Download Differentiation of "AV Junctional Rhythms"

Differentiation of "A-V Junctional Rhythms"
By BENJAMIN J. SCHERLAG, PH.D., RALPH LAZZARA, M.D.,
AND
RICHARD H. HELFANT, M.D.
SUMMARY
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Considerable controversy exists regarding the site(s) of origin of so-called junctional rhythms.
However, experimental and clinical evidence indicates that a more precise identification of the
origin of these rhythms is now possible. Microelectrode recordings from the atrioventricular (A-V)
junction have clearly demonstrated that all three zones of the A-V node (upper nodal [AN], midnodal [NI, and lower nodal [NH] regions) exhibit action potentials which are functionally different
from those recorded in contiguous atrial and His bundle cells. In addition, the amplitude and rate
of rise of A-V nodal action potentials are markedly depressed by acetylcholine, a relative sensitivity
not shared by atrial and His bundle cells. Cells of the AN and NH regions of the A-V node do show
pacemaker activity as do His bundle cells. Experimental studies using His bundle recording techniques indicate significant differences in heart rate between nodal rhythms produced by sinus node
isolation or suppression (average: 94 ± 22 beats/min) and His bundle rhythms caused by A-V
nodal destruction (average: 39 ± 9 beats/min). Nontoxic doses of ouabain significantly reduced
the average A-V nodal rate to 55 beats/min whereas the same dose regimen did not change the
average rate of His bundle rhythms. Several clinical studies have claimed that the absence of "A-V
nodal" potentials during so-called middle and lower A-V nodal rhythms indicate a site of origin in
the His bundle and not the A-V node. However, the nondescript, sometimes spurious nature of A-V
nodal recordings severely Lrmnts th.s approach to differentiation of junctional rhythms. Recent clinical
studies using His bundle recordings showed that patients with complete heart block and narrow
QRS complexes could be clearly divided into two groups. In one group the heart rates ranged from
45-60 beats/min and invariably increased significantly following atropine administration (A-V nodal
pacemakers). In the other group heart rates ranged from 35-45 beats/min and there was no significant response to atropine (His bundle pacemakers). Intra-His bundle block could be documented in
several patients in the latter group, confirming the His bundle location of the ventricular pacemaker.
In conclusion, evidence gained from experimental in vivo and in vitro animal studies and from
clinical investigations clearly suggests the existence of at least two pacemakers in the A-V junction.
The two A-V junctional pacemakers are distinctly different in both heart rate and chronotropic
response to cholinergic or cholinergic-blocking agents.
Additional Indexing Words:
Atrioventricular node
Atrial pacing
His bundle recordings
His bundle pacing
Atrioventricular conduction
Tl' HE LOCALIZATION of pacemaker activity
in the atrioventricular (A-V) node and the
His bundle region has been a subject of considerable debate. As many as five different pacemaker
sites have been described in the A-V junction:
coronary sinus ostium, the upper, middle, and lower
A-V node,' and more recently, the His bundle.2 In
Heart rate
the past, the distinction between these various
pacemakers was made primarily on the basis of the
temporal relationship between the retrograde P
wave and the QRS. The latter ordinarily shows the
same shape and duration as seen during supraventricular rhythms. It has since become clear that
these temporal relationships can be affected by
relative antegrade and retrograde conduction times
as well as by the location of the pacemaker.3
Despite abundant accumulated evidence for the
existence of A-V nodal automaticity,4 in recent
years some experimental findings have fostered the
concept that the A-V node is devoid of automaticity.5 Rhythms once attributed to the A-V node are
now referred to as low atrial or His bundle
rhythms.5' 6 The inability to resolve this controversy
has led to a semantic compromise: the term
"junctional rhythm."7 The purpose of this paper is
From the Division of Cardiology, Department of Internal
Medicine, Mount Sinai Medical Center, Miami Beach,
Florida; The University of Miami School of Medicine, Coral
Gables, Florida; and the Division of Cardiology, Department
of Medicine, Presbyterian-University of Pennsylvania, Philadelphia, Pennsylvania.
