British Journal of Anaesthesia 104 (5): (2010) doi: /bja/aeq080 Advance Access publication March 30, 2010

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1 RESPIRATION AND THE AIRWAY Lung recruitment and positive airway pressure before extubation does not improve oxygenation in the post-anaesthesia care unit: a randomized clinical trial A. B. Lumb 1, S. J. Greenhill 12, M. P. Simpson 1 * and J. Stewart 1 1 St James s University Hospital, Leeds Teaching Hospitals NHS Trust, Beckett Street, Leeds LS9 7TF, UK. 2 Present address: The Queen Elizabeth Hospital, Gayton Road, King s Lynn PE30 4ET, UK *Corresponding author. mpsimpson@doctors.org.uk Background. Atelectasis is known to develop during anaesthesia and after operation atelectasis 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 oxygenation 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 H 2 Ofor15 s, 30 min before the end of anaesthesia, followed by 10 cm H 2 O of PEEP and then 10 cm H 2 Oof CPAP from return of spontaneous breathing until extubation; or no lung recruitment manoeuvre, 5 cmh 2 O PEEP, and no CPAP. Arterial blood gases were taken at randomization and 1 h after extubation. The primary endpoint of the study was the change in (A a)do 2 between these times. Statistical analysis of the two groups was done by x 2 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 (A a)do 2 between the groups (P¼0.82). 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 Identification number: ISRCTN ( Br J Anaesth 2010; 104: British Journal of Anaesthesia 104 (5): (2010) doi: /bja/aeq080 Advance Access publication March 30, 2010 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 IPPV 1 2 and, along with altered ventilation perfusion relationships, causes an increase in alveolar to arterial oxygen partial pressure difference (A a)do 2. 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 positive end-expiratory pressure (PEEP) and the avoidance of high inspired oxygen fractions (FI O2 ). 5 6 Once formed, atelectatic lung regions may be effectively recruited by maintaining a sustained airway pressure of 40 cmh 2 O 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 journals.permissions@oxfordjournal.org

2 Lumb et al. 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 oxygenation does not persist into the postoperative period. 9 If an intraoperative recruitment manoeuvre is followed by the use of 10 cm H 2 O of PEEP, atelectasis is prevented from recurring even in the presence of a high FI O2. 9 We hypothesized that if positive airway pressure were maintained after a recruitment manoeuvre and throughout emergence 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 limiting (APL) valve to generate continuous positive airway pressure (CPAP). We tested the hypothesis that by performing a recruitment manoeuvre near the end of the anaesthetic followed by PEEP and then CPAP until extubation, the (A a)do 2 1 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 (Identification number: ISRCTN ). 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 procedures 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 there was any contraindication to the use of 10 cm H 2 O of PEEP or the recruitment manoeuvre or the clinical requirement for the use of.5 cmh 2 O of intraoperative PEEP. Patients were also excluded if any perioperative cardiovascular 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 FI O2 of , PEEP 5 cmh 2 O, tidal volume 7 10 ml kg 21, and ventilatory frequency as appropriate to maintain end-tidal carbon dioxide partial pressure of kpa. Thirty minutes before the anticipated end of the anaesthetic, an arterial blood sample was obtained for measurement of arterial PO 2 and PCO 2, and the FI O2 was recorded. The patients 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 anaesthesia, patients in the intervention group received a lung recruitment manoeuvre consisting of lung inflation to an airway pressure of 40 cm H 2 O sustained for 15 s. Immediately after this recruitment manoeuvre, ventilation continued as previously but with PEEP increased to 10 cm H 2 O. IPPV continued at the same rate until evidence of return of spontaneous ventilation. At this point, CPAP was maintained at 10 cm H 2 O by adjusting the APL valve and providing a fresh gas flow of.10 litre min 21 to maintain the positive airway pressure during inspiration. Circuit disconnection 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 settings including any intraoperative PEEP (5 cmh 2 O). No CPAP 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 FI O2 was set to 1.0 with fresh gas flow exceeding 10 litre min 21 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 FI O2 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 PO 2 and PCO 2. The (A a)do 2 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 as described above. Alveolar PO 2 was calculated using the following version of the alveolar gas equation: alveolar P O2 ¼ PI O2 Pa CO 2 RQ ð1 FI O 2 ð1 RQÞÞ RQ assumed to be 0.8. The standard deviation (SD) of(a a)do 2 for the purposes of the power calculation was derived from preinduction values in a previous study of a similar population 644

