- i 0
* VOL 60 NO 3
NWllla^
c/In Official Journal ofthe aAmerican Heart c./Issociation, Inc.
CURRENT TOPICS
Second-degree Atrioventricular Block
DOUGLAS P. ZIPES, M.D.
WENCKEBACH"1 2 AND HAY,3 by analyzing the
A, C and V waves in the jugular venous pulse,
described two types of second-degree atrioventricular
(AV) block. After the introduction of the electrocar-
diograph, Mobitz4 classified the two types of block as
type I and type II. Electrocardiographically, typical
type I second-degree AV block is characterized by
progressive PR prolongation culminating in a noncon-
ducted P wave, while in type II second-degree AV
block, the PR interval remains constant before the
blocked P wave. In both instances, the AV block is in-
termittent, generally repetitive and may involve
several P waves in a row. Usually, the eponym Mobitz
Downloaded from http://ahajournals.org by on February 2, 2019
type I and Mobitz type II AV block is applied to the
two types of block, while the term "Wenckebach
block" refers to type I AV block only.
The purpose of this paper is to provide both a brief
review of clinically relevant electrophysiologic and
electrocardiographic concepts of AV conduction and
block, and a critical evaluation of the present
classification of second-degree AV block.
Electrophysiological Characteristics of the AV Node
and His-Purkinje System
Since the difference between type I and type II AV
block, in most instances, probably relates to the site at
which the block occurs, it is important to review the
electrophysiological properties of the tissues involved.
Transmembrane action potentials recorded from
cells within the AV node differ markedly from those
recorded in the His-Purkinje system. AV nodal cells
display reduced action potential amplitude, duration,
resting potential, conduction velocity, maximum rate
From the Krannert Institute of Cardiology, the Department of
Medicine, Indiana University School of Medicine, the Veterans Ad-
ministration Hospital, Indianapolis, Indiana.
Supported in part by the Herman C. Krannert Fund, grants HL-
06308, HL-07182 and HL-18795 from the NHLBI, NIH, Bethesda,
Maryland, and by the American Heart Association, Indiana
Affiliate, Inc.
Aadress for reprints: Douglas P. Zipes, M.D., Indiana University
School of Medicine, 1100 West Michigan Street, Indianapolis, In-
diana 46202.
Received January 15, 1978; revision accepted March 8, 1979.
Circulation 60, No. 3, 1979.
NV -%-SEPTEMBER 1979
of rise of the upstroke (dV/dt), overshoot, safety fac-
tor for conduction and threshold of activation, com-
pared with cells in the His-Purkinje system.56
Recovery of excitability in AV nodal cells is delayed
beyond the time for restoration of the membrane
potential to its full diastolic potential (time
dependence),7 while refractoriness is voltage-
dependent in normal cells of the His-Purkinje system.
Summation is another feature of AV nodal cells.5 8
Based on studies in the rabbit AV node,9 the middle or
N portion does not exhibit automaticity, while normal
cells of the His-Purkinje system commonly undergo
spontaneous diastolic depolarization.
The ionic currents responsible for the depolariza-
tion and repolarization of cardiac cells appear to be
different for AV nodal cells and cells in the His-
Purkinje system. In the His-Purkinje system, the fast,
inward, sodium current, which is responsible for the
rapid upstroke of the cardiac action potential, triggers
a second, slower current carried by calcium (and
possibly sodium) ions, which is responsible primarily
for the plateau phase of the cardiac action potential.
These two inward currents, interdependent and more
complex than simply a rapid current followed by a
slow component, are present in specialized conducting
tissues and in atrial and ventricular muscle cells.'0-13 In
the N region of the AV node, it is possible that only
the second, slow current may be operative, and
propagation through this area may occur normally
without engaging the fast component.6 14-16 Cells on
either side of the AV node may demonstrate a con-
tinuum: Depending upon their distance from the N
region, these cells show progressively less dependence
on the slow-current contribution to depolarization.17
Slow-channel blockers, such as manganese'4' 15 and
verapamil,'5' 16 strikingly depress AV nodal propaga-
tion without significantly affecting conduction in the
His-Purkinje system or in ventricular or atrial muscle.
