Unusual Cardiac Arrhythmias in

Myocardial Infarction
A Case with S-A Block, Paroxysmal A-V Nodal Tachycardia
with Varying 21 and 3: 1 Block, Dissociation between
Pacemakers Situated within the Conducting System and
Premature Beats in A-V Rhythm and A-V Dissociation*
L. M. SANGHVI, M.R.C.P. (London), D.T.M. & H. (England)

Jaipur, India

S
INOATRIALBLOCKWITH coronarysinusrhythm ELECTROCARDIOGRAMS
is stated to be rare if indeed it exists at all.
Figure 7. A, taken on February 2, shows a pattern
Clinical reports of dissociation between two
of inferior and anteroseptal myocardial infarction;
ectopic pacemakers, both situated within the elevated P-Q segments in leads II, III and aVF are
A-V conducting system,2-5 and of effects of suggestive of atria1 infarction. The atria1 rate is
premature beats upon A-V rhythm6-g are few. 172 per minute and ventricular rate, 86 per minute.
A case of myocardial infarction with a combina- The P waves are low positive in lead I, inverted in
tion of these rare arrhythmias with several II, III and aVF and upright in aVR, indicating a
interesting features has, therefore, been con- focus low in the atrium near the atria1 part of the
sidered worth recording. A-V node or in the A-V node. Change in relation of
the P waves to QRS suggests that the paroxysmal
tachycardia is associated with 2 : 1 A-V block and
CASE REPORT variable conduction time or that there is A-V
A sixty year old man was first admitted to the dissociation. Slowing of the ventricular rate with
hospital on February 2, 1959, when the first electro- increase of block to 3 : 1 or 4 : 1 after carotid sinus
cardiogram was taken. He had a history of attacks pressure (bottom strip) shows the presence of the
of pain over the precordium and left shoulder during former.
the last three months. He left the hospital two days B (upper three strips are continuous, bottom strip
later against advice and was readmitted on March 2. after carotid sinus pressure), taken on March 2,
1959. He had not taken any digitalis preparation. shows persistence of the ectopic tachycardia. The
On examination the pulse was slightly irregular with atrial rate is 162 per minute. The P-P intervals are
a rate of about 75 beats per minute, the blood pressure absolutely constant at 0.37 second; the R-R intervals
160/100 mm. Hg, the heart was considerably enlarged vary. Groups of faster beats are separated by longer
and there was moderate congestive cardiac failure. ventricular pauses. The third, ninth, twelfth,
A series of electrocardiograms were taken during his thirteenth and sixteenth QRS complexes which
stay in the hospital. They showed paroxysmal A-V terminate the longer pauses are conducted at a P-R
nodal tachycardia with varying A-V block until interval of 0.34 to 0.36 second. The P-R intervals of
March 5, escape-capture type of bigeminal rhythm the second to the sixteenth QRS complexes are 46,
from March 5 to 14, and mostly A-V dissociation 34, 40, 44, 44. 45, 46, 36, 40, 46, 36, 36, 40, 46 and 34
with ventricular capture beats from March 14 until (hundredths of a second), respectively, and the R-R
the patient was discharged on April 18. Transient intervals are 75, 99, 81, 78, 76, 76, 75, 101, 81, 79,
A-V rhythm was seen spontaneously on April 8 and 102, 112, 84, 75 and 100 (hundredths of a second),
during administration of Bellafolline from April 14 respectively. Thus, within the faster groups of beats
to 16. the P-R interval progressively increases and the R-R

* From the Department of Cardiology, Sawai Man Singh Hospital and Medical College, Jaipur, India.

JULY 1961 147

 Sanghvi

Fig. 1. A, taken on February 2, 1959; B, taken on March 2, 1959. See text.

interval decreases. The increasing P-R interval is A-V junction, leading to 3 : 1 conduction in the beats
clearly noted in the increasingly visible blocked P terminating the long pauses. The bottom strip after
waves just preceding the QRS complexes. The last carotid sinus pressure shows increase in block to
R-R interval before the pause is shorter than the 4 : 1.
first one after the pause except when there is 3 : 1 Figure 2. A, electrocardiograms taken on March
conduction in the twelfth and thirteenth successive 5 show A-V dissociation with escape-capture bige-
beats when the R-R interval is three times the P-P miny or reciprocal rhythm with first degree A-V
interval. All this is characteristic of Wenckebach block. The direction of the P waves is the same (other
periods of the alternate effective impulses in the lower leads not shown here) as in Figure 1A demonstrating

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 Unusual Cardiac Arrhythmias 149

FIG. 2. A, electrocardiograms taken on March 5, 1959; B, taken after an intravenous injection of atropine.
See text.