Address for reprints: Dr. B. J. Scherlag, Division of
Cardiology, Mount Sinai Medical Center, 4300 Alton Road,
Miami Beach, Florida 33140.
Received January 12, 1973; revision accepted for
publication March 20, 1973.
304
Circulation, Volume XLVIII, August 1973
JUNCTIONAL RHYTHMS
to examine evidence gained from microelectrode
and catheter electrode recordings in experimental
and clinical situations as they apply to the site of
origin of junctional rhythms. On the basis of these
data, a more precise classification of some of these
rhythms is suggested.
Definition of Terms
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The terms to be discussed are defined as follows:
1) The A-V junction, according to the concept of
Pick and Langendorf,' includes the specialized
atrial fibers in the low right atrium or coronary
sinus near the A-V node, the A-V node itself, and
the common bundle or His bundle. 2) The A-V
node, according to the concept of Hoffman and
Cranefield,2 includes "the entire complex of fibers
functionally interposed between the atrial fibers
proper and the His bundle proper." On the basis of
differences in electrical properties, the A-V node has
been subdivided into an upper nodal (AN) region,
a midnodal (N) region, and a lower nodal (NH)
region.8' 9, 10 The action potentials of the AN are
morphologically intermediate between those of the
atrium and the N region. Those of the NH region
similarly bridge the N region and the His bundle.
In all these regions (AN, N, NH) conduction is
slower than in the atrium or the His bundle. The
upstroke velocity and action potential amplitude
are correspondingly low. 3) The common bundle or
His bundle is that structure which sits on the crest
of the intraventricular septum connecting the A-V
node with the bundle branches. According to Lev
and Widran,"1 Hudson,12 and more recently,
Rosenbaum et al.,13 the bundle of His is composed
of two segments. "The penetrating portion of the
bundle travels from the distal end of the A-V node
to a point where the initial radiations of the left
bundle are given off." The branching portion stems
from the point where the bundle starts to emit the
most posterior fibers of the left bundle to the point
which marks the origin of the right bundle branch
and the most anterior fibers of the left bundle
branch.'3
Microelectrode Recordings
from the A-V Junction
Microelectrode techniques have been utilized to
ascertain the differential responses of the cells of
the A-V node and His bundle to various physiological and pharmacological interventions. Block of
premature impulses may occur in any of the three
regions.'4' 15, 16 All of these cells in the A-V node
share a far greater sensitivity to acetylcholine than
Circulation, Volume XLVIII, August 1973
305
those of the His bundle proper.'7 The loss of
amplitude and upstroke velocity of the action
potential of the A-V nodal cells with acetylcholine is
a response which is qualitatively different from
ordinary atrial cells or the cells composing the His
bundle. In common with His bundle cells and some
specialized atrial cells (sinus node), cells of the
NH5 and AN'8 regions of the A-V node show
pacemaker activity.
The action potentials of His bundle cells have
greater amplitude and upstroke velocity than those
of the A-V nodal cells.2 In contrast to the A-V nodal
cells, the amplitude and upstroke velocity of the His
bundle cells are relatively constant over a wide
range of heart rates and are relatively insensitive to
acetylcholine.17 His bundle cells display slow
diastolic depolarization, and pacemaker activity can
occur when complete heart block is produced by
acetylcholine.2 The rate of diastolic depolarization
is relatively unaffected by acetylcholine.17
Thus the response of the action potentials of the
A-V node and His bundle to rate changes, as well as
their responses to acetylcholine, are clearly different. However, specific A-V nodal cell types and His
bundle cells do show spontaneous depolarization
characteristic of pacemakers.
