Brit. J. Anaesth. (1973), 45,1013
FACTORS INFLUENCING THE DEVELOPMENT OF EXPIRATORY
MUSCLE ACTIVITY DURING ANAESTHESIA
S. U. KAUL, J. R. HEATH AND J. F. NUNK
SUMMARY
Expiratory muscle activity has been studied in the external oblique muscle during
anaesthesia with spontaneous breathing in twenty-two patients. Expiratory muscle activity
was absent in all subjects before induction but developed within 29 minutes of induction
in twenty patients, remaining absent in the other two. Deepening the level of halothane
anaesthesia reduced, but in only one case abolished, expiratory muscle activity. Endotracheal intubation and passage of a pharyngeal airway had no effect other than initial
stimulation and relief of obstruction when present. Topical analgesia of larynx had no
effect. Surgical stimulation and respiratory obstruction both caused marked increase in
expiratory muscle activity.
It is now well established that there is no detectable
expiratory muscle activity (EMA) during quiet
breathing in the normal, conscious, supine man.
Freund, Roos and Dodd (1964), however, found that
expiratory muscle activity invariably appeared after
the induction of light anaesthesia, without use of
relaxants or endotracheal tubes, and was sustained
throughout the period of anaesthesia, terminating
only on recovery from anaesthesia. They demonstrated the sudden disappearance of this pattern of
breathing during transient recovery of consciousness
as, for example, on calling out the subject's name
or in response to other mild stimuli.
In the course of measurements of functional
residual capacity of the lungs in progress in our
laboratory (Hewlett et al., in preparation) it was
found that expiratory muscle activity did not invariably occur during anaesthesia. Details of their anaesthetic technique differed in several respects from the
study of Freund, Roos and Dodd and this study was
undertake to throw further light on the factors influencing expiratory muscle activity in anaesthetized
man.
METHODS
muscle giving the maximum contraction was located
with a Wakeling peripheral nerve stimulator while
the patient was conscious but after premedication
(table I). Electromyograms were obtained by silver
foil surface electrodes. Both the electromyogram
(e.m.g.) and its integral were recorded using the a.c.
high gain channel of a Devices M19 recorder. The
amplifier gain setting was varied for different patients
but full scale deflection was usually of the order
of 0.3 mV. The integrator had a decay time-constant
of approximately 0.5 sec.
Satisfactory recordings of e.m.g. and its integral
were obtained in all patients. Although phasic activity
of the expiratory muscles was absent during normal
breathing in all patients while conscious, there was
vigorous activity in response to phonation, coughing
and raising the head. A clear electrocardiogram was
obtained in all cases from the e.m.g. electrodes and in
most cases the integral of the cm.g. showed deflections in phase with the e.c.g., which were minimi?*^
but not abolished by minor changes in position of
the reference electrode. The e.c.g. artefact was, in
fact, a useful indication of consistent response of the
e.m.g.
As an indication of the phase of respiration, the
pressure waveform was recorded from the corrugated
tubing of the Magill system (Mapleson A) near the
expiratory valve (range 0-2 mm Hg).
After recording the expiratory muscle e.m.g. in
The study comprised 22 patients anaesthetized for
routine minor surgery. All were in excellent general
health; none was suffering from respiratory disease
and all were non-smokers. The ages ranged from
20 to 40 years and informed consent was obtained S. U. KAUL, B.SC, M.B., BS., F.F.A.RX.S.; J. R. HEATH,
in each case, in addition to general approval by the PH.D.; J. F. N U N N , MJD., PH.D., F.F.A.R.C.S.; Division of
Anaesthesia. Northwick Park Hospital and Clinical
Hospital Ethical Committee.
Research Centre, Watford Road, Harrow, Middlesex
The motor point of right or left external oblique HA1 3UJ.
BRITISH JOURNAL OF ANAESTHESIA
1014
TABLE I
Parian:
no. Age
1
2
21
27
Sex
M
M
3
50
M
4
33
M
5
50
M
6
7
27
29
F
M
8
28
F
9
10
22
33
M
F
11
26
F
12
29
F
13
14
33
26
M
F
15
18
F
16
31
F
17
18
21
40
M
M
19
29
F
20
22
F
21
20
F
22
23
F
Premedication
None
Morphine 10 mg,
atropine 0.6 mg
Papaveretum 15 mg,
hyoscine 0.3 mg
Morphine 10 mg,
atropine 0.6 mg
Morphine 10 mg,
atropine 0.6 mg
None
Papaveretum 15 mg,
hyoscine 0.3 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
None
Papaveretum 10 mg,
hyoscine 0.2 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
None
Papaveretum 20 mg,
hyoscine 0.4 mg
Morphine 5 mg,
atropine 0.6 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
None
Morphine 10 mg,
atropine 0.6 mg
Papaveretum 15 mg,
hyoscine 0.3 mg
Papaveretum 15 mg,
hyoscine 0.3 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
Papaveretum 10 mg,
hyoscine 0.2 mg
Thiopentone
(mg)
300
300
325
500
350
250
400
the conscious state, anaesthesia was induced with
thiopentone in the dosage shown in table I, and
maintained with inhalation of nitrous oxide/oxygen
mixtures. Circumstances were then varied to investigate the influence of a number of different factors
on expiratory muscle activity (table II). In addition,
transient respiratory obstruction occurred from time
to time and we were able to observe its effects on
expiratory muscle activity. In some cases recordings
were continued during surgery and any changes in
activity of the expiratory muscles occurring during
surgical stimulation were observed.