that the upper pacemaker is located low in the wandering pacemaker with intermittent shift of the
atrium or in the A-V node. Its rate is 22 per minute. atria1 focus, probably to the sinus node. The last
The identical QRS contour of the escape and the strip reveals return of the bigeminal rhythm with
conducted beat shows that the lower pacemaker is inverted P waves which continue with return to the
situated in the conducting system above the bi- original P-P intervals.
furcation of the bundle of His, probably in the lower Figure 3. Electrocardiograms taken on March 14
part of the A-V node. when change of rhythm was again noted. There is
B (the strips are continuous), taken after an A-V dissoc:ation with ventricular captures. A,
intravenous injection of 0.6 mg. atropine, suggests demonstrates inverted P waves in leads II, III and aVF.
that the bigeminy in record A is due to A-V dis- B (the three strips are cuttings from a long tracing
sociation with capture beats and not to reciprocal of lead III), shows that the rate of the lower pace-
rhythm. A change in relation of the P waves to maker is 33 per minute and that of the upper pace-
the QRS is clearly seen in the fifth cycle in the first maker varies between 22 and 33 with uneven P-P
strip and third cycle in the second strip; there is intervals varying between 1.80 and 2.60 seconds.
considerable variation in the R-P (0.20 to 0.46 The R-R intervals between the conducted beat and
second) intervals and in the P-R (0.26 to 0.48 the next nodal escape are shorter than the internodal
second) intervals of the conducted beats. The change interval due to delay of the conducted impulse below
in shape and direction of the P waves suggests a the site of the escaping pacemaker. The P-P intervals

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 Sanghvi

FIG. 3. Electrocardiograms taken on March 14, 1959. A, demonstrates inverted P waves in leads II, III and
aVF; B, demonstrates rates of pacemakers; C, demonstrates abolition of the ventriculophasic arrhythmia and
acceleration of rates of pacemakers after administration of atropine. See text.

which include the conducted QRS are usually shorter interval of 0.20 to 0.22 second. A, the two strips are
due to ventriculophasic arrhythmia. At two places continuous. A-V dissociation is present, with
the P-P interval lengthens to 2.6 seconds and gives shifting rate of both the pacemakers. In a long
rise to bigeminy. The P-P interval in the bigeminal tracing on this occasion the P-P intervals varied
rhythm in Figure 2A is similar (2.64 seconds). between 1.32 and 1.68 seconds and R-R intervals
C, taken after intravenous injection of 1.2 mg. between 1.48 and 1.60 seconds except at one place, the
atropine, shows abolition of the ventriculophasic second P and QRS in the lower strip. The first P in
arrhythmia and acceleration of the rates of the upper this strip just precedes the first QRS complex which is
and the lower pacemakers to 52 and 56 per minute, partly superimposed on the later part of the P.
respectively. A-V dissociation with capture beats is The second P occurs after a P-P interval of 0.90
still present. There is no change in the direction of second. Such a short P-P interval was never seen
the P waves as is noted after administration of during A-V dissociation, even when the rate was
atropine in Figure 2B. considerably accelerated after the administration of
Figure 4. Spontaneous change of rhythm on atropine (Fig. 3C). This is, therefore, a premature
April 8. The P waves are inverted in leads II, beat arising from the upper pacemaker. A QRS
III, aVF and Vt-VS, and upright in I and aVR. complex follows after 0.22 second at an R-R interval
They precede the QRS at a P-R interval of 0.24 of 1.04 seconds. The next P and QRS occur after a
second indicating low atria1 or A-V nodal rhythm P-P interval of 1.60 and R-R interval of 1.54 seconds,
with A-V block. The QRS duration is 0.15 second respectively. The premature beat is apparently
with intrinsicoid deflection after 0.09 second in Vi conducted to the ventricles and shifts the timetable of
and after 0.06 second in Vs. This suggests the both the pacemakers. A-V dissociation continues.
presence of right bundle branch block with probable B, ventricular premature beat (fourth cycle) in A-V
peri-infarction block. The change of rhythm was rhythm interferes with the upper pacemaker, causes
transient as another tracing the same day again nodal escape and sets up A-V dissociation. C, A-V
revealed A-V dissociation. dissociation with ventricular capture beat simulating
Figure 5. Bellafolline was administered orally in ventricular premature beat. D, the two strips are
doses of three tablets daily from April 12 to 16. continuous. Termination of A-V dissociation by
Strips A to G are cuttings from tracings obtained on interpolated premature beat (seventh cycle in upper
April 14 to 16. All are of lead III except D which is of strip) which sets up A-V rhythm. E and F, inter-
lead Vi. During A-V nodal rhythm, the P waves are polated ventricular premature beats in A-V rhythm
inverted and precede the QRS complexes by an arising from different foci and causing prolongation of

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 Unusual Cardiac Arrhythmias 151

FIG. 4. Spontaneous change in rhythm on April 8, 1959. See text.

