JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gander, S.
Right arrow Articles by Magnusson, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gander, S.
Right arrow Articles by Magnusson, L.

Anesth Analg 2005;100:580-584
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000143339.40385.1B

GENERAL ARTICLES

Positive End-Expiratory Pressure During Induction of General Anesthesia Increases Duration of Nonhypoxic Apnea in Morbidly Obese Patients

Sylvain Gander, MD*, Philippe Frascarolo, PhD*, Michel Suter, MD{dagger}, Donat R. Spahn, MD*, and Lennart Magnusson, MD, PhD*

Departments of *Anesthesiology and {dagger}Surgery, University Hospital, Lausanne, Switzerland

Address correspondence and reprint requests to Lennart Magnusson, MD, PhD, Department of Anesthesiology, University Hospital, CHUV BH-10, CH-1011 Lausanne, Switzerland. Address e-mail to lennart.magnusson{at}chuv.hospvd.ch.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Positive end-expiratory pressure (PEEP) applied during induction of anesthesia prevents atelectasis formation and increases the duration of nonhypoxic apnea in nonobese patients. PEEP also prevents atelectasis formation in morbidly obese patients. Because morbidly obese patients have difficult airway management more often and because arterial desaturation develops rapidly, we studied the clinical benefit of PEEP applied during anesthesia induction. Thirty morbidly obese patients were randomly allocated to one of two groups. In the PEEP group, patients breathed 100% O2 through a continuous positive airway pressure device (10 cm H2O) for 5 min. After induction of anesthesia, they were mechanically ventilated with PEEP (10 cm H2O) for another 5 min until tracheal intubation. In the control group, the sequence was the same but without any continuous positive airway pressure or PEEP. We measured apnea duration until Spo2 reached 90% and we performed arterial blood gases analyses just before apnea and at 92% Spo2. Nonhypoxic apnea duration was longer in the PEEP group compared with the control group (188 ± 46 versus 127 ± 43 s; P = 0.002). Pao2 was higher before apnea in the PEEP group (P = 0.038). Application of positive airway pressure during induction of general anesthesia in morbidly obese patients increases nonhypoxic apnea duration by 50%.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Whatever the clinical preoperative evaluation, unexpected difficult airway may occur. Therefore, administration of 100% O2 has been a common practice for decades in order to increase the possible duration of nonhypoxic apnea, the so-called margin of safety. However, general anesthesia, even in the lung-healthy nonobese subject, causes an increase in intrapulmonary shunt (1), which may impair oxygenation (2). The magnitude of shunt is correlated with the formation of pulmonary atelectasis (3–5), which appears within minutes after induction of anesthesia (6) in 85%–90% of all patients (7). Atelectasis is larger in morbidly obese patients (8) or when a high fraction of inspired oxygen (Fio2) is used (9,10). Using low Fio2 during administration of O2 prevents atelectasis formation during induction of general anesthesia (10); however, this technique is not recommended because it reduces the duration of nonhypoxic apnea. Indeed, a recent study has shown that even Fio2 as high as 0.8 may prevent atelectasis formation but at the cost of a reduction in the duration of nonhypoxic apnea of 90 s (11).

We have previously shown that atelectasis formation can be effectively prevented by application of positive end-expiratory pressure (PEEP) during anesthesia induction despite the use of 100% O2 in nonobese patients (12). Moreover, the duration of nonhypoxic apnea is not only maintained but is increased from 8 to 10 min in nonobese patients with this technique (13).

Morbidly obese patients are at increased risk of difficult airway management (14,15) and, at the same time, their O2 reserve is decreased because they will develop much more atelectasis during induction of general anesthesia than nonobese patients (8). Consequently, the O2 reserve in morbidly obese patients is diminished (16). As we have shown that prevention of atelectasis formation by application of PEEP during induction is also effective in morbidly obese patients (17), it may be that this technique will also increase the duration of nonhypoxic apnea in these patients.

