POSTGRAD. MED. J. ,(1966), 42, 421

PULMONARY FUNCTION IN THE SURGICALPATIENT

K. N. V. PALMER, M.A., M.D.(Camb.), F.R.C.P.(Lond.)Reader in Medicine, University of Aberdeen. Hon. Consultant Physician, Aberdeen Royal

Infirmary

THE introduction of improved methods of spiro-metry and of relatively simple methods of meas-uring arterial oxygen saturation and the bloodgas tensions, has stimulated much research re-cently into disturbances of pulmonary functionin the surgical patient. In this paper the effectof anaesthetic drugs and operative procedureson a number of aspects of pulmonary functionwill be considered, and the significance of thesefindings in the prevention and treatment ofpulmonary complications after operations willbe discussed.

First, some relevant aspects of the physiologyof respiration will be reviewed.

IntroductionThe function of respiration is to arterialise

venous blood and maintain the partial pressuresof oxygen and carbon dioxide in the arterialblood within narrow limits throughout a widerange of physiological activity. To accomplishthis, ventilation must add oxygen to and removecarfbon dioxide from alveoiar3gas at a rate deter-mined by the metabolic requirements withoutthe expenditure of excessive work. To achieverapid gas exchange there must 1be no barrierto the diffusion of gases across the alveolarmembrane, pulmonary iblood flow must beadequate, and the distribution of the pulmonaryblood must approximately equal the ventilationpattern throughout the lung.

Adequacy of VentilationThis depends not only upon the volume of

air passing the lips per minute (minute ventila-tion) ibecause ajbout a third of the tidal volumeremains in the conducting airways i(anatomicaldead space) and does not take part in gas ex-change. In addition, as a result of disturbedpulmonary function there may be alveoli whichare inadequately perfused with blood and theywill therefore also not partake fully in gasexchange (alveolar dead space). The anatomicaland alveolar dead spaces together constitutethe physiological dead space. In health, theanatomical and physiological dead spaces are

approximately equal, but in many disorders ofthe lungs the voluime of the physiological deadspace exceeds the anatomical because there isan appreciajble alveolar dead space. If the par-tial pressure of caribon dioxide in expired gas(PE-o2) and arterial blood (Paco2) and the tidalvolume (VT) are measured, the physiologicaldead space (VD) can be calculated from Bohr'sEquation and related to the tidal volume.

VD Paco2-PECo2

VT Paco2(1)

Normally the ratio, physiological dead space:tidal volume does not exceed 0.3. If it is in-creased, parts of the lung are assumed to haveventilation to perfusion ratios.above average.

Effective or alveolar ventilation is the tidalvolume minus the physiological dead space xthe frequency of 'breathing. The level of alveolarventilation is adjusted through the respiratorycentre to maintain the carbon dioxide tensionof arterial blood near 40 mm.Hg. If the alveolarventilation is halved the arterial Pco2 is doubledand i(f the alveolar ventilation is doubled thearterial Pco2 is halved.

Vol. of CO. excreted x barometric pressureArterial Pco2 =

Alveolar ventilation

(2)Thus, measurement of the arterial Pco2 is asensitive indication of the rate of alveolar ven-tilation.

If the arterial Pco2 level rises above 44mm.Hg. ventilatory failure is present (unlessthe raised Paco2 level is compensatory in thepresence of a primary non-respiratory or meta-bolic alkalosis).

Ventilatory failure is followed iby a fall inarterial pH !(respiratory acidosis) and whenbreathing air, by the development of arterialdesaturation and hypoxaemia.As the arterial Pco2 rises and the pH falls,

bicarbonate is retained 'by the kidney whichwill tend to restore the arterial pH -level tonormal (compensated respiratory acidosis). This

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is apparent from the Henderson-HasselbalchEquation.

(HCO3)-pH - 6.1 + log (3)

0.03 x PaCO2Although hypercapnia (raised arterial Pco2)

does not result from lung disease without therebewing redluced alveolar ventilation, arterial de-saturation may occur although alveolar venti-latUon is adequate due to uneven distriibution of,gas and blood within the lung (ventilation-pvrrus-on imbalance), or more rarely lbecausethe transfer of oxygen across the alveolar mem-brane is impaired. (Carbon dioxide transfer isnot affected because it is about 20 times morediffusilble than oxygen.)

Central cyanosis cannot thereCore ibe relieduLpon as an indication of inadequate ventilationand ventilatory failure can be diagnosed withcertainty only when 'the arterial Pco2 ismeasLired. Moreover, it must be rememberedthat ventilatory fai-lure and severe respiratoryacidosis may 'be present in a pink patient whois ibreathing oxygen-enriched air as, for example,during anaesthesia.

Oxygenation of Arterial BloodThe arterial oxygen tension depends on, first,

the tension of oxygen in the alveoli; secondly,whether there is any ibarrier to the diffusion ofoxygen through the alveolar membrane and intothe red cells, and thirdly, the degree of venousadmixture or shunt effect due to blood comingfrom areas of lung which are ventilated ipoorlyor not at all, although adequately perfusedwith pulmonary capillary blood. In additionblood 'from 'bronchial, pleural and Thbebesianveins by by-passing the pulmonary capillariescontrilbutes to the venous admixture effect.The alveolar Po2 dcepends upon the inspired

Po2, the alveolar Pco2 and th. respiratory-ex-change ratio. Because the volume of nitrogenis constant for inspired and expired gas andbecause the sum of the partial pressures ofgases in the alveoli is equal to atmosphericpressure, the alveolar Po2 can be readily cal-culated from the alveolar-air equation whichstates that

Arterial Pco.Mean Alveolar Po., = Inspired Poa.-

Respiratory ExchangeRatio

(4)

*The arterial and alveolar Poo2 tension are assumedto be equal.

In health, the alveolar-arterial 02 tensiondifference is less than 10 mm.Hg.-most of thisarises !because of variations in regional ventila-tion to perfusion ratios especialily in the erectposture, when blood from the lower lobes isless well oxygenated than that from other partsof the lung and so contributes to the venousadmixture effect. In disordered pulmonary func-tion these inequalities are often much increasedand may give rise to signifidant hypoxaermia.

Barriers to diffusion across the alveolar mem-brane become important in the iproduction ofhypoxaemia when the alveolar Po2 is reduced.Although 02 transfer across a thickened alveolarmembrane may be impaired on exercise whenthe alveolar Po2 is normal ibecause the rate ofdiffLlsion is less, diffusional impairment is sel-dom important clinically at rest if the alveolarPo., is normal.

Mechanical Factors in BreathingInspiratory muscular contraction is required

to overcome the elastic forces oif the lungs andthorax and the resistance to airflow 'throughthe 'bronchial airways. Expiration is passive inthe absence of airway cdbstruction. The mainmuscles of inspiration are the diaphragm andto a lesser extent the intercostal muscles. Theefficiency of the bellows action of tthe chest canbe assessed by measuring the Vital Capacity(VC) which is the volume of gas that can bebreathed out after a maximal inspiration, with-out any restriction as to time. It depends uponthe inspiratory muscle power, the mobility ofthe thorax and the distensiibility of the lungs.A reduction in Vital Capacity therefore indi-cates mainly a restrictive ventilatory defect. Theamount of gas 'thiat can be expired after amaximal inspiration in a given time is a sen-sitive 'indicator o-f obstruction of the bronchialairways. The volume expired in one second isthe Forced Expiratory Volume in 1 sec. (FEV1).Alternatively the Peak Expiratory Flow Rate(PEFR) in litres per minute may be measured.

In pure restrictive ventilatory insufficiencythe VC and FEV, are 'both reduced, but theratio FEV, is, as in health, greater than 75 percent. Where there is airwav obstruction thisratio is reduced and in severe cases it may beless than 40 per cent. The amount of obstructiveventilatory defect due to reversilble airway ob-struction can 'be determined iby measuring theFEV1 before and after the aerosol inhalationof a ibronchodilator drug such as 1 per centisoprenaline. Reversible airway obstruction is

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indicated lby an absolute increase in FEV,(rather than increases in ratios).At the end of a normal quiet expiration, the

amount of air in the lungs is the FunctionalResidual Capacity 4(FRC). At the position offull expiration i.e. after the vital capacity hasbeen exhaled, airway closure occurs, and thegas then remaining in the lung which cannotbe exhaled is the residual voluime (RV). TheVital Capacdity and the Residual Volume makeup the total ilung capacity (TLC). If the TLCis reduced, the VC is reduced also, but theVC may 'be reduced because the RV is in-creased, as for example, when the lungs areoverinflated. When the FRC is reduced, theVC and TUC will also be reduced, breathingis more in the expiratory or deflated positionand small airway closure may occur even atthe resting respiratory level.

Effects of Anaesthesia and Surgical Operationson Pulmonary PhysiologyVentilatory FunctionImpaired alveolar ventilation due to the de-

pressant effects of the anaesthetic on the res-piratory centre may occur during and brieflyimmediately after operations when 'breathing isspontaneous but not when it is controlled (Dun-dee, 1952; Hobsley, 1963). Where abdominalincisions have ibeen made there is a persistingrestrictive impairment of pulmonary mechanicalfunction due mainly to reduced diaphragmaticmovement which is greatest during the firsttwo postoperative days and persists for manydays afterwards. The Vital Capacity is reducedto less than half the pre-operative level, andthe Forced Expiratory Volume in 1 sec. andPeak Expiratory Flow Rate are similarly re-duced (Palmer, 1961; Palmer and Gardiner,1964). The total lung capacity is reduced andthere is a consistent and significant decreasein functional residual capacity (Beecher, 1933 b)so that the patient is 'breathing in a more ex-piratory position than normal. The tidal volumeis reduced 'but the respiratory rate is inicreasedso there is little or no change in Minute Volume(Beecher, 1933a; Palmer and Gardiner, 1964).The normal pattern of breathing is altered, how-ever, being at a low and fixed tidal volumewith an absence of periodic deep breaths. T'hismay lead to a fall in lung compliance, and toprogressive alveolar atelectasis, an effect whichcan ibe prevented by periodic hyperinflation ofthe lungs (Bendixen, Hedley-Whyte and Laver,1963).The impairment of pulmonary function is

more marked after upper than lower abdominaloperations and occurs whether or not post-operative bronchopneumonia occurs. Those inwhom this complication develops show a some-what greater restrictive venti'latory defect thannormals and they often show in addition revers-ible airways obstruction during the first threepostoperative days as shown by atbsolute in-creases in FEV1 and PEFR after the inhalationof a bronchodilator drug >(Palmer, 1961; Palmerand Gardiner, 1964).

Fig. 1 shows measurement of FEV1 beforeand after gastric surgery in two groups ofpatients-one was uncomplicated but the otherdeveloped postoperative 'bronchopneumonia.FEV1 was recorded at daily intervals before(interrupted lines) and after (continuous lines)aerosol inhalation of isoprenaline. In those whosubsequently developed lbronchoppneumoniathere was a slight increase in FEV1 before theoperation after the bronchodilator indicatingsome reversible airways dbstruction. Aifter thheoperation there was a considerable reduction inFEV1 in both groups; this was maximal onthe first postoperative day and gradually becameless marked afterwards. The reduction in FEV1was greater in those who developed broncho-pneumonia and in these patients there was amean increase of FEV1 after the bronchodilatorduring the first three postoperative days. Thiswas especially marked in the suibjects with themost severe chest complications.

It is apparent therefore that laparotomy hasa profound effect on pulmonary mechanicalfunction leading to a marked restrictive ventila-tory diefect, and breathing that is shallow, rapid,at a fixed tidal volume predominantly in theexpiratory position, and lacking in periodicdeep breaths. In those who develop 'broncho-pneumonia these changes are more marked andthey may also show reversilble airway obstruc-tion during the first three postoperative days.

Blood Gas Tensions and Acid-Base BalanceCarbon DioxideHypercapnia sometimes occurs during and

immediately after operation when breathing isspontaneous and unassisted. For example inpatients undergoing uterine dilatation and curet-tage the mean arterial Pco2 level rose from acontrol value of 40 mm.Hg. to 55 mm.Hg. dur-ing the anaesthetic, fallinig to 45 mm.Hg. anhour afterwards (Taylor, Scott and Donald,1964). However, these patients were operatedupon in the lithotomy position and it seemsthat this position during operation rather than

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424 POSTGRADUATE MEDICAL JOURNAL July, 1966

3000

\M~~~^^>N~~~ Normals

1 Bronchopneumonia

2000 //

1000 0 Before bronchodilator*After bronchodilator

Pre-op 1 2 3 4 5 Days Post-op.

FIG. 1.- FEV1 mis. (BPTS) before and after gastric surgery

the effect of the anaesthetic was responsible forthe production of slight alveolar ,hypoventila-tion. The development of hypercapnia is notinevitable either during or immediately aftersurgical procedures under general anaesthesia.In a group of patients undergoing carotid angio-graphy and other minor surgical operationswhen Ibreathing was spontaneous, no significantchange in arterial CO2 tension levels from thecontrol measurements Iwas found (Gardiner andPalmer, 1964). On the other hand, when breath-ing is controlled during the anaesthetic patientsare often somewhat hyperventilated leading toa fall in arterial Pco2 levels and hypocapnia.Thus, with modern anaesthesia, skilfully ad-ministered, any effect on the arterial carbon-dioxide tension is slight and short-lived.

After abdominal incisions have Ibeen madethere is a marked restrictive 'impairment ofpulmonary ventilatory function and the patternof breathing is altered, but, in spite of this,slight hypocapnia rather than hypercapnia isfound postoperatively. After gastric surgery, forexample, the mean arterial Pco2 fell from 38mm.Hg. Ibefore the operation to 35 mm.Hg. onthe second and third 'postoperative days. Inthose who developed postoperative broncho-pneumonia the arterial Pco2 level fell from amean preoperative level of 40 mm.,Hg. to 30mm.Hg. on the 5th postoperative day-so that

these patients had a mild respiratory alkalosis(Palmer and Gardiner, 1964). These changesreflect the increased physiological dead/tidalvolume ratios which have been measured aftergastric surgery and which indicate the presenceof areas of lung with high ventilation: perfusionratios '(probably at the upper parts of the lung)due to over-ventilation (Palmer, Gardiner andMcGregor, 1965).Hypocapnia develops postoperatively only in

those patients in whom the arterial Pco2 levelis normal Ibefore the operation. In subjects withobstructive lung disease who have some degreeof carbon dioxide retention, serious postopera-tive hypercapnia and respiratory acidosis mayoccur. This cannot be readily detected clinic-ally and for the proper 'management of thesepatients measurement of the arterial Pco2 levelbefore and after the operation is essential.

Acid-Base BalanceA primary metabolic adidosis has been found

after major operations especially when largedoses of anaesthetic agents have 'been used andthe operation has taken a long time. It is mostcommonly associated with a respiratory acidosisproduced tby depression of the respiratory centreby the anaesthetic drugs (IHoladay, ,Ma andPapper, 1957; Hobsley, 1963). The cause of themetabolic acidosis is not clear and several fac-

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tors are probably responsible such as the effectsof trauma, of the anaesthetic, starvation andhypoxaemia. This combined metabolic and res-piratory acidosis is short-lived, and a mild res-piratory alkalosis is commonly found for somedays after abdominal operations. This mightresult from anoxic stimulation of the carotidand. #ortic bodies but this is unlikely as *thelowet arterial Pco2 ilevels do not occur on thedays postoperatively when the arterial Po2 levelsare 'most reduced. It probably results fromalteration in the pattern of ibreathing 'leading toslight overall alveolar hyperventilation. The ten-dency to over-ventilation and hypocapnia iscompensated for by the development of a mildmetabolic acidosis the extent of which closelyparallels the lowered Pco2 levels '(Palmer andGardiner, 1964).Oxygen

While it has been recognised for some timethat arterial saturation commonly follows openchest surgery (Maier and Coumaud, 1943), itis only comparatively recently that arterialsaturation has 'been reported during and imme-diately after other operations under generalanaesthesia, and this arises 'whether breathingis spontaneous or controlled during the anaes-thetic (Nunn and Payne, 1962; Conway andPayne, 1964). Nevertheless, this is not an in-variable occurrence and no hypoxaemia hasbeen ifound after carotid angiography or uterinedilatation and curettage under general anaes-thesia when breathing was spontaneous (Gar-diner and Palimer, 1964; Taylor and others,1964). Apart from major thoracic and cardiacsurgery muscular incisions are probably neces-sary for the development of significant post-operative hypoxaemia. After gastric surgery, forexample, hypoxaemia constantly occurs andpersists for at least five days. Falls in arterialPo2 levels of about 20 mm.Hg. from preopera-tive values are commonl:y found on the firstpostoperative day and arterial Po2 levels of70 mm.Hg. or below i(equivalent to an arterialsaturation of 92 per cent) are usual when thearterial Po2 levels are within the normal rangebeforehand. When postoperative bronchopneu-monia develops arterial Po2 levels as low as55 mm.Hg. corresponding to an arterial 02saturation of 85 -per cent 'may occur. Postopera-tive hypoxaemia is not due to overall hypo-ventilation, however, as it occurs in the absenceof hypercapnia, nor does -it strictly parallel thereduction in Vital Capacity and there is moreusually slight overall hyperventilation leadingto reduced arterial Pco2 levels. There is a sig-

