Accelerated isorhythmic ventricular rhythms

Accelerated isorhythmic ventricular rhythms

Reviews Accelerated lsorhythmic Ventricular Rhythms RASHID A . MASSUMI, MD, FACC NAYAB ALI Washington, D . C. Thirty cases of accelerated ventricul...

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Reviews

Accelerated lsorhythmic Ventricular Rhythms

RASHID A . MASSUMI, MD, FACC NAYAB ALI Washington, D . C.

Thirty cases of accelerated ventricular rhythms occurring in patients with a variety of cardiac diseases and in normal individuals are presented . Acute myocardial infarction was present in only 4 cases . The attribute "isorhythmic" is suggested to underline the constant and important feature of equality or proximity of the rate of the ectopic ventricular pacemaker and that of the dominant rhythm . It is shown that an identical arrhythmia can easily be produced by electrical stimulation of the ventricle at an isorhythmic rate and that an isorhythmic ectopic atrial pacemaker is capable of producing a similar arrhythmia involving the atria only. The benign nature of the arrhythmia and the underlying reasons are pointed out . Three cases are presented of an unusual type of isorhythmic ventricular rhythm caused by propulsion of the catheter tip toward the right ventricular endocardium at the time of atrial contraction. It is concluded that the various arrhythmias having the common feature of a relatively rapid idioventricular rate are determined by a multitude of mechanisms including parasystole, atrioventricular dissociation with an idioventricular focus and also a mechanism similar to that of the demand or stand-by ventricular pacemakers .

Intermittent ectopic idioventricular rhythms at rates faster than ventricular escape (30 to 40/min) but considerably slower than those of ventricular tachycardia (generally 120 to 180/min) have been reported with increasing frequency since the inception of coronary care units . The inference is that the arrhythmia is peculiar to acute myocardial infarction . The long list of terms used to describe this arrhythmia includes active ectopic ventricular rhythm at rate under 100, 1

From George Washington University, Division of Medicine, and the Cardio-Pulmonary Laboratory, D . C . General Hospital, Washington, D. C . Manuscript received August 12, 1969, accepted October 24, 1969. Address for reprints : Rashid A . Massumi, MD, District of Columbia General Hospital, Washington, D . C . 20003 .

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slow ectopic ventricular rhythm, 2 nonparoxysmal ventricular tachyca.rdia 3 (following Pick and Dominguez's 4 example of nonparoxysmal A-V nodal tachycardia), idioventricular rhythm in acute myocardial infarction used by the same authors 5 as those who described nonparoxysmal ventricular tachycardia . accelerated ventricular rhythm,° slow ventricular tachycardia,7 ventricular tachycardia at slow rates parasystolic ventricular paroxysmal tachycardia causing intermittent A-V dissociation° and A-V dissociation with idioventricular rhythm . 10 Occasionally, an author" has used the general term ventricular tachy-

cardia and elected to ignore the slow rate even though it contradicted his own criterion for ventricular tachycardia . Other terms used are idioventricular tachycardia 12 isorhythmic A-V dissociation, 13 and intermittent slow ventricular parasystolic tachycardia .'^

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There is considerable disagreement concerning the applicability of the term tachycardia when the discharge rate of a pacemaker is faster than the normal expected rate but still considerably glower than that customarily associated with tachycardias . Moreover, Marriottl , wonders if such terms as nonparoxysmal, which describe what the arrhythmia is not without stating what it is . add much to our understanding of the rhythm disturbance . For these semantic reasons, he and others prefer the term accelerated rhythm in the strict sense that the discharge rate is faster than that ordinarily associated with the idioventricular foci .15' 16 This point of view is adopted here and is further qualified by the word isorhythmic to highlight the critical importance of the proximity of the rates of the ectopic and the dominant descending rhythms . This report presents 30 cases of this arrhythmia, most of which occurred in conditions unrelated to acute myocardial infarction, and suggests the tern) accelerated isorhythmic ventricular rhythm . The word isorhythmic connotes-following the suggestion of Marriott and Mcnendez'"-the proximity of two independent rates and does not signify actual synchronization or accrochage 17-10 Selection of this term is based on the observation that in the majority of the published and in all of the presently reported cases the basic ventricular and the ectopic ventricular rates have been either equal or reasonably close to one another ; the proximity of the two rates is a central feature of the arrhythmia, accounting for its intermittent or nonparoxysmal appearance and its benign nature_ This work demonstrates that any ectopic rhythm-whether atrial, A-V junctional or ventricular, spontaneous or electrically induced, so long as it possesses a discharge rate close to that of the basic mechanism-is capable of competing with the latter in an intermittent, nonparoxysmal manner . In a few patients the idioventricular rhythm recurred several times at different rates, always keeping pace with the prevailing sinus rate, and there were relatively slower rates of idioventricular discharge in cases of sinus bradycardia and incomplete A-V block . These findings suggest that the proximity of the dominant and the ectopic rhythms may not always be purely coincidental . This study presents an experimental model of accelerated isorhythmic ventricular rhythm readily produced by electrical stimulation of the right ventricle at a rate equal to or slightly slower than the dominant sinus rate . This rhythm may usurp control of the ventricles irrespective of whether or not it dominates the atria by means of retrograde V-A conduction ; however, ectopic rhythm is likely to last much longer if it does take over the control of the atria . Finally, three examples of an unusual and hitherto

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undescribed type of accelerated isorhythric ventricular rhythm occurring during right heart catheterization will be presented . In the patients studied, ectopic ventricular heats occurred after each P wave when the catheter tip lay against the wall of the right ventricle, but the beats disappeared when the catheter was drawn away from the wall . It was believed that the jolt imparted to the catheter by the atrial contraction and transmitted to the tip lying within the right ventricle caused ectopic ventricular heats to occur between the sinus P and the normal QRS .