Characteristics of Junctional Pacemakers
in Experimental Studies
Rate
Recent studies in animals and man, employing
electrode catheter recordings from the A-V junction, have established criteria for differentiating
junctional rhythms. Experimental studies in dogs
with A-V nodal escape rhythms, induced after
cooling or crushing of the sinoatrial node (SA),
showed A-V nodal escape rates during pentobarbital anesthesia of 94 ± 22 beats/min.19 On the other
hand, in animals with heart block, caused by local
injection of the A-V node with formaldehyde, the
QRS configuration and duration remained essentially unchanged and the heart rate averaged 39 +9
beats/min. Figure 1 shows typical recordings in a
dog with sinus rhythm, A-V nodal rhythm, and His
bundle rhythm during complete heart block.
During A-V nodal rhythm, the His bundle potential
precedes atrial and ventricular activity, a recording
which is characteristic of the mid A-V nodal
rhythm. With the induction of complete heart
block, atrial and ventricular activity are completely
dissociated but the His bundle potential still
precedes the essentially unchanged QRS complex
SCHERLAG, LAZZARA, HELFANT
306
A
NSR
L-2
HBe
S
A
1.-
1-
a
&
g -1- -y-
-1
l BH
130/min
I
1
k-
.
=
1
1 l-
I
BH
AV = 79/min
A jS
0
.1,
-.
*1
BH
I.15II,
&
BH
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C
I LH 1-
ll- AL ~L
wmru
~
~
49/min
(Complete Heart Block)
BH
_
-1i
---1I
a
WA~
lONSOOP
~~~
=
LL
BH I
v-rl11'
L
--dmmmmmb&
-JL- W..
BH
tl
Figure 1
Atrial, His bundle, and ventricular relationships in a dog during normal sinus rhythm (NSR), A-V rhythm
(AV) and His bundle rhythm (BH). The top trace in each panel is a standard lead II electrocardiogram (L-2); below is the His bundle electrogram (HBe) showing atrial, A; His bundle, BH; and
late activity in the base of the ventricular septum, S. A) Normal sinus rhythm at a rate of 130/min
with His bundle activity occurring during the P-R interval of the surface electrocardiogram. B)
A-V nodal rhythm at a rate of 79 beats/mim produced by cooling the sinoatrial node. Note that His
bundle activity precedes atrial activity which in turn occurs just prior to ventricular activity. C) His bundle rhythm at 49 beats/mim with complete heart block produced by injection of A-V node with formaldehyde. Note the dissociation of atrial activity from ventricular activity. A His bundle deflection precedes each ventricular complex and a normal QRS configuration persists. The interval between time lines
equals 1 sec. Reproduced with permission of the Amer Heart J (81: 227, 1971).
by the same interval as that seen during normal
sinus rhythm and A-V nodal rhythm.
In addition to these physiologic differences, A-V
nodal and His bundle rhythms also have differential
chronotropic responses to ouabain.19 With progressively increasing (nontoxic) doses of ouabain, the
mean rate of A-V nodal rhythm decreased from 94
to 55 beats/min. In contrast, in animals with His
bundle rhythms, there was no significant change in
heart rate over the same range of ouabain dosages
(average rate, 40 beats/min).
Thus, experimentally created A-V nodal and His
bundle rhythms have markedly different "escape"
rates and chronotropic responses to ouabain.