nificant correlation lbetween the postoperativePo2 and the age of 'the patient .(Nunn, 1965) anda regression equation 'has been derived:

Postoperative Po2 = 94.3 -0.455 '(age)There is, however, consideraible scatter of Po2levels within any decade, which indiicates thatthere is considerable variation in the factorswhich result in postoperative hypoxaemia.

It has been suggested that premedicationmight be a factor in the development of post-operative hypoxaemia as arterial desaturationwas found after atropine and before the opera-tion (Tomlin, Conway and Payne, 1964; Payneand Conway, 1966). However arterial saturationor reduced 02 tensions have not been foundwhen atropine is given to healthy volunteers,(Daly, Ross and Behnke, 1963; Nunn andand Bergmann, 1964) 'and in further experi-ments premedication with atropine or withpapaveretum and scopolamine in surgicalpatients was not followed by a change in con-trol arterial blood measurements-eitherarterial 02 saturation or 02 tension-bothvalues 'being directly measured (Taylor, Scottand Donald, 1964; Gardiner and Palmer, 1964).

Recently total cardiopulmonary by-pass 'hasbeen shown to 'be frequently complicated bypostoperative hypoxaemia and in this instanceit arises especially when homologous perfusedblood is 'u'sed, which it is suggested, leads toan immune reaction in the lungs. Congestion,thickening of the interalveolar walls, patchycollapse and intra-alveolar haemorrhage occurso 'that an appreciable portion of the cardiacoutput traverses the lungs without 'being oxy-genated '(Nahas, Melrose, Sykes and Robinson,1965).The combination of hypoxaemia without

hypercapnia in surgical patients has been sug-gested to 'be due 'to an increased venous admix-ture effect from regional ventilation/pedusioninequality in the lungs and possibly also fromshunting of pulmonary capillary blood throughunventilated areas of alvedlar collapse.

This hypothesis is su'pported by the observa-tion that normal saturation is rapidly restored-by breathing moderately enriched oxygen-airmixtures (which reverses the effect of regionalalveolar hypo-ventilation) and by studies inwhich alveolar-arterial 02 tension gradients weredirectly measured before and for five days aftergastric surgery. These have shown that the hy-poxaemia was associated with a proportionateincrease in alveolar-arterial tension gradient(Palmer, Gardiner and McGregor, 1965)-aneffect which may be equivalent to a 'right to leftshunt of 25 iper cent of the pulmonary 'blood

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flow. Alveolar 02 tensions were normal so thatimpaired diffusion is unlikely to play a part inthe development of hypoxaemia. Because alveo-lar-arterial oxygen tension differences weregreater when lbreathing 100 per cent oxygenafter major abdominal surgery than before theoperation the presence of shunts due to pul-monary collapse is also indicated (Gordh, Lin-derholm and Norlander, 1958). During anaes-thesia also there is an increased alveolar-arterial02 tension difference and increased venous ad-mixture which can largely be prevented whenlarge tidal volumes are used during controlledventilation (Sykes, Young and Robinson, 1965).

Thus, it seems that after operations wheremuscular incisions have ibeen made there is re-duced diaphragmatic movement and an inabilityto take periodic deep breaths. This leads to lowventilation/perfusion ratios at the lung basesand possibly to areas of alveolar collapse whichmay 'be present without X-ray evidence (Hamil-ton, McDonald, Fischer and Bethards, 1961).The development of slight hypoxaemia is

therefore almost inevitable after ajbdominal sur-gery but it 'becomes less marked as the restric-tive ventilatory defect improves during convales-cence and it is unlikely to 'be of much signifi-cance to patients in good health. But in oldersu'bjects (who start with lower Po, levels) andin those with cardiac and cerelbrovasculardisease it is of greater significance. Changes inblood gas tensions are of most importance tothose with chronic respiratory diseases 'becausethere is commonly 'hypoxaemia with or with-out hvpercapnia before the operation. Theyare also most prone to develop postoperativebronchopneu;monia.