Material and Methods Thirty patients with intermittent idioventricular rhythms at rates identical or close to the basic heart rate were studied, Table I shows for each patient age, sex, diagnosis, state of digitalization, the basic and ectopic rates, the mode of onset and end of the arrhythmia and the presence or absence of retrograde conduction of the ectopic rhythm to the atria . Selection of patients was based on the finding of an ectopic ventricular rhythm lasting for at least four consecutive heats and characterized by grossly abnormal QRS complexes that were clearly idioventricular in origin and not conducted from the artria . The abnormal QRS configuration could not be explained by aberration of intraventricular conduction of supraventricular beats taking into consideration the coupling intervals and the preceding R-R intervals . Complete medical history, physical examination, routine laboratory studies and at least one electrocardiogram were available in all cases, and the majority of the patients were under observation in this hospital for several days . Multiple rhythm strips were obtained every day in many patients until the arrhythmia ceased or as long as the patients were available for study . The factors responsible for the emergence of the isorhythmic idioventricular rhythm and those contributing to or determining its termination were carefully studied, The experimental model of this arrhythmia was easily produced in patients by electrical stimulation of the right ventricular endocardium at rates equal to or slower than the basic sinus discharge rate . The isorhythmic idioventricular rhythm so produced was able to usurp control of the heart for short periods lasting up to 22 beats . Right ventricular stimulation was carried out by means of bipolar catheter electrodes and a Medtronic pacemaker, model 5840 . The experimental tracings were recorded on an Electronicsfor-Medicine photographic recorder and consisted of a direct atrial or esophageal lead and generally two limb and two chest leads . Results Only 4 patients had recent myocardial infarction, and I had had an infarction several years previously . Altogether 14 patients were receiving digitalis, and an

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TABLE I . Summary of Thirty Clinical Cases Case no . 1

2

Age & Sex

Dig .

Dig. Tax .

Basic Rhythm, Rate

Ectopic Rate

81F

No

No

NSR 70 124 NSR 49

74 120 48

63M

Yes

No

3

80F

Yes

Yes

4*

67F

Yes

No

5

62M

No

6

71M

7

Diagnosis HCVD

HCVD

NSR 86 NSR 59-62

86

ASHD

61

Acute MI

No

NSR 62-70

62 once 84 once

Acute MI

Yes

1

A . fib . 55-80

58

ASHD

85F

No

No

60-69

ASHD

8

76F

No

No

49

ASHD

9

48M

Yes

No

A . fib . 48-88 2° A-V block 48 NSR 108

104

RHD ; AR

lot

32M

Yes

Yes

NSR 68-78

71

HCVD

11

35F

No

No

83

No HD

12

30M

Yes

No

58

13

22F

No

No

60

T .R . 2` to drug addiction Tetralogy

14t

27F

none none

NSR 83 NSR 58 NSR 60 NSR 90 102

90 94

No HD

15

61M

Yes

No

16`

10F

No

No

17

67F

No

No

18

48M

No

No

19

56M

Yes

No

2° A--V block 48 2° A-V block 39-40 2-1 A-V block 40 NSR 87 NSR 46-72

48 40 42 54

Variable 48-106

Ectopic Rhythm Brought on by (1) PVB ; 2) PAB, gradual, fusion forms Slowing of sinus rhythm

Ectopic Rhythm Terminated by Gradual, through fusion forms

(1) Slowing of ectopic pacemaker (2) Speeding up of sinus rhythm Gradual, fusion Gradual, through forms fusion forms (1) Slowing of sinus ; (1) Speeding up of (2) gradual, fusion sinus : (a) spontaforms neous ; (b) atropine ; (c) valsalva ; (2) gradual Post PVB slowing ; Speeding up of sinus post PAB once ; PVB once Post PVB slowing (1) Capture by fibrillating; (2) exit block Unexplained ? Exit block Gradual, fusion forms PVB

Slowing of sinus, gradual, multiple fusions Unknown PVB most common Unknown

Slowing of sinus rhythm, gradual via fusion forms ASHD Gradual, multiple fusions Congenital Gradual, multiple heart block fusions ASHD Gradual, fusion forms Old MI PVB, 1 min after end of treadmill exercise ASHD PVB

Capture by sinus P

V-A Conduction No

No No No No

No

Impossible, A. fib. Impossible, A . fib . No

Sinus capture, no Yes change in rate, multiple fusion forms Speeding of sinus, No gradual with multiple fusions Unknown Impossible, sinus P before QRS ? Exit block Impossible, sinus P before QRS 7 Exit block Impossible, sinus P before PVB Speeding up of sinus, No gradual via fusion forms Gradual, fusion forms No Gradual, fusion forms ; No no speeding Gradual, fusion forms No Return of sinus activity and A-V conduction Sinus capture exit block

Probable

After 2nd beat

' Case studied and tracing supplied by Dr . James Waters, Georgetown Univ . Hospital, Wash . D .C . t Case studied and tracings supplied by Dr. James Bacos, Director, Section of Cardiology, Washington Hospital Center, Wash ., D.C . t Case studied and tracings supplied by Dr . W- P . Nelson, Col ., Chief of Cardiology Branch, Fitzsimmons Gen . Hosp ., Denver, Col; Case studied and tracings supplied by Dr . Louis Scott, Director of Cardiology, Childrens Hasp . of Washington D .C . A . fib . = atrial fibrillation ; AR = aortic regurgitation ; ASHD = arteriosclerotic heart disease ; Dig. Tox . = digitalis toxicity; HCVD = hypertensive heart disease ; MI = myocardial infarction ; No HD = no heart disease, NSR = normal sinus rhythm, PAB = premature atrial beat ; PMD = primary myocardial disease; RHO = rheumatic heart disease ; T.R . = tricuspid regurgitation ; PVB = premature ventricular beat . Continued

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TABLE I (continued) Case no.

Age & Sex

Dig .

Dig. Tox .

Basic Rhythm Rate

20

66M

Yes

?

21

68F

Yes

?

