Effects of Alveolar Recruitment on Arterial Oxygenation in Patients After Cardiac Surgery: A Prospective, Randomized, Controlled Clinical Trial

Effects of Alveolar Recruitment on Arterial Oxygenation in Patients After Cardiac Surgery: A Prospective, Randomized, Controlled Clinical Trial Leonid Minkovich, MD, PhD, George Djaiani, MD, FRCA, Rita Katznelson, MD, Fergal Day, MD, Ludwik Fedorko, MD, PhD, Jens Tan, MD, Jo Carroll, RN, Davy Cheng, MD, FRCPC, and Jacek Karski, MD, FRCPC Objective: Pulmonary atelectasis and hypoxemia remain considerable problems after cardiac surgery. The objective of this study was to determine the efficacy of consecutive vital capacity maneuvers (C-VCMs) to improve oxygenation in patients after cardiac surgery. Study Design: Randomized, controlled clinical trial. Setting: Tertiary referral teaching center. Participants: Ninety-five patients requiring elective cardiac surgery with cardiopulmonary bypass (CPB). Intervention: Patients were randomly allocated to either C-VCM or control groups. In the C-VCM group, lung inflation at pressure of 35 cmH2O was sustained for 15 seconds before separation from CPB and at 30 cmH2O for 5 seconds after admission to the intensive care unit (ICU). Measurements and Main Results: The primary outcome was the ratio of arterial oxygen tension to inspired oxygen

fraction measured at the following predetermined time intervals: after induction of anesthesia, 15 minutes after separation from CPB, after admission to the ICU, after 3 hours of positive-pressure ventilation, after extubation, and before ICU discharge. C-VCM resulted in better arterial oxygenation extending from the immediate postoperative period to approximately 24 hours after surgery at the time of ICU discharge. There were no significant adverse events related to C-VCM application. Conclusion: C-VCM is an effective method to reduce hypoxemia associated with the formation of atelectasis after cardiac surgery with CPB. © 2007 Elsevier Inc. All rights reserved.

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mg/kg/h and isoflurane. After completion of surgery, patients were transferred to the cardiac intensive care unit (ICU). Propofol infusion was continued until extubation criteria were fulfilled. All patients underwent median sternotomy. Management of CPB included systemic temperature drift to 33°C to 34°C, alpha-stat pH management, mean perfusion pressure between 50 and 70 mmHg, pump flow rates of 2.0 to 2.4 L/min/m2, and hematocrit ⬎20%. A 32-␮m filter (Avecor Affinity, Minneapolis, MN) was used in the arterial perfusion catheter. Before separation from CPB, patients were rewarmed to 36°C to 37°C. Mechanical ventilation was terminated during CPB. The lungs were deflated, and the endotracheal tube was left connected to the anesthesia machine with fresh gas flow of air at 1 L/min. Positive end-expiratory pressure (PEEP) was not applied during CPB. Before separation from CPB, the C-VCM group received sustained manual lung inflation at a pressure of 35 cmH2O for 15 seconds with an FIO2 of 0.4. The second VCM was administered within 20 to 30 minutes after arrival in the ICU. The lungs were inflated by using the CPAP mode of the ICU ventilator (FIO2 0.4). Duration and inflation pressure of the second VCM were limited to 30 cmH2O for 5 seconds. It was decided to limit inspiratory pressure and duration of the second VCM to avoid potential adverse hemodynamic effects related to persistently elevated intrathoracic pressure. The control group received standard management including re-establishment of mechanical ventilation before separation from CPB. Patients in both groups were managed according to a standard fast-track protocol postoperatively.10 During the transfer from the operating room to the ICU, all patients were manually ventilated by an

ETERIORATION IN ARTERIAL oxygenation is common after cardiac surgery with cardiopulmonary bypass (CPB). Although the causes of postoperative hypoxemia are multifactorial, the formation of atelectasis appears to be the primary factor responsible for increased intrapulmonary shunt after cardiac surgery with CPB.1-4 Experimental animal studies have shown that vital capacity maneuver (VCM) (ie, sustained lung inflation for 15 seconds at maximum pressure of 40 cmH2O) appeared to abolish formation of atelectasis after CPB.5,6 In human trials, a VCM administered at completion of CPB decreased intrapulmonary shunt; however, this improvement in oxygenation was limited only to a few hours postoperatively.7-9 Consequently, it was hypothesized that application of consecutive vital capacity maneuvers (C-VCMs) would result in improved oxygenation beyond the immediate postoperative period in patients undergoing elective cardiac surgery with CPB. METHODS After institutional review board approval, informed consent was obtained from all participants. Patients undergoing elective primary coronary artery bypass graft surgery with CPB or single-valve repair/ replacement surgery were randomly allocated to 1 of 2 groups: group C-VCM (consecutive vital capacity maneuver) and group C (controls). Computer-generated randomization code in blocks of 4 was used for group assignment. Patients undergoing emergency or redo surgery; patients requiring chest re-exploration in the immediate postoperative period; patients with preoperative congestive heart failure, cardiogenic shock, requiring inotropic and/or intra-aortic balloon pump supports; patients who were unstable hemodynamically at the time of ICU admission; patients requiring prolonged mechanical ventilation for reasons other than respiratory failure; patients with chronic obstructive lung disease; and patients with significant sleep apnea requiring continuous positive airway pressure support were excluded. Premedication was standardized to lorazepam, 2 to 4 mg sublingually, 1 hour before surgery. Anesthesia was induced with midazolam, 0.05 mg/kg, fentanyl, 10 to 15 ␮g/kg, and propofol, 0.5 to 1 mg/kg. Pancuronium, 0.1 mg/kg, was administered to facilitate tracheal intubation. Anesthesia was maintained with a propofol infusion at 1 to 4

KEY WORDS: postoperative atelectasis, prevention of hypoxemia, lung recruitment, cardiac surgery, cardiopulmonary bypass

From the Department of Anesthesia and Pain Management, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada. Address reprint requests to George Djaiani, MD, FRCA, Department of Anesthesia and Pain Management, Toronto General Hospital, 200 Elizabeth Street, 3EN-410, Toronto, Ontario M5G 2C4, Canada. E-mail: [email protected] © 2007 Elsevier Inc. All rights reserved. 1053-0770/07/2103-0010$32.00/0 doi:10.1053/j.jvca.2006.01.003

Journal of Cardiothoracic and Vascular Anesthesia, Vol 21, No 3 (June), 2007: pp 375-378

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Ambu-type resuscitation bag (Ambu SPUR; Ambu Inc, Linthicum, MD) with FIO2 equal to 1.0 and no PEEP. At the ICU admission, mechanical ventilation of the lungs was started with a 760 Ventilator System (Nellcor Puritan Bennett Inc, Pleasanton, CA), using the volume-targeted, assist-control mode. Initial ventilator parameters were set at a tidal volume of 8 to 10 mL/kg, a respiratory rate of 12 to 14/min, PEEP of 5 cmH2O, an inspiratory trigger of 1 L/min of inspiratory flow, and an FIO2 of 0.5. The peak inspiratory flow was initially set at 50 L/min and adjusted subsequently to maintain inspiratory-expiratory ratio of 1:2. Increments of 2 cmH2O of PEEP until 10 cmH2O, with subsequent increments of FIO2, were used to achieve the SaO2 ⬎92%. Pressure support mode of ventilation (PSV) was applied to wean all patients from mechanical ventilation. Extubation was performed if the patient was hemodynamically stable, fully awake, with no signs of respiratory distress and/or clinically significant hypoxemia after one hour of minimal respiratory support (5 cmH2O and PEEP of 5 cmH2O). Glycopyrrolate (0.005 mg/kg) and neostigmine (0.035 mg/ kg) were used to reverse neuromuscular blockade in all patients. After extubation, the physiotherapist provided hourly vigorous chest physiotherapy to all patients. Deep breathing, coughing exercises, incentive spirometry, and early ambulation of patients after surgery were parts of the standard fast-track protocol. All patients received oxygen by Venturi-type oxygen mask (Airlife; Cardinal Health Inc, McGaw Park, IL) with FIO2 ranging from 0.24 to 0.5. Patients who required higher FIO2 were managed with high oxygen flows system (DHD Healthcare Corporation, Wampsville, NY) that provided FIO2 in a range of 0.6 to 0.95. The primary outcome was the ratio of arterial oxygen tension to inspired oxygen fraction (PaO2/FIO2). This ratio is an accepted parameter allowing for comparison of oxygenation between patients who receive a wide range of FIO2. It was measured at the following predetermined time intervals: (1) in the operating room 10 to 15 minutes after intubation of the trachea and establishment of mechanical ventilation, (2) 15 minutes after separation from CPB, (3) immediately after arrival in the ICU, (4) 3 hours after ICU admission (while mechanical ventilation was still in progress), (5) 30 minutes after tracheal extubation, and (6) immediately before ICU discharge. The secondary outcomes were duration of mechanical ventilation, ICU, and hospital length of stay. The data are presented as mean ⫾ standard deviation if not otherwise stipulated. Differences in continuous data between the 2 groups were analyzed by using unpaired, 2-tailed Student t test after conformation of the normal distribution of the data. Differences in nominal values were analyzed by using chi-square test. Comparison of PaO2/FIO2 values between the C-VCM and control groups was analyzed with repeatedmeasures analysis of variance. A p value ⬍0.05 was considered statistically significant. Mann-Whitney U test was used to compare duration of mechanical ventilation, ICU, and hospital length of stay. RESULTS

