FUNCTIONAL RESIDUAL CAPACITY DURING ANAESTHESIA II: SPONTANEOUS RESPIRATION

FUNCTIONAL RESIDUAL CAPACITY DURING ANAESTHESIA II: SPONTANEOUS RESPIRATION

Br. J. Anaesth. (1974), 46, 486 FUNCTIONAL RESIDUAL CAPACITY DURING ANAESTHESIA E : SPONTANEOUS RESPIRATION A. M. HEWLETT, G. H. HULANDS, J. F. NUNN ...

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Br. J. Anaesth. (1974), 46, 486

FUNCTIONAL RESIDUAL CAPACITY DURING ANAESTHESIA E : SPONTANEOUS RESPIRATION A. M. HEWLETT, G. H. HULANDS, J. F. NUNN AKD J. R. HEATH SUMMARY

A number of studies have shown that the functional residual capacity (FRC) is reduced during anaesthesia with spontaneous respiration. Those studies in which supine patients have been used as their own controls before the induction of anaesthesia are listed in table I. More recently it has been demonstrated that the reduction in FRC is related to the well-known increase in alveolar-arterial Po, difference during anaesthesia. Hickey et aL (1973) have shown a significant correlation between reduction in FRC and increase in alveolar-arterial Po, difference, while Alexander et al. (1973) have shown a similar relationship during the postoperative period. The reduction in FRC which accompanies the induction of anaesthesia remains unexplained and the present studies were designed to explore further the influence on change in FRC of age, weight/ TABLE I. Studies of change in FRC during anaesthesia with spontaneous respiration in the supine position. Mean % reduction of FRC compared with No. of Date Authors pre-induction patients 1963 27.0 5 1968 Colgan and Whang 3.1% increase 8 1970 Don et al. 31.4 11 1972 Don, Wahba and Craig 19.0 17 233 1973 Westbrook et al. 5 1973 Hickey et aL 12.6 16 26 Present study 16.1 This table does not include studies without controls obtained before anaesthesia.

height ratio, expiratory reserve volume, duration of anaesthesia and inspired oxygen concentration. In addition we have obtained new data on the influence of expiratory muscle activity on FRC during anaesthesia. METHODS

The patients taking part in this study, which had been approved by the Hospital Ethical Committee, were 26 males (table II) undergoing routine minor surgery, all of whom had previously given informed consent to the procedures used in measurement of the FRC and recording of the electromyogram (ejn.g.). No patient had a history or clinical evidence of significant cardiopulmonary disease. The day before the operation, each patient visited the laboratory for familiarization with the equipment, involving practice measurements of FRC in the supine position, and for location, by a nerve stimulator, of the motor point of an external oblique muscle. The following day, after premedication, the e.m.g. electrodes were attached in the anaesthetic room, and satisfactory signals obtained. While the patient was awake the FRC was then measured, in duplicate unless precluded by pressure of time. In the A. M. HEWLETT,* M J . , CH.B., FJ.A.R.C»S.; G. H. HULANDS, M.B., CHJL, F.FJLR.CS.; T. F. NONN, PHJJ., MJ>,

F.F.A.R-CS.; J. R. HEATH, PH.D.; Division of Anaesthesia,

Clinical Research Centre, Watford Road, Harrow, Middlesex HA1 3UJ. • Dr Hewlett is supported by a Wellcome Research Fellowship.

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Functional residual capacity has been measured by helium dilution in 26 spontaneously breathing patients before and immediately after anaesthesia, which was induced with thiopentone and maintained with halothane. The mean reduction was 390 ml (16.1% of pre-induction value) and the change was highly significant (P<0.001). The decrease in FRC correlated with age (r=0.41; P<0.005) and less satisfactorily with the weight/height ratio (r=0.30; P<0.05) which itself correlated with age. Inspired oxygen concentration, expiratory reserve volume and the presence of phasic expiratory muscle activity bore no significant relationship to the decrease in F R C There was no evidence of any progressive change in FRC between 6 and 20 min after the induction of anaesthesia.

Height Patient (years) (cm) Aae

1 2 3 4

5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22

23 24 25 26

39 47 42 54 44 34 26 27 37 25 24

58 31 36 31 45 43 43 34 32 24 37

68 38 40 19

171

168 174 165 179 190 173 170 167 176 194 154 177 181 170 171 172 179 171 175 182 175 174 176 179 169

Weight (kg) 66.5 64.2 79.0 71.5 68.5 80.0 74.5 66.6 56.0 92.0 85.0 64.0 85.0 74.0 61.0 69.8 90.0 53.0 76.7 75.0 73.5 80.0 68.2 75.0 93.0 56.5

10 10 10 10 10 10 10 10 15 nil 10 10 20 20 20 20 20 20 20 10 15

15 20 nil

0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6 0.6

During anaesthesia

FRC

FRC

(mcflD

(mean of 2)

Floj

of 2)

0.21 0.21 0.21 0.21 0.21 0.21 0.21 0.21 035 0.35 0.35 0.35 0.35 035 035 0.35 0.35 0.35 0.35 0.35 0.35 0.35 0.35 035 0.35 0.35 Mean SD

2.184 2.733 1.846 1.755 2.606* 1.551 1.934* 2.647 1.347 2.188 3.096 1.808* 1.443* 2.571 1.571* 2.251 2.093 4.771 2.206 2.527 1.732 2.553* 2.651* 3.625 1.061 2.611 2.283 0.771

ERV 1.17 0.71 0.58 0.36 0.75 0.53 0.47 0.94 0.57 0.45

no, 1.0 1.0 1.0 1.0 1.0 1.0 1.0 1.0 035

0.35 0.35 0.35 0.35 035

0.596 0.83 0.54 0.536 0.73

1.26 0.45 0.983

0.35 0.35 0.35 0.35 0.35 035

0.35 035 0.35 035 0.35 0.35 Mean SD

1.934 2.300 1.535 1.535* 1.960* 1.611 1.772* 2.640* 1.118* 1.872 2.830* 1.519 1.381 1.527* 1.123* 1.886 1.435* 3.290* 1.251 2.931 1.656 2.271 2.245* 2.473 0.822* 2.301 1.893 0.610

Changes following induction 0/ /o

cm.g.

reduction in FRC conscious anaesth. 11.45 +H +++ 15.84 0 0 16.85 -)_ +^ 0 12.54 0 0 24.79 0 0 -3.87 0 838 0 0 0.26 17.00 14.44 8.59 15.98 430 e.m.g..recordings 40.61 not available 28.52 16.22 31.44 31.04 0 0 43.29 0 0 -15.99 X %*%A *A%? ^ 4 \J LA

439

11.05 15.31 31.78 22.53 11.87

*Single measurement only. M=morphine; P^papaveretum; A=atropine. All volumes are expressed in litres (BTPS).

0 0 0

+0+

0

-f 0

a

VIS

Prc-induction Premcuiuuii drugs (ma) P M A

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TABLE II. Data of individual patients.

*•

i

9 o

c

S M

9 z

488

FRC measurement. Measurements of FRC were made using a Jaeger Spirotest Mk II and a katharometer. To assess the magnitude of error in the system taken as a whole, and including non-linearity of the katharometer, repeated measurements of the space between a bottle and a contained self-inflating bag of fixed volume, were made. TheTe was no significant systematic error but the coefficient of variation of the random error was 1.3% (SD 59 ml). Further details of the technique are described in a previous paper which considers methodology of the helium dilution technique as applied to anaesthesia (Hewlett et al., 1974). For measurements using 35% oxygen, the spirometer was filled to a standard position with air and then the correct volume of oxygen, originally determined by trial and error, was introduced to bring the concentration to 35%. This was then checked with a paramagnetic analyser (Servomex OA 150), and a concentration of 35 % ± 1 was accepted. The halothane concentration in the circuit at the end of FRC measurement was determined using an ultra-violet absorption meter (Hook & Tucker Ltd). 0.1% halothane was found to decrease the katharometer reading by 0.46% of full scale deflection and the appropriate corrections were made to the final helium reading.