22

36M

No

No

23

58F

Yes

No

24

71F

Yes

No

NSR 70-72 NSR 62-64 NSR 62-74 NSR 90-94 NSR 62-68

25

51F

No

No

26

62M

No

No

27

82M

Yes

7

28

58M

No

No

29

79M

Yes

Yes

30

44M

No

No

Ectopic Rate 86

Ectopic Rhythm Terminated by

V-A Conduction

Unexplained

Sinus capture

PMD

Gradual, fusion forms Yes

56

PMD

Gradual, fusion forms PVB

102

PMD

PVB

64-68

PMD

Speeding of sinus, fusion forms ? not available

No

No No

(1) Slowing of sinus Speeding of sinus No rhythm ; (2) post PVB slowing PMD Slowing of sinus Speeding of sinus No rhythm Acute MI Gradual, fusion Gradual, fusion forms No forms ASHD PVB, also probably Return of A-V conduc Impossible ; slowing of vention A . fib . tricular rate Hypothermia Slowing of sinus Speeding up and Impossible to tell, capture by basic muscle tremor 90° No HD rhythm rhythm Not available No ASHD Slowing of sinus rhythm Acute MI Slowing of sinus Speeding up of sinus, No rhythm, gradual, fusion forms fusion forms

64 72 59

62

58-62 70

overdose was suspected in 3 of them . The basic rhythm was normal sinus in 22, atrial fibrillation 4 and second degree heart block in 4 . The intrinsic cetopic rate was within ± 10 beats/min of the dominant ventricular rate in 28 eases, and within ± 4 beats of it in 18 cases . The ectopie mechanism emerged with a

in

premature ventricular beat of the same configuration in 7 cases, after post .extrasystolic pauses in 4, after spontaneous slowing of the dominant rhythm in 10 and by an unexplained gradual process through several fusion forms in 10 cases . In several cases, more than one mechanism was involved . The ectopie rhythm, once in control, lasted from a few seconds to as long as 1 minute . Termination of the ectopie rhythm was unexpected (probably exit block) in 9 cases, related to speeding of the dominant rhythm in 10, occurred gradually through fusion forms in 7 and not recorded in 4 cases .

Illustrative Cases Thirteen of the clinical cases and 2 of the experimental cases will be reported in detail . In addition, I case not included in Table I of isorhythmic atrial rhythm in which an ectopie pacemaker somewhere in the atria discharged at a rate very close to that of the sinoatrial node and competed with the latter for the control of the heart will he presented .

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Ectopic Rhythm Brought on by

ASHD

62-64

NSR 71 NSR 62 A . fib . with nodal at 52 NSR approx . 65 A . fib . 40-70 NSR 68

Diagnosis

Clinical Cases Case 1. The three strips of lead V l in Figure 1 were recorded 4 hours after a surgical lumbar sympathectomy was performed on the left side for relief of ischemie symptoms in the left lower limb in this 81 year old woman with known hypertension and chronic congestive heart failure . She had stopped taking digitalis 3 weeks before surgery . The basic rhythm was one of sinus tachyeardia (rate 124 beats/ min), probably secondary to postoperative hypovolelnia . It was interrupted at frequent intervals by runs of an ectopie idioventricular rhythm at about the same rate and not exceeding 20 beats in duration . The onset was precipitated occasionally (Fig . 1C) by a premature ventricular beat (beat 381 but more often was ushered in after a premature atrial beat (beats 4 and 22) which served 10 unmask or activate the ventricular focus . In either case, the first beats of the accelerated isorhythnuic ventricular rate were not preceded by long pauses and were coupled to the preceding beats by intervals of 0 .44, 0 .46 and 0 .47 see, respectively, compared to the basic R-R interval of 0 .48 . The first and last beat or two of each run displayed various grades of fusion between sinus and ectopie beats (beats 11, 12, 25, 39 and 42) . No treatment was given, and the patient was monitored in the cardiac care unit . The ectopie focus continued to be active, but its rate of discharge varied in time with the sinus rate . On the following day, both the basic

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Figure 1 . Case 1 . Tracings during early postoperative period when sinus tachycardia probably secondary to hypovolemia was in evidence .

sinus and ectopic rates had decreased to about 86 heats/min, and on the third day, both rates had fallen to about 70 to 74/min (Fig . 2) . At this point the atrial mechanism had switched to one of ectopic, probably coronary sinus rhythm . No further ectopic activity was detected beyond this date . In the hottom strip of Figure 2, the P waves occurring after beats 38 to 41 may be retrograde . Comment : In this individual with hypertensive heart disease, an ectopie ventricular pacemaker continued to be active for 3 (lays during which its rate of discharge seemed to have been tuned to the basic sinus rhythm . The proximity of the two rhythms explained the multiplicity of fusion beats, which occurred both at onset and offset of the runs of idioventricular rhythm . Aberrant intraventricular conduction of supraventricular beats was not tenable since the ectopic rhythm was in fact slightly slower than the sinus rhythm and the first beat in each run of idioventricular rhythm was not preceded by a long cycle . The emergence of the ectopic mechanism was not occa1 74

sioned by slowing of the basic sinus rhythm . Rather it was precipitated by a premature beat . It is postulated that the ectopic ventricular pacemaker was not depolarized by the premature beats 4, 22 and 38 because of an entrance block and was therefore provided with a longer period (intervals between beats 3 to 5, 21 to 23 and 37 to 39) in which to recover completely and become active . Moreover, the surrounding myocardium was provided with a longer interval and, therefore, more complete recovery . When the normal sinus rhythm was in control, the ectopic ventricular pacemaker was probably depolarized by every descending sinus beat and was therefore unable to elicit any discharges . However, its slower rate of recovery in comparison with the remaining parts of the ventricle protected it from being depolarized when the premature atrial heat arrived . As a result, it succeeded in initiating an impulse in the wake of the premature beat . Figure 2 includes two strips of lead V3 and one of lead II recorded on the third day of arrhythmia at a The American Journal of CARDIOLOGY

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time when the atrial rate had fallen to 70 to 74/min (beats 1 through 16 and 281 . The pacemaker for the idioventricular rhythm likewise was discharging at a slower rate of 78 to 89 . During transition from the basic rhythm to idioventricular rhythm, simultaneous discharges of two isorhythmic foci gave rise to a number of fusion beats tbeats 17, 29 through 31) . That the abnormal beats 18 through 27 and 33 through 41 were in fact. ectopic and did not represent aberrancy of intraventricular conduction because of the minimal acceleration of the rate is indicated by the lack of anv relation with the P waves . Case 2. The three continuous strips of lead V, in Figure 3 were recorded in this 63 year old man with hypertensive heart disease . He had been taking digoxin regularly but was not shown to be intoxicated . Beats 1, 2 and 10 through 13, 23, 24 and 33 are of sinus origin at a rate of 49 beats/min and display slightly widened QRS complexes . The heats with right bundle branch block configuration occur at a rate of 48/min, are clearly unrelated to the P waves and are ectopic ventricular in origin . The slightly longer interectopie intervals of about 1 .23 see as compared with the cycle lengths of approximately 1 .18 see for sinus beats makes deviation of A-V junctional beats most improbable . The runs of ectopic beats are separated both at onset and offset by a series of fusion beats 3, 8 and 16 through 20, 25 and 29 through

Figure 2 . VOLUME 26, AUGUST 1970

32 . Note that beats 3, 25 and 29 possess a narrow, "normalized" QRS because activation of the ventricles from the descending sinus P and from the ectopic ventricular focus was almost simultaneous and in a manner analogous with the normal ventricular activation . Comment : In this case of sinus bradycardia, the accelerated isorhythmic ventricular rate discharged at a rate very close to the dominant sinus rhythm, suggesting a mechanism which dictated the proximity of the two rates . Case 3 . The three strips of lead V, in Figure 4 were obtained in quick sequence from an 80 year old woman admitted in severe congestive heart failure and after she had received three oral doses of 0 .25 fig digoxin at hourly intervals . The same arrhythmia persisted for several days even though no more digoxin was given, and it was considered probably not due to digitalis toxicity, Beats 1, 2, 12 and 13 are normal sinus beats with narrow QRS complexes . Beats 10, 12, 17 through 25 and 27 through 33 display features of complete right bundle branch block . Beats 3 through 9 and heats 14 and 15 display various, grades of fusion (F I . The presence of normal P waves at normal P-R intervals before beats with right bundle branch block may suggest a normal sinus mechanism with aberrant intraventric_ular conduction . However, the premature

Case 1 . Tracings taken on second postoperative day . 175

MASSUMI AND ALI

Figure 3 . Case 2 . Accelerated isorhythmic ventricular rhythms in the presence of slow sinus rate. beat 26 disturbs the relation between P and QRS and discloses the ectopic idioventricular nature of those beats, The rates of the sinus and the ectopie pacemakers are so close to one another as to make it possible for the two discharges to remain inseparable, and consequently fused, for many beats . Comment : In this case of normal sinus rhythm, an accelerated isorhythmic ventricular rhythm appeared without any appreciable slowing of the sinus rate and without any recognizable reason . After fusing with the basic QRS for 7 heats, the idioventricular beats achieved complete control . Retrograde V-A conduction played no role in this case . The extreme proximity of the two rates made it impossible to recognize the true nature of the arrhythmia until a premature beat disturbed the synchrony of the two rhythms . True synchronization in the sense of beating in unison of two independent structures through some active, dominating influence of one structure over the other need not be invoked in this case . Case 4 . In a 67 year old woman with acute anteroseptal myocardial infarction, the arrhythmia shown in Figure 5 developed from the third day of infarction to the sixth day . She had been taking 0 .5 mg of digoxin daily for a long time before the acute infarction and may well have been intoxicated by it . The idioventricular rhythm shown here was observed intermittently at frequent intervals and became manifest without any appreciable slowing of the basic sinus rhythm . The rate of discharge of the ventricular focus, however, was slightly faster than the sinus rate (61/min vs . 60/min) . The onset and offset of the isorhythmic ventricular rhythm were marked by a series of fusion beats (beats 6, 7, 19 to 21, 28 to 30 and 39) . Increasing the basic sinus rate by coughing, Valsalva maneuver or intravenous injection of atropine sulfate was regularly sufficient to sub-

176

due the idioventricular pacemaker for as long as the sinus rate remained significantly faster than the idioventricular rate . At times the idioventricular rhythm was in control for over 1 minute but generally lasted for 20 to 30 seconds . Several times during control by the idioventricular pacemaker, a premature supraventricular heat disturbed the continuity and allowed the sinus pacemaker to resume control . Comment : In this ease of acute myocardial infarction and possibly digitalis intoxication, an idioventricular rhythm was present intermittently for 3 days and competed with the sinus rhythm . Its emergence was more often than not unprovoked and spontaneous . Normal sinus rhythm returned after premature supraventricular beats interrupting idioventricular rhythm . This observation suggests that the idioventricular pacemaker was invaded, depolarized and extinguished by the premature beat, that is, it was not, protected by an entrance block . It should be noted that the ectopie idioventricular beats failed to enter the atrium and the sinus mechanism remained undisturbed during the periods of ectopic rhythm . Case 5 . This was a 62 year old man with acute diaphragmatic myocardial infarction . The three rhythm strips in Figure 6 are from a monitor lead, and the lower two strips are continuous, In the top strip, beats 1 through 4 are normal sinus heats at a rate of 60/min . Beat, 5 is probably a premature ventricular beat and is followed by an accelerated isorhythmic ventricular rhythm at a rate of approximately 62/ min . The latter is short-lived, lasting only 5 beats and ends because the sinus mechanism accelerates and the P of beat 11 depolarizes the ventricles at about the time the next idioventricular beat is due to arrive . In the middle strip the sinus rate is slightly faster at 68/min . The idioventricular rhythm is again ushered in by a premature atrial beat (beat 191 and

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Figure 4. Case 3 . Accelerated isorhythmic ventricular rhythms with multiple fusion forms .

Figure 5 . Case 4 . Accelerated isorhythmic ventricular rhythms in acute anterior myocardial infarction .

Figure 6. Case 5 . Accelerated isorhythmic ventricular rhythms in acute diaphragmatic myocardial infarction .