A total of 104 patients were enrolled in the study. Nine patients were excluded (5 from R-VCM and 4 from control groups); 5 patients underwent resternotomy to control postoperative bleeding, 2 patients required prolonged mechanical ventilation because of cardiogenic shock requiring intra-aortic balloon pump, and 2 suffered perioperative stroke. The remaining 95 patients completed the study and were followed until discharge from the hospital. Both groups were similar with respect to their demographic data and surgical characteristics (Table 1). VCMs were accomplished successfully in all patients. Minor reduction in systolic blood pressure (⬍15% of baseline value) was encountered during application of the second VCM in all

Table 1. Demographic Data and Surgical Characteristics

Age (y) Males, n (%) Body weight (kg) Height (cm) Body surface area (m2) Body mass index (kg/m2) Left ventricular grade (Grade 1-4)* Smokers, n (%) Coronary artery bypass surgery, n (%) Valvular surgery, n (%) Duration of cardiopulmonary bypass (min) Duration of aortic crossclamp (min)

C-VCM Group (n ⫽ 47)

Control Group (n ⫽ 48)

p Values

62 ⫾ 11 39 (83) 81 ⫾ 18 172 ⫾ 11 1.96 ⫾ 0.3 27.2 ⫾ 4.3

62 ⫾ 10 41 (85) 80 ⫾ 15 171 ⫾ 8 1.93 ⫾ 2.0 27.3 ⫾ 4.7

0.65 0.34 0.71 0.45 0.32 0.66

1.7 ⫾ 0.7 18 (38)

1.6 ⫾ 0.7 19 (40)

0.43 0.54

39 (83) 8 (17)

41 (85) 7 (15)

0.57 0.44

84 ⫾ 23

88 ⫾ 21

0.29

66 ⫾ 28

70 ⫾ 22

0.31

NOTE. Data are presented as mean ⫾ SD or number of patients (percentage). *LV Grading; Grade 1 (LV ejection fraction [EF] ⬎60%; Grade 2, EF 41%-60%; Grade 3, EF 20%-40%; Grade 4, EF ⬍20%).

patients; however, it was self-limiting and returned to baseline within a few seconds after termination of VCM. All patients remained in sinus rhythm during and immediately after VCM. Tidal volume, respiratory rate, PaCO2, peak and mean airway pressures, and amount of PEEP were similar between the 2 groups during the study period. Compared with the control group, application of C-VCM was associated with significantly higher values of PaO2/FIO2 ratio and, thus, better oxygenation after separation from CPB, 3 hours after ICU admission, and before ICU discharge (Fig 1). Duration of mechanical ventilation, ICU and hospital length of stay were comparable between the 2 groups (Table 2). DISCUSSION

The main finding of this study is that consecutive VCM resulted in better arterial oxygenation extending from the immediate postoperative period to approximately 24 hours after surgery, at the time of ICU discharge. Impaired arterial oxygenation after cardiac surgery is a wellrecognized problem.1-3 Multiple mechanisms are responsible for acute lung injury after CPB. Oxidant-mediated lung damage as a sequela of ischemia-reperfusion injury; adhesion and sequestration of neutrophils; activation of complement; and mediators of inflammatory cascade such as tumor necrosis factor, interleukins 1, 6, 8, and 10, and thromboxane A24,11-13 may play a major role in development of postoperative lung injury. Even though the precise mechanisms of CPB-related acute lung injury are still unknown, a formation of collapsed unstable alveolar units1,13 is the final pathway of this type of lung injury that clinically manifests as atelectasis, increased intrapulmonary shunt, and hypoxemia. As many as 64% of patients have radiologically confirmed atelectasis after CPB.4,14 Although general anesthesia and intrathoracic surgical intervention alone are associated with increased risk of atelectasis,15-17 Magnusson

