Nature of the Gap Phenomenon in Man
By Delon Wu, Pablo Denes, Ramesh Dhingra, and Kenneth M. Rosen
ABSTRACT
The atrioventricular (AV) gap phenomenon occurs when the effective refractory
period of a distal site is longer than the functional refractory period of a proximal site
and when closely coupled stimuli are delayed enough at the proximal site to allow distal site recovery. According to previous studies, in type 1 gap, the distal site of block is
distal to the His bundle (ventricular specialized conduction system) and the proximal
site of block is in the AV node. In type 2 gap, both the proximal and the distal sites of
conduction block are within the ventricular specialized conduction system. Using His
bundle recordings and atrial extra-stimulus techniques in man, we observed three
previously undescribed types of gaps between (1) the AV node (distal) and the
atrium (proximal), (2) the His bundle (distal) and the AV node (proximal), and (3) the
ventricular specialized conduction system or a bundle branch (distal) and the His
bundle (proximal). The delays at the His bundle in the second and third types of gaps
seen in this study were demonstrated as splitting of His bundle potentials. Gaps between the AV node or the His bundle and the ventricular specialized conduction
system were more easily demonstrated at long cycle lengths, but gaps between the
atrium and the AV node were more easily demonstrated at short cycle lengths. Therefore, the previous subdivision of gaps into two types is an oversimplification, because
gaps can occur between multiple sites in the conduction system. The gap phenomenon may be potentiated by both long and short cycle lengths; long cycle lengths increase the effective refractory period of a distal site, e.g., the His bundle and the
ventricular specialized conduction system, and the short cycle lengths decrease the
functional refractory period of a proximal site, e.g., the atrium and the AV node.
KEY WORDS
atrial extra stimuli
functional block
cycle length
His bundle electrogram
supernormal conduction
refractory period
split His bundle potentials
intra-atrial conduction delay
• One type of supernormal conduction, i.e., the
paradoxical propagation of closely coupled
stimuli when stimuli at longer coupling intervals
are blocked, reflects a gap phenomenon (1-6).
This phenomenon occurs when the refractory
period of a distal conduction site limits conduction. With closely coupled stimuli, enough
proximal delay occurs so that the impulse arrives
at the distal conducting site late enough to be
conducted. Gallagher and co-workers (5) have
defined two types of gaps. In type 1 gap, the initial distal site of block is distal to the His bundle
recording site, and the proximal site of delay is
in the atrioventricular (AV) node. In type 2 gap,
both the distal and the proximal site of conduction delay are distal to the His bundle recording
site (5). A third kind of gap has recently been
From the Section of Cardiology, Department of Medicine,
Abraham Lincoln School of Medicine of the University of
Illinois College of Medicine, and the West Side Veterans
Administration Hospital, Chicago, Illinois 60612.
This work was supported in part by the Myocardial Infarction Program Contract 71-2478 from the National Heart
and Lung Institute and by Basic Institutional Support, West
Side Veterans Administration Hospital.
Received September 17, 1973. Accepted for publication
February 20, 1974.
682
described by Agha and co-workers (6) in a patient
with AV block; however, this kind of gap appears
to reflect supernormal conduction, and proximal
and distal sites of delay have not been defined (6).
In the present study, previously undescribed
types of gaps between (1) a bundle branch or
ventricular specialized conduction system
(distal) and the His bundle (proximal), (2) the
AV node (distal) and the atrium (proximal), and
(3) the His bundle (distal) and the AV node
(proximal) were demonstrated. These findings
suggest that classification of gap phenomena into
types 1 and 2 is an oversimplification. Gap
phenomena can occur between any two portions
of the AV conducting system from the atrium to
the distal Purkinje system. The two conditions
necessary for development of a gap are (1) a
distal site with an effective refractory period
that is longer than the functional refractory
period of proximal conducting tissues and (2) a
proximal site with a relative refractory period
that allows enough delay between impulses to
ensure that the effective refractory period of the
distal site is exceeded.
The effects of cycle length on the gap phenomenon were also investigated in this study.
Circulation Research, Vol. XXXIV, May 1974
683
GAP PHENOMENON
Methods
Electrophysiological studies were performed in
three patients during diagnostic cardiac catheterization in the supine, postabsorptive, nonsedated state.