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remains in control for 18 beats . Its rate is now also faster than in the top strip, and averages 72/min . This run of accelerated isorhythmic ventricular rhythm terminates with what appears to be a blocked premature aerial beat (the inverted P after beat 37) . This is interpreted as an indication that the ectopic pacemaker was situated within the right or left bundle branch . The premature P was able to penetrate in a concealed manner through the A-V junction and far enough into the bundle branch to extinguish the ectopic focus without reaching the myocardium . Comment : In this case, two runs of accelerated isorhythmic ventricular rhythm were observed . Both were precipitated by premature beats which were followed by long pauses . The discharge rate of the idioventricular rhythm, while not very close to that of the sinus rhythm prevailing at the time, did vary in accordance with the sinus rate . Termination of the ventricular rhythm was effected by concealed conduction of a premature atrial beat into the ectopic focus, which was thought to be situated within one of the bundle branches . Case 6 . A 71 year old man with ischemic heart disease had been receiving 0 .25 trig of digoxin daily . The four strips of lead II in Figure 7 are segments of a longer rhythm tracing . The basic mechanism is one of atrial fibrillation with a slow ventricular rate of

60 to 70/min . Beats 1, 3 to 5, 8, 10, 11, 20 to 25, 27, 33, 37 and 39 to 42 are conducted with left bundle branch block configuration . Beats 2, 7, 9, 12 to 19, 29, 31, 32 and 34 to 36 have an unusual right bundlee branch block pattern . They occur at perfectly regular R-R intervals of 1 .16 see (rate 51/lain) and originate from idioventricular pacemaker . Fusion between the two types of QRS results in fusion heats 6 and 38 . The emergence of the ectopic, rhythm is preceded by R-R intervals of conducted beats exceeding 1 .02 see . However, occasionally R-RR intervals as long as 1 .16 sec fail to unearth the ectopic mechanism . Similarly, although the premature beat 28 with the ensuing long pause was followed by an ectopic discharge, the premature beat 26 was not so followed . Comment : In this case of atrial fibrillation with possible digitalis intoxication and a slow ventricular rate, accelerated isorhvthmic ventricular rhythm discharging at a commensurately slow rate competed with the conducted beats . Failure of the ectopic discharge to appear after some long pauses suggested either an intermittent exit block or resetting of the ectopic pacemaker by the premature beat . Case 7 . This was an 85 year old woman with a diagnosis of arteriosclerotic heart disease . The three strips of Figure 8 were taken on 3 consecutive days . She had not received digitalis before . The basic rhythm is atria] fibrillation . In the top row conducted beats

a

5a

It

L

Figure 7 .

1 78

Case 6 . Accelerated isorhythmic ventricular rhythms in the presence of atrial fibrillation .

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Figure 8 . Case 7 . Accelerated isorhythmic ventricular rhythms in the presence of atrial fibrillation . An A-V nodal rhythm with aberrant intraventricular conduction cannot be ruled out . with narrow QRS (beats 1 to 4) are interrupted by a run of an almost . regular rhythm (beats 5-9 and 11, 12) with right. bundle branch block configuration . The first beat of the accelerated isorhvt .hmic ventricular rhythm is coupled to the last conducted beat by a relatively short interval (beat 4 to 5 = 0 .90 see) . Similar beats with right bundle branch block configuration recur after beat 10 . The interectopic intervals range between . 088 and 0 .96 see (rate 67/mini ; which is slightly faster than the rate of the conducted QRS . In the middle strip taken on the following day, the ventricles are driven by a regularly discharging pacemaker at a rate of 62/min ; in the bottom strip, the rate is 60 to 61/min . It may be argued that the middle strip shows an idioventricular rhythm and the bottom strip an A-V junctional rhythm . However, an

alternative explanation is thatt the ectopic beats in all three strips originated front an A-V junctional focus ; and that the right bundle branch block configuration in the top and middle strips is due to slightly more rapid rate of discharge than in the bottom strip (critical rate of intraventricular aberrance( . Comment : lit this second case of atrial fibrillation the ectopic mechanism appeared to originate from an actively discharging pacemaker . It, emergence did not depend on slowing of the basic rhythm . Case 8 . This was a 76 year old woman . The top two strips of lead V, iFig . 91 were taken from a routine tracing submitted for interpretation . Similar arrhythmia was found the next . day (bottom strip) and for several weeks thereafter ; the basic rhythm is

Figure 9. Case 8 . Accelerated isorhythmic ventricular rhythms in the presence of 2 :1 heart block of Mobitz II type .

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Case 9 . This was a 48 year old man with rheumatic aortic regurgitation . Of the three strips of lead V, (Fig . 10), the top two are continuous . An accelerated isorhythinic ventricular rhythm begins with beat 8 and persists through beat 16 . Beats 17 through 21 are fusion beats . Beats 25 through 41 are again of ventricular origin with one major difference of being followed by retrograde P waves at a 1 : 1 relation . The occurrence of retrograde V-A conduction enabled the ectopie ventricular pacemaker to maintain and control the entire heartt for several hours . Comment : Here the accelerated isorhythmic ventricular rhythm discharged at a rate exactly equal to the sinus rate . Its emergence was not provoked by slowing of the basic rhythm and its termination was equally unexplained . The relation of the premature beat 6 to the onset of the ventricular rhythm is not clear. Retrograde V-A conduction allowed the ventricular rhythm to remain active for longer periods .

Figure 10 . Case 9 . Accelerated isorhythmic ventricular rhythms in the presence of sinus tachycardia . 2 :1 A-V block with left bundle branch block in beats 2 to 4, 13, 14, 17, IS and 24 . The actual mechanism is one of bilateral bundle branch block consisting of complete block of the left bundle branch and 2 :1 block of the right branch . Beats 1, 7 to 12, 16 and 19 to 22 arc idioventricular and display features of right bundle branch block . The ectopiec ventricular pacemaker discharges at a rate of 50/ruin in all three strips, whereas the ventricular beats resulting from A -V conduction occur at a rate of 49/min in the top two tracings and 54/min in the bottom strip . The emergence of the accelerated isorhythmic ventricular rhythm in the top strip seems spontaneous and unprovoked, but it is occasioned by a pause (interval 18 to 19) in the bottom strip and could therefore be considered an idioventricular escape mechanism, The conducted beats with left bundle branch block and the ventricular beats with right bundle branch block fuse together both at onset and end of the isorhythmic ventricular rhythm and give rise to a variety of fusion forms (beats 5, 6, 15, 16, 23) . Comment : In this case of Mobitz Type II with 2 :1 A-V block and left bundle branch block, an accelerated isorhythmic ventricular rhythm at a rate close to the basic rate of the conducted beats occurred and persisted for several weeks . Slowing of the basic rhythm or progression to the more advanced grades of A-V block was not always required for emergence of the ventricular rhythm . Its rate was constant and was therefore lower, equal or faster than the basic rate depending on the latter.