Electromyography. During the measurement of FRC, the e.m.g. activity was recorded from the motor point of an external oblique muscle, using a pair of silver surface electrodes (arranged so as to minimize, but not obliterate, the e.c.g. artefact). Signals were amplified and the activity recorded on a Devices multi-channel recorder. This activity was also displayed as an integral on a separate channel, with time constant 0.5 sec. Evidence of continuing function of the e.m.g. was shown by constant amplitude of the e.c.g. (as recorded on the e.m.g.) and by the very marked activity during fasciculation following the injection of suxamethonium. In most cases this produced a mavimai response on the channel recording the integrated e.m.g. After attachment of the electrodes, patients were asked to count aloud or cough so that die gain on the e.m.g. recording and the resulting integral could be adjusted to a reasonable range. Further details of the technique are given by Kaul, Heath and Nunn (1973). RESULTS

Induction of anaesthesia resulted in a reduction of FRC in 24 out of the 26 patients. The mean change for all patients was a reduction of 0.390 1. (BTPS) (SD 0.403). As a percentage of the pre-induction value, the mean reduction was 16.1% (SD 13.4%). The change was highly significant (P<0.001). Individual changes are listed in table H. Inspired oxygen concentration. Patients breathing the higher concentration of oxygen showed the smaller mean fall of FRC (10.8%) compared with 18.5% for the group breathing 35% oxygen. The two means are not significantly different from one another at the 95% level of confidence. Other relevant data are listed in table i n . Electromyography. Lack of an absolute standard made it impossible to compare the level of e.m.g. activity between different patients. However, by comparison with the e.c.g. artefact, it was possible to detect changes in the level of e.m.g. activity in any one patient. Satisfactory e.m.g. recordings were made in 15 patients, and these results were grouped into three categories (table IV): (1) Three patients in whom the e.m.g. activity was absent before anaesthesia, but was present during measurement of FRC after induction. These patients showed a mean decrease in FRC of 11.5% (SD 0.4%).

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first 8 patients, the inspired oxygen concentration was 2 1 % while awake and 100% during anaesthesia. Because of the possibility that the high oxygen concentration might result in absorption collapse, the routine was changed for observations on the last 18 patients who breathed 35% oxygen in nitrogen throughout. Patients were anaesthetized with thiopentone and, after relaxation with suxamethonium, and spraying of the larynx with 2 ml of lignocaine 4%, were intubated with a cuffed endotracheal tube. Spontaneous respiration was re-established with inspired halothane concentrations ranging from 1 to 2.5 %. FRC was measured again, where possible in duplicate (time between the two measurements being 10-20 min), with the inspired oxygen concentration held constant for the group breathing 35% oxygen (i.e. helium partially replacing nitrogen in the spirometer circuit). For patients breathing 100% oxygen, the inspired oxygen concentration was reduced by 5-10% when helium was added to the spirometer for FRC determinations. All measurements were completed before surgery began, and anaesthesia in all cases was uneventful.

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FRC DURING ANAESTHESIA: SPONTANEOUS RESPIRATION TABLE III. Patients grouped according to inspired oxygen concentration* Halothane Halothane vaporized in vaporized in 100% oxygen 30-35% oxygen

DISCUSSION

We have demonstrated a mean reduction in FRC of 16.1% between the pre-induction period and the first half-hour of anaesthesia with spontaneous respiration. This change is highly significant (P<0.001) and accords with other studies reported previously (table I). At least six factors have been considered at some time or other to be related to the reduction in FRC and these are considered below. Where possible we have also pooled our data with those of Don et al. (1970) and Don, Wahba and Craig (1972). Other studies in table I have not included sufficient details of individual patients. Age. Figure 1 shows our data and those of Don et aL (1970) and Don, Wahba and Craig (1972) with percentage reduction in FRC related to age.

TABLE IV. Patients grouped according to expiratory muscle activity {EMA).