ALVEOLAR RECRUITMENT

377

500

*

*

*

PO2/F I O2

400 300 200 100 0 1

2

3

4

5

6

Time Points Control

VCM

Fig 1. Comparison of PaO2/FIO2 ratio between the repeated vital capacity maneuver (C-VCM) and control groups. Measurements were taken at the following predetermined time intervals: (1) operating room after tracheal intubation, (2) 10 to 15 minutes after separation from cardiopulmonary bypass, (3) after arrival in the ICU, (4) 3 hours after ICU admission, (5) 30 minutes after tracheal extubation, and (6) immediately before ICU discharge. *Significant differences.

et al5,6 showed that CPB played a leading role in formation of atelectasis after cardiac surgery. Different techniques have been proposed to diminish postCPB atelectasis with no apparent success.4,18 Mechanical ventilation of the lungs18-20 or continuous positive airway pressure during CPB with different FIO2 have proven to be of limited or no benefit.21-23 Several experimental and clinical trials have shown that alveolar recruitment strategy is an effective and safe method to resolve atelectasis related to general anesthesia.15-17 It consists of combination of VCM applied to recruit collapsed alveoli and followed by application of PEEP to stabilize compromised lungs units. In a pig model, repeated VCM abolished formation of atelectasis after CPB.5,6 Although 2 recent clinical trials showed that single application of VCM before separation from CPB initially improved oxygenation,7,8 this improvement could not be sustained beyond 1 hour after ICU admission. Tschernko et al9 showed longer improvement in oxygenation in a small group of patients in whom 3 consecutive VCM maneuvers were applied immediately before termination of CPB.9 In contrast with previous clinical trials, the authors studied the effect of VCM on oxygenation in a relatively large group of patients. Moreover, consecutive VCMs were used, first, before separation from CPB and, second, after arrival in ICU. This distinction is important because during the transfer from the operating room to the ICU patients often receive manual ventilation with an FIO2 equal to 1.0 and no PEEP. This type of practice, which is accepted in many institutions, may predispose to development of derecruitment of compromised lung units and recurrence of atelectasis. It corresponds with the results of this trial as well as other studies.7,8 Application of a second VCM (despite the fact that it was limited in pressure and duration) appeared to be sufficient in preserving better oxygenation not only after separation from CPB but also 3 hours after ICU admission while mechanical ventilation was still in progress. However, there was no difference in the PO2/FIO2 ratio between the 2 groups immediately after extubation.

This finding agrees with the results from previous clinical trials that found no benefit of VCM beyond tracheal extubation.7,8 Cessation of positive-pressure ventilation may cause collapse of unstable alveolar units and thus deterioration in oxygenation. However, it was found that at the time of ICU discharge, the C-VCM group had a significantly higher PO2/FIO2 ratio reflecting faster recovery of lung function in this group of patients. “Atelectotrauma” is a well-recognized mechanism contributing to development of acute lung injury because of the cyclic “opening-closing” of unstable lung units. Partially atelectatic, asymmetrically stretched lung units are most vulnerable. They locate in segments opposed to fully collapsed lungs and are prone to cyclic recruitment and derecruitment with creation of shear stress that cause tangential distortion of the cell membranes.24,25 The authors suggest that patients in the C-VCM group developed less atelectasis, less lung injury, and thus faster recovery. Pasquina et al26 found that noninvasive pressure-support ventilation applied 4 times a day for 30 minutes after tracheal extubation preserves oxygenation in patients after cardiac surgery. It is possible that a combination of C-VCM strategy with noninvasive pressure support ventilation may be an optimal approach in management of pulmonary dysfunction after cardiac surgery. However, this hypothesis would need to be explored in subsequent studies. The present study has several limitations. First, the authors studied a group of patients who underwent either elective coronary artery bypass graft surgery or single-valve repair/replacement surgery with relatively short duration of CPB. Consequently, the results of this study are limited to this particular group of patients. Second, the duration (5 seconds) and inflation pressure (30 cmH2O) of the second VCM applied immediately after ICU admission were limited because of the potential of hemodynamic compromise related to a sustained increase in intrathoracic pressure.27 As a result, all patients in this study tolerated VCM well without any significant cardiovascular side effects. In a recent study, Dyhr et al28 used an alveolar recruitment maneuver in ICU patients after cardiac surgery inflating lungs for 10 seconds with inspiratory pressures as high as 45 cmH2O. No adverse cardiac effects were reported. Consequently, increasing duration and/or inspiratory pressure of VCM may enhance its efficacy in resolving atelectasis. However, the risk/benefit ratio of this approach should be evaluated in further studies. Furthermore, there is a theoretic risk of stretching a left internal mammary artery graft during the lung recruitment maneuver, although the actual incidence of this is unknown. Good communication between surgeon and anesthesiologist is critical to avoid this complication. The authors success-

Table 2. Comparison of Intubation Times and Length of Stay Between the C-VCM and Control Groups

Intubation time (h) ICU-LOS (h) Hospital-LOS (d)

C-VCM Group (n ⫽ 47)

Control Group (n ⫽ 48)

p Value

5.2 (2-19) 22.0 (13-48) 7.0 (4-11)

6.0 (3-32) 22.5 (18-72) 7.1 (5-21)

0.28 0.06 0.36

NOTE. Data are presented as median (range). Abbreviations: LOS, length of stay; ICU, intensive care unit; NS, not significant.

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fully accomplished a vital capacity maneuver in all patients with no consequence to left internal mammary artery grafts. However, it is likely that more caution should be exercised in patients with preoperative pulmonary comorbidities. Third, the study period was limited to 24 hours after surgery; the usual ICU length of stay in the fast-track cardiac surgery setting. Consequently, the authors did not evaluate the primary outcome beyond the 24-hour period. Although Shenkman et al29 found that maximum deterioration in oxygenation occurred during the second day after cardiac surgery, the study was performed before the fast-track protocol was introduced into clinical practice and thus their results would not be applicable to the present clinical setting. Further studies should also address the impact of VCM on clinical outcomes after cardiac surgery. Incidence of pneumonia, acute respiratory distress syndrome, and other respiratory compli-

cation after uncomplicated cardiac surgery is reported in the range of 0.8% to 2%, whereas patients with preoperative pulmonary dysfunction and patients undergoing complicated cardiac surgery requiring prolonged CPB (more than 140 minutes) and/or massive blood transfusions have considerably higher risk of pulmonary complications, ranging from 7% to 20%.4,11,12,30 Thus, further studies should be adequately powered to determine whether VCM improves clinically relevant outcomes. In summary, consecutive VCM applied before separation from CPB and immediately after ICU admission improves oxygenation after elective cardiac surgery. VCM is a safe and simple method that attenuates formation of atelectasis associated with general anesthesia and CPB. Application of consecutive VCM may have significant clinical implications as part of a multimodal approach in management of acute lung dysfunction after cardiac surgery.

