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RESPIRATION AND THE AIRWAY

Lung recruitment and positive airway pressure before extubationdoes not improve oxygenation in the post-anaesthesia

care unit: a randomized clinical trialA. B. Lumb 1, S. J. Greenhill 1 2, M. P. Simpson 1* and J. Stewart 1

1St Jamess University Hospital, Leeds Teaching Hospitals NHS Trust, Beckett Street, Leeds LS9 7TF, UK.2Present address: The Queen Elizabeth Hospital, Gayton Road, Kings Lynn PE30 4ET, UK

*Corresponding author. E-mail: [email protected]

Background. Atelectasis is known to develop during anaesthesia and after operation atelecta-

sis leads to impaired oxygenation. Lung recruitment manoeuvres, positive end-expiratory

pressure (PEEP), and continuous positive airway pressure (CPAP) have been proposed for

reduction of atelectasis but their benefits have not been shown to persist after operation. We

proposed that a combination of these techniques before extubation would improve oxygen-ation after operation.

Methods. Adult patients undergoing elective surgery requiring tracheal intubation and an arterial

catheter were randomized to receive either: a lung recruitment manoeuvre of 40 cm H2O for 15

s, 30 min before the end of anaesthesia, followed by 10 cm H2O of PEEP and then 10 cm H2O of

CPAP from return of spontaneous breathing until extubation; or no lung recruitment manoeuvre,

5 cm H2O PEEP, and no CPAP. Arterial blood gases were taken at randomization and 1 h afterextubation. The primary endpoint of the study was the change in (Aa)DO2 between these times.

Statistical analysis of the two groups was done by x2 or unpaired t-test as appropriate.

Results. Twenty-two patients were recruited to each group. There were no significant differences

between the groups before randomization. There was no significant difference in the change in

(Aa)DO2 between the groups (P0.82).

Conclusions. Postoperative oxygenation is not improved by a combination of a lung recruitment

manoeuvre and maintenance of a positive airway pressure until extubation. Further research is

needed to elucidate the mechanism of atelectasis on emergence from anaesthesia and to evaluate

more invasive clinical strategies such as post-extubation CPAP.

Trial registered at URL http://www.controlled-trials.com

Identification number: ISRCTN32464251

(http://www.controlled-trials.com/ISRCTN32464251)

Br J Anaesth 2010; 104: 6437

Keywords: complications, atelectasis; lung, atelectasis; ventilation, continuous positive

pressure; ventilation, positive end-expiratory pressure

Accepted for publication: February 20, 2010

Atelectasis in dependent lung units is an almost inevitable

consequence of general anaesthesia with IPPV1 2 and,

along with altered ventilation perfusion relationships,

causes an increase in alveolar to arterial oxygen partial

pressure difference (A a)DO2. Atelectasis, which can

persist into the postoperative period,3 is resistant to simple

techniques normally used to improve lung function such

as patient posture and may contribute to postoperative

pulmonary complications.4 Studies using computerized

tomography (CT) during anaesthesia have shown that

atelectasis formation can be attenuated by the use of posi-

tive end-expiratory pressure (PEEP) and the avoidance of

high inspired oxygen fractions (FIO2).5 6 Once formed,

atelectatic lung regions may be effectively recruited by

maintaining a sustained airway pressure of 40 cmH2O for

15 s.7 This is the only lung recruitment manoeuvre that

# The Author [2010]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved.

For Permissions, please email: [email protected]

British Journal of Anaesthesia 104 (5): 6437 (2010)

doi:10.1093/bja/aeq080 Advance Access publication March 30, 2010
http://www.controlled-trials.com/http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/ISRCTN32464251http://www.controlled-trials.com/http://www.controlled-trials.com/http://www.controlled-trials.com/http://www.controlled-trials.com/http://www.controlled-trials.com/


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has been shown to be effective in CT studies,7 is safe in

clinical use,8 and improves intraoperative oxygenation.

When performed in isolation, this improvement in oxygen-

ation does not persist into the postoperative period.9

If an intraoperative recruitment manoeuvre is followed

by the use of 10 cm H2O of PEEP, atelectasis is prevented

from recurring even in the presence of a high FIO

2.9 We

hypothesized that if positive airway pressure were main-tained after a recruitment manoeuvre and throughout emer-

gence from anaesthesia, there would be a reduction in

atelectasis even in the presence of 100% oxygen and so an

improvement in oxygenation in the postoperative period.