Mean percentage reduction in FRC Number of patients Mean age Mean wt/ht ratio Number breathing halothane in 100% oxygen

EMA increased during anaesthesia 11.5 •3 31.7 039

EMA absent or unchanged before and during anaesthesia 13.6 10 40.1 0.43

EMA present before operation but decreased during anaesthesia 19.7 2 41.0 0.49

1:3

5:10

1:2

(2) Ten patients showing either no activity or the same degree of activity before and during anaesthesia. In this group the mean decrease in FRC was 13.6% (SD 17.1%) after the induction of anaesthesia. (3) In 2 patients e.m.g. activity was present before induction and decreased during anaesthesia. Mean FRC was reduced by 19.7% (SD 4.0%) during anaesthesia. Serial changes of FRC during anaesthesia. Pairs of determinations of FRC were obtained during anaesthesia in 14 patients, the first measurement being at a mean time of 6 min after induction and the second at a mean time of 20 min. The mean reduction was 3.2%, which was not significant. Four of these patients were breathing halothane vaporized

Although there is much scatter, the correlation coefficient is 0.41 :P for this number of patients is less than 0.005 and the correlation is thus significant at an acceptable level of confidence. Nevertheless, the scatter of points is such that age is of little value for predicting the decrease in FRC of individual patients. Pulmonary venous admixture, derived from alveolar-arterial Po, difference, during anaesthesia shows a similar correlation with age (r=0.36) (Nunn, Bergman and Coleman, 1965). Weight/height ratio. Don et al. (1970) demonstrated a strong correlation (r=0.9) between weight/height ratio and reduction in FRC after induction of anaesthesia (fig. 2). This was for 11 patients; but in a subsequent paper (Don, Wahba and Craig, 1972) report-

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This study Mean percentage 18.5 10.8 reduction in FRC 18 8 Number of patients 36.9 39.1 Mean age 0.42 0.42 Mean wt/ht ratio Number showing increased 1 1 expiratory muscle activity Pooled data Don et al. (1970) and Don, Wahba and Craig (1972) and this study Percentage reduction 19.6 in FRC mean 20.8 13.7 SD 14.3 30 24 Number of patients 37.0 38.0 Mean age 0.41 0.40 Mean wt/ht ratio 30% oxygen was used in the studies of Don et al. (1970) and Don, Wahba and Craig (1972) and 35% in the present studies.

in 100% oxygen and their mean reduction was only 2.2%, which was also not significant.

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10

10

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.

&-20

-20

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-30

8 -40

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-50

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-60

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2O

3O

4O

SO

60

70

AGE

FIG. 1. Percentage reduction in FRC following induction of anaesthesia in relation to the age of the patients. O=present study; A=Don et al (1970); • = D o n , Wahba and Craig (1972). Regression equation of pooled data: % reduction in FRC=4.0+0.43Xage (r=0.41; P<0.005).

ing 17 patients, the relationship was only poorly described by the regression linp derived from the previous study. We have pooled all of Don's data together with our own and the combined results indicate a correlation (r=0.30) which for 54 patients is just significant at the 95% confidence limit. There is, furthermore, a significant correlation between age and weight/height ratio of the pooled data (r=0.35), suggesting that the relationship shown in figure 2 is secondary to the relationship between weight/height ratio and age and that the strongest correlation of the pooled data is with age. Expiratory reserve volume (ERV). It appeared a reasonable hypothesis that any reduction in FRC might be related to the ERV which is known to be very variable in the supine position (Caltagirone, Mistretta and Vagliasindi, 1969). However, our data from 18 patients show no significant correlation between change in FRC and ERV ( r = 0.31). Furthermore, change in FRC expressed as a

•3

-4 , weight Kg) neight(cm)