REFERENCES 1. Magnusson L, Zemgulis V, Wicky S, et al: Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: An experimental study. Anesthesiology 87:1153-1163, 1997 2. Johnson D, Hurst T, Thomson D, et al: Respiratory function after cardiac surgery. J Cardiothorac Vasc Anesth 10:571-577, 1996 3. Taggart DP, El-Fiky M, Carter R, et al: Respiratory dysfunction after uncomplicated cardiopulmonary bypass. Ann Thorac Surg 56: 1123-1128, 1993 4. Weissman C: Pulmonary complications after cardiac surgery. Semin Cardiothorac Vasc Anesth 8:185-211, 2004 5. Magnusson L, Wicky S, Tyden H, et al: Repeated vital capacity manoeuvres after cardiopulmonary bypass: Effects on lung function in a pig model. Br J Anaesth 80:682-684, 1998 6. Magnusson L, Zemgulis V, Tenling A, et al: Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass: an experimental study. Anesthesiology 88:134-142, 1998 7. Murphy GS, Szokol JW, Curran RD, et al: Influence of a vital capacity maneuver on pulmonary gas exchange after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 15:336-340, 2001 8. Claxton BA, Morgan P, Mckeague H, et al: Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass. Anaesthesia 58:111-116, 2003 9. Tschernko EM, Bambazek A, Wisser W, et al: Intrapulmonary shunt after cardiopulmonary bypass: The use of vital capacity maneuvers versus off-pump coronary artery bypass grafting. J Thorac Cardiovasc Surg 124:732-738, 2002 10. Cheng DC, Karski J, Peniston C, et al: Early tracheal extubation after coronary artery bypass graft surgery reduces costs and improves resource use. Anesthesiology 85:1300-1310, 1996 11. Rady MY, Ryan T, Starr NJ: Early onset of acute pulmonary dysfunction after cardiovascular surgery: Risk factors and clinical outcome. Crit Care Med 25:1831-1839, 1997 12. Milot J, Perron J, Lacasse Y, et al: Incidence and predictors of ARDS after cardiac surgery. Chest 119:884-888, 2001 13. Matuschak GM: Pulmonary dysfunction after surgery involving cardiopulmonary bypass: Do we understand the mechanisms? Crit Care Med 25:1778-1780, 1997 14. Jain V, Rao TL, Kumar P, et al: Radiographic pulmonary abnormalities after different types of cardiac surgery. J Cardiothorac Vasc Anesth 5:592-595, 1991 15. Rothen HU, Sporre B, Engberg G, et al: Prevention of atelectasis during general anaesthesia. Lancet 345:1387-1391, 1995

16. Magnusson L, Tenling A, Lemoine R, et al: The safety of one, or repeated, vital capacity maneuvers during general anesthesia. Anesth Analg 91:702-707, 2000 17. Tusman G, Bohm SH, Vazquez de Anda GF, et al: “Alveolar recruitment strategy” improves arterial oxygenation during general anaesthesia. Br J Anaesth 82:8-13, 1999 18. Wall MH, Royster RL: Pulmonary dysfunction after cardiopulmonary bypass: Should we ventilate the lungs on pump? Crit Care Med 28:1658-1660, 2000 19. Stephan L, Kalweit G, Tarnow J: Effects of ventilation and nonventilation on pulmonary venous blood gases and markers of lung hypoxia in humans undergoing total cardiopulmonary bypass. Crit Care Med 28:1336-1340, 2000 20. Cogliati AA, Menichetti A, Tritapepe L, et al: Effects of three techniques of lung management on pulmonary function during cardiopulmonary bypass. Acta Anaesthesiol Belg 47:73-80, 1996 21. Berry CB, Butler PJ, Myles PS: Lung management during cardiopulmonary bypass: Is continuous positive airway pressure beneficial? Br J Anaesth 71:864-868, 1993 22. Loeckinger A, Kleinsasser A, Lindner KH, et al: Continuous positive airway pressure at 10 cm H2O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg 91:522-527, 2000 23. Magnusson L, Zemgulis V, Wicky S, et al: Effect of CPAP during cardiopulmonary bypass on postoperative lung function: An experimental study. Acta Anaesthesiol Scand 42:1133-1138, 1998 24. Suh GY, Koh Y, Chung MP, et al: Repeated derecruitments accentuate lung injury during mechanical ventilation. Crit Care Med 30:1848-1853, 2002 25. Pinhu L, Whitehead T, Evans T, et al: Ventilator-associated lung injury. Lancet 361:332-340, 2003 26. Pasquina P, Merlani P, Granier JM, et al: Continuous positive airway pressure versus noninvasive pressure support ventilation to treat atelectasis after cardiac surgery. Anesth Analg 99:1001-1008, 2004 27. Pinsky MR: The hemodynamic consequence of mechanical ventilation: An evolving story. Intensive Care Med 23:493-503, 1997 28. Dyhr T, Nygard E, Laursen N, et al: Both lung recruitment maneuver and PEEP are needed to increase oxygenation and lung volume after cardiac surgery. Acta Anaesthesiol Scand 48:187-197, 2004 29. Shenkman Z, Shir Y, Weiss YG, et al: The effects of cardiac surgery on early and late pulmonary function. Acta Anaesthesiol Scand 41:1193-1199, 1997 30. Cavner CC, Chanda J: Intraoperative and postoperative risk factors for respiratory failure after coronary bypass. Ann Thorac Surg 75:855-858, 2003