRS. These oscillations were irregular because of frequent premature atrial contractions, and the period varied from 15 to 45 sec. The variations in arterial blood pressure Circulation, Volume XLII, October 1970 associated with the changes in P-R interval are apparent in figure 6. When the P wave was located on the ascending limb of the T wave (first four beats), the blood pressure was only 85/40 mm Hg. As the P gradually advanced in front of the QRS, the blood pressure increased to 105/45 mm Hg. The influence of P-R interval on blood pressure is also evident in the record by virtue of the occurrence of two premature atrial contractions. After each of these atrial contractions (sixth and tenth beats), there was a significant reduction in the systolic arterial blood pressure resulting from the corresponding ventricular contractions. The excessively prolonged P-R intervals were evidently well beyond the optimum value. Case 5: Arteriosclerotic Heart Disease with Digitalis Toxicity This 80-year-old man was admitted to the hospital in congestive heart failure, with a history of three previous myocardial infarctions. He had been treated with digitoxin, antihypertensive agents, and diuretics. His electrocardiogram on admission exhibited signs of the remote infarctions, a prolonged P-R interval (0.22 sec), and other effects of digitalis. On the third hospital day, the sinus rhythm was replaced by one in which the P waves consistently occurred shortly after the QRS complex (fig. 7A) but were upright in leads II, III, and aVF. LEVY, EDELSTEIN 694 I- D~~~ Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 lFigure Electrocardiog:ram (lead III) from a patient 7 with toxicity (case 5). A continuous strip was recorded arteriosclerotic heart At the beginning of strip B, the carotid sinus regions were massaged. strips: A-B, 35 sec; B-C, 19 sec; C-D, 18 see; D-E, 24 see; E-F, Seven segments from a continuous tracing (lead III) are shown in figure 7. The most frequent position of the P wave was in the ST segment (as in the last five beats in strip A). However, the R-P interval occasionally became more prolonged so that the P wave appeared just before the summit of the T wave (as in the first several beats of strip A). During the 35 sec which elapsed between strips A and B, the P wave remained in the same position as in the last few beats of strip A. During the first two beats of strip B, pressure was applied to the carotid sinuses. This resulted in a significant prolongation of the next R-R interval of 0.30 sec, but produced a lengthening of the corresponding P-P interval of only 0.04 sec. As a consequence, the P wave preceded the QRS by 0.20 sec (presumably sinus rhythm) during the last four beats in strip B. During the subsequent 2 or 3 min, the atria and ventricles became dissociated. In the 19 sec between strips B and C, the P-P and R-R intervals gradually diminished, but the R-R interval decreased slightly more rapidly than did the P-P interval. Consequently, the P-R interval was gradually reduced, and it measured only 0.11 sec in strip C. Both P-P and R-R intervals gradually increased during the 18 sec period between strips C and D, but the increments in R-R slightly exceeded those in P-P. Therefore, the P-R interval gradually increased again and was 0.20 sec in strip D. Subsequently, the S-A and junctional pacemakers again accelerated, the junctional slightly more disease and digitalis from which seven segments were selected. Time 33 see; intervauls betwJeen and EG, 49 sec. than the sinus nodal; again the P-R interval gradually diminished. The P-R interval decreased from 0.16 sec to 0.12 sec in strip E (recorded 24 sec after D), and was 0.06 sec in strip F (recorded 33 sec after E). There was a slight, transient prolongation of the P-R interval after strip F was recorded. The P-R interval then gradually diminished until the P wave finally moved into and through the QRS. It reappeared on the ST segment, where it remained thereafter in a relatively fixed position. Forty-nine seconds elapsed between strips F and C. Repetitive determinations of systolic arterial blood pressure were made by the usual sphygmomanometric method during the above observations. Measurements were made by a cardiology resident who was not apprised in advance of the purpose of the measurements nor of the existing relationship between the P waves and QRS complexes at the time of each blood pressure determination. Before and during strip A, the mean level of the systolic pressure was 116 mm Hg. While the P wave preceded the QRS (strips B through F), the systolic pressure averaged 130 mm Hg. When the P returned to its relatively fixed position after the QRS (strip G), the systolic pressure fell to 100 mm Hg. Case 6: Complete Heart Block with Ventricular Pacing A transvenous pacemaker was inserted into the right ventricle of this 68-year-old man for the treatment of complete heart block with recurrent Circulation, Volume XLII, October 1970 ISORHYTHMIC DISSOCIATION 695 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Figure 8 Continuous strip (lead I) recorded from case 7. 4~~~~~~4A4c~~~~~~~~ {iMf. S-M. ......... -M* *- .:(L it + min ATROPINE 0.8 MG min t+10 6~ ATROPINE min 0.8 MG Figure 9 + 35 min Segments of lead II recorded fromt case 7, 1 min before (strip 1) and 6 min after (strip 2) atropine sulfate, 0.8 mg iv. A second injection of atropine, 0.8 mg iv, was given 7 min after the first injection. Strips 3 and 4 were recorded 10 and 35 min, respectively, after the first injection. episodes of syncope. When the frequency of ventricular pacing was different from the spontaneous S-A nodal frequency by 2 beats/min or more, there was little tendency evident for synchronization of atria and ventricles. When the P waves preceded the QRS complexes, then the arterial pressure was greater than when the P waves occurred just after the QRS. However, the changes in arterial pressure were not great (10 to 15 mm Hg change in systolic pressure and about 5 mm Hg change in diastolic pressure). When the ventricular pacing frequency was within 2 beats/min of the spontaneous atrial frequency, persistent synchronization did occur. In this patient, however, there was no characteristic oscillation of the P about the QRS. Instead, the P wave remained in a rather constant position near the beginning of the T wave. Circulation, Volume XLII, October 1970 Case 7: Arteriosclerotic Heart Disease with Digitalis Toxicity Figure 8 shows a continuous rhythm strip (lead I) recorded from a 58-year-old man in congestive heart failure, who was treated with digoxin and ethacrynic acid. At the beginning of the top strip, the P wave is located in the ST segment. The R-P interval gradually diminished, so that in beats 3 to 5 in the bottom strip, the P is manifested simply as a slurring of the downstroke of the R wave. The R-P interval then increased again, and the P is clearly evident in the ST segment at the end of the bottom strip. Similar changes in R-P interval were also recorded in leads II, III, and aVF. In all these leads, the P wave was upright. The changes in the electrocardiographic pattern associated with the intravenous injections of 696 atropine sulfate are displayed in figure 9. One minute prior to the first injection, the heart rate was 80 beats/min, and the P wave in lead II was upright and located in the ST segment. Six minutes after administration of atropine (0.8 mg), the heart rate increased to 100 beats/min, and the P wave was largely obscured by the QRS. A second injection of atropine was given 7 min after the first, and 3 min later, the heart rate was still 100 beats/min, but now the beginning of the P was evident just in front of the QRS (P-R interval, 0.04 sec). At 35 min after the first injection, the Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 mechanism had reverted briefly to a normal sin7ts rhythm, with a heart rate of 90 beats/min and a P-R interval of 0.15 sec. This persisted only 3 min; then the pattern returned to that observed 6 min after the first injection (second tracing, fig. 9). Discussion In isorhythmic dissociation, the relationship between the P waves and QRS complexes appears to fall into two distinct patterns. The first type of pattern is characterized by a rhythmic fluctuation of the interval between the P and QRS waves, most often with the P oscillating gradually back and forth across the QRS; that is, with periodically varying P-R and R-P intervals. This pattern, which has been described previously by numerous observers,5 9-16 was characteristic of cases 1 through 4 in the present study. Furthermore, this pattern occurred consistently in the dog with experimentally induced A-V block in which ventricular pacing was used.8 In the second type of electrocardiographic pattern, the P-R or R-P interval did not undergo rhythmic fluctuations, but the P and R waves were in a relatively fixed position with respect to each other. This pattern, which has also been reported frequently,6 15,17-21 was observed in cases 5 through 7 of the present study. It did not appear during synchronization in the experimental animal with complete heart block.8 Pattern I: Rhythmical Variations in P-R and R-P Intervals The mechanism of A-V synchronization in this type of isorhythmic dissociation has been elicidated by recent studies on dogs with experimentally induced complete heart block.8 A classical biologic control system was shown to be operative. The dissociated atrial and LEVY, EDELSTEIN ventricular pacemaker sites are differentially responsive to the level of the arterial blood pressure. The frequency of the usual atrial pacemaker (that is, the S-A node) varies inversely as the arterial pressure, primarily via the sino-aortic baroreceptor reflex. Idioventricular pacemaker cells are presumably less responsive to reflex alterations in autonomic neural activity, and with artificial ventricular pacing, the ventricular contraction frequency would, of course, be totally independent of the level of the arterial blood pressure. The phase difference (the P-R interval) between the beginnings of atrial and ventricular activation is a determinant of stroke volume, and hence of the arterial blood pressure.22-28 The correlation between the A-V contraction delay and the arterial blood pressure in animals was described originally by Gesell22 in 1911, and analogous phenomena have subsequently been reported in human subjects.2 34 In the patients analyzed in the present study who exhibited the pattern I type of isorhythmic dissociation (cases 1 to 4), there was a characteristic relationship between the P-R interval and the arterial blood pressure. As shown in figures 2, 4, and 6, as the P wandered rhythmically back and forth across the QRS, the blood pressure increased significantly as the P moved in front of the QRS, and fell as the P moved into and behind the QRS. This relationship between the P-R interval and the blood pressure closely resembled that seen in the experimental animal under analogous conditions.8 In the dog with experimentally induced complete A-V block, it was demonstrated that the rhythmic fluctuations in blood pressure were essential for synchronization.8 When the amplitude of the fluctuations was severely attenuated, synchronization ceased. In patients with the pattern I type of isorhythmic dissociation, the same mechanism producing synchronization undoubtedly prevails. As the P moves to the right and passes beyond the QRS, the blood pressure decreases, and this reflexly accelerates the S-A node. The P then begins to move to the left relative to the QRS, and when the P passes in front of the QRS, Circulation, Volume XLII, October 1970 ISORHYTHMIC DISSOCIATION Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 the blood pressure begins to rise. The motion of the P to the left relative to the QRS is thereby decelerated, and within a few beats, the P begins moving to the right again, to complete the cycle. Synchronization can be sustained by this mechanism when the steady-state gains of two of the elements in this biologic feedback loop are of sufficient magnitude.8 One of these gains is the change in blood pressure per unit change of P-R interval, and the other gain is the change in S-A nodal frequency per unit change in blood pressure. It was very difficult to produce persistent synchronization in patient 6. The probable reason is that the first of these system gains was inadequate. In this patient, the arterial pressure was affected only slightly by the position of the P relative to the QRS. Perhaps atrial contractility was severely depressed, so that the extent of the atrial contribution to ventricular filling was minimal even when the P-R interval was optimal. Pattern II: Relatively Fixed Relationship Between P and QRS In this type of isorhythmic dissociation, the P wave is in a fairly constant position relative to the QRS complex. It is usually coincident with and therefore hidden by the QRS complex, or it is located on the ST segment or first half of the T wave.6' 15. 17-21 This pattern was observed in cases 5 through 7 of the present study (fig. 7, panels A and G; fig. 8). Since the beginning of atrial activation occurs synchronously with or later than the beginning of ventricular excitation, any small change in the R-P interval is not likely to affect arterial blood pressure significantly. Therefore, the mechanism proposed to explain the pattern I type of isorhythmic dissociation cannot account for synchronization in the pattern II of this arrhythmia. Several other mechanisms have been proposed which could explain synchronization in this form of isorhythmic dissociation. The most widely cited hypothesis is that advanced by Segers,35 who demonstrated electrical and mechanical interactions in separate segments of frog heart. It has been postulated that there is an electrical interaction between dissociated Circulation, Volume XLII, October 1970 697 atrial and ventricular pacemakers which is analogous to that between two coupled relaxation oscillators.'3' 36 The mechanical pulsation in the S-A node artery has been shown to have a synchronizing effect on the pacemaker cells in that node.37 It is conceivable, therefore, that arterial pulsations could also produce a synchronizing effect on pacemaker cells in the A-V junctional or ventricular conducting tissue, thereby synchronizing atria and ventricles. It is also possible that some reflex mechanism might be involved, other than that responsible for the pattern I type of