-5

-6

FIG. 2. Percentage reduction in FRC following induction of anaesthesia in relation to the weight/height ratio of the patients. #=present study; A =Don et aL (1970); • = D o n , Wahba and Craig (1972). The lower line is the regression line for the data of Don et al. (1970) while the upper line is the regression line for the pooled data: % reduction in FRC=—6.7+ 65.2X

height

(r=0.30; P<0.05) percentage of ERV has no significant correlation with age (r=0.16). Duration of anaesthesia. D&y et al. (1965) reported a progressive fall in FRC during anaesthesia for patients breathing 100% oxygen but not for those breathing 50% oxygen. Hickey et aL (1973) reported a significant mean decrease of 8% in FRC measured 50-70 min after induction compared with measurements made 20-40 min after induction. Our data show a mean decrease of 3.2% in all patients on whom duplicate measurements were made and a mean reduction of 2.4% in the 4 patients who were breathing high oxygen concentrations. Neither of these changes is significant, and there is agreement with Don et al. (1970) who found no significant progressive changes with

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^ -30

FRC DURING ANAESTHESIA: SPONTANEOUS RESPIRATION

Inspired oxygen concentration. D£ry et aL (1965) reported that the FRC was reduced during anaesthesia only when the patients breathed high concentrations of oxygen. This observation strongly suggested that the decrease in FRC was the result of absorption collapse. However, this finding has not been confirmed. Hickey et al. (1973) studied patients breathing high oxygen concentrations but found decreases in FRC which were rather less than other studies with lower concentrations of oxygen (table I). Don et al. (1970) reported a mean reduction of 34.8% in FRC in a group of 6 patients (mean age 45) breathing halothane in 100% oxygen. In a comparable group breathing halothane in 30% oxygen in nitrogen, 5 patients (mean age 39) showed a mean reduction of 27.2%. He later reported mean decreases of 20.3% in 10 patients of mean age 33 breathing halothane in 100% oxygen, and 17% in 7 patients of mean age 36 breathing halothane in 30% oxygen (1972). In neither study does the difference approach the level of significance. If Don's results are pooled with those of the present study, the 24 patients breathing 100% oxygen have a mean reduction of FRC of 2 1 % (SD 14.3%) of pre-anaesthetic level and the 30 patients breathing 30 or 35 % oxygen have a mean reduction of 20% (SD 14%). These data do not suggest that the inspired oxygen concentration plays an important pan in the reduction of F R C This is supported by evidence that during anaesthesia high inspired oxygen concentrations are not associated with higher pulmonary venous admixture than when lower concentrations of oxygen are breathed (Nunn, 1964). Expiratory muscle activity. The studies of Freund, Roos and Dodd (1964)

and Kaul, Heath and Nunn (1973) have shown that phasic expiratory muscle activity commonly appears shortly after anaesthesia is induced. Don et al. (1970) recognized the possibility that this was the cause of the reduction in FRC but dismissed it on the grounds that neuromuscular block produced only a small increase (80 ml) in the FRC of anaesthetized patients breathing spontaneously. Thus it appeared unlikely that expiratory muscle activity was being used to maintain the tidal range substantially below the F R C It is scarcely possible to quantify overall expiratory muscle activity but we have been able to record whether the activity of one external oblique muscle increased, decreased or was unchanged after the induction of anaesthesia. Our technique of anaesthesia differed from that of Freund, Roos and Dodd (1964) and resulted in a low incidence of expiratory muscle activity. Therefore we had only a small group of patients in whom there was a detectable increase in expiratory muscle activity. In the majority, no expiratory muscle activity developed as determined either by palpation of the abdomen or by recording the e.m.g. In table IV we have separated our patients according to expiratory muscle activity and related changes in FRC to age and weight/height ratio, and inspired oxygen concentrations of the two groups. Within the limits of this study, the development of expiratory muscle activity during anaesthesia did not appear to exert any major effect upon the change in F R C although it would seem inevitable that expiratory muscle activity must always reduce the FRC if it is present at the end of expiration. What is perhaps more important is that we have demonstrated a substantial reduction in FRC (13.6%) in 10 patients who had no detectable expiratory muscle activity. In our studies on conscious subjects we were able to detect e.m.g. activity with the degree of expiratory muscle activity required to reduce lung volume 100-200 ml below FRC. Thus, considering the additional fact that a fall in FRC occurs in paralysed, anaesthetized patients (Laws, 1968), there can be little doubt that this phenomenon is the result of factors other than expiratory muscle activity. The cause of the reduction in FRC This study has not explained the mechanism by which the FRC is reduced during anaesthesia and it is not easy to postulate any remaining cause which is feasible. There appear to be five basic possibilities which are shown diagramatically in figure 3.