380

Case 10 . A 32 year old man had a 3 year history of "leaking valve," right bundle-branch block and a recurrent arrhythmia treated with orally administered quinidine sulfate which he took sporadically . Within 2 months 2 admissions to the Washington Hospital Center were occasioned by tachycardia and left ventricular failure associated with anginal pain . The first attack of tachycardia was precipitated by lifting a heavy weight (Fig . 11, top row) . The tachycardia responded to digitalis, procainandde and propranolol hydrochloride . After discharge the patient failed to take his medication and was readmitted 7 weeks later with a similar tachycardia . He was given digitalis and quinidine sulfate and discharged with this therapy . Cardiac examination after relief of the tachycardia revealed no cardiomegaly, valvular disease or other structural abnormalities . The QRS complexes during tachycardia displayed complete left bundle branch block and left axis deviation (Fig . 11, top cow) . During the second hospital day the rhythm switched frequently from normal sinus with right bundle branch block (second row, A, lead 1) to an idioventricular rhythm with retrograde 1 :1 A-V conduction . The rate for this accelerated isorhythmic ventricular rhythm was faster than the sinus rate and varied considerably from 104 to 90/ min tA,B) . The QRS complexes of the. accelerated isorhytlunic ventricular rhythm had complete left bundle branch block and left axis deviation with no features distinguishing them from those seen during the tachycardia . The tracings on the fourth hospital day are represented by the third and fourth stripe (Fig . 11) which show frequent change of rhythm from normal sinus with right bundle branch block to the ventricular rhythm at approximately the same rate . Noteworthy is that the ventricular rhythm emerges when the sinus rate slows (note P-P intervals 1-2 and 2-3 in the third strip and 16-I7, 17-I8 and 18-19 in the fourth

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strip)- The intrinsic discharge rate of the ventricular rhythm, however, is not constant and is subservient to the prevailing sinus rate . With a sinus rate of just under 60/min in the third strip, the rate of the ventricular rhythm is 60/min, while corresponding values in the fourth strip, which is lead V, of the same electrocardiogram, are 66 to S0/min for the sinus and approximntely 72/min for the ventricular rhythm . Again fusion forms are seen at the time of rhythm transition . Comment : This is the only case in the present group in which a recurrent severe taehycardia complicated the picture of accelerated isorhythuic ventricular rhythm . The discharge rate of the latter remained ill close proximity of and changed with the prevailing sinus rhythm . It is uncertain whether the tachveardia originated from the same ectopic ventricular pacemaker which gave rise to the slower isorhythmic ventricular rhythm . The resemblance between the two rhythms in terms of the QRS configuration and frontal axis suggests that the two pacemakers were either one and the same or juxtaposed .

Catheter-Induced Cases Cases 11 to 13 . These 3 cases are presented together because of the identical and unique mechan-

Figure 11 . cardia .

VOLUME 26 . AUGUST 1970

isin responsible for the apparent arrhythmia . In all the 3 cases, the apparent accelerated isorhythmic ventricular rhythm with left bundle branch block developed during right heart catheterization (Fig . 121 . Each strip begins with normal sinus beats displaying narrow QRS complexes . Later beats in each strip display complete left bundle branch block and also fusion beats of various grades . Inn each case the eetopic rhythm disappeared when the catheter was moved from the particular position in the right ventricle . The presence of fusion forms in Cases 11 and 12 (beats 5, 6, 9 of Fig . I IA and 5 . 11, 12, 15 and 16 of Fig . 11131 is in favor of an eetopie rhythua especially because fusion beats are noted to occur after relatively normal P-R intervals . Beats with pure left bundle branch block occur earlier and indicate mechanical stimulation of the right ventricular myocardium a few hundredths of a second in advance of the arrival of the sinus discharge . Comment : An isorhythmic idioventricular rhythm with true synchronization would immediately suggest itself . However, we are certain that the arrhythmia presented by these 3 patients was one of mechanical stimulation of the right ventricle by the catheter tip . The latter occupied al critical position so that atrial contraction caused it to strike the right ventricular

Case 10. Accelerated isorhythmic ventricular rhythms complicated

by

ventricular tachy-

let

MASSUMI AND ALI

Figure 12 . Cases 11 to 13 . Accelerated isorhythmic ventricular rhythms induced mechanical contact of the right ventricle with the tip of the cardiac catheter . endocardium and elicit a right ventricular beat with left bundle branch block configuration . Slight variations in the time of occurrence of the catheter-induced beats explain the variations ill the degree of fusion . Experimental Cases (Pacemaker-Induced) Case 31 . This 37 year old man was suspected of having pulmonary embolism . The basic mechanism of sinus rhythm (beats 1 to 3, Fig . 13) was overtaken by artificial stimulation of the right ventricle at a rate very close to the sinus rate . A direct right atrial lead (RA) was recorded simultaneously with leads V, and V, ; at a paper speed of 25 mm/sec . Complete control of the ventricles was maintained for up to five beats; after this time sinus P waves that occurred sufficiently ahead of the electrical stimuli (marked Si penetrated the ventricles . Fusion forms (marked FI occurred both at the onset and at the termination of the ectopic ventricular rhythm . The

by

basic sinus mechanism remained undisturbed during the ectopic rhythm . Comment : An accelerated isorhythmie ventricular rhythm was easily produced by electrical stimulation of the right ventricle at a fixed rate . The mechanism was that of a true parasystole in which the pacemaker is protected from the dominant sinus heats . The resemblance between this and the spontaneously occurring isorhythmic ventricular rhythm in some cases is striking . Case 32 . In this case of to 45 year old man with severe pulmonary fibrosis and eor pulmonale the mechanism of production of arrhythmia (Fig . 14) was identical with that of Case 31 . Here, however, the ectopic ventricular beats activated the atria in a retrograde fashion and depolarized the sinus node . The retrograde P waves marked P can he best recognized by the notch at the apex of the T waves in lead V, in beats 6 through 13 . By virtue of the retrograde conduction, the ectopic artificial pacemaker was able to remain in control of the whole heart for indefinite periods of time It was not until after the pacemaker rate was slowed by more than 10 heats per minute below the sinus rate thatt the sinus P waves managed to recapture control of the ventricles . Comment : This case saves to demonstrate that retrograde V-A conduction in accelerated isorhythmie ventricular rhythm enables the vetopic pacemaker to remain in control for long periods and also at rates even slower than the dominant mechanism . The mechanism here resembles that seen in Case 9 (Fig . 10) .