synchronization. Recent studies have demonstrated that discrete bursts of impulses in the efferent cardiac vagus nerves tend to synchronize the pacemaker activity in the S-A node with the rhythmic neural action potentials.38 3 Such bursts of activity in the efferent vagal pathways could originate from the effect of ventricular ejection on the arterial baroreceptors,40' 41 and they could thereby synchronize atrial contraction with ventricular ejection. In one patient in the present study (case 7), isorhythmic dissociation ceased briefly after atropine (fig. 9). However, the effect did not occur until 35 min after atropine and was so transient that this incident cannot be considered convincing evidence in support of a vagal reflex mechanism. One final possibility which must be considered as an explanation for electrocardiographic pattern II is that this pattern does not really represent isorhythmic dissociation. Waldo and his associates2' have recently proposed that during this arrhythmia, true A-V dissociation is only a transient phenomenon and that the persistent mechanism is actually an A-V junctional rhythm. Their hypothesis may be illustrated by referring to cases 5 and 7. In case 5, the P wave occurred during the early portion of the T wave (fig. 7A), and it appeared to be upright in leads II, III, and aVF. However, Waldo and associates2' presented cogent evidence which indicates that upright-appearing P waves in these leads are not incompatible with an origin in the A-V junction. Hence, according to their hypothesis, the arrhythmia in figure 7A and G is not LEVY, EDELSTEIN 698 Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 isorhythmic dissociation but merely an A-V junctional rhythm with retrograde P waves appearing as positive deflections in leads II, III, and aVF. After carotid sinus stimulation in this patient, a brief period of normal sinus rhythm was followed by true A-V dissociation. In segments C through F, there was a rhythmic variation in the P-R interval, which was associated with the expected changes in arterial blood pressure. Segments C through F, therefore, probably represent the pattern I type of isorhythmic dissociation, as described above. Subsequently, this presumably reverted to a junctional rhythm (segment G). The observations made in case 7 may also be explained by the hypothesis proffered by Waldo and associates. Despite the upright P waves in leads II, III, and aVF, the continuous rhythm strip in figure 8 might represent a junctional rhythm, with some slow variations in the ratios of antegrade to retrograde conduction time to account for the changing R-P intervals. Atropine might also have produced some changes in the ratio of antegrade to retrograde conduction time or in the location of the pacemaker site within the junction, as well as a transient reversion to a normal sinus rhythm (fig. 9). It seems less likely that the apparent synchronization observed in case 6 can be explained by the hypothesis of Waldo and associates, although this possibility cannot be excluded entirely. In this patient with complete heart block, when synchronization was achieved by careful adjustment of the artificial ventricular pacemaker, the P wave occurred in a fixed position on the ST segment. To be compatible with the hypothesis of Waldo and co-workers, this would have to represent retrograde transmission to the atria. In a patient with complete heart block, this is unlikely, although valid instances have been 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. und Ventrikel: Erk1arung des partiellen Herzblocks. Z Klin Med 110: 401, 1929 FiscHER R: Uber das Vorkommen einfacher zahlenmassiger Beziehungen zwischen der Frequenz dissoziiert schlagender Herzabschnitte. Z Klin Med 116: 466, 1931 KisCm B: Boebachtungen bei einem Kranken mit totalem Block. Cardiologia 2: 47, 1938 SEGERS M, LEQUIME L, DENOLIN H: Synchronization of auricular and ventricular beats during complete heart block. Amer Heart J 33: 685, 1947 MARRIOTT HJL: Atrioventricular synchronization and accrochage. Circulation 14: 38, 1956 BURCHELL HB: Experiences with electronic pacemakers. In Mechanism and Therapy of Cardiac Arrhythmias, edited by LS Dreifus, W Likoff. New York, Grune & Stratton, Inc, 1966, pp 535-541 LEVY MN, ZIESKE H: The mechanism of synchronization in isorhythmic A-V dissociation: I. Experiments on dogs. Circulation Research, In press GALLAVARDIN L, VEIL P: Sur un cas de bradycardie permanente 'a 40: Rhythme nodal avec P positif ou dereglage auriculo-ventriculaire. Arch Mal Coeur 21: 210, 1928 ENESCU I, VACAREANU N: Dissociation auriculoventriculaire isorhythmique transitoire. Arch Mal Coeur 27: 691, 1934 MAHAIM I, TANNER A: Dissociation iso-rhythmique provoquee avec automatisme ventriculaire accelere: Myocardite gommeuse de la cloison. Acta Cardiol 3: 296, 1948 SEGERS M, ENDERLE J, PIRART J: Un cas de dissociation isorhythmique. Acta Cardiol 8: 417, 1953 GRANT RP: The mechanism of A-V arrhythmias, with an electronic analogue of the human A-V node. Amer J Med 20: 334, 1956 14. MARRIOTr HJL, SCHUBART AF, BRADLEY SM: A- 15. 16. 17. reported.'7 References 18. 1. LEWIS T: The Mechanism and Graphic Registration of the Heart Beat, ed 3. London, Shaw and Sons, Ltd, 1925, p 178 2. VAN BUCHEM FSP: Dissoziation zwischen Atrium 19. V dissociation: A reappraisal. Amer J Cardiol 2: 586, 1958 SCHOTT A: Atrioventricular dissociation with and without interference. Progr Cardiovasc Dis 2: 444, 1959 ScHERF D, COHEN J: The Atrioventricular Node and Selected Cardiac Arrhythmias. New York, Grune & Stratton, Inc, 1964 pp. 288-295 MARRIoTT HJL: Interactions between atria and ventricles during interference dissociation and complete A-V block. Amer Heart J 53: 884, 1957 SCHUBART AF, MARRIOTT HJL, GORTEN RJ: Isorhythmic dissociation: Atrioventricular dissociation with synchronization. Amer J Med 24: 209, 1958 AVERILL KH, LAMB LE: Less commonly Circulation, Volume XLII, October 1970 ISORHYTHMIC DISSOCIATION recognized actions of atropine on cardiac rhythm. Amer J Med Sci 237: 304, 1959 20. JACOBS DR, DONOSo E, FRIEDBERG CK: A-V dissociation: A relatively frequent arrhythmia. Medicine 40: 101, 1961 21. WALDO AL, VrrIKAINEN KJ, HARRIS PD, ET AL: The mechanism of synchronization in isorhythmic A-V dissociation. Circulation 38: 880, 1968 22. GESELL RA: Auricular systole and its relation to ventricular output. Amer J Physiol 29: 32, Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 1911 23. BROCKMAN SK: Dynamic function of atrial contraction in regulation of cardiac performance. Amer J Physiol 204: 597, 1963 24. SKINNER NS, JR, MITCHELL JH, WVALLACE AG, ET AL: Hemodynamic effects of altering the timing of atrial systole. Amer J Physiol 205: 499, 1963 25. MITCHELL JH, GUPTA DN, PAYNE RM: Influence of atrial systole on effective ventricular stroke volume. Circulation Research 17: 11, 1965 26. BENCHIMOL A, MAROKO P, GARTLAN J, ET AL: Continuous measurements of arterial flow in man during atrial and ventricular arrhythmias. Amer J Med 46: 52, 1969 27. BENCHIMOL A, STEGALL HF, MAROKO PR, ET AL: Aortic flow velocity in man during cardiac arrhythmias measured with the Doppler catheter-flowmeter system. Amer Heart J 78: 649, 1969 28. RUSKIN J, MCHALE PA, HARLEY A, ET AL: Pressure-flow studies in man: Effect of atrial systole on left ventricular function. J Clin Invest 49: 472, 1970 29. BRAUNWALD E, FRAHM CJ: Studies on Starling's law of the heart: IV. Observations on the hemodynamic functions of the left atrium in man. Circulation 24: 633, 1961 30. SAMET P, JACOBS W, BERNSTEIN WH, ET AL: Hemodynamic sequelae of idioventricular Circulation, Volume XLII, October 1970 699 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. pacemaking in complete heart block. Amer J Cardiol 11: 594, 1963 SAMET P, BERNSTEIN W, LEVINE S: Significance of the atrial contribution to ventricular filling. Amer J Cardiol 15: 195, 1965 CARLETON RA, PASSOVOY M, GRAE`TTINGER JS: The importance of the contribution and timing of left atrial systole. Clin Sci 30: 151, 1966 TSAGARIS TJ, BUSTAMANTE RA, FRIESENDORF RA: Unusual complication of transvenous electrical pacing of the heart. Dis Chest 53: 110, 1968 LEINBACH RC, CHAMBERLAIN DA, KASTOR JA, ET AL: A comparison of the hemodynamic effects of ventricular and sequential A-V pacing in patients with heart block. Amer Heart J 78: 502, 1969 SEGERS M: Les phenomenes de synchronisation au niveau du coeur. Arch Internat Physiol 54: 87, 1946 NADEAU RA, ROBERGE FA: The mechanism of A-V arrhythmias: In Electrical Activity of the Heart, edited by GW Manning, SP Ahuja. Springfield, Charles C Thomas, Publishers, 1969, pp 117-128 JAMES TN: Pulse and impulse in the sinus node. Henry Ford Hosp Med Bull 15: 275, 1967 REID JVO: The cardiac pacemaker: Effects of regularly spaced nervous input. Amer Heart J 78: 58, 1969 LEVY MN, MARTIN PJ, IANO T, ET AL: Paradoxical effect of vagus nerve stimulation on heart rate in dogs. Circulation Research 25: 303, 1969 IRIUCHIJIMA J, KUMADA M: Efferent cardiac vagal discharge of the dog in response to electrical stimulation of sensory nerves. Jap J Physiol 13: 599, 1963 IRIUCMJIMA J, KUMADA M: Activity of single vagal fibers efferent to the heart. Jap J Physiol 14: 479, 1964 The Mechanism of Synchronization in Isorhythmic A-V Dissociation: II. Clinical Studies MATTHEW N. LEVY and JOSEF EDFLSTEIN Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017 Circulation. 1970;42:689-699 doi: 10.1161/01.CIR.42.4.689 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 1970 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/42/4/689 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. 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