Informed consent was obtained from all patients. His
bundle electrograms were recorded using previously
described techniques (7). A bipolar electrode catheter
was percutaneously introduced into the right femoral
vein and passed to the tricuspid valve for His bundle
recording. A second quadripolar electrode catheter
was introduced into an antecubital vein and positioned fluoroscopically against the lateral wall of
the high right atrium. The distal two electrodes were
used for atrial stimulation and the proximal two were
used for recording high right atrial electrograms.
Lead I, II, and III electrocardiograms (ECG) and
ventricular, high right atrial, and His bundle electrograms were recorded on a multichannel oscilloscopic
photographic recorder (Electronics for Medicine
DR-16) at paper speeds of 100 mm/sec and 200 mm/sec.
The stimulus was a 2-msec square wave that was approximately twice diastolic threshold; it was provided by a digital programmable pulse generator.
The basic intervals were recorded during sinus
rhythm or with atrial pacing at varied rates. Refractory
periods were measured with the atrial extra-stimulus
technique. The test stimulus (S2) was introduced after
every eighth driving (Si) or spontaneous sinus beat.
The coupling interval was decreased in increments
of 5-10 msec.
DEFINITIONS
Ai, Hi, and Vi are the low right atrial, the His
bundle, and the ventricular electrograms, respectively,
of driven or spontaneous sinus beats recorded from
the His bundle catheter, and A2, H2, and V2 are the
low right atrial, the His bundle, and the ventricular
responses, respectively, to the test stimuli (S2). HRAi
and HRA2 are the high right atrial electrograms of
driven or spontaneous beats and of test stimuli, respectively. A-H, H-V, Hi-H2, and Vi-V2 intervals
were measured as described by Wit et al. (8). H is
the initial portion and H' is the delayed portion of
split His bundle potentials. H2-H'2 is the interval
between the initial (H2) and the delayed split His
bundle potential (H'2) of the test cycle; Hi-H'2 is
the interval between the His bundle potential of the
driven or spontaneous beat (Hi) and the delayed portion of the split His bundle potential of the test
beat (H'2).
The relative refractory period of the ventricular
specialized conduction system was defined as the
longest H!-H2 interval at which H2 was conducted
to the ventricles with an increase in the H2-V2 interval relative to the H-V (H1-V1) interval of driven
beats. The effective refractory period of the ventricular specialized conduction system was defined as
the longest H]-H2 interval at which H2 failed to
propagate to the ventricles. The relative refractory
period of the His bundle was defined as the longest
H1-H2 interval at which H2 duration relative to Hi
duration was prolonged or at which splitting of the
Circulation Research, Vol. XXXIV, May 1974
H2 potential occurred. The refractory period of the
left or right bundle was defined as the longest Hi-H2
interval at which H2 was conducted to the ventricles
with electrocardiographic aberrancy of the left or
right bundle branch block pattern. If splitting of H2
was observed, the Hi-H'2 interval was used to measure the refractory period of the bundle branch. The
functional refractory period of the AV node was the
shortest attainable Hi-H2 interval conducted from
the atrium. The effective refractory period of the AV
node was the longest A^Aj. interval that failed to
propagate to the His bundle. The functional refractory
period of the atrium was the shortest attainable Ai-A2
interval. The effective refractory period of the atrium
was the longest Si-S2 (or HRA!-S2) interval at which
S2 failed to capture the atrium.
Results
Case 1 was a 48-year-old woman evaluated
because of chest pain. Her electrocardiogram
was within normal limits; electrophysiological
studies during sinus rhythm revealed a rate ol
73 beats/min, an A-H interval of 90 msec, and
an H-V interval of 34 msec.
Atrial premature stimuli were introduced at a
cycle length of 650 msec (Figs. 1 and 2). The
refractory period of the right bundle branch was
480 msec (H!-H 2 ). The effective refractory period
of the AV node was 300 msec (Fig. 1A and B). At
S1-S2 intervals between 300 and 250 msec, the
corresponding HRA1-HRA2 and Ai-A2 intervals
were also between 300 and 250 msec; A2 was
not conducted to the His bundle (Fig. IB and C).
As the S1-S2 interval was decreased from 240
msec to 200 msec, the HRA1-HRA2 interval decreased similarly. However, the Ai-A2 interval
increased to 310 msec, which allowed conduction
through the AV node (Fig. 2A and B). The effective refractory period of the atrium was 190 msec
(Fig. 2C).
In this patient, the initial distal site of block
was in the AV node, and the effective refractory
period of the AV node was longer than the functional refractory period of the atrium. Proximal
delays in the atrium at shorter coupling intervals
between the high and the low right atrium
allowed the AV node to recover. Thus, the gap
was between the atrium and the AV node.
Case 2 was a 23-year-old male with coarctation of the aorta. His electrocardiogram showed
sinus rhythm at 86 beats/min with a P-R interval of 160 msec and left ventricular hypertrophy. Electrophysiological studies during sinus
rhythm revealed an A-H interval of 103 msec
684
A
WU, DENES, DHINGRA, ROSEN
CL=650
S, V 3 I 0
HRA,,-HRA2=3l0 .A, A2=3l0 H, H2= 375
HBE
FIGURE 1
AE.!S
B
S.Si=3OO
HRArHR;A2=3OO A, A/300
AE
S.^250
n
HRA,-HRA2=250 A, A2=250 I
Demonstration of the gap
phenomenon between the
AV node (distal) and the
atrium (proximal) in case 1.
Records of the lead II
ECG (II) and ventricular
(V,), His bundle (HBE), and
high right atrial (AE) electrograms are shown. See
text for definitions of other
abbreviations. Paper speed
is 100 mm/sec and time
lines represent 1 second on
this and all subsequent illustrations. The basic driving cycle length was 650
msec. Arrows indicate the
first high-frequency atrial
spikes of both driven and
test beats recorded from the
His bundle electrogram. A:
At an S,-S2 interval of 310
msec, S2 was conducted to
the ventricles with an A,-A2
interval of 310 msec. B and
C: At an S,-S2 interval between 300 and 250 msec,
S2 was blocked in the AV
node because the A,-A2 interval was less than the
effective refractory period
of the AV node (300 msec).
The HRA2-A2 interval was
equal to the
HRA,-A,
interval.
V,
HBE
AE
Circulation Research, Vol. XXXIV, May 197-4
685
GAP PHENOMENON
=240 HRA,-HRA=i40 . A , A/310
H,H2=375
L4U
Hi'
HBE
AE
FIGURE 2
HBE!
HBE
Circulation Research, Vol. XXXIV, May 1974
Demonstration of the gap
phenomenon between the
AV node (distal) and the
atrium (proximal) in case 1.
A and B: At an Si-S2 interval between 240 and 200
msec, S2 was again conducted to the ventricles
because of sufficient intraatrial conduction delay; the
HRA2-A2 interval was longer than the HRA,-A, interval, which allowed the
AV node to recover. The
fourth beat in B was a premature atrial contraction
(PAC). C: At an S,-S2 interval of 190 msec, the effective refractory period of the
atrium was achieved.
686
and an H-V interval of 40 msec. The His bundle
potential duration was 30 msec and prolonged (9).
Extra stimuli were introduced during sinus
rhythm (cycle length 755 msec) (Fig. 3). At an
Ai-A2 interval of 385 msec, H2 was conducted
to the ventricles with an Hi-H2 interval of 425
msec (Fig. 3A). At an Ai-A2 interval of 375 msec,
the Hi-H 2 interval was 420 msec, and the H2
potential duration increased. Thus, the relative
refractory period of the His bundle was 420 msec
(Fig. 3B). The QRS complex was essentially unchanged. As the Ai-A2 interval was further decreased to 370 msec, the H1-H2 interval decreased
to 400 msec and splitting of H2 potentials occurred. H2 was conducted to the ventricles with
a QRS complex characteristic of left bundle
branch block (QRS 145 msec) during an H,H'2 interval of 425 msec (Fig. 3C). The refractory period of the left bundle was 425 msec.