Conduction
In another study from our laboratory, on the
intact dog heart, retrograde conduction from the
His bundle to the sinus node area was significantly
longer during His bundle rhythms, produced by
pacing the His bundle, than during spontaneous
mid A-V nodal rhythms at the same heart rate.20
Figure 2 illustrates a lead II electrocardiogram
recorded in conjunction with electrograms taken
from the area of the sinus node (SA), the region of
the His bundle (Hb), and the area of the coronary
sinus (CS). Changes in sequence of activation of
different recording sites are noted as the rhythm
changes from sinus rhythm to A-V nodal rhythm
and His bundle pacing rhythm. In panel B a mid
A-V nodal rhythm was produced by crushing the
sinus node. Note that the sequence of atrial activation then proceeded from the low atrium to the high
right atrium with coronary sinus and atrial activity
in the region of the His bundle preceding sinus
node activation. The P wave is coincident with
Circulation, Volume XLVIII, August 1973
JUNCTIONAL RHYTHMS
A Sinus
307
Rhythm
Hb ,^jp
CS
v
1
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C His Bundle Pacing
pi
HR =
62/min
PI-R
33 msec
=
PI
H-SA = 115 msoc
H-CS =100 mseccl
Figure
;
2
A comparison of retrograde His bundle to atrium conduction in the dog during mid A-V nodal (Middle "Nodal" Rhythm) and electrically induced His bundle rhythm showing atrial (A), His bundle (H),
and ventricular (V) activation. Traces in panels A and B, starting from the top: Lead II ECG (L-2);
bipolar electrograms from the sinus node area (SA), the His bundle (Hb), and coronary sinus ostium
(CS). In panel C traces are Lead II ECG and bipolar electrograms from SA and CS. A) During sinus
rhythm (heart rate 120 beats/min) initial activity occurred in the sinus node area. Then the atrium was
activated in the A-V-node-His-bundle region (A). Atrial activation in the area of the coronary sinus ostium followed. The H-V time was 32 msec. B) After crushing the sinus node, a mid A-V nodal rhythm
(heart rate 65 beats/min) was produced with the P wave temporally coincident with the QRS. His bundle activation preceded all activity and the H-V time remained unchanged (32 msec). However, atrial
activity in the His bundle electrogram was coincident with the early portion of the ventricular activation (note V complex in panel A) and was the earliest atrial activation recorded. Activation in the area
of the coronary sinus ostium (CS) and sinus node (SA) followed. The retrograde conduction time from
the onset of His bundle activity to the CS and SA activation was 35 and 50 msec, respectively. C)
During His bundle pacing at essentially the same rate as the spontaneous mid A-V nodal rhythm (panel
B), the time from delivery at the pacing impulse (PI) to activation of the CS and of the SA was 100
and 115 msec, respectively. Note that the time from PI to the onset of ventricular activity closely corresponded to the previously measured H-V time (panels A and B) and the QRS was identical to that
seen during sinus and mid A-V nodal rhythm. The interval between time lines equals 1 sec.
ventricular activation and thus is not seen on the
surface electrocardiogram. The His bundle deflection (H) precedes ventricular activation by 32
msec, the same as that seen during sinus rhythm. If
this mid A-V nodal rhythm actually arises in the His
bundle, as has been suggested by Damato et al.,6 it
should be possible to pace the His bundle at
approximately the same rate as the mid A-V nodal
Circulation, Volume XLVIII, August 1973
rhythm and show that the time from the paced
impulse back to any part of the atrium is essentially
the same as that seen during the spontaneous mid
A-V nodal rhythm. In panel C (fig. 2), His bundle
pacing was achieved at a slightly lower heart rate
than the mid A-V nodal rhythm (A-V nodal
rhythms can be readily suppressed by overdrive).
Note that the QRS is unchanged from that recorded
SCHERLAG, LAZZARA, HELFANT
308
Table 1
Comparison of Spontaneous Mid Nodal Rhythm and
His Bundle Rhythm at Similar Heart Rates in Dogs*
Spontaneous mid A-V
nodal rhythm
HR
BH-SA
(beats/min) (msec)
Exp.
1
2
3
4
108
92
95
6
7
Average
SD
109
90
124
103
103l1
His bundle pacing
BH-SA
HR
(msec)
75
50
45
65
39
45
50
150
62
105
105
75
65
93
53 12t
94
2St
(beats/min)
108
93
90
103
95
12 5
104
103 9
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Abbreviations: HR = heart rate; BH = bundle of His;
SA = sinus node.