The key period for developing atelectasis at the end of

anaesthesia is likely to be the period after discontinuation

of IPPV and PEEP but before extubation. During this

period, patients often cough and zero end-expiratory

pressure (ZEEP) is commonly used and will accentuate

flow- and volume-related airway collapse. ZEEP may be

avoided in the spontaneously breathing, intubated patient

by preventing disconnection of the breathing system from

the tracheal tube and by using the adjustable pressure lim-iting (APL) valve to generate continuous positive airway

pressure (CPAP).

We tested the hypothesis that by performing a recruit-

ment manoeuvre near the end of the anaesthetic followed

by PEEP and then CPAP until extubation, the ( A a)DO21 h after extubation would be improved compared with

patients in whom these interventions were not performed.

Methods

The study was approved by the Leeds Local Research

Ethics Committee (Ref: 06/Q1205/17 COREC Locked

Code: AB/66109/2) and registered at http://www.controlled-

trials.com (Identification number: ISRCTN32464251).

Written informed consent was obtained from all the study

subjects.

Patients were recruited from elective surgical lists at the

two large teaching hospitals in the Leeds Teaching

Hospitals NHS Trust. Patients deemed eligible for

inclusion were adults undergoing elective operative pro-

cedures that were expected to last .45 min, and whose

anaesthesia technique was to include tracheal intubation,

muscle relaxation, IPPV, and the insertion of an arterial

catheter for clinical care. Patients were excluded if therewas any contraindication to the use of 10 cm H2O of

PEEP or the recruitment manoeuvre or the clinical require-

ment for the use of.5 cm H2O of intraoperative PEEP.

Patients were also excluded if any perioperative cardiovas-

cular or respiratory event occurred which the anaesthetist

with clinical responsibility for the patient thought would

make the study intervention clinically unacceptable.

Patient factors recorded before operation were age, sex,

BMI, and smoking status. Apart from the requirements for

inclusion in the study described above, the anaesthetic

technique was left to the discretion of the anaesthetist.

Intraoperative IPPV settings were an FIO2

of 0.3 0.8,

PEEP 5 cm H2O, tidal volume 710 ml kg21, and venti-

latory frequency as appropriate to maintain end-tidal

carbon dioxide partial pressure of 4 5.5 kPa. Thirty

minutes before the anticipated end of the anaesthetic, an

arterial blood sample was obtained for measurement of

arterial PO2 and PCO2, and the FIO2 was recorded. Thepatients allocation was concealed from the investigators

until this point when an envelope prepared at the start of

the trial (by a non-investigator) bearing only a number on

the outside and the allocation group on the inside was

opened.

Fifteen minutes before the anticipated end of anaesthe-

sia, patients in the intervention group received a lung

recruitment manoeuvre consisting of lung inflation to an

airway pressure of 40 cm H2O sustained for 15 s.

Immediately after this recruitment manoeuvre, ventilation

continued as previously but with PEEP increased to 10 cm

H2O. IPPV continued at the same rate until evidence of

return of spontaneous ventilation. At this point, CPAP wasmaintained at 10 cm H2O by adjusting the APL valve and

providing a fresh gas flow of.10 litre min21 to maintain

the positive airway pressure during inspiration. Circuit dis-

connection was avoided at all times before extubation of

the trachea to maintain the positive airway pressure.

The control group received no lung recruitment

manoeuvre and ventilation continued with the current set-

tings including any intraoperative PEEP (5 cm H2O). NoCPAP was applied on return of spontaneous ventilation,

with the APL valve left fully open. Circuit disconnection

was permitted, for example, when moving the patient.

In both groups, the FIO2

was set to 1.0 with fresh gas

flow exceeding 10 litre min21 before extubation of the

trachea. This occurred when deemed appropriate by the

anaesthetist with clinical responsibility for the patient.

In the post-anaesthesia care unit (PACU), both groups

received standard post-anaesthetic care. A Venturi mask

(Lifecare Hospital Supplies, Edinburgh, UK) providing

an FIO2

of 0.4 was used for all patients from 45 min

post-extubation until an arterial blood sample was obtained

at 1 h post-extubation for measurement of arterial PO2and PCO2.

The (A a)DO2 gradient at 1 h post-extubation was used

as the endpoint of the study. Arterial oxygen partial

pressure was measured from the arterial blood samples asdescribed above. Alveolar PO2 was calculated using the

following version of the alveolar gas equation:

alveolar PO2 PIO2 PaCO2

RQ1 FIO21 RQ

RQ assumed to be 0.8.

The standard deviation (SD) o f (A a)DO2 for the pur-

poses of the power calculation was derived from preinduc-

tion values in a previous study of a similar population

Lumb et al.

644
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(3.91 kPa).9 A significance level for the study of 5%

(P0.05) and a power of 80% were used for the calcu-

lation. Two groups of 22 subjects were calculated to be

needed to detect a difference of 3.33 kPa (0.8 times the

previously published SD).

Statistical analysis of the two groups was done by x2 or

unpaired t-test as appropriate with significance assumed with

P,0.05 using SPSS 15.0 (SPSS Inc., Chicago, IL, USA).

Results

A total of 52 patients were enrolled between June 2006

and February 2009 (Fig. 1). There were no significant

differences between the groups with regard to preoperative

characteristics, duration, and nature of operation, and arter-

ial gases at randomization and in PACU (Table 1).

The mean (SD) (A a)DO2 during anaesthesia was 12.3

(8.4) kPa and this increased slightly in PACU to 14.1

(5.2) kPa. The change in individual (A a)DO2 between

randomization and PACU displayed no particular pattern

(Fig. 2).

Using each patient as their own control, the meanchange in (A a)DO2 was 1.98 (6.52) in the standard group

and 1.52 (6.71) in the intervention group (P0.82). This

showed that there was no statistical difference or clinical

benefit accruing from the intervention.

Discussion

This study has shown that patients undergoing general

anaesthesia develop abnormal (A a)DO2 and that this

persists into the postoperative period. We have also shown

that a lung recruitment manoeuvre followed by positive

airway pressure until extubation does not improve the

(A a)DO2 in PACU.

In the usual absence of a significant alveolar to pulmon-

ary capillary diffusion barrier, abnormalities of (A a)DO2result from intrapulmonary shunting and areas of lung

with low ventilationperfusion ratios.10 During anaesthe-

sia, intrapulmonary shunting through areas of atelectasis is

the most significant contributor; so, in the absence of

acute lung pathology before operation, it may be assumed

that changes in (A a)DO2 are mostly secondary to the

development of atelectasis.

Our results are comparable with a previous study which

also used (A a)DO2 as a marker of atelectasis,9 and

demonstrate high (A a)DO2 values at the end of the

Consented, n=52

Analysed, n=22Excluded from analysis, n=1

Lost to follow-up, n=0Required FIO2

>0.4 in PACU, n=1

Allocated to standard group, n=23Received allocated treatment, n=23

Lost to follow-up, n=0Discontinued intervention, n=0

Analysed, n=22Excluded from analysis, n=2

Randomized, n=47

Allocated to intervention group, n=24Received allocated treatment, n=22

Protocol violation circuit disconnection, n=2

Operation cancelled, n=2Investigator unavailable, n=1

Required PEEP >5 cm H2O, n=2

Fig 1 Consort flow chart showing patients progress through the trial.

Table 1 Comparison of the two study groups showing mean (range), mean ( SD)

or number of occurrences of factors that could potentially affect (A a)DO2.

None of the factors differed significantly between the groups, P.0.05. PACU,

post-anaesthesia care unit. Operation: AO, abdominal open; AL, abdominal

laparoscopic; P, peripheral

Standard group Intervention group

Age (yr) 61.8 (42 85) 68.3 (49 89)

BMI (kg/m2) 28.4 (7.7) 27.3 (4.5)

Sex (male/female) 18/4 14/8

ASA (I/II/III) 7/7/8 2/15/5

Smoker/non-smoker 4/18 2/20

Operation (AO/AL/P) 12/4/6 15/4/3Duration of surgery (min) 255 (150) 319 (122)

(A a)DO2 at randomization (kPa) 12.5 (8.7) 12.1 (8.4)

FIO2

at randomization 0.475 (0.119) 0.467 (0.094)

Arterial PCO2 at randomization (kPa) 5.59 (0.72) 5.53 (0.80)

Arterial PCO2 in PACU (kPa) 5.77 (0.61) 5.70 (0.37)

Lung recruitment and (A a)DO2 in PACU

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anaesthetic that become even higher at 1 h after operation.

As demonstrated by the large standard deviations in our

data, there is a wide variation between patients, particu-

larly during anaesthesia, results which are again compar-

able with the previous study,9 which also studied the

effects of manual inflations every 30 min throughout

surgery and before extubation. Although details of themanual inflation used and how long before extubation it

was applied are not clear, they, like us, failed to demon-

strate any beneficial effect on (A a)DO2 in PACU.