3 Lung recruitment and (A a)do 2 in PACU Consented, n = 52 Randomized, n = 47 Operation cancelled, n = 2 Investigator unavailable, n = 1 Required PEEP >5 cm H 2 O, n = 2 Allocated to standard group, n = 23 Received allocated treatment, n = 23 Allocated to intervention group, n = 24 Received allocated treatment, n = 22 Protocol violation circuit disconnection, n = 2 Lost to follow-up, n = 0 Required F I O2 >0.4 in PACU, n = 1 Lost to follow-up, n = 0 Discontinued intervention, n = 0 Analysed, n = 22 Excluded from analysis, n = 1 Analysed, n = 22 Excluded from analysis, n = 2 Fig 1 Consort flow chart showing patients progress through the trial. (3.91 kpa). 9 A significance level for the study of 5% (P¼0.05) and a power of 80% were used for the calculation. 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 x 2 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 arterial gases at randomization and in PACU (Table 1). The mean (SD) (A a)do 2 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)do 2 between randomization and PACU displayed no particular pattern (Fig. 2). Using each patient as their own control, the mean change in (A a)do 2 was 1.98 (6.52) in the standard group and 1.52 (6.71) in the intervention group (P¼0.82). 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)do 2 and that this 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)do 2. None of the factors differed significantly between the groups, P 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/m 2 ) 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 15/4/3 Duration of surgery (min) 255 (150) 319 (122) (A a)do 2 at randomization (kpa) 12.5 (8.7) 12.1 (8.4) FI O2 at randomization (0.119) (0.094) Arterial PCO 2 at randomization (kpa) 5.59 (0.72) 5.53 (0.80) Arterial PCO 2 in PACU (kpa) 5.77 (0.61) 5.70 (0.37) 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)do 2 in PACU. In the usual absence of a significant alveolar to pulmonary capillary diffusion barrier, abnormalities of (A a)do 2 result from intrapulmonary shunting and areas of lung with low ventilation perfusion ratios. 10 During anaesthesia, 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)do 2 are mostly secondary to the development of atelectasis. Our results are comparable with a previous study which also used (A a)do 2 as a marker of atelectasis, 9 and demonstrate high (A a)do 2 values at the end of the 645

4 Lumb et al. Intervention Standard (A a)do 2 (kpa) (A a)do 2 (kpa) Randomization PACU 0 Randomization PACU Fig 2 Individual patients (A a)do 2 at randomization and in PACU (post-anaesthesia care unit) for each treatment group. 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, particularly during anaesthesia, results which are again comparable with the previous study, 9 which also studied the effects of manual inflations every 30 min throughout surgery and before extubation. Although details of the manual inflation used and how long before extubation it was applied are not clear, they, like us, failed to demonstrate any beneficial effect on (A a)do 2 in PACU. It is known that CPAP at induction prevents the formation of atelectasis 11 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 recovery period. Our results show that our management strategy, used at the end of anaesthesia, has not provided a significant improvement in patient oxygenation in PACU. There are a number of possible explanations for this. First, (A a)do 2 may be affected by the FI O2 or the arterial PCO 2, 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 H 2 O is greater than or equal to that shown to be effective during previous studies at other periods of anesthesia 6 11 and was the maximum level we felt we could use without risking clinically unacceptable cardiovascular depression. Fourthly, we did not apply CPAP by a facemask after extubation. It was hoped that after extubation, normal vocal fold function would quickly return and provide auto-cpap by the normal physiological mechanism 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 phase when 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, encouraging 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 H 2 O 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 care should 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)do 2 as a surrogate marker of the severity 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 646

5 Lung recruitment and (A a)do 2 in PACU 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 oxygenation that occurs in PACU, further research is needed both to 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 developed, 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 preventing 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. References 1 Warner DO, Warner MA, Ritman EL. Atelectasis and chest wall shape during halothane anesthesia. Anesthesiology 1996; 85: Lundquist H, Hedenstierna G, Strandberg A, Tokics L, Brismar B. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995; 36: Strandberg A, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Atelectasis during anaesthesia and in the postoperative period. Acta Anaesthesiol Scand 1986; 30: Duggan M, Kavanagh BP. Pulmonary atelectasis. A pathogenic perioperative entity. Anesthesiology 2005; 102: Rothen HU, Sporre B, Engberg G, Wegenius G, Högman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a re-expansion manoeuvre during general anaesthesia. Anesthesiology 1995; 82: Neumann P, Rothen HU, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 1999; 43: Rothen HU, Neumann P, Berglund JE, Valtysson J, Magnusson A, Hedenstierna G. Dynamics of re-expansion of atelectasis during general anaesthesia. Br J Anaesth 1999; 82: Magnusson L, Tenling A, Lemoine R, Högman M, Tydén H, Hedenstierna G. The safety of one, or repeated, vital capacity maneuvres during general anesthesia. Anesth Analg 2000; 91: Clarke JP, Schuitemaker MN, Sleigh JW. The effect of intraoperative ventilation strategies on perioperative atelectasis. Anaesth Intensive Care 1998; 26: Lumb AB. Distribution of pulmonary ventilation and perfusion. In: Lumb AB, ed. Nunn s Applied Respiratory Physiology, 6th Edn. Philadelphia: Elsevier Butterworth Heinemann, 2005; Rusca M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg 2003; 97: Kathirgamanathan A, McCahon RA, Hardman JG. Indices of pulmonary oxygenation in pathological lung states: an investigation using high-fidelity, computational modelling. Br J Anaesth 2009; 103: Lumb AB. Pulmonary ventilation. In: Lumb AB, ed. Nunn s Applied Respiratory Physiology, 6th Edn. Philadelphia: Elsevier Butterworth Heinemann, 2005; Tatar M, Hanacek J, Widdicombe J. The expiration reflex from the trachea and bronchi. Eur Respir J 2008; 31: Squadrone V, Coha M, Cerutti E, et al. Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. J Am Med Assoc 2005; 293: