Anaesthesia.

1982, Volume 37, pages 1190-1 194

CASE REPORT

Anaesthesia in first degree

atrioventricular block

R. H A Y W A R D . N . DOMANIC, G. E. H . ENDERBY AND L. M c D O N A L D

Summary
.4 parient with un intrucurdia(.conduction defect charucterised by,first degree atrioventricular block due
to slowed rransmission through the utrioventriculur node with increased refractoriness of the node, is
described. Asyniptomutic first degree block, rarelv progressing to transienl Wenckebach (type I second
degree) block had been present for a period of 32 ?’ears until generul unaesthesia wus required, when
profound bradycardia uttributable to complete atrioventricular block developed ubruptly. Subsequent
investigations located delajwd intracardiac conduction through the atrioventricular node, und indicated
e.xcess vugal activity rather than structural disease as the cause.
The significance if’ first degree heurt block i s discussed in relation to other .forms of atrioventriculur
conduction drfect und he current recommenda[ion.sfi,r temporary pucingfor elective general anuesthesiu.

Key words
Anursthelic trchniques.
Heart; atrioventricular node, conduction block.

A previously healthy SO-year-old woman with
long-standing first degree atrioventricular (A-V)
block on electrocardiogram (ECC) abruptly de-
veloped episodes of profound bradycardia as-
sociated with hypotension while under general
anaesthesia for cosmetic facial surgery (blepharo-
plasty and rhytidectomy). It was necessary to
discontinue the operation prematurely. Subse-
quently there was no evidence of peri-operative
cardiac ischaemia or infarction, and sinus rhythm
with first degree A-V block was again present.
In this patient first degree A-V block (P-R
interval greater than 0.2 seconds) had been
documented over thc preccding 32 years (Fig.
I), having first been observed during rheumatic
fever at age 18. The duration of the P-R interval
varied spontaneously over the years. between
0.24 and 0.32 seconds. though never falling within
the normal range. Cardiovascular symptoms
were entirely absent. Arterial blood pressure was
1 10/70 mmHg, physical signs, chest radiograph
and standard laboratory investigations were
consistently normal. She was preniedicated with
pethidine 100 mg, hyoscine 0.4 nig and anaes-
thesia induced with thiopentone 375 mg with
decamethonium S mg and suxamethoniurn 10 mg

Roger Hayward,* MB, MRCP, Registrar in Cardiology, Nergiz Domanic, MD, Research Fellow in Cardiology,
Lawson McDonald, MD, FRCP, Consultant Cardiologist, National Hcart Hospital and Cardiothoracic Institute,
Westmoreland Street, London W I G.E.H. Enderby, MA. FFARCS, Hon. Consultant Anaesthetist, Queen Victoria
~

Hospital, East Grinstead, West Sussex.

*Present address and address for correspondence: Cardiac Department, Middlesex Hospital, London WI .

0003-2409:82/121190 + 05 $03.00/0 0 1982 The Association of Anaesthctists of Gt Britain and Ireland 1190