It is known that CPAP at induction prevents the for-

mation of atelectasis11 and that PEEP applied after a

recruitment manoeuvre during anaesthesia prolongs the

time taken for atelectasis to reform.6 We hoped that by

applying the same principle at the end of anaesthesia and

up until the moment of extubation, we could reduce the

effects of atelectasis upon oxygenation in the early recov-

ery period. Our results show that our management strategy,

used at the end of anaesthesia, has not provided a signifi-

cant improvement in patient oxygenation in PACU. There

are a number of possible explanations for this. First,

(A a)DO2 may be affected by the FIO2

or the arterial

PCO2,12 but this is unlikely to have affected our results as

the values for these factors were the same in each group

(Table 1). Secondly, despite using high fresh gas flow

rates, our method of applying CPAP during spontaneous

respiration may have been ineffective during inspiration,

particularly at high inspiratory flow rates. Thirdly, the

positive airway pressures used (PEEP and CPAP) after

the lung recruitment manoeuvre may have been too low;

10 cm H2O is greater than or equal to that shown to be

effective during previous studies at other periods ofanesthesia6 11 and was the maximum level we felt we

could use without risking clinically unacceptable cardio-

vascular depression. Fourthly, we did not apply CPAP by

a facemask after extubation. It was hoped that after extuba-

tion, normal vocal fold function would quickly return and

provide auto-CPAP by the normal physiological mechan-

ism of vocal fold adduction during expiration, which

retards expiration to reduce pulmonary collapse.13 It seems

that this aspect of respiratory muscle activity may not

return immediately after extubation. Finally, the

mechanism of atelectasis at the end of anaesthesia may

differ from that so widely studied at other times. When a

patient attempts to cough with a tracheal tube in situ, an

unphysiological phenomenon occurs. A normal cough has

three phases: an inspiratory phase when lung volume is

increased, a compressive phase when there is a forced

expiration against a closed glottis, and an expulsive phasewhen the glottis is quickly opened and extremely high

expiratory flows generated. This differs from the expiration

reflex which occurs after direct stimulation of the upper

airway and involves only the last two phases of the cough

reflex.14 Both these protective reflexes are likely to be

active immediately before extubation, and both will be

ineffective due to the inability of the glottis to close for

the compressive phase. Instead, the expiratory muscles

will be contracting strongly against an open airway, so

actively reducing lung volume to very low levels, encoura-

ging pulmonary collapse. Although only occurring for a

short time, the positive intrathoracic pressure generated

during the compressive phase of a cough is very high, and

therefore, our strategy of 10 cm H2O positive airway

pressure will have had no impact on ameliorating the

effects of the cough reflex on lung collapse.

Our study shows that lung recruitment manoeuvres that

have been shown to improve atelectasis temporarily may

not provide a benefit that persists into the postoperative

period.

The patients we studied may have influenced the poor

oxygenation observed. In order to be included in the

study, all patients were required to have an arterial line

inserted on clinical grounds and so were mostly ASA II or

III having major and prolonged surgery, and therefore careshould be taken when applying our results to other patient

populations.

CT is the best technique for quantifying atelectasis but

this is impossible during surgery, and is difficult in the early

postoperative period when close monitoring is required. We

therefore used (A a)DO2 as a surrogate marker of the sever-

ity of atelectasis, allowing an assessment to be made at both

the time points in which we were interested.

We did not document whether individual patients

coughed, or to what extent, so are unable to comment

40

Intervention

30

(Aa)DO2(kPa)

20

10

0Randomization PACU

40

Standard

30

(Aa)DO2(kPa)

20

10

0Randomization PACU

Fig 2 Individual patients (A a)DO2 at randomization and in PACU (post-anaesthesia care unit) for each treatment group.

Lumb et al.

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further on whether this mechanism could explain our

results. However, it is interesting to speculate whether the

trend in recent years to extubate patients when awake

enough to protect their airway from aspiration may be

causing widespread impairment of lung function in the

postoperative period.

In order to prevent the significantly impaired oxygen-

ation that occurs in PACU, further research is needed bothto elucidate the mechanism of atelectasis on emergence

from anaesthesia and to evaluate more invasive clinical

strategies.

Future studies using ventilators specifically designed to

offer CPAP while spontaneously breathing, or iatrogenic

CPAP immediately after extubation, may prove effective

in reducing atelectasis. CPAP has been shown to be an

effective treatment once postoperative hypoxia has devel-

oped,15 but a functional seal between the mask and patient

may be difficult to achieve immediately post-extubation.

In conclusion, the use of a recruitment manoeuvre and

positive airway pressure strategy, which is effective in pre-

venting atelectasis on induction and during anaesthesia,has not been shown to improve oxygenation after operation

when used on emergence from anaesthesia and therefore

cannot be recommended.

Conflict of interest

None declared.

Funding

All funding was from departmental sources.

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