At an Ai-A2 interval of 330 msec, the Hi-H2
interval was 390 msec and the Hi-H' 2 interval
increased to 440 msec, which allowed recovery
of the left bundle branch. As the A:-A2 interval
decreased from 330 msec to 230 msec, the H t -H 2
interval decreased from 390 msec to 315 msec,
the H 2 -H' 2 interval increased, and therefore
the Hi-H' 2 interval was lengthened. The configuration of the QRS complex was partially
normalized at all Hi-H' 2 intervals equal to or
greater than 425 msec (Fig. 3D and E). The
effective refractory period of the atrium of 170
msec limited AV conduction. When the atrium
was driven at a cycle length of 520 msec, splitting of the His bundle potentials and left bundle
branch block were not observed even at the
shortest attainable Hs-H2 interval of 360 msec.
In this patient, the initial distal site of block
was in the left bundle branch, and the refractory
period of the left bundle was shorter than the
functional refractory period of the His bundle.
Conduction delay in the common His bundle
(proximal) allowed the left bundle branch (distal)
time to recover. Therefore, this gap was between
the His bundle and the left bundle branch.
Shortening of the cycle length eliminated both
the proximal and the distal sites of delay.
Case 3 was a 65-year-old male with angina
pectoris. His electrocardiogram revealed sinus
rhythm of 68 beats/min, a P-R interval of 160
msec, and a QRS complex of 170 msec; the characteristics of the QRS complex revealed left
bundle branch block. Electrophysiological
studies during sinus rhythm revealed an A-H
WU, DENES, DHINGRA, ROSEN
interval of 90 msec and an H-V interval of
65 msec.
Atrial test stimuli were coupled to spontaneous sinus rhythm (cycle length 879 ± 40
msec) (Figs. 4 and 5A). With an Ai-A2 interval
of 505 msec, the Hi-H2 and Vi-V2 intervals were
525 msec (Fig. 4A). With Ai-A2 intervals between
500 and 450 msec, Hi-H2 intervals were between
520 and 475 msec, and H2 failed to propagate to
the ventricles. Thus, the effective refractory
period of the ventricular specialized conduction
system was 520 msec (Fig. 4B). With an Ai-A2
interval between 445 and 400 msec, the Hi-H2
interval decreased from 470 msec to 435 msec.
With this decrease in the Hi-H2 interval, splitting of H2 was observed, and the H:-H'2 interval
increased from 495 msec to 520 msec. The HiH'2 interval was equal to or less than the effective
refractory period of the ventricular specialized
conduction system and no conduction to the
ventricles was observed (Fig. 4C). At an Ai-A2
interval between 395 and 370 msec, the Hi-H2
interval decreased from 430 msec to 420 msec;
splitting of H2 increased with an Hi-H' 2 interval
of 530-550 msec, which allowed conduction to
the ventricles, because the Hi-H' 2 interval was
greater than the effective refractory period of
the ventricular specialized conduction system
(Fig. 4D). At an Ai-A2 interval between 365 and
355 msec, the Hi-H2 interval increased because
of AV nodal refractoriness; this increase allowed
the His bundle to recover partially—a decrease
in splitting and a decrease in the Hi-H' 2 interval to 520-500 msec occurred. Thus, conduction to the ventricles again failed, because the
Hi-H'2 interval was shorter than the effective
recovery period of the ventricular specialized
conduction system (Fig. 4E). At the closest
A,-A2 interval (350-340 msec), the H^H-. interval became longer than both the relative refractory period of the His bundle and the effective refractory period of the ventricular specialized conduction system; therefore, splitting of H2
disappeared and conduction to the ventricles
was resumed (Fig. 4F).
When the atria were driven at a cycle length of
770 msec, Aj-A2 intervals of 420 msec or more
produced corresponding Hi-H2 intervals of 465
msec or more. As the Ai-A2 interval was decreased to 410 msec, the Hi-H2 interval decreased to 460 msec, and H2 was not propagated
to the ventricles (Fig. 5B). Thus, the effective
refractory period of the ventricular specialized
Circulation Research, Vol. XXXIV, May 1974
687
GAP PHENOMENON
CL=755
It-
FIGURE 3
Left: Records from case 2 showing prolongation of His bundle duration, splitting of His bundle
potentials, and the gap phenomenon between the left bundle branch (distal) and the His bundle
(proximal). The atrial extra stimuli were coupled to normal sinus rhythm at a cycle length of
755 msec. Right: Magnified His bundle potentials of the test beats. A: At an A,-A2 interval of
385 msec, A2 was conducted to the ventricles with an H,-Ht interval of 425 msec. Both H, and
H2 duration were 30 msec. B: At an A,-Ai interval of 375 msec, A2 was conducted to the ventricles
with prolongation of H2 duration (40 msec). C: At an A,-A: interval of 370 msec, the H,-H2
interval was 400 msec, splitting of the H2 potentials occurred, and H2 was conducted to the ventricles with functional left bundle branch block. D: At an At-A2 interval of 330 msec, the H,-H2
interval was 390 msec; H2 was conducted to the ventricles with less left bundle branch block,
because the delay in the His bundle allowed the left bundle branch to recover partially. E: At
an A,-A2 interval of 255 msec, H2 was conducted to the ventricles with even less left bundle
branch block, because of increased delays in the His bundle.
Circulation Raearch, Vol. XXXIV, May 1974
688
WU, DENES, DHINGRA, ROSEN
conduction system was 460 msec. At Ai-A2 intervals between 390 and 360 msec, H,-H 2
intervals ranged from 430 to 415 msec, and splitting of the H2 potential (H,-H' 2 interval 455-460
msec, and H2-H' 2 interval 20-40 msec) occurred; H' 2 was still not conducted to the
ventricles. As the Ai-A2 interval was decreased
from 350 msec to 340 msec, the Hi-H 2 interval
increased from 450 msec to 460 msec, and splitting of the His bundle potential disappeared. At
A]-A2 intervals between 340 and 320 msec,
H r -H 2 intervals were greater than 465 msec,
which was less than the effective refractory
period of the ventricular specialized conduction
system, and AV conduction was resumed. As the
Si-S2 interval was decreased to 310 msec, the
effective refractory period of the AV node was
achieved at an Ai-A2 interval of 310 msec (Fig.
6A and B). Further decreases in the coupling
intervals resulted in a slight increase in latency
CL=879
HBE
FIGURE 4
Records from case 3 showing the AV gap phenomena. The atrial extra stimuli were coupled to sinus rhythm at a cycle length of
879 msec. A: At an A,-A2 interval of 505 msec, H2 was conducted to the ventricles with an H,-H2 interval of 525 msec. B: At an
A,-A2 interval of 500 msec, H2 was blocked in the ventricular specialized conduction system, because the effective refractory
period of the ventricular specialized conduction system was achieved (520 msec). C:At an A,-A2 interval of 400 msec, splitting of
H2 potentials occurred because the H,-H2 interval (435 msec) was less than the relative refractory period of the His bundle
(470 msec). H'2 was still blocked in the ventricular specialized conduction system, since theH,-H'2 interval (520 msec) was equal
to the effective refractory period of the ventricular specialized conduction system. D: At an A,-A2 interval of 395 msec, AV conduction resumed because the H,-H'2 interval (545 msec) was now longer than the effective refractory period of the ventricular
specialized conduction system. E: At an A,-A2 interval of 360 msec, the degree of splitting of H2 decreased because of the increasing delay in the AV node, which allowed the His bundle to recover partially. However, H'2 was blocked in the ventricular
specialized conduction system, because the H,-H'2 interval was equal to the effective refractory period of the ventricular specialized conduction system. F: At an A,-A2 interval of 340 msec, AV conduction resumed because the H,-H2 interval (525 msec) was
longer than both the relative refractory period of the His bundle and the effective refractory period of the ventricular specialized
conduction system.
Circulation Research, Vol. XXXIV, May 1974
689
GAP PHENOMENON
GL=879
msec
700
A
A
A V,V,
A
600 H,H,
A
v*v,
500
3
o
°°o
rf>°
oo°
400 1
1
B.
msec
700
CL=770
A
A V, V,
A
A
600
H,H,
H,H;
A
A
A
500
A
o
400
'
1
300
400
I
500
<
600
700 msec
A, A,
FIGURE 5
Atrioventricular conduction curves in case 3 showing multiple gap phenomena and their relations to the changes in
cycle length. Abscissa: A,-A2 intervals. Ordinate: H,-H2
intervals (open circles), H,-H'2 intervals (solid circles),
and V;-V2 intervals (triangles). A: Cycle length = 879 msec.