FIG. 5. Electrocardiograms taken on April 14 to 16,1959. See text.

the P-R interval of the postextrasystolic beats. G, 2B) the P waves are inverted in leads II, III
single ventricular premature beat in A-V dissociation and aVF, and upright in I and aVR. This
which does not disturb either pacemaker. indicates a focus either in the lower atrium
near the atria1 part of the A-V node or in the
COMMENTS A-V node.g JO The prolonged P-R interval of
In all the records of this case except the one the capture beats in A-V dissociation suggests
taken after the administration of atropine (Fig. the presence of first degree A-V block. Inverted

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 Sanghvi

P waves in the conducted beats in Figures complete elimination of the S-A node in ani-
4 and 5 precede the QRS complexes at a mals, when the A-V node became the sole
P-R interval of 0.20 to 0.24 second. This type active pacemaker governing the heart, positive
of rhythm with a P-R interval of 0.12 second P waves in leads II, III and aVF have been
or more has been considered to represent A-V found.15
nodal rhythm with A-V block by Langendorf, Besoain-Santander and co-workers16 described
Simon and Katz. It has also been interpreted concealed conduction and variable penetration
as coronary sinus rhythm,1J0J2 the beats origi- of the ineffective impulses, the presence of
nating in the extension of the A-V node toward two zones of impedance in the junctional tis-
the area of the orifice of the coronary sinus sues and Wenckebach periods of alternate ef-
vein, an area which has a high degree of au- fective impulses in the lower A-V junction in
tomatism.13 In the present case, even after the atria1 flutter. The arrhythmia in Figure 1 illus-
paroxysmal tachycardia subsided, the direction trates all these features and is thus analogous.
of the P waves remained the same during A-V The 3 : 1 odd conduction ratio in the presence of
dissociation as well as during A-V rhythm, Wenckebach periods of alternate effective im-
during a period of nearly six weeks of further pulses is most unusual. The baseline between
observation. This suggests that the focus for the P waves is, however, isoelectric and the
atria1 activation remained unchanged. The atria1 rate, the varying degree of A-V block,
lower pacemaker during A-V dissociation was the increase in the block after carotid sinus pres-
probably located in the lower part of the A-V sure and the persistence of the tachycardia for
node. All this favors the assumption that the several weeks are findings similar to those de-
pacemaker during the paroxysmal tachycardia scribed in the hybrid arrhythmia of paroxys-
and A-V rhythm and the upper pacemaker mal atria1 tachycardia with block. A-V nodal
during the A-V dissociation were situated in tachycardia with concealed conduction, Wencke-
in the upper part of the A-V node, probably in bath phenomenon and irregular beating of the
its extension in the coronary sinus region. atria and the ventricles has been described9 but
Upper nodal rhythm with P-R longer than the combination of the various features in this
0.12 second does occur when A-V block is also case is unique.
present9 Absolute localization and distinction Figure 2A shows a bigeminal rhythm with
between low atrial, coronary sinus rhythm and inverted P waves sandwiched between two QRS
upper nodal rhythm is not possible to obtain complexes of identical contour and an R-P
with certainty.O interval of 0.50 second. This is suggestive of
The records also favor the assumption that reciprocal rhythm with A-V block. Figure
there was probably complete sinus block with 2B, taken soon after 2A and following an
shift of the pacemaker to the A-V node. The injection of atropine, shows A-V dissociation.
possibility of permanent suppression of sinus Again, Figure 3B shows occurrence of similar
activity by retrograde discharge by the nodal bigeminy during A-V dissociation. Further-
impulses seems unlikely. A regular normal more, during A-V nodal rhythm in Figure 4
sinus rhythm was never noted in this case and, the P waves precede the QRS complexes by an
therefore, the normal sinus contour of the P interval of 0.24 second. There is, therefore,
wave or the normal P-R interval could not be little doubt that the bigeminy represents A-V
established. Positive P waves suggestive of dissociation with escape-capture sequence. Es-
sinus activity were observed transiently on only cape-capture bigeminy associated with com-
one occasion, in the record taken after adminis- plete sinus block does not seem to have been
tration of atropine (Fig. 2B) which shows A-V reported previously although a few instances
dissociation. This record shows wandering of associated with 2 :l or 3 :l S-A block have
the pacemaker with some P waves inverted and been reported.10J8-21
others positive. It is conceivable that atropine S-A Block and Interference Dissociation: Miller
relieves the sinus block and allows the sinus and Sharrett22 described the theoretic possibili-
pacemaker to activate the atria. It is also con- ties concerning the foci between which inter-
ceivable that the impulse may originate in the ference dissociation could occur, including
A-V node and yet be represented by a positive dissociation between two pacemakers situated
although abnormal P wave, an idea defended within the A-V junction. Records in Figures
by Scherf and Shookhoff many years ago and 2 and 3 illustrate this latter type of dissociation.
confirmed by recent experimental work. After It has been produced experimentally and the