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patients breathing both 30 and 100% oxygen during observations extending into the second and third hour of anaesthesia. Thus it seems unlikely that there are major progressive decreases in FRC during the course of an anaesthetic and this parallels observations of Panday and Nunn (1968) who found that the alveolar-arterial Po, difference increased soon after induction but, in the majority of patients, did not thereafter increase by a significant amount. A minority of patients showed a progressive increase in alveolar-arterial Po, difference and a few responded favourably to positive pressure inflations. It seems likely that such patients develop pulmonary collapse in the manner proposed by Bendixen, Hedley-Whyte and Laver (1963).

491

492

Increase in central blood volume (A->B) would result in a displacement of gas from the chest, provided that the diaphragm and chest wall were unchanged in position. This would result in a decrease in FRC. However, the observed reduction in FRC is of the order of 300-500 ml and there is no evidence that central Hood volume increases by this amount during anaesdiesia. In fact, dilatation of peripheral capacitance vessels is an obvious feature of anaesthesia and this would tend to reduce central blood volume. Few measurements of central Hood volume have been reported but these suggest a small reduction during anaesthesia (Johnson, 1951). Elevation of the diaphragm (A->C) would certainly cause a reduction in FRC, and an elevation of only about 1 cm would be sufficient to explain the observed changes. A possible cause is that, in the conscious state, the diaphragm might not be fully relaxed at the end of a normal expiration, thus maintaining some "inspiratory tone". Certainly this holds for the earlier part of the expiratory phase, where "braking action" of the diaphragm has often been described (Basmajian, 1967). Anaesthesia is known to change the pattern of breathing towards a more abrupt and passive expiration, which closely approximates to an exponential decay. This is thought to be the result of an earlier release of inspiratory muscle braking action during expiration. However, this would only result in a reduction in FRC if inspiratory muscle tone were to persist throughout expiration in the conscious state and

there is at present no evidence that this is the case in supine man. Collapse of the chest wall (A->D) has been suggested as a possible cause of the reduction in FRC which accompanies the induction of anaesthesia. While it is extremely unlikely that anaesthesia could influence die mechanical properties of the chest wall, variations in tone of die muscles surrounding and influencing the chest, similar to the mechanism described above for the diaphragm, cannot be ruled out. Trapping of gas (A->E) would result in a reduction of FRC as measured by an inert tracer gas, but not by body plethysmography. It is scarcely conceivable that the induction of anaesthesia could result in an increase of airway muscle tone sufficient to cause die degree of trapping necessary to decrease the measured FRC by 400 mL Conversely, if die FRC is reduced by some other mechanism, dien the volume of trapped gas will be increased in patients whose FRC is reduced below dieir closing volume. This has been investigated by Don, Wahba and Craig (1972) who did, in fact, demonstrate an increase in trapped gas volume following induction of anaesthesia in older patients whose closing volume was close to FRC. However, only 3 patients out of 17 showed the large increases in die volume of trapped gas (VTG) which would be required to explain the reduction in FRC following induction of anaesdiesia. That is to say, the F R C + V T G after induction was nearly always substantially less dian F R C + V T G before induction and in only 3 cases did increase in VTG approach reduction in FRC. Additional evidence against trapped gas being die explanation of die reduction in FRC is provided by two studies of die effect of anaesthesia on FRC in the sitting position. In one of diese (Rehder, Sittapong and Sessler, 1972) FRC was measured by inert tracer gas (nitrogen washout) and no reduction in FRC was found. In die odier study (Shah et al., 1971) FRC was measured by plediysmography and a rapid reduction in FRC was found, which was related to the concentration of nitrous oxide inhaled. It is still not clear why diere should be a difference between the results of these two studies but, had the reduction of FRC been die result of trapped gas, the results would have been reversed, widi die reduction being detected by die nitrogen washout study but not by die plediysmographic study. The plediysmographic study employed nitrous oxide, which would have been rapidly absorbed under the conditions of the study. Furthermore, the plethys-