300
RESULTS
350
250
Appearance of expiratory muscle activity following
induction of anaesthesia.
There was no detectable phasic expiratory muscle
activity in any patient during the preinduction
period. In all patients except two, phasic activity
appeared after spontaneous respiration was re-established following injection of thiopentone (fig. 1). The
interval between the re-establishment of spontaneous
breathing and the appearance of expiratory muscle
activity was less than 5 tnin in 16 cases but between
5 and 29 min in 4 cases. Patients 13 and 18 showed
no trace of expiratory muscle activity except during
a bout of coughing. It continued for 5 min after
termination of the coughing but eventually subsided
completely. Both these patients were men: all female
patients developed expiratory muscle activity.
300
200
400
400
300
300
300
350
300
300
300
350
Insertion of oropharyngeal
airway.
In 8 patients (1, 2, 3, 4, 5, 12, 16, 17) insertion of
an
oropharyngeal airway produced no alteration in
TABLB II. Conditions investigated m relation to development
expiratory
muscle activity in the absence of airway
of expiratory muscle activity (EMA).
obstruction. In 1 patient (4) the airway was repeatNo. of
patients edly inserted and removed without any effect on the
expiratory muscle activity which was present. In 2
1 Insertion of an oropharyngeal airway after
patients with mild airway obstruction, insertion of
8
EMA developed
the airway reduced the activity but did not abolish it.
2 4% lignocaine spray to the laryngopharynx
4
after EMA developed
In 1 patient (9) transient but total airway obstruc3 Endotracheal intubation:
tion
inadvertently occurred and was accompanied
with
halothane
alone
after
EMA
(a)
by a gross rise in activity. Insertion of an airway
1
developed
(b) with lignocaine spray and halothane
relieved the obstruction and rapidly reduced the
after EMA developed
2
expiratory muscle activity (fig. 2).
(c) with suxamethonhim and halothane
after EMA developed
with suxamethonium, lignocaine spray
and halothane after EMA developed
(<0 with suxamethonium, lignocaine spray
and halothane before EMA developed
4 Suxamethonhim without intubation
5 Depth of anaesthesia
6 Painful stimuli
3
(d)
3
5
3
7
8
4% lignocaine spray to the laryngopharynx.
In 4 patients (6, 7, 8, 9) spraying was studied in
isolation from other factors, while the patient was
inhaling 0.5-1% halothane. In each case there was
an immediate increase in expiratory muscle activity,
presumably in response to the stimulation of laryn-
EXPIRATORY MUSCLE ACTIVITY DURING ANAESTHESIA
PHONATION
&IAUGH
IHIOPtNTONE350n)g
1015
MASK APPIIED
T l « MARKER
AIRWAY
PRESSURE
r*
L
INTEGRATED EMC
EMC WITH
ECG ARTEFACT
FIG. 1. Appearance of expiratory muscle activity immediately after induction of anaesthesia.
Respiratory phase is indicated by the airway pressure trace which commenced only when the
mask was applied. Downward deflection indicates inspiration. Note how phasic expiratory muscle
activity is much easier to recognize in the integrated trace. The e.c.g. artefact is of constant
amplitude throughout the trace. Time marker, 1-min intervals.
OBSTRUCTION
AIRWAY
FIG. 2. Powerful activity of the expiratory
muscles is present at the beginning of the
trace when the patient was obstructed
(integrated trace off scale). The obstruction
was relieved by passage of a pharyngeal airway after which the expiratory muscle activity
rapidly subsided.
1 minute
goscopy and spray, with a gradual return to preexisting levels: in 3 of the patients there was also
obvious clinical evidence of laryngeal irritation. In
no case did local anaesthesia abolish expiratory
muscle activity. Further studies were done in combination with the administration of suxamcthonium
and endotracheal intubation (see below).
Endotracheal intubation
Endotracheal intubation was carried out in five
different ways as is shown in table II.
In 1 patient (14) intubation was carried out under
deep halothane anaesthesia; there was no immediate
effect on expiratory muscle activity.
In 2 patients (7, 8), intubation was carried out
BRITISH JOURNAL OF ANAESTHESIA
1016
during light halothane anaesthesia with topical anaesthesia of the laryngopharynx but without the use of
muscle relaxants. This was accompanied by an immediate increase of activity, apparently in response
to the stimulation of the spray, which then gradually
subsided to pre-existing levels.
In 3 patients (2, 4, 5) induction was followed by
a period of spontaneous breathing during which
expiratory muscle activity was present. Intubation
was then carried out during muscle relaxation obtained with suxamethonium but without local analgesia. In each patient expiratory muscle activity
reappeared within 4 min of the return of spontaneous
respiration and gradually returned to the pre-existing
level.
In 3 patients (11, 15, 16) intubation was carried
out under the circumstances described in the preceding paragraph but with the addition of spraying
the laryngopharynx with 4% lignocaine. Expiratory
muscle activity returned to its previous level within
2 min in 2 patients, but in the third (11) it did not
return for 11 min from the re-establishment of
spontaneous respiration and then only following, and
apparently in response to, surgical stimulation.
In 5 patients (18, 19, 20, 21, 22) induction was
immediately followed by injection of suxamethonium and topical anaesthesia of the laryngopharynx
prior to intubation: apnoea caused by the suxamethonium was continuous with the apnoea caused by thiopentone. In 1 patient expiratory muscle activity did
not develop but did in the other 4, although in 1
case not until 29 min after return of spontaneous
respiration, and even then the activity was minimal
and only lasted for a period of 1 min.
HALOTHANE
Suxamethonium without intubation.
In 3 patients (9, 15, 16) suxamethonium was administered without intubation and in each case
expiratory muscle activity returned within 1 min of
the resumption of spontaneous breathing, with no
change in its intensity.
Effect of deepening of anaesthesia.
In 7 patients (6,7, 8,11, 14,17,19), the expiratory
muscle activity present while breathing 80% nitrous
oxide/20% oxygen was compared with that seen
during the inhalation of various concentrations of
halothane. Figure 3 shows expiratory muscle activity
arbitrarily measured as peak deflections of the integral of the electromyogram plotted against the concentration of halothane in the inspired gas mixture. A
a 5*
*
HALOTHANE
FIG. 3. Expiratory muscle activity plotted against inspired
concentration of halothane. The figures within the graph
indicate the number of minutes of inhalation of each
particular concentration.
4»
5*
AIRWAY
PRESSURE
INTEGRATED
E.M.G.
E.M.G.
TIME MARKERS
VVWWVVWV /WWVVVWW *vvw\.'./ww\/i/v> MVWVWW *
FIG. 4. Traces of expiratory muscle
activity at different inspired concentrations of halothane. The horizontal bars
indicate periods of 30 sec.
EXPIRATORY MUSCLE ACTIVITY DURING ANAESTHESIA
tendency for the activity of the expiratory muscles
to diminish with increasing concentrations of halothane is apparent. In only 1 patient (17) was it
possible to abolish the activity by deepening of
anaesthesia. Figure 4 shows actual records of 1
patient (14) with different concentrations of halothane.
Painful stimuli.
Relatively mild stimulation such as squeezing of
the ear lobe or application of a tetanic stream of
stimuli by the Wakeling peripheral nerve stimulator
produced no change in expiratory muscle activity.
Surgical stimulation, e.g. skin incision, stripping
periosteum (fig. 5), application of a tourniquet, etc.,
produced an increase in 7 of 8 patients studied, even
though iq some there was no discernible change in
either the rate or the depth of breathing.
SUHGICAL STIMULATION
t
+
AIRWAY PRESSURE
tmln)
INTEGRATED
E.M.G.
E.M.G.-
FIG. 5. Response of expiratory muscle activity to stripping
of periosteum. Note diat the respiratory trace (airway
pressure) is unaffected. Time marker, 1-min intervals.
DISCUSSION
In the upright position, the abdominal muscles are
concerned in the maintenance of posture and their
tone varies during the respiratory cycle. For a resting conscious subject in the supine position, however, there is no detectable expiratory muscle
activity at any phase of respiration (Floyd and Silver,
1950; Campbell, 1952). This is in contrast to the
long-standing observation of anaesthetists and
surgeons that expiratory muscle activity is usually
present in the lighdy anaesthetized patient and it is,
in fact, often relied upon as an indication of depth of
anaesthesia. Freund, Roos and Dodd (1964) have
confirmed the presence of expiratory muscle activity
in every one of a series of 24 male volunteers lightly
anaesthetized with thiopentone followed by nitrous
oxide or halothane.
In the present study, expiratory muscle activity
1017
developed during quiet breathing in 20 of 22 patients
but there was no apparent reason why it should have
been absent in the remaining 2 patients. Studies
within our department involving measurement of
functional residual capacity (Hewlett et al., in preparation) have also shown a number of patients who
do not develop expiratory muscle activity again without anything to indicate in which patients it will fail
to appear.