Tetrodotoxin, the poison obtained from the puffer
fish, blocks the fast channel,'8 19 making His-Purkinje
cells inexcitable, and fails to inhibit AV nodal ac-
tivity. 14
These distinctive electrophysiologic differences
between normal cells in the AV node and normal cells
in the His-Purkinje system account for differences in
465
 466 ClIRCULATION
the nature of conduction and block.20 Subjecting cells
in the His-Purkinje system to a variety of interven-
tions, such as ischemia, elevated potassium concen-
trations or other ionic perturbations, depolarizing
currents, or superfusion with ionic blockers such as
tetrodotoxin, may depress the normal fast response
and, under appropriate circumstances, may evoke
slow conduction that can be a typical slow response, a
depressed fast response, or possibly a mixture of the
two (for review, see Cranefield'3). Such depressed His-
Purkinje conduction may respond more like the nor-
mal AV node and show large increments in conduc-
tion time before a blocked impulse.
Mechanisms of Block
Various mechanisms have been proposed to explain
the nature of type I block, including fatigue,2' ac-
cumulation of extracellular potassium ions22 and en-
croachment of succeeding impulses on incompletely
recovered tissue,23 24 possibly due to prolongation of
the absolute and relative refractory periods.25 Slow
conduction can result in lengthening of the action
potential duration and the refractory period,26 27
leading to a positive feedback interplay of RP and PR
intervals that progresses to the point of block.28 The
block then shortens the action potential duration and
refractoriness in fibers that were activated proximal to
the site of block, and the sequence restarts.
Decremental conduction, in which the properties of
the fiber change along its length so that the action
potential loses its efficacy as a stimulus for the unex-
Downloaded from http://ahajournals.org by on February 2, 2019
cited fiber ahead of it, may be responsible for type I
block.5' 29 Alternatively, electrotonus may play an im-
portant role.30 Decreased stimulating efficacy of a
transmitted electrotonic potential, rather than a
regenerative, propagating impulse, has been suggested
as the cause of Wenckebach periodicity.3'
Recently, it was demonstrated during 4:3 AV nodal
Wenckebach cycles in the dog, that the effective
refractory period after the fourth (blocked) beat was
shorter than after any other beat. The effective refrac-
tory period cumulatively and progressively increased
in succeeding cycles, so that the effective refractory
period of the third beat exceeded the duration of the
basic cycle length, and caused the fourth beat to
block.32 The functional refractory period, on the other
hand, decreased in succeeding Wenckebach cycles,
primarily because the control conduction time in-
creased in successive beats of the cycle.33
Other phenomena implicated in the genesis of block
include automaticity,34 3 geometric configuration of
the tissue,36 the role of intercellular connections,37 uni-
formity of the propagating wavefront,38 alterations in
excitability,39 and concealed re-entry.40 All of these
factors may be modulated in vivo by potential
hemodynamic alterations and the influence of the
autonomic nervous system.4"
Despite multiple mechanisms that may be responsi-
ble for causing type I AV block, relatively few
hypotheses have been advanced to explain the elec-
trophysiologic basis of type II AV block.42 Recently, it
VOL 60, No 3, SEPTEMBER 1979
has been suggested that the two types of block may be
different manifestations of the same electro-
physiologic mechanism.43-45
Evaluation of Electrophysiologic Evidence
for One Type of Second-degree AV Block
El-Sherif et al.43 showed that dogs subjected to liga-
tion of the anterior septal artery developed second-
degree AV block in the proximal His-Purkinje system.
After coronary artery occlusion, the block was ini-
tially preceded by no perceptible or only 1-2-msec in-
crements in conduction time. After 1-2 hours, the in-
crement in conduction time before the block increased
100-200 msec. Upon recovery of the excised tissue
during superfusion in vitro, the large increments that
occurred before the blocked impulse once again
decreased, but not consistently in each preparation.44
These observations were offered as support for the
concept that second-degree AV block encompassed a
spectrum that ranged from no perceptible or small in-
crements preceding the blocked impulse "at an early
stage of departure from normal" to increments of
several hundred milliseconds as the abnormality in-
creased. The authors suggested that type I and type II
AV block "represent various degrees of the same elec-
trophysiologic mechanism," differing only quan-
titatively, in the size of the increments.45
While these studies43"- demonstrated that ischemia
can alter conduction and block in the His-Purkinje
system, the data do not support the conclusion that the
mechanism giving rise to the block preceded by small
increments was the same as when the block was
preceded by large increments. In these studies, El-
Sherif and colleagues compared the response of cells
in the His-Purkinje system exposed to short periods of
ischemia with that of cells exposed to long periods of
ischemia. If these cells were electrophysiologically
different - and it is likely that they were after ex-
posure to different durations of ischemia - the cause
of the initial block may have differed from the
mechanism that caused the later block. Also, the site
of early and late block may have changed. These in-
vestigators observed that paroxysmal AV block (that
is, block of multiple, successive P waves) only oc-
curred early, when the increments were still small, and
could not be produced in their preparation when the
increments were large.45 This finding also supports the
concept that the two types of block are different.
From these43"- and other studies of block in the
His-Purkinje system, several facts emerge: I) Most,46
but possibly not all,42' 47 examples of apparent type II
AV block in the His-Purkinje system are preceded by
small increments in conduction time that can be found
if carefully searched for. 2) The His-Purkinje system,
both in animals and in patients who appear to have
typical type II AV block, can be perturbed by
ischemia48 or other factors (figs. 1 and 2) to show large
increments in conduction before the blocked impulse.
However, increments in conduction time before a
blocked impulse, whether large or small or present or
absent, are descriptive phenomena and cannot be
 SECOND-DEGREE AV BLOCK/Zipes 467

HH467-SV268212-5

FIGURE 1. Type II second-degree A V block in a patient with left-axis deviation and right bundle branch
block. During right atrial pacing at a constant cycle length (510 msec), P waves intermittently blocked in the
His-Purkinje system, distal to the His bundle recording site. No change occurred in the duration of the PR
interval (188 msec), AH interval (125 msec) or HV interval (42 msec) before or after the blocked P wave.
A = atrial deflection; H = His deflection; V = ventricular deflection; RA = right atrial electrogram;
S = stimulus. Leads I, II, III and V1 are scalar leads. The paper speed was 100 mm/sec; time lines = I
second.
equated with the electrophysiologic mechanisms that second-degree AV block may be too simplistic, as it is
give rise to the block. Block can result from complex based on a description of only input and output data:
interactions of multiple mechanisms.5' 21-42 A certain number of atrial impulses enter a "black
The present classification of only two types of box," i.e., the AV node and His-Purkinje system, and
Downloaded from http://ahajournals.org by on February 2, 2019

Vi

AH ~~ ~~
~~~~~~A
~h H
RA- UVH H4

s ~~~~~~~~~~~~~~~~~~~~~~~~~~~HH4
8212-5
V26 70-S

FIGURE 2. Increase in the HV interval before block in the same patient as in figure 1. Continuous record-
ing: The stimulus and part of the last paced atrial complex (unlabeled) in the top recording are repeated as
the first stimulus andfirst paced atrial complex in the bottom recording. Right atrial pacing at a shorter cy-
cle length (450 msec) than in figure 1 resulted in 3:2 conduction. The HV interval increased from 44 to 81
msec before the blocked P wave and shortened to 44 msec after the block. The PR interval only increased
from 197 to 226 msec before the block, because ofshortening of the AH intervalfrom 133 to 125 msec. Note
a slight change in the contour of the second QRS complex, when the HV interval prolonged. A = atrial
deflection; H = His deflection; V = ventricular deflection; RA = right atrial electrogram; S = stimulus.
Paper speed was 250 mm/sec.
 468 CIRCULATION
a certain number of His-Purkinje or ventricular im-
pulses exit in a certain pattern. From an analysis of
these patterns, one attempts to deduce the mech-
anisms that cause the block. Probably, different elec-
trophysiologic mechanisms within the "black box"
can cause similar patterns to emerge, and, conversely,
similar electrophysiologic mechanisms can produce
different emerging patterns. Even if the "black box" is
partially opened, and the cells are studied by the
microelectrode technique," depressed transmem-
brane potentials may appear remarkably similar,'3
but be ionically and therefore, "mechanistically"
distinct.
Differentiating Type I and Type II
Second-degree AV Block
Although the classification is descriptive, clinically
separating second-degree AV block into type I and
type II serves a useful function, and, in most instances,
the differentiation can be made easily and reliably
from the surface ECG.