*From reference 20.
tPaired t test, P < 0.01.
during spontaneous A-V nodal rhythm or sinus
rhythm and that the time from the pacer impulse to
the R wave (PI-R) is equal to 33 msec, the same as
the H-V time as measured in panels A and B during
spontaneous rhythm and mid A-V nodal rhythm,
respectively. However, the time from the stimulus
applied at the His bundle to activation of the SA
node electrogram and the coronary sinus electrogram was 115 and 100 msec, respectively. This is
ECG
P8EQ
A-V Nodal Potentials
Several recent studies have utilized catheter
recordings of A-V nodal potentials2 to differentiate
the origin of junctional rhythms.6 22 Damato et al.6
indicated that recordings of A-V nodal potentials
were made in three patients with so-called middle
and lower A-V nodal rhythm. Pacing of the atrium
at a faster rate than the nodal rate resulted in a
sequence consisting of atrial depolarization, a small
slow potential, His bundle activation, and ventricular activation. During A-V nodal rhythm the slow
S
:QR
HBE
markedly longer than the time measured from the
recorded His bundle deflection to the SA nodal
electrogram or the coronary sinus electrogram
during the spontaneous mid A-V nodal rhythms.
The significant increase of conduction time during
His pacing reflects the delay of the impulse across
the entire A-V node. During mid A-V nodal
rhythms the impulse must traverse only a portion of
the A-V node. The average values and standard
deviations recorded for retrograde conduction time
during mid A-V nodal rhythms and during His
bundle pacing at the same heart rate show that the
retrograde conduction time during the His bundle
pacing is significantly increased when compared
with conduction time during spontaneous A-V
nodal rhythm (table 1).
Xi.~~~~~~~~.
l
: Qf*0;120
Q
.
4 P'@
4
He
Z
., .e . .0
..
1.
Figure 3
Influence of electronic filtering on slow waves in the P-R interval in a patient. The two traces above are
standard lead 11 and a His bundle electrogram recorded with bandpass fiters of 0.1 to 200 Hz. Note
that the His deflection in the second trace occurs on the crest of a slow wave. In the bottom trace, the
His bundle electrogram frequency settings of 40-500 Hz show a deflection resembling an N potential at
the end of atrial depolarization but prior to His bundle depolarization. cps= Hz. (From Circulation 39:
13, 1969).
Circulation, Volume XLVIII, August 1973
I
JUNCTIONAL RHYTHMS
,;1;0__L
t S
t
oVR
t
m
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vi
t
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1 320 msec
H-V
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309
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V4
Vt6
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Li-R
aVR _
a V F~~~~~~~~~~~~~~~~~~~~~~~~~~
Figure 4
His bundle electrocardiographic analysis of a patient with complete heart block in which the lesion
was localized proximal to the recording of the bundle of His electrogram. At the top are 12 standard
ECG leads showing a narrow QRS complex with atrioventricular dissociation. The His bundle recording
showed His bundle activity (BH) constantly linked to ventricular activity (V) and QRS complexes (H-V
= 40 msec, R-R = 1320 msec). Atrial activity (A) occurs at a cycle length of 770 nsec and is independent of ventricular activation. (Modified from Circulation 41: 437, 1970).
A-V nodal or "N potentials" did not precede His
bundle activity but were associated with atrial
activity, the latter usually occurring during or after
ventricular activation. However, each QRS complex
was preceded by a His bundle potential. The
authors interpreted these data as evidence that the
site of origin of these rhythms was the His bundle,
not the A-V node. However, an isoelectric segment
was usually interposed between the A-V nodal
deflection and the His deflection. Since activation of
A-V node is continuous throughout the interval
between activation of the atrium and the His
bundle,'0 a portion of A-V nodal activation must
occur during the isoelectric interval present in the
recordings reported in the study by Damato et al.,
as well as in the isoelectric interval recorded
in another similar study in the experimental
animal." 22 This argues against the authors' contention that the absence of an A-V "nodal potential"
preceding a His deflection localizes the pacemaker
in the His bundle, because the A-V nodal activity
occurring during the isoelectric interval may be
unrecorded or undetectable.23
Circulation, Volume XLVIII, August 1973
Slow deflections recorded at the A-V junction
should be interpreted cautiously. False potentials
were recorded by Scher et al.24 In addition, slow
potentials are invariably present during the P-R
interval in unfiltered records (fig. 3). These slow
EkontrD
t i
--
HR 401-'n
1-2
FVigure 5
Electrocardiogram shzowinig the response of a patient with
complete heart block to atropine. A previous His bundle
study indicated block was proximal to the recorded His
bunldle electrogram. A) Note the slow ventricular rate of
40 beats/mmn and dissociated atrial rate of 73 beats/mzn.