Figure 13. Case 31 . The experimental model of accelerated isorhythmic ventricular rhythms produced by right ventricular pacing without retrograde V-A conduction .

182

Case 33 . A 30 year old woman with rheumatic heart disease, not receiving digitalis, exhibited an atrial arrhythmia characterized by changing configuration of the P waves without much change in rate (Fig . 151 . In the top strip are shown two sets, lead, I, 11, V, and Vs, taken within 2 hours . In the left

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ACCELERATED ISORHYTHMIC VENTRICULAR RHYTHMS

Figure 14. duction .

Case 32 . Experimentally produced accelerated isorhythmic ventricular rhythms with retrograde V-A con-

set, the P waves are flat in lead 1, inverted in 11 and and negative-positive in V, . This superior orientation of the P together with the short P-R intervals of 0 .15 see suggests a low atrial pacemaker, most probably in the left atrium .202L The right set shows conversion to the pattern of normal sinus rhythm with a P-R interval of 0 .19 sec . The middle and bottom strips are continuous and demonstrate the gradual change from the normal to the ectopic P with two fusion P waves interposed (P waves 4 and 5) ; and again from ectopic to sinus with fusion beats (P waves 16 to 18) . The P-P intervals are not constant . A slightt acceleration of the ectopic rate occurs in beats 4 to 9, thereby accounting for the take-over by the ectopic pacemaker . A similar acceleration of the sinus pacemaker in beats 16 onward explains the return of the sinus rhythm . V6

Comment : The existence of an isorhythmic ectopic pacemaker in the atrium discharging at a rate very close to that of the prevailing sinus rhythm created

Figure 15 .

VOLUME 26, AUGUST 1970

a picture identical with that observed in accelerated isorhythmic ventricular rhythm with the only difference that in the former the ectopic pacemaker was situated in the atrium . Based on our own observation, this type of isorhythmic ectopic atrial rhythm is relatively frequent and is found both in healthy individuals and in association with heart disease .

Discussion The idioventricular origin of the arrhythmia in the cases presented here and those reported can be scarcely questioned because (1) aberrant iutraventricular conduction of a supraventricular rhythm cannot be supported either on the basis of the coupling intervals between the first ectopic beat and the preceding normal beat or of the preceding R-R cycles, and (2) the presence of numerous fusion forms at the time of rhythm change speaks strongly in favor of ventricular ectopy . From the standpoint of the site of

Case 33 . Accelerated isorhythmic atrial rhythm .

183

MASSUMI AND ALI

origin the arrhythmia described here differs from isorhythmic A-V dissociation of Waldo and associates'-' in which the latent ectopic pacemaker was in the A-V junction and the QRS complexes were identical with those of the dominant rhythm_ The proximity of the rates of the dominant and the ectopic mechanisms and their tendency to keep in pace with one another probably represent a similarity in the response of the two rhythms to such external influences as the autonomic reflexes and blood volume among others . 'J'he experimental study reported here (Fig . 13 and 14) demonstrates that an ectopic ventricular focus discharging at a rate equal to or even slightly slower than the basic heart rate can take the control away from the dominant supraventricular impulse-formning focus and drive the heart from the number of beats which it takes to place the supraventricular discharge sufficiently ahead of the ectopic beat to recapture the ventricles . Assuming a continuous, independent discharge by the ectopio focus (parasystolic), it is easy to visualize the manner in which the normal and the ectopic pacemakers may compete for control of the heart and give rise to a gradual, intermittent and nonparoxysmal emergence of the ectopic rhythm much like the competitive pacing which occurs in cases of heart block with implanted fixed-rate pacemakers after 1 : 1 A-V conduction has resumed .23 This is not to suggest an exact analogy between the spontaneous accelerated isorhythmicc ventricular rhythm and those produced by artificial ventricular pacemakers . Nor is it the intention to suggest that a parasystolic mechanism operates in all cases of isorhythmic ventricular rhythms . In the case of fixed-rate artificial pacemakers, discharges of high intensity occur anywhere within the cardiac cycle and capture the ventricles whenever the latter are sufficiently recovered . True "exit block" must he extremely rare in cases of properly functioning pacemakers, while entrance block is the rule in fixed-rate pacing . The cctopic idioventricular focus responsible for the accelerated isorhythinic ventricular rhythm shares none of these features with consistency . The factt that the ectopio idioventricular focus in some eases can be reset by beats coming front other sources indicates that the focus of the isorhytlunic ventricular rhythm does not enjoy protection or "entrance block" in all cases and therefore cannot be looked upon as a parasystolic focus . The emergence of the ectopic ventricular rhythm is said by many authors'' 4 '" to be secondary to a slowing of the dominant rhythm or to an acceleration of the idioventricular pacemaker . In the present study, this was true in only 7 patients . In others the first beat of the cctopic rhythm occurred anywhere within the R-R cycle of the basic rhythm or was precipitated