Clinically, type II AV block often antedates the
development of Adam-Stokes syncope and complete
AV block, while type I AV block with a normal QRS
complex is generally more benign, and does not
progress to more advanced forms of AV conduction
disturbance.495' In the patient with an acute myocar-
dial infarction, type I AV block usually accompanies
an inferior myocardial infarction, is transient and does
not require temporary pacing, while type II AV block
results in the setting of an acute anterior myocardial
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infarction, may require temporary or permanent pac-
ing, and is associated with a high mortality.50 52
While type I conduction disturbance is ubiquitous
and may occur in any tissue in the in situ heart, as well
as in vitro, the site of block for the usual forms of
second-degree AV block can be judged with sufficient
reliability from the surface ECG to permit clinical
decisions without requiring invasive electrophysiologic
studies in most instances (table 1). Type I AV block
with a normal QRS complex almost always takes
place at the level of the AV node (proximal to the His
bundle).5 An exception is the uncommon patient with
TABLE 1. Site of Second-degree Atrioventricular Block
Type of block Normal QRS BBB
Type I AVN > > > > HPS AVN > HPS
Type II HPS>AVN HPS> > > >AVN
1:1-s2:1; fixed
2:1 or greater HPS = AVN HPS > > AVN
Except for the location of type I atrioventricular block with
a normal QRS and type II atrioventricular block with a
bundle branch block, quantitative data regarding the other
sites of block are not available and these statements must be
regarded as the author's impressions.
Abbreviations: AVN = atrioventricular node; HPS
His-Purkinje system; BBB = bundle branch block. Arrows
( >) indicate relative frequency of second-degree atrioven-
tricular block at different sites, with one arrow meaning
slightly more frequenit, anid four arrows meaning far more
frequent.
VOL 60, No 3, SEPTEMBER 1979
type I intrahisian block."4 Type II AV block, par-
ticularly when it occurs with a bundle branch block, is
localized in the His-Purkinje system."-"' Type I AV
block in a patient with a bundle branch block may
represent block in the AV node or in the His-Purkinje
system." Type II AV block in a patient with a normal
QRS complex may be due to intrahisian AV block,
but the block is likely to be type I AV nodal block,
which exhibits small increments in AV conduction
time."6
The above generalizations encompass the vast ma-
jority of patients who present with second-degree AV
block. However, certain caveats must be heeded to
avoid misdiagnosis because of subtle ECG changes or
exceptions:
1) Two:one AV block may be a form of type I or
type II AV block (fig. 3). If the QRS complex is nor-
mal, the block is more likely to be type I, located in
the AV node, and one should search for a transition of
the 2: 1 block to 3:2 block, during which the PR inter-
val lengthens in the second cardiac cycle. If a bundle
branch block is present, the block may be located
either in the AV node or in the His-Purkinje system.
2) AV block may occur simultaneously at two or
more levels, and render the distinction between type I
and type II difficult.
3) If the atrial rate varies, it may alter conduction
times and cause type I AV block to simulate type II or
change type II AV block into type I. For example, if
the shortest atrial cycle length that just achieved 1:1
AV nodal conduction at a constant PR interval is
decreased by as little as 10 or 20 msec, the P wave of
the shortened cycle may block at the level of the AV
node without an increase in the antecedent PR inter-
val.4' Apparent type II AV block in the His-Purkinje
system (fig. 1) may be converted to type I in the His-
Purkinje system (fig. 2) in some patients by increasing
the atrial rate.
4) Concealed premature His depolarizations may
create electrocardiographic patterns that simulate
type I or type II AV block (fig. 4).57, 58
5) Abrupt, transient alterations in autonomic tone
may cause sudden block of one or more P waves
without altering the PR interval of the conducted P
wave before or after the block.'9 Thus, apparent type
II AV block would be produced at the A-V node. In
the absence of atrial pacing, a burst of vagal tone
would probably lengthen the PP interval as well as
produce AV block.4'
6) The response of the AV block to autonomic
changes, either spontaneous or induced, to distinguish
type I from type II AV block, may be misleading.
Though it is considered that vagal stimulation
generally increases and atropine decreases the extent
of type I AV block,60 61 such conclusions are based on
the assumption that the intervention acts primarily on
AV conduction and fail to consider rate changes. For
example, an injection of atropine that minimally im-
proves conduction in the AV node, but markedly in-
creases the heart rate, can increase AV conduction
time and the degree of block as a result of the faster
atrial rate. Conversely, if an increase in vagal tone,
 SECOND-DEGREE AV BLOCK/Zipes 469

HH220
677006

A VI A

I II) N N % N

I 0~~~~~~~~~~~~~~~~~~~~~~~~~~~~I

II

W 8 \ l l ~~~~~~~~~~~~~~~~~~~~~~~205965
BAE__, - ¢ 1{* '

AHA A
H{i
BHrL,-- --- gA
AH75 ,
HV30
BEE -

FIGURE 3. Two: one second-degree A V block distal (top panel) and proximal (bottom panel) to the His
bundle recording site in two different patients. Conventions as in figure 1. BEE = bipolar esophageal re-
Downloaded from http://ahajournals.org by on February 2, 2019

cording; BAE = bipolar atrial electrogram; BHE = bipolar His electrogram. (Reproduced with permission
from Zipes DP, Watanabe A W, Besch HR: Clinical electrophysiology and electrocardiography, In The
Science and Practice of Clinical Medicine. Clinical Cardiology, edited by Wilkerson JT, Sanders CA. New
York, Grune and Stratton, 1977, pp 235-248.)

produced pharmacologically or by carotid sinus PR Shortening after the Blocked P Wave

massage, minimally prolongs AV conduction time,
but greatly slows the heart rate, the net effect on type I
AV block may be an improvement in conduction.
Analogous examples can be proposed for changes
effected by alterations in adrenergic tone due to infu-
sion of isoproterenol or after exercise.
7) During type I AV block with high ratios of con-
ducted beats, the increment in the PR interval may be
quite small and simulate type II AV block if only the
last few PR intervals before the blocked P wave are
measured. By comparing the PR interval of the first
beat in the long Wenckebach cycle with that of those
beats immediately preceding the blocked P wave, the
increment in AV conduction becomes readily ap-
parent.62
8) Finally, the classic AV Wenckebach structure
depends on a stable atrial rate and a maximum incre-
ment in AV conduction time for the second PR inter-
val of the Wenckebach cycle, with progressive
decrease in subsequent beats. Unstable or unusual
alterations in the increment or atrial rate, often seen
with long Wenckebach cycles, result in atypical forms
of type I AV block and are quite common.32 63
The duration of the PR interval of the first P wave
that conducts to the ventricle after AV block is a
source of disagreement. After discounting AV junc-
tional escape complexes that follow a nonconducted
sinus P wave at a short interval, the question is: In
type II AV block, can the PR interval after the
blocked P wave shorten and if so by how much? Does
"marked" shortening (i.e., >20 msec)64 eliminate the
possibility of type II AV block?
During type I or type II second-degree AV block,
the PR interval after the blocked P wave generally is
the shortest, because the pause after the blocked P
wave provides a period of recovery for conduction dis-
tal to the site of block. Increments in AV conduction
time that accrued during the sequence of conducted
beats before the block are lost in this recovery period,
and the PR interval usually shortens by an amount
equal to this increment.
During the usual type I AV nodal block, the in-
crements in AV conduction time are fairly large, and
the decrease in the PR interval after the blocked P
wave will be similarly large. During the usual type II
 470 CIRCULATION
H-HIM
,
I liI
OOOM%
I I iv
Downloaded from http://ahajournals.org by on February 2, 2019
AV block in the His-Purkinje system, the increments,
if any, in His-Purkinje conduction time are small or
nonmeasurable. In this instance, the PR interval after
the blocked P wave will shorten minimally or not at
all. However, if the increments in the His-Purkinje
conduction time are large (fig. 2), the reduction in the
PR interval will also be large, even exceeding 20 msec.
However, the argument is sophistic because, given the
latter situation, the block is called type I in the His-
Purkinje system, rather than type II, and large in-
crements, as well as marked PR shortening, are ex-
pected.
Finally, the PR interval in the scalar ECG is made
up of conduction through the atrium, the AV node and
the His-Purkinje system. An increment in HV conduc-
tion can be masked in the scalar ECG by a reduction
in the AH interval, and the resulting PR interval will
not reflect the entire increment in His-Purkinje con-
duction time (fig. 2). The AH interval can shorten due
to changes in autonomic tone, multiple AV nodal
pathways, concealed conduction or other reasons.
Also, a shorter AH interval must shorten the HH in-
terval of the preceding cycle, a change that can be con-
ducive to His-Purkinje conduction delay or block.
These potential variations in the duration of the PR
interval make difficult the accurate deduction of the
type of block based on a particular pattern of the
duration of the PR interval immediately before and
after the blocked P wave.45 Nevertheless, certain
generalizations about the PR interval can be made.
First, very long PR intervals (>200 msec) are more
VOL 60, No 3, SEPTEMBER 1979
FIGURE 4. Concealed discharge from the
bundle of His mimicking first-degree (top
panel), type I (middle panel) and type II
(bottom panel) second-degree A V block.
Numbers are in milliseconds. Time
lines- 1 second (magnification not the
same in all three panels). Conventions as in
figure 1. Numbers in the bipolar His elec-
trogram (BHE) indicate the A H interval;
the HV interval was constant. Numbers in
lead II indicate the PR interval. HH refers
to the interval between His responses in nor-
mally conducted cycles. HH' refers to the in-
terval between the last normal His discharge
and premature His discharge. H'-A refers to
the interval between the premature His
depolarization and the following normal
sinus-initiated atrial discharge. H' blocked
before reaching the atria retrogradely and
the ventricles antegradely. H' invaded the
A V node and resulted in lengthening of the
A H interval or, in A V nodal block, of the
following atrial depolarization. (Repro-
duced with permission from Bonner AJ,
Zipes DP: Lidocaine and His bundle extra-
svstoles. His bundle discharge conducted
normally, conducted with functional right or
left bundle branch block or blocked entirely
(concealed). Arch Intern Med 136: 700,
1976.)
likely to result from AV nodal conduction delay (and
block), with or without concomitant His-Purkinje
conduction delay. Second, when second-degree AV
block occurs during incomplete AV dissociation,
variations in the PR interval that reflect the usual in-
verse relationship between RP and PR intervals
generally are due to changes in AV nodal conduction
time and suggest that the block is type I; constant PR
intervals during ventricular captures are more consis-
tent with the presence of type II AV block.64 Finally,
although it is clear that large increments in the PR in-
terval before the blocked P wave and a large decre-
ment in the PR interval after the blocked P wave may
occur with His-Purkinje block, such PR changes
would be more consistent with, though not diagnostic
of, type I AV nodal block.
Some patients may require an electrophysiologic
(His bundle) study to determine with certainty the
nature and site of block. For example, patients with
type I AV block and a bundle branch block, those with
type II AV block and a normal QRS complex, those
with fixed 2: 1, or greater, degrees of block and those
with a type of block that does not appear to conform
to any of the patterns mentioned, may profit from
such a study.
Limitation of Measurements
Measurement errors may prevent small changes in
conduction time from being detected. At the standard
electrocardiographic paper speed of 25 mm/sec, a
 SECOND-DEGREE AV BLOCK/Zipes
finely drawn line or the tip of the commonly used
caliper has a width equal to approximately 5 msec; at
a paper speed of 100 mm/sec (the usual recording
speed for electrophysiologic studies in man) the line or
caliper tip has a width of 1 or 2 msec. Recording
speeds in the range of 250 mm/sec may be required to
detect 1- or 2-msec changes (fig. 2).
Summary
1) While it is possible only one type of second-
degree AV block exists electrophysiologically, the
available data do not justify such a conclusion and it
would seem more appropriate to remain a "splitter,"
and advocate separation and definition of multiple
mechanisms, than to be a "lumper," and embrace a
unitary concept.
2) The clinical classification of type I and type II
AV block, based on present scalar electrocar-
diographic criteria, for the most part accurately
differentiates clinically important categories of
patients. Such a classification is descriptive, but serves
a useful function and should be preserved, taking into
account the caveats mentioned above. The site of
block generally determines the clinical course for the
patient. For most examples of AV block, the type I
and type II classification in present use is based on the
site of block. Because block in the His-Purkinje
system is preceded by small or nonmeasurable in-
crements, it is called type II AV block; but the very
fact that it is preceded by small increments is because
it occurs in the His-Purkinje system. Similar logic can
Downloaded from http://ahajournals.org by on February 2, 2019
be applied to type I AV block in the AV node. Excep-
tions do occur. If the site of AV block cannot be dis-
tinguished with certainty from the scalar ECG, an
electrophysiologic study will generally reveal the
answer.
References
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2. Wenckebach KF: Beitrage zur Kenntnis der mensclichen Hertz-
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3. Hay J: Bradycardia and cardiac arrhythmia produced by
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4. Mobitz W: (Jber die unvollstandige Storung der
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