B) After 0.5 mg atropine, the ventricular rate increased to
75 beats/mmn. The QRS retained its configuration duration
and complete A-V block is still evidenlt. (From Circulation
41: 437, 1970).
SCHERLAG, LAZZARA, HELFANT
310
evidence for the existence of pacemakers in the A-V
node and His bundle. Both physiological and
pharmacological studies were performed on 25
patients with complete heart block and a narrow
QRS complex.26 Figures 4-6 illustrate examples of
the two groups of patients which were defined. In
fig. 4 a bipolar His bundle recording (BE) was
made in a patient with complete heart block and a
narrow QRS complex (see 12 lead ECG above and
three simultaneously recorded ECG leads I, aVR,
and aVF below ).27 It can be seen that the ventricular activity was preceded in each cycle by a
His bundle deflection. Atrial activity was not
related to either His bundle or ventricular activation. With the administration of a small dose of
potentials are presumably associated with atrial
repolarization.25 The application of the conventional filter settings to record the His bundle electrogram (40-200 Hz) can convert the slow potentials
into A-V "nodal humps" or "N potentials" (see fig.
3). Indeed, Hoffman et al. have suggested that
upstroke velocities of cells of the A-V node are too
slow to be recorded by commonly used extracellular
techniques.25
Thus, the nondescript, spurious nature of A-V
nodal recordings would severely limit if not totally
exclude their usefulness in differentiating the site of
origin of junctional rhythms.
Clinical Studies
Recent studies in man have provided further
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BE
- v
A
-YU*VR
W
lA
't
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i
i 1
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'
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II
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940
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40
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940
o
.Hl90
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RH
440
150
125
SN
600
40
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c
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vP
5
t
Bs
7f -il
Pi-1
40
BHR
085/m
L-3 t
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Figure 6
His bundle electrocardiographic analysis of patient with complete heart block and narrow QRS complex.
At the top are the 12 standard ECG leads showing QRS complex and dissociated atrial activity. A) The
His bundle electrogram (BE) indicates two rapid deflections, one associated wtih atrial activity, the other
associated with ventricular activity (BH and BH', respectively). Premature atrial stimulation (PI = pacer
impulse) shows that the A to BH time widens from 90 to 150 msec. B) C) Validation of the BH' potential was performed by His bundle pacing at a heart rate of 57-85 beats/min. Note that the QRS is the
same as that recorded during spontaneous ventricular activity, (panel A), and the stimulus to R wave
interval (PI-R = 40 nsec) is exactly the same as the measured BH'-V interval. (From Circulation 41: 77,
1970.)
Circulation, Volume XLVIII, August 1973
JUNCTIONAL RHYTHMS
311
Table 2
Electrophysiological and Pharmacological Characteristics of Pacemakers in Patients with Complete
Heart Block
Group A
Group B
QRS duration
(msec)
Heart rates
(beats/min)
Site of block by His
electrogram
recording
0.08-0.10
45-60
Proximnal to His
36-43
recording
Distal to His
0.08-0.10
recording
or
Response to atropine
Marked increase in rate
(35-45 beats/min)
No appreciable rate
change ( 5 beats/min)
Probable
site of
pacer
A-V node
His
bundle
intra-His lesion
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atropine the heart rate accelerated from a rate of 40
to 75 beats/min (fig. 5).