I II
aVR aV L
Fig. 1. Electrocardiogram showing first degree A-V block (P-R interval = 0.26
seconds).
for intubation. Anaesthesia was maintained with
nitrous oxide and oxygen (1 : 1) and halothane
(0.5-1.5x) using a circle absorber system with a
fresh gas flow of 4 litres/minute. Pentolinium 7
mg i.v. allowed controlled hypotension to 6&70
mmHg (at heart level) using a foot down tilt and
manual ventilation with deliberate positive ex-
piratory pressure. Arterial pressure was moni-
tored continuously by an oscillometer, though
continuous ECG monitoring was not performed.
After 20 minutes, profound bradycardia (20/
minute) developed suddenly during eyelid reduc-
tion with an ,issociated severe fall in arterial
pressure noted as ‘almost an arrest’. The rate
was however unaltered until the episode ter-
minated after 1-3 minutes during which time
blood pressure was restored by a reduction of
the tilt and relief of the positive expiratory
pressure. It u a s not necessary to administer
positive chronotropic agents such as isoprenaline
or atropine.
Two further such episodes occurred, one when
arterial systolic: pressure was at 70 mmHg, and
one when it had been restored to 100 mmHg.
The operation was terminated prematurely, and
no further attack was noted during recovery
which was uneventful. A year later the aban-
doned rhytidectomy was accomplished satisfac-
torily without tlysrhythmia, under local analgesia
supplemented by oral and intravenous diazepam.
In view of these experiences and of this
woman’s past history, it was considered probable
that paroxysms of high grade A-V block had
First degree atrioventricular block 1191
Ill
aV F
occurred under anaesthesia. To clarify possible
mechanisms involved, a standard intracardiac
electrophysiological investigation was subse-
quently undertaken. Under lignocaine local anal-
gesia ( 5 ml273, three bipolar recording electrodes
were introduced percutaneously via the right
femoral vein and located in the right side of
the heart. One was used for pacing, while intra-
cardiac signals were recorded using the other
two, from a position adjacent to the bundle of
His and from the right atrial wall, together with
four surface ECG leads. First degree block was
confirmed, and was shown to be due to slowed
conduction entirely at A-V node level (Table l),
reflected in a long A-H time. Transatrial conduc-
tion (P-A time) and His bundle-Purkinje system
conduction (H-V time) were normal. A-V nodal
refractoriness was increased in parallel with
slowed conduction. Wenckebach A-V block was
easily provoked by overdrive right atrial pacing
at 90/minute (cycle length 650 mseconds), pro-
ducing extreme prolongation of A-V transmis-
sion time (A-H time) without delay elsewhere
(Fig. 2). Atropine 0.6 mg i.v. had little effect
on the slow A-V conduction, but normal conduc-
tion was achieved when a total of 1.8 mg had
been given (Table 1).
Discussion
The underlying abnormality here consists of a
defect of intracardiac conduction localised at,
and confined to, the A-V node level. The result
 Fig. 2. Results of intracardiac electrophysiological investigation. (a) Simultaneous record during normal sinus
rhythm of (from above downwards): 1 second time marker signal; surface ECG leads I. 11, 111 and V; His
bundle electrogram (HBE) and high right atrial electrogram (RAE) in which depolarlsdtion of atrium, His bundle
and ventricles are denoted by A, H and V. respectively: and diagrammatic representation to illustrate course
ofconduction through right atrium (A), A-V nodc (AVN) and ventricles (V). Note long A-H time (175 rnscconds)
indicating first degree block at A-V node level. (b) Recordings in identical format in sinus rhythm after atropine
1.8 mg i.v. Heart rate has increased. and A-H time has decreased to 120 maeconds. (c) Wenckebach A-V
nodc block initiated by right atrial pacing at 90/minute. cycle length 650 mseconds. before atropine. Pacing
$titnull WI-clabcllcd S . Dotted line in thc diagram beneath indicates thc longest A-H time preceding the dropped
atrial heat.

of high dose atropine administration under lab- vagal influence upon the A-V node. either due
oratory conditions w8as to achieve normal A-V to high vagal tone. or alternatively abnormal
conduction. The mechanism involved may there- sensitivity to vagal discharge, rather than to any
fore be considered to be long-standing excessive structural conducting system defect. Spnntane-