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FIG. 3. Possible mechanisms for reduction of FRC. For explanation see text

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and thereafter remains stable for 2 or 3 hours after induction. Such a change might be explained if anaesthesia abolished inspiratory muscle tone continuing into late expiration, but there is currently no firm evidence for the existence of inspiratory muscle tone continuing to the end of expiration in conscious supine man. An alternative explanation is that anaesthesia, or some aspect of it such as endotracheal intubation, might result in a rapid stepwise increase in pulmonary elastic recoil and this is supported by the findings of Westbrook et aL (1973). Possible explanations for this hypothesis include stimulated contraction of alveolar muscle or changed properties of surfactant. ACKNOWLEDGEMENTS

We are indebted to Mr A. G. Cox for permission to study patients under his care and to Miss Susan Chinn T ror statistical advice. We would like to thank Miss Brcoda Dobson who typed the manuscript. REFERENCES

Alexander, J. I., Spence, A. A., Parikh, R. K., and Stuart, B. (1973).- The role of airway closure in postoperative hypoxaemia. Br. J. Anaesth., 45, 34. Basmajian, J. V. (1967). Muscles Alive, their Functions Revealed by Electromyography, 2nd edn, p. 300. Baltimore: Williams and Wilkias. Bendixen, H. H., Hedley-Whyte, J., and Laver, M. B. (1963). Impaired oxygenation in surgical patients during general anaesthesia with controlled ventilation. N. Engl. J. Med., 269, 991. Bergman, N. A. (1963). Distribution of inspired gas during anesthesia and artificial ventilation. J. AppL Physiol., 18, 1085. Caltagirone, S., Mistretta, A., and Vagliasindi, M. (1969). Normal Values for Respiratory Function in Man, p. 77, Italy: Panminerva Medica. Colgan, F. J., and Whang, T. B. (1968). Anesthesia and atelectasis. Anesthesiology, 29, 917. Dery, R., Pelletier, J., Jacques, A., Qavet, M., and Houde, J. (1965). Alveolar collapse induced by denitrogenation. Can. Anaesth. Soc. J., 12, 531. Don, H. F., Wahba, W. M., and Craig, D. B. (1972). Airway closure, gas trapping, and functional residual capacity during anesthesia. Anesthesiology, 36, 529. Cuadrado, L., and Kelkar, K. (1970). The effect of anesthesia and 100 per cent oxygen on the functional residual capacity of the lungs. Anesthesiology, 32, 521. Freund, F., Roos, A., and Dodd, R. B. (1964). Expiratory activity of the abdominal muscles in man during general anesthesia. J. Appl. Physiol, 19, 693. Hewlett, A. M., Hulands, G. H., Nunn, J. F., and Minty, K. M. (1974). Functional residual capacity during anaesthesia. I: Methodology. Br. J. Anaesth., 46, 479. Hicfcey, R. F., Visick, W. D., Fairley, H. B., and Fourcade, H. F. (1973). Effects of halothane anesthesia on functional residual capacity and alveolar-arterial oxygen tension difference. Anesthesiology, 38, 20. Johnson, S. R. (1951). The effect of some anaesthetic agents on the circulation in man. Acta Chhr. Scand., 102, (Suppl.) 158.