The effective refractory period of the ventricular specialized
conduction system was 520 msec; the relative refractory
period of the His bundle was 470 msec. The first gap between
the ventricular specialized conduction system (distal) and
the His bundle (proximal) occurred at an A,-Az interval between 500 and 400 msec; the second gap between the His
bundle (distal) and the AV node (proximal) occurred at an
A,-A2 interval between 445 and 340 msec; the third gap between the ventricular specialized conduction system (distal)
and the AV node occurred at an A,-A2 interval between 365
and 355 msec. B: Cycle length = 770 msec. The effective
refractory period of the ventricular specialized conduction
system was 460 msec; the relative refractory period of the His
bundle was 430 msec. The first gap between the ventricular
specialized conduction system (distal) and the AV node
(proximal) occurred at an A,-A2 interval between 410 and 345
msec; the second gap between the His bundle (distal) and
the AV node (proximal) occurred at an A,-A2 interval between
390 and 360 msec. As the cycle length shortened, both the
relative refractory period of the His bundle and the effective
refractory period of the ventricular specialized conduction
system decreased, and the pattern of the gaps changed.
Circulation Research, Vol. XXXIV, Slay 1974
and a progressive increase in the A,-A2 intervals
due to intra-atrial conduction delays (prolongation of HRA2-A2 interval). As the Si-S 2 interval
was decreased to 265 msec or less, the Ai-A2
interval was increased to 320 msec and A2 again
conducted to the ventricles (Fig. 6C and D). The
effective refractory period of the atrium was
250 msec.
These relationships are graphically demonstrated in Figure 5. Figure 5A shows the AV
conduction curve at a cycle length of 879 msec.
The Hi-H 2 interval of 520 msec was the effective
refractory period of the ventricular specialized
conduction system, the H!-H 2 interval of 470
msec was the relative refractory period of the His
bundle. The first gap between the His bundle
and the ventricular specialized conduction
system occurred at an Ai-A2 interval between
500 and 400 msec; the second gap between the
AV node and the His bundle occurred at an
Ai-A2 interval between 445 and 340 msec; the
third gap between the AV node and the ventricular specialized conduction system occurred
at an A!-A2 interval between 365 and 355 msec.
Figure 5B shows the AV conduction curve at a
cycle length of 770 msec. The H,-H 2 interval of
460 msec was the effective refractory period of
the ventricular specialized conduction system;
the Hi-H 2 interval of 430 msec was the relative
refractory period of the His bundle. The first
gap between the AV node and the ventricular
specialized conduction system occurred at an
Ai-A2 or Sj-S2 interval between 410 and 345
msec; the second gap between the AV node and
the His bundle was concealed on the surface
electrogram and occurred at an A,-A2 or Si—S2
interval between 390 and 360 msec. The third
gap between the atrium and the AV node occurred at an S,-S2 interval between 310 and
270 msec and is not shown in Figure 5B.
In this patient the left bundle branch block
was probably complete. Thus, block distal to the
His bundle (ventricular specialized conduction
system) could reflect the effective refractory
period of the right bundle. During sinus rhythm,
three gaps were demonstrated. The first gap was
between the ventricular specialized conduction
system (distal) and the His bundle (proximal);
splitting of the His bundle potential allowed the
ventricular specialized conduction system to
recover. The second gap was between the His
bundle (distal) and the AV. node (proximal).
Relative refractoriness in the AV node allowed
690
WU, DENES, DHINGRA, ROSEN
CL=77O
S,S2=3I5
HRA,-HRA=3I5
A,A2=320
HRA.-HRA/3IO
A,A2=3IO
H, H/470
HBE—
B.