Table 1. lntracardiac conduction times and A-V nodal refractory periods
Pre-atropine
Sinus rate 62/min
Sinus CL 970 ms
Conduction times
P-A time 25 ms
A-H time 175 ms
H-V time 30 ms
P-R interval 230 ms
Refractory periods
A-V nodal ERP 535 ms
A-V nodal FRJ? 730 ms
A-V nodal RRP 760 ms
CL = cycle length; ERP = effective refractory period; FRP = functional
refractory period; RRP = relative refractory period. (See text for explanation
of conduction times.)
ous variation over the preceding years in the
degree of A-V block may be explained on the
basis of changes in the level of vagal stimulation,
which may summate with extrinsic factors cap-
able of suppressing A-V conduction.
This case contrasts with a previously reported
example of chronic first degree A-V block,z
coincidentally also documented over a period of
three decades, in which the defect was of struc-
tural rather than functional type, probably repre-
senting increased anatomical length of the A-V
node. Here conduction was slow but refractori-
ness was normal, characteristics which effectively
exclude significant involvement of the vagus.
Predictably on these grounds. general anaesthesia
for abdominal surgery was tolerated without
difficulty.
The usually benign nature of conduction im-
pairment at 4 - V node level has been d e ~ c r i b e d , ~
though prekalence and relative importance of
functional v(:rsus structural block have not been
detailed. Isdated first degree block is not an
indication for temporary pacing, and has been
described as of no great significance as regards
anaesthesia;'' indeed a P-R interval greater than
normal ( m o x than 2 standard deviations from
the mean) may be expected in 2.5% of the popula-
tion. Co-existent episodes of Wenckebach phen-
omenon pu1.s the subject into a smaller sub-
category, although a relatively high incidence of
this combination has been recorded in healthy
subjects such as highly trained athletes.5
The significance is different if first degree block
is accompanied by bundle branch block. Conduc-
First degree utrioventricular block 1193
After After
atropine atropine Normal
0.6 mg i.v. 1.8 mg i.v. values
86/min 109/rnin
700 ms 550 ms
25 ms 25 ms 25-45 ms
165 rns 120 ms 50-120 ms
35 ms 30 rns 3 5 4 5 ms
225 ms 175 ms 120-200 rns
490 rns 375 mb 265425 ms
630 ms 485 ms 330-520 ms
640 ms 415 ms ~
tion disturbancc is then usually more extensive,
sited in the His bundle branch system in vagally
insensitive territory." Temporary pacing during
anaesthesia and surgery is recommended,' but
is considered to be unnecessary for bundle branch
block with a normal P-R interval.8 Marked varia-
tion in the severity of A-V block with a changing
P-R interval and periods of Wenckebach phen-
omenon suggests lability of vagal effect. Chron-
icity of conduction impairment and the absence
of related symptoms offers no guarantee that
the block will not increase under provocation.
This calls for a more cautious approach, which
should include accurate pre-operative siting of
the block, assessment of the effectiveness o f vagal
blockade in improving conduction, and measure-
ment of its response to atropine. This is best
achieved by an intracardiac study as described
here. A possible alternative course of action
would involve taking three precautionary steps.
Firstly prernedication in such cases should be
with atropine, avoiding the greater negative
chronotropic activity of hyoscine which could
possibly further depress intracardiac conduction.
Pethidine is indicated for sedation in viefir of
its mild but significant atropine-like activity
which would be expected slighly to favour con-
duction through the A-V node. Secondly, con-
tinuous ECG monitoring should be available,
ideally with a paper print-out facility to aid pre-
cise diagnosis and recording. We now consider
this step advisable with any incomplete atrio-
ventricular conduction defect. Thirdly, there
should be a preparedness to use relatively high
1194 R . H u p v a r d er al.
doses of intravenous atropine (up t o 1.8 mg or
more) t o deal with any tendency towards higher
grades of A-V block that might develop during
induction of anaesthesia. Such a n occurrence
would present either as dropped beats indicating
second degree A-V block, or as profound slowing
consistent with onset of third degree (complete)
block. Temporary cardiac pacing to cover anaes-
thesia in this rare subgroup of patients appears
necessary, firstly where atropine responsiveness
has been shown t o be inadequate or attenuated,
high doses being needed for restoration of normal
A-V conduction and refractoriness, as in this
example. and secondly when d o u b t s a b o u t the
relative contributions o f functional versus struc-
tural factors in partial A-V block cannot be
resolved, for example when the simple intra-
cardiac investigative techniques discussed above
a r e not accessible.
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HL,
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