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mographk study employed spontaneous breathing while the nitrogen washout study used artificial ventilation. However, a later study of patients in the supine position by Westbrook et aL (1973) showed that the manner of breathing did not influence the FRC during anaesthesia, and our own studies are in agreement with this. It should also be noted that the study by Westbrook et al. showed a large decrease of FRC during anaesthesia (table I) measured by the pleythsmographic technique, and this would not be so if the change were entirely the result of trapped gas. Increased elastic recoil of the respiratory system (A->F) would reduce the FRC if other factors remained constant. There are many conflicting reports of the effect of anaesthesia on the mechanical properties of the lungs and chest wall but information relating to the absolute lung volume is seldom available. This is an important omission, since it is the intercept of the pressure/volume curve on the absolute lung volume axis which determines FRC, rather than merely the slope of the pressure/volume curve (compliance). The position has been greatly clarified by the study of Westbrook et al. (1973) who have related airway, oesophageal and transpulmonary pressure to absolute lung volume, showing a major shift to the right of both airway pressure/volume and pulmonary pressure/volume curves during anaesthesia by an amount corresponding to their observed 23.3% reduction in FRC. They did not establish the cause of the change in mechanical properties and this question remains open. One possible cause of a reduction in compliance is pulmonary collapse of the miliary type suggested by Bendixen, Hedley-Whyte and Laver (1963). At first sight this would provide a very plausible explanation of the reduction of FRC, which was favoured by Dery et al. (1965). However, we have noted above that many of the original observations supporting the theory of "miliary atelectasis" have not been confirmed, and it is our opinion that progressive absorption collapse is a relatively uncommon feature of general anaesthesia using the techniques which we have studied. In conclusion it appears that there is currently no obvious explanation for the substantial reduction in FRC which accompanies the induction of anaesthesia. Various factors, such as expiratory muscle activity and oxygen absorption collapse have been eliminated and the time course of the change has been clarified. In a typical patient, the reduction seems to be complete within 10 min of induction

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494 Kaul, S. U., Heath, J. R., and Nunn, J. F. (1973). Factors influencing the development of expiratory muscle activity during anaesthesia. Br. J. Anaesth., 45, 1013. Laws, A. K. (1968). The effects of induction of anaesthesia and muscle paralysis on functional residual capacity of the lungs. Can. Anaesth. Soc. J., 15, 325. Nunn, J. F. (1964). Factors influencing the arterial oxygen tension during halothane anaesthesia with spontaneous respiration. Br. J. Anaesth., 36, 327. Bergman, N. A., and Coleman, A. J. (1965). Factors influencing the arterial oxygen tension during anaesthesia with artificial ventilation. Br. J. Anaesth., 37, 898. Panday, J., and Nunn, J. F. (1968). Failure to demonstrate progressive falls of arterial Poj during anaesthesia. Anaesthesia, 23, 38.

Rehder, K., Sittapong, R., and Sessler, A. D. (1972). The effects of thiopental-mepcridine anesthesia with succinylcholine paralysis on functional residual capacity and dynamic lung compliance in normal sitting man. Anesthesiology, 37, 395. Shah, J., Jones, J. G., Galvin, J., and Tomlin, P. J. (1971). Pulmonary gas exchange during induction of anaesthesia with nitrous oxide in seated subjects. Br. J. Anaesth., 43, 1013. Westbrook, P. R., Stubbs, S. E., Sessler, A. D., Rehder, K., and Hyatt, R. E. (1973). Effects of anesthesia and muscle paralysis on respiratory mechanics in normal man. J. Appi Physiol., 34, 81.

One-week Course in PRACTICAL ASPECTS OF MEASUREMENT IN ANAESTHESIA A course of practical instruction and tutorials designed to help trainee anaesthetists will be held in the Department of Anaesthesia during the week December 16-20, 1974. Numbers will be limited in order to allow those accepted to gain first-hand experience in operating the equipment. The course will consist of practical exercises illustrating the use of selected types of measuring equipment of interest in the specialty of Anaesthesia. Topics will include: basic electronics; statistics; gas flows and volumes; gas analysis; blood flow, pressure and temperature measurements; gas chromatography; recorders and the use of radioisotopes. Participants will be expected to have done some preliminary reading. Further particulars and application forms from: The Secretary, University Department of Anaesthesia, 24 Hyde Terrace, Leeds, LS2 9LN.

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DEPARTMENT OF ANAESTHESIA : THE UNIVERSITY OF LEEDS