In fig. 6 another patient who exhibited complete
heart block and a narrow QRS complex was studied
using His bundle-electrocardiography. In this case
the His bundle recording showed that there were
two deflections recorded on the His bundle
electrogram (BE )-one associated with atrial
activity (BH) and the other preceding ventricular
activity (BH' )27 That both these deflections emanate from the His bundle was validated by
recordings during an induced premature beat (PI)
which widened the A-H interval from 90 to 150
msec, an increase that indicates that this deflection
(BH) was not part of atrial activity. In addition,
panels B and C illustrate that pacing from the His
bundle recording electrodes produced capture of
the ventricles with 1:1 conduction. During pacing
the same QRS morphology was produced as in the
unpaced state in all leads, and the time interval
from the pacer impulse to ventricular activation
(PI-R) was the same as the unpaced H-V time seen
in panel A (40 msec). Atropine induced no
significant change of rate (an increase of 5 beats or
less) in contrast to its marked effect on the first
patient discussed.
In table 2 this series of patients with complete
heart block is separated into two groups, each
showing a narrow QRS complex. In group A the
heart rates ranged from 45 to 60 beats/min and
invariably increased significantly with atropine. In
group B the heart rates ranged from 35 to 45
beats/min and the block was located distal to the
recorded His bundle deflection. In several cases
intra-His bundle lesions could be discerned by
recording of double but dissociated His bundle
deflections (see fig. 6). There was no appreciable
effect of atropine on heart rate in these patients.
These differential responses to atropine in patients
with block proximal to the recorded H deflection or
blocks localized within the His bundle have also
Circulation, Volume XLVIII, August 1973
been reported recently by Rosen et al.29 Thus, the
site of block in patients with complete heart block
and narrow QRS can be differentiated on the basis
of escape rates and heart rate response to
atropine.
Conclusion
In summary, studies in both the experimental
animal and in man indicate that rhythms arising in
the A-V junction can be differentiated into at least
two groups. Basic electrophysiologic studies indicate that action potentials in the A-V node and His
bundle clearly respond differently to rate changes
and to acetylcholine. Experimentally created A-V
nodal and His bundle rhythms have different
escape rates and chronotropic responses to ouabain.
In addition, conduction times from His bundle to
atrium in A-V nodal rhythms and during His
bundle pacing at the same rate are significantly
different. In man, A-V nodal escape rhythms are
relatively fast (45-60 beats/min) and the rate
increases markedly in response to atropine. Escape
rhythms arising in the His bundle are somewhat
slower (35-45 beats/min), and their rate is relatively
unchanged by atropine.
References
1. ZAHN A: Experimentelle untersuchungen ueber die
reizbildung und reizleitung im atrioventrikular knoten. Arch Ces physiol 151: 247, 1913
2. HOFFMAN BF, CRANEFIELD PF: Electrophysiology of
the Heart. New York, McGraw-Hill, 1960, ch 6
3. SCHERF D, SHOOKHOFF C: Experimentelle unter
suchungen ueber die umker-extrasystole. Wein Arch
Inn Med 12: 501, 1926
4. SCHERF D, COHEN J: The Atrioventricular Node and
Selected Cardiac Arrhythmias. New York, Grune and
Stratton, 1964, pp 48-58
5. HOFFNIAN BF, CRANEFIELD PF: The physiological basis
of cardiac arrhythmias. Amer J Med 37: 670, 1964
6. DAMATO AN, LAU SH: His bundle rhythms. Circulation
40: 527, 1969
312
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7. PICK A, LANGENDORF R: Recent advances in the
differential diagnosis of A-V junctional arrhythmias.
Amer Heart J 76: 553, 1968
8. HOFFMAN BF, PAES DE CARVALHo A, DEMELLO WC:
Electrical activity of single fibers in the A-V node.
Nature 181: 66, 1958
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Circulation, Volume XLVIII, August 1973
Differentiation of "A-V Junctional Rhythms"
BENJAMIN J. SCHERLAG, RALPH LAZZARA and RICHARD H. HELFANT
Circulation. 1973;48:304-312
doi: 10.1161/01.CIR.48.2.304
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