The aim of this study was therefore to evaluate the clinical benefit, in terms of duration of nonhypoxic apnea, of PEEP applied during the induction period of general anesthesia in morbidly obese patients.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After local ethics committee approval and written informed consent, 30 ASA physical status II–III patients aged 18–60 yr, with a body mass index (BMI) >35 kg/m2 and scheduled for elective surgery were enrolled in this prospective, single-blinded study and randomly assigned to 1 of 2 groups. The estimation of the sample size was based on previous studies (16). This size was calculated to detect a difference of 60 s of nonhypoxic apnea duration, accepting a type I error of 5% and type II error of 20%. Exclusion criteria were pregnancy, cardiac or pulmonary disease, and Spo2 at ambient air <94%. Patients were also excluded if they had known carotid stenosis, pulmonary hypertension, or a history of neurological disorder. Sleep apnea syndrome was not considered to be an exclusion criterion.

No patients received premedication before surgery. In the operating room, patients were positioned with pillows or towels under their shoulders, with their head elevated and neck extended. Routine monitoring was initiated and the same pulse oximetry (type F-CU8-22-05; Datex-Engstrom, Helsinki, Finland) was used for all patients. General anesthesia was induced with propofol (effect site target: 4 µg/mL), remifentanil (effect site target: 6 ng/mL), and cisatracurium (0.2 mg/kg). For maintenance, drugs were adjusted to obtain a clinically adequate depth of anesthesia and bispectral index between 40 and 50.

In the PEEP group, awake patients were administered 100% O2 through a continuous positive airway pressure (CPAP) device (Dräger CF800; Drägerwerk, Lübeck, Germany) set at 10 cm H2O for 5 min. After induction of anesthesia, patients were mechanically ventilated with the pressure-controlled mode (type A-ELEC 00; Datex-Engstrom 5/5, Bromma, Sweden) (pressure-controlled ventilation at 14 cm H2O, PEEP 10 cm H2O, respiratory rate 8/') for another 5 min until tracheal intubation.

In the control group, patients had the same induction technique but without any PEEP or CPAP. They breathed spontaneously through the CPAP device without any positive pressure. After induction of general anesthesia, they were mechanically ventilated with the same settings but without any PEEP.

After tracheal intubation, no pressure was applied to the airway and correct placement of the endotracheal tube was confirmed by fibroscopy. The endotracheal tube was left open to air at atmospheric pressure and the patient was left apneic until Spo2 reached 90%. Capnography was used to monitor involuntary breathing. Patients were then administered 100% O2 and the recruitment maneuver (increasing airway pressure to 40 cm H2O for 15 s) was applied until Spo2 reached initial values.

Nonhypoxic apnea was defined as the time needed to reach 90% Spo2 from the end of mechanical ventilation. Arterial blood gases were measured twice: first, just before the beginning of the period of apnea and, second, when Spo2 decreased to 92%.

Values were expressed as mean ± sd. Paired and unpaired Student’s t-test was used for comparisons within and between groups. {chi}2 was used to compare discrete variables. The Pearson product-moment correlation coefficient was calculated to assess the relationship between the duration of nonhypoxic apnea and other variables. P value < 0.05 was considered significant. The statistical package used was JMP (version 5.01; SAS Institute, Cary, NC).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Three patients of the PEEP group were excluded after randomization because of an Spo2 at ambient air <94% in the operating room and, because of technical difficulties, only 11 arterial catheters could be inserted in each group (PEEP group: 12 patients, 11 patients with blood gases analysis; control group: 15 patients, 11 patients with blood gases analysis). The two study groups did not differ with respect to age, sex, BMI, smoking, and Spo2 at ambient air (Table 1). No patients had a difficult intubation, only one attempt was necessary, and the duration of intubation did not exceed 1 min in any patient.


View this table:
[in this window]
[in a new window]
  		Table 1. Patient Demographics

 

Nonhypoxic apnea duration was significantly longer in the PEEP group than in the control group (188 ± 46 versus 127 ± 43 s; P = 0.002) (Fig. 1).



View larger version (26K):
[in this window]
[in a new window]
  		Figure 1. Duration of nonhypoxic apnea and Pao2 before apnea in control and positive end-expiration pressure (PEEP) patients. *P = 0.002 and {dagger}P = 0.038 for comparison between groups.

 

Just before apnea, Pao2 was higher in the PEEP group than in the control group (376 ± 145 versus 243 ± 136 mm Hg, respectively; P = 0.038) (Fig. 1). No difference was seen for Paco2 before apnea (Table 2). At 92% Spo2, there was no difference for Pao2 or Paco2 between the two groups (Table 2).


View this table:
[in this window]
[in a new window]
  		Table 2. Blood Gases

 

We found a negative correlation between BMI and nonhypoxic apnea duration in the control group (R2 