S, S2=3IO
FIGURE 6
HBE—
S,S2=270
HRA,-HRA2=3O5
A,A2=3IO
V
Records from case 3 showing gap phenomenon between the AV node (distal) and the atrium (proximal). The
arrows in A and B indicate S2. A: At
an S,-Sg interval of 315 msec, S2 was
conducted to the ventricles with an
A,-A2 interval of 320 msec. B: At an
S,-S2 interval of 310 msec, S2 was
blocked in the AV node because the
effective refractory period of the AV
node was achieved (310 msec). C: At
an S,-S2 interval of 270 msec, the
latency of S2 increased; S2 was still
blocked in the AV node because the
A,-A2 interval (310 msec) was equal
to the effective refractory period of
the AV node. D: At an S,-S2 interval
of 265 msec, the A,-A2 interval increased because of an increase in both
latency (S2-A2) and intra-atrial conduction delay (HRA2-A2). S2 was conducted to the ventricles because the
A,-A2 interval (320 msec) was longer
than the effective refractory period
Of the AV node-
S,S2=265
HRA,- HRA2=300 A,A2=320
H, H/465
Circulation Research, Vol. XXXIV, May 1974
691
GAP PHENOMENON
recovery of the His bundle and disappearance of
splitting. The third gap was between the ventricular specialized conduction system (distal)
and the AV node (proximal) and was identical
to type 1 gap previously described by Gallagher
and co-workers (5).
Discussion
Microelectrode studies have shown that action
potential durations and refractory periods in the
canine His-Purkinje system increase progressively from the His bundle toward the peripheral
Purkinje tissue. The area of maximum action
potential duration and refractoriness, the
"gate," is located 2-3 mm proximal to the termination of the His-Purkinje system in the myocardium (10, 11). Studies in intact dogs and
humans that used His bundle and proximal
bundle branch recordings have revealed functional blocks between the His bundle and the
bundle branches with coupled stimulation
(12, 13). In the present study, functional block in
the His bundle was demonstrated by prolongation of the His bundle potentials, splitting of His
bundle potentials, or both. The exact site of the
delay that resulted in splitting of the His bundle
potential could not be delineated, because the
origin of catheter-recorded His bundle electrograms is controversial. Sano et al. (14), using
isolated rabbit and dog hearts, have suggested
that the His bundle electrogram is a composite
resulting from depolarization of the entire His
bundle. In contrast, Kupersmith et al. (15),
using direct recordings of His bundle activity
during open heart surgery, have suggested that
the catheter-recorded His bundle electrogram is
generated from the proximal His bundle. We
propose that the site of splitting is somewhere in
the His bundle.
Therefore, the possible potential sites of delay
or block with coupled atrial extra stimuli are (1)
the distal gate of the His-Purkinje system, (2) the
more proximal bundle branches, (3) the His
bundle, (4) the AV node, and (5) the atrium. It is
also possible that several sites of block could
occur in the His bundle or in the AV node.
Occurrence of the gap phenomenon depends
on two conditions. The first condition requires
that the effective refractory period of a distal
tissue must be longer than the functional refractory period of proximal tissues, so that during a
critical coupling interval there is block in a
distal site. The second condition requires that
Circulation Research, Vol. XXXIV. May 1974
the relative refractory period of a proximal tissue
at close coupling intervals permits enough proximal delay so that the initially blocked distal
tissue can recover. Gallagher et al. (5) classified
gaps into two types. In type 1 gap the distal site
of block was in either a bundle branch or the
ventricular specialized conduction system (both
distal to the His bundle), and the proximal site
of delay was in the AV node. In type 2 gap both
the distal and the proximal site of delay were
within the ventricular specialized conduction
system. In the present study, we described three
new types of gaps between the AV node (distal)
and the atrium (proximal), between the His
bundle (distal) and the AV node (proximal),
and between the ventricular specialized conduction system or a bundle branch (distal) and the
His bundle (proximal). Gallagher et al. (5) have
described the occurrence of type 1 and 2 gaps in
the same heart. In the present study (case 3),
three gaps were observed in one patient. We also
observed that gaps could be concealed on the
surface electrocardiogram; for example, splitting
of His bundle potentials was not apparent on the
surface electrocardiogram and it was reversed as
proximal delays in the AV node increased the
interval between impulses entering the His
bundle.
The previous classification of gaps into types
1 and 2 is thus an oversimplification because of
the multiple sites of occurrence of the gap phenomenon. We recommend that this classification
be eliminated and that gaps be described by
noting both the distal and the proximal site of
delays.