Postoperative BronchopneumoniaThis develops almost exclusively in patients

with varying degrees of chronic bronchopul-monary disease, especially chronic broncthitis,who undergo abdominal surgery (Palmer, 1962).Bronchitics commonly have a restrictive ventila-tory defect and reduced vital capacity with air-way obstruction and reduced FEV1 or PEFR,and are therefore less able to tolerate thechanges in ventilatorv function that occur afterlaparotomy. They have increased 'bronchialsecretion, low grade pulmonary infection anddepressed ciliary activity. The amount of bron-chial secretion increases after the operation and,because coughing is impaired and ciliary acti-vity further depressed, it cannot ibe expectorated.Small symptomless areas of pulmonary collapsewhich in the normal gradually re-expand, ex-

tend, giving rise to larger areas of segmentalcollapse which!become infected leading to bron-chopneumonia. This causes a worsening in thedegree of hypoxaemia.

Aerosol inhalations of bronchodilators withassisted postural drainage (Palmer and Sellick,1953) or intermittent positive pressure breathingwith isoprenaline (Anderson, Dossett and Ham-ilton, 1963) overcome the restrictive ventila-tory defect, reduce airway obstruction, and aidthe expectoration of ibronchial secretion. Inthese ways they prevent the start of a train ofevents which lead to postopperative pneumonia.

Because of the great importance of recognis-ing the high-risk case, especially those withchronic obstructive lung disease, preoperativespirometry should tbe carried out in all patientsa'bout 'to undergo major abdominal surgery.Where abnormalities are found, (blood gas ten-sions must also be measured. If these are ab-normal, careful monitoring of 'blood gas ten-sions postoperatively is mandatory and, whendangerous hypoxaemia or hypercapnia develop,postoperative tracheostomy and oxygen therapywith or without assisted ventilation will 'be re-quired. It is only iby these measures that themorbidity and mortallity from postoperativechest infection will be reduced.SummaryWith modern anaesthetics iskilfu'lly adminis-

tered, 'there is little risk of serious hypo-ventila-tion and carbon dioxide retention during orimmediately after even a miajor operation. Ar-terial desaturation is also not a problem duringanaesthesia 'because oxygen is usually added toinspired gas, but an increased alveolar-arterialoxygen tension difference and increased venousadmixture exist because of ventilaition/perfusionimbalance in the lungs. The continuing effectsof surgery on pulmonary function are almostwholly confined to operations where muscularincisions have been made. After 1aparotomythere is marked restrictive ventilatory impair-ment, 'breathing is rapid, shallow and pre-dominantly in an expiratory position, and thereis an inability to take deep 'breaths. Thesechanges lead to hypoxaemia but without hyper-capnia, due to an increased venous 'admixtureeffect from ventilation / perfusion inequality inthe lungs and 'probably 'from true shunts throughunventilated areas of alveolar collapse. Whilethese changes are not important to the patientin good health, they'are of great importance inolder subjects and in those with chronic bron-chopullmonary disease who are especially proneto develop postoperative bronchopneumonia.

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July, 1966 PALMER: Pulmonary Function in the Surgical Patient 427

These patients require preoperative spirometryand measurement of blood gas tensions beforeand after operation to detect alveolar hypo-ventilation and dangerous hypoxaemia.

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NUNN, J. F. (1965): Influence of Age and OtherFactors on Hypoxaemia in the Postoperative Period,Lancet, ii, 466.

NUNN, J. F. and BERGMANN, N. A. (1964): TheEffect of Atropine on Pulmonary Gas Exchange,Brit. J. Anaesth., 36, 68.

NUNN, J. F., and PAYNE, J. P. (1962): Hypoxaemiaafter General Anaesthesia, Lancet, ii, 631.

PALMER, K. N. V. (1961): Changes in VentilatoryFunction after Abdominal Operations, Lancet, i,191.

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