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 Unusual Cardiac Arrhythmias 153

possibility of such an arrhythmia occurring in and Winterberg3? and Lewis, White and
specific cardiac tissue has been considered.23 Meakins33 investigated this problem and the
Only five cases of this arrhythmia have, how- conditions prevailing in extrasystolic arrhythmia
ever, been reported. 2-5 The rates of the upper in A-V rhythm were further clarified by the
pacemaker in the reported cases have varied work of Scherf and Shookhoff. Figure 5
between 44 and 86 per minute and are, there- illustrates occurrence of A-V nodal rhythm and
fore, slow in comparison to the rate in non- of premature beats, many of them interpolated,
paroxysmal A-V nodal tachycardia.24 The during administration of Bellafolline. It also
arrhythmia in two cases2*5 was due to enhance- illustrates disturbances of impulse formation and
ment of activity of the A-V centers by digitalis impulse conduction in A-V rhythm and in A-V
intoxication. In cases with slower rates the dissociation caused by concealed conduction35z36
arrhythmia is believed to represent marked and variable penetration of the junctional
depression of the sinus node as a result of true tissues by the premature beats. Ventricular
sinus depression or some degree of S-A block.5 premature beats cause change from A-V rhythm
In the present case digitalis was not admin- to A-V dissociation and vice versa (strips B and
istered. The rate of 22 of the upper pacemaker D). Strip A is of interest in that the premature
in Figure 2A is very slow and the lowest so far beat arises in the upper A-V nodal pacemaker
reported. Sinus bradycardia with a rate of as during A-V dissociation and that it shifts the
low as 24 has been reported to occur as a result timetable of both the pacemakers; A-V
of ischemic changes or occlusion of the artery dissociation then continues. Another interesting
supplying the S-A node.25J6 In order to feature in this record is the occurrence of
obtain rhythms with bradycardia Scherfz? interpolated ventricular premature beats during
had to damage the sinus node and depress the A-V nodal rhythm. The beats cause pro-
A-V node as well. A-V rhythm with a slow longation of the P-R interval of the post-
rate may result if the sinus node has ceased to extrasystolic A-V beats. The prolongation was
function or is so slow that the A-V centers are related to the ratio between the coupling of the
able to escape; this form is seen in complete premature beat to the preceding QRS complex
sinus block or when a pathologic process in the and the R-P interval between the premature
area of the sinus node has depressed it ab- beat and the next P wave.
normally, the most common cause being
SUMMARY
occlusion of the artery supplying the sinus
node. It has been stated that this form of A patient with myocardial infarction is
coronary sinus rhythm is rare if, indeed, reported whose electrocardiograms revealed the
it exists at all. In the present case in the following: (1) S-A block with shift of the
presence of extensive myocardial infarction pacemaker to the upper part of the A-V node,
and other disturbances of conduction the S-A probably in the coronary sinus area; (2) A-V
block is probably due to a pathologic process nodal tachycardia with varying 2 : 1 and
in the area of the sinus node. Marked depres- 3 : 1 A-V block and Wenckebach periods of alter-
sion of the junctional tissues due to vagus tone nate effective impulses; (3) escape-capture bige-
is demonstrated by the acceleration of both the miny; (4) dissociation between two pacemakers,
pacemakers after administration of atropine. both located in the A-V node; and (5) disturb-
Figures 4 and 5 in the present case may be ances caused by premature beats, including in-
interpreted to represent this rare type of slow terpolated ones, in A-V rhythm and A-V
coronary sinus rhythms1 Figure 3, which shows dissociation.
abolition of ventriculophasic sinus arrhythmia ACKNOWLEDGMENT
by atropine, supports the view that the vagus Dr. L. R. Sarin, Superintendent, Sawai Man Singh
tone is a factor in producing this irregularity.28-30 Hospital, kindly permitted the publication of this
Premature Beats in A-V Nodal Rhythm: Oc- report.
currence of nodal rhythm attributed to in- REFERENCES
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JULY 1961
 Sanghvi

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