184

by a premature beat . In the latter case, the ectopic focus was not penetrated by the premature atrial beat and thus found sufficient time to recover completely and discharge The pause following a premature ventricular beat occasioned the emergence of the idioventricular rhythm in 4 instances . In several patients, more than one mechanism was found to be responsible . The emergence of the ectopic rhythm upon slowing of the dominant rhythm or after a postextrasystolic pause compels one to consider an idioventricular escape mechanism, albeit at a rather accelerated inherent rate . This is probably true in one third of the cases but cannot explain the ventricular rhythm in the remaining two-thirds . The escape explanation appears to be particularly applicable to cases of atrial fibrillation with superimposed accelerated isorhythmic ventricular rhythm . The mechanism of termination of the ventricular rhythm was no more uniform than its emergence . Most frequently, the ectopic rhythm ceased when the descending P waves appeared sufficiently ahead of the cctopic beats to traverse the A-V junction and enter the ventricles in advance of the next cctopic discharge . This mechanism was usually predictable, much like the return to the normal sinus rhythm in artificially produced idioventricular rhythms IFig . 13 and 141 . In some cases of dominant sinus rhythm and in all cases of atrial fibrillation, cessation of the ectopic rhythm was unpredictable . It could have been a manifestation of fatigue of the ectopic focus of an exit block . The atrial mechanism during the sieges of the accelerated isorhythmic ventricular rhythm remained unchanged in all cases of atrial fibrillation and in those in which a sinus rhythm was associated with second degree antegrade A-V block . In a few cases of normal sinus rhythm, retrograde penetration of the atria was present . These cases resemble the artificially induced ventricular rhythm with 1 :1 retrograde conduction (Fig. 14) . More commonly, however, the idioventricular beats failed to propagate in retrograde fashion, and the sinus node remained in control of the atria . The ectopic rhythm in the latter situation is likely to be of shorter duration, lasting only a few beats . However, in the presence of 1 :1 retrograde V-A conduction, the ectopic mechanism could theoretically remain in control of the entire heart for an indefinite period . What is the relation of the accelerated isorhythmic ventricular to the more familiar A-V dissociation? It may be said that during the time when the ectopic pacemaker is in command of the ventricles without involving the atria, the rhythm is one of true A-V dissociation in which an idioventricular focus-and not the usual A-V junctional focus-is in charge of the ventricles . The emergence of retrograde V-A conduc-

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ACCELERATED ISORHYTHMIC VENTRICULAR RHYTHMS

tion would place the arrhythmia in the category of "synchronized"

A-V

dissociation ."'"

the patient in Case 10, no patient ill our study re-

The clinical significance of this arrhythmia is in-

quired treatment, and the arrhythmia was self-limiting in all . The benign nature of the arrhythmia is due

completely understood at this time . That the arrhyth-

primarily to the isorhythmic discharge rate, which

mia is relatively benign is suggested by the clinical

makes paroxystnal emergence and appearance in the

experience in all the present observations . Except for

vulnerable period of the preceding basic heat unlikely .

References 1 . Spann JF, Moellering RC, Haber E, et al : Arrhythmias In, Mechanisms and Therapy of Cardiac Arrhythmias in acute myocardial infarction . (Dreifus LS, Likoff W, Moyer JH, ed) . New York, Grune & Stratton, 1966, p 535 New Eng J Med 271 :427-431, 1964 14 . Chung EKY : Parasystole . 2 . Bashour FA, Jones E, Edmonson R : Cardiac arrhythProgr Cardiovasc Dis 11 :64-81, 1968 mias in acute myocardial infarction . II Incidence of 15 . Marriott HJL : Personal communication the common arrhythmias with special reference to ventricular tachycardia . Dis Chest 51 :520-524, 1967 16 . Church G : Accelerated idionodal and idioventricular rhythms . Presented at the 1969 Scientific Sessions of 3 . Rothfeld EL, Zucker IR, Alinsonorin C : Nonparoxysmal ventricular tachycardia . the Heart Association of Southern Maryland 17 . Marriott HJL, Menendez MM : A-V dissociation reCirculation 35 : Suppl 2 :227, 1967 visited . Progr Cardiovasc Dis 8 :522-538, 1966 4 . Pick A, Dominguez P: Nonparoxysmal A-V nodal tachy18 . Segers M : Synchronization of auricular and ventricular cardia . Circulation 16:1022-1032, 1957 beats during complete heart block . 5 . Rothfeld EL . Zucker RI, Parsonnet V, et al : Idioventricular rhythm in acute myocardial infarction . Amer Heart J 33:685-691, 1947 Circulation 37 :203-209, 1968 19 . Segers M, Enderle J, Pirart J : Un cas de dissociation isorhythmique . Ada Cardiol 8:417-422, 1953 6. Hurst J, Myerburg R : Introduction to Electrocardiography . New York, McGraw-Hill, 1968, p 260 20 . Massumi RA, Tawakkol AA : Direct study of left atria) P 7 . Killip T : The Current Status of Intensive Coronary waves . Amer J Cardiol 20 :331-340, 1967 Care. New York, The Charles Press, 1966, p 88 21 . Massumi RA, Sarin R, Tawakkol AA, et al : Time se8 . Lown 8 : The Current Status of Intensive Coronary squence of right and left atrial activation in recognition Care, in Ref 7, p 45 of the origin of ectopic P waves. Amer J Cardiol 24 :28-36, 1969 9 . Katz LN, Pick A : Clinical Electrocardiography . The Arrhythmias . Philadelphia, Lea & Febiger, 1956 22 . Waldo AL, Vitikainen K, Harris PD, et al : The mechanism of synchronization in isorhythmic A-V dissocia10 . Hiss RG, Averill KH, Lamb LE : Electrocardiographic findings in 67,375 asymptomatic subjects . III . Ventriction . Circulation 38:880-898, 1968 23 . Burchell HB, Connolly DC, Ellis FH Jr. Indications for ular rhythms . Amer J Cardiol 6 :96-107, 1960 and results of implanting cardiac pacemakers . 11 . Bellet S . Clinical Disorders of the Heart Beat . PhilaAmer J Med 37 :764-777, 1964 delphia, Lea & Febiger, 1963, p 479 24 . Schubart AF, Marriott HJL, Gorten RJ : Isorhythmic 12 . Schamroth L: Idioventricular tachycardia . J Electrocardiology 1 :205-212, 1968 dissociation : atrioventricular dissociation with synchronization . Amer J Med 24 :209-214, 1958 13 . Burchell HB: Experiences with electronic pacemakers .

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