The effect of cycle length on the gap phenomenon is predictable. Refractory periods of both
the atrium and the His-Purkinje system decrease
as the cycle length shortens (1, 16). Gaps with a
distal site of block in the His-Purkinje system
are less likely to occur at faster heart rates. At
long cycle lengths, the atrium may limit AV conduction. Decreasing the cycle length results in
shortening of the effective refractory period of
the atrium and reveals a gap phenomenon not
seen when the atrium limits AV conduction. The
AV nodal responses to changes in cycle length
vary; however, the effective refractory period of
the AV node tends to lengthen and the functional refractory period tends to shorten with a
decrease in cycle length (16). The effect of
changes in cycle length on gaps involving' the
AV node depends on whether the AV node is
692
WU, DENES, DHINGRA, ROSEN
serving as the distal or the proximal site of delay
and on relative changes in the effective refractory period and the functional refractory period
of the AV node compared with those of other
conducting tissue.
7.
SCHERLAG, B.J., LAU, S.H., HELFANT, R.H., BERKOWITZ, W.D., STEIN, C , AND DAMATO, A.N.: Catheter
technique for recording His bundle activity in man.
Circulation 39:13-18, 1969.
8.
WIT, A.L., WEISS, M.B., BERKOWITZ, W.D., ROSEN,
K.M., STEINER, C , AND DAMATO, A.N.: Patterns of
atrioventricular conduction in the human heart.
Circ Res 27:345-359, 1970.
Acknowledgment
9.
R.P.: Atrioventricular block: Localization and classification by His bundle recordings. Am J Med 50:
146-165, 1971.
We wish to acknowledge the secretarial help of Ms. Mary
Jo Moore in the preparation of this manuscript.
10.
2.
3.
4.
MOE, G.K., MENDEZ, C , AND HAN, J.: Aberrant A-V
impulse propagation in the dog heart: Study of functional bundle branch block. Circ Res 16:261-286,
1965.
DURRER, D.: Electrical aspects of human cardiac activity: Clinical physiological approach to excitation
and stimulation. Cardiovasc Res 2:1-18, 1968.
GOLDREYER, B.N., AND BIGGER, J.T., JR.: Spontaneous
and induced reentrant tachycardia. Ann Intern Med
70:87-98, 1969.
5.
GALLAGHER,
J.J.,
DAMATO,
A.N.,
12.
LAU, S.H., BOBB, G.A., AND DAMATO, A.N.: Catheter re-
cording and validation of left bundle branch potentials
in intact dogs. Circulation 42:375-383, 1970.
13.
ROSEN, K.M., RAHIMTOOLA, S.H., SrNO, M.Z., AND GUN-
NAR, R.M.: Bundle branch and ventricular activation
in man. Circulation 43:193-203, 1971.
14.
SANO, T., NAKAI, M., AND SUZUKI, F.: Nature of His
potential in His electrogram. Jap Heart J 13:521-536,
1972.
15.
KUPERSMITH, J., KRONGARD, E . , AND WALDO, A . L . :
Conduction intervals and conduction velocity in
human cardiac conduction systems: Studies during
open heart surgery. Circulation 47:776-785, 1973.
AGHA, A.S., CASTELLANOS, A., JR., WELLS, D., ROSS,
M.D., BEFELER, B., AND MYERBURG, R.J.: Type I,
type II and type III gaps in bundle branch conduction. Circulation 47:325-330, 1973.
MYERBURG, R.J., GELBAND, H., AND HOFFMAN, B.F.:
Functional characteristics of the gating mechanism in
the canine AV conducting system. Circ Res 28:136147, 1971.
CARACTA,- A.R.,
VARGHESE, P.J., JOSEPHSON, M.E., AND LAU, S.H.:
Gap in A-V conduction in man: Type I and II. Am
Heart J 85:78-82, 1973.
6.
11.
WIT, A.L., DAMATO, A.N., WEISS, M.B., AND STEINER,
C : Phenomenon of gap in atrioventricular conduction
in the human heart. Circ Res 27:679-689, 1970.
MYERBURG, R.J., STEWART, J.W., AND HOFFMAN, B.F.:
Electrophysiological properties of the canine peripheral AV conducting system. Circ Res 26:361-378,
1970.
References
1.
NARULA, O.S., SCHERLAG, B.J., SAMET, P., AND JAVIER,
16.
DENES, P., Wu, D., DHINGRA, R., PIETRAS, R.J., AND
ROSEN, K.: Effects of cycle length on cardiac refractory
periods in man. Circulation 49:32-41, 1974.
Circulation Research, Vol. XXXIV, May 1974