None of the circumstances which we have studied
appear to be important in determining whether
expiratory muscle activity will be present or absent.
It seems dear that deepening halothane anaesthesia
will diminish diis activity but it will not generally
abolish it altogether, except perhaps at unacceptably
deep levels. Topical anaesthesia of the larynx had
no effect other than a transient stimulation and it
appears that laryngeal afferents are not essential for
the development of expiratory muscle activity.
We were surprised to see the extent to which
respiratory obstruction augmented expiratory muscle
activity, and these observations contrast with the
inhibition of this activity in response to lung inflation observed by Freund, RQOS and Dedd (1964).
The only effects of passage of an endotracheal tube
or pharyngeal airway were transient stimulation in
some cases, and the relief of obstruction where it
was present.
The administration of suxamethonium, with or
without intubation, usually caused only transient
abolition of expiratory muscle activity which generally returned shortly after the resumption of spontaneous breathing. However, when intubation
followed the administration of suxamethonium given
directly after thiopentone and before the resumption
of spontaneous breathing (i.e. following the customary procedure for intubation), then in one case
expiratory muscle activity never developed and in
another only did so feebly after 29 min. Thus, once
it was established during anaesthesia, it was almost
impossible to abolish. However, the use of thiopentone/suxamethonium/intubation sequence in some
cases resulted in spontaneous respiration without
expiratory muscle activity. Hewlett and associates (in
preparation) in their studies of functional residual
capacity during anaesthesia have found that expiratory muscle activity frequendy failed to develop
under these circumstances.
Surgical stimuli consistendy increased the level
of expiratory muscle activity. This was present even
when the patient appeared to be in the stage of
"surgical anaesthesia" (e.g. inhaling 1% halothane
1018
in nitrous oxide/oxygen mixture for 13 min), and
did not display any obvious increase in respiratory
depth or frequency in response to the stimulation.
It is dear that minimal alveolar concentrations for
anaesthesia (MAC) may prevent gross movement in
response to incision of the skin but do not necessarily
prevent other responses to surgical stimulation.
Although this study confirms the frequent, if not
universal, development of expiratory muscle activity
during anaesthesia with spontaneous breathing, it
still does not answer the pulling question of why
anaesthesia should so consistently cause this change
in the pattern of breathing. Certain possibilities havebeen eliminated. Sensitization of laryngeal reflexes
does not seem to be a likely explanation and expiratory muscle activity dearly does not depend upon
the presence of foreign bodies such as pharyngeal
airways. Freund, Roos and Dodd (1964) considered
various possibilities, induding increase in airway
resistance which in our study, but not that of Freund
and associates, caused a marked increase in activity.
Our observations would thus tend to support an
increase in airway resistance as one possible cause of
the devdopment of expiratory musde activity during
anaesthesia. Widely differing values for airway resistance have been reported during anaesthesia, but it is
dear from the study of Gold and Helrich (1965)
that substantial increases in upper airway resistance
may occur in patients without pharyngeal airways or
endotracheal tubes.
There is now widespread agreement that reduction of functional residual capadty occurs during
anaesthesia (Laws, 1968; Don et al., 1970). Observations in our own department accord with the
Canadian studies (Hewlett et al., in preparation). In
BRITISH JOURNAL OF ANAESTHESIA
the supine position, reduction of functional residual
capadty of the magnitude which has been observed
may be expected to have a number of effects on lung
function. There will inevitably be some increase in
airway resistance, and increased airway dosure may
be expected in older patients. Gas trapping may also
occur. It is not possible at present to say whether
expiratory musde activity occurs during anaesthesia
in response to peripheral changes in the lungs or is
due to an alteration in the pattern of discharge of the
respiratory neurones in the medulla. It would be
valuable to know whether expiratory musde activity
can be abolished during anaesthesia by vagal
blockade.
ACKNOWLEDGEMENTS
We are indebted to Mr A. Cox, Mr A. E. Fisher, Mr E.
Lance, Mr I. F. McFadyen and Mr B. B. Porter, for
agreement to study patients admitted under their care.
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Don, H. F., Wahba, M., Cuadrado, L., and Kelkar, K.
(1970). The effects of anesthesia and 100 per cent
oxygen on the functional residual capacity of the lungs.
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Floyd, W. F., and Silver, P. H. S. (1950). Electromyographic study of patterns of activity of the anterior
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Freund, F., Roos, A., and Dodd, R. B. (1964). Expiratory
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anesthesia. J. appl. Physiol., 19, 693.
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adequacy. Anesthesiology, 16, 751.
Laws, A. K. (1968). Effects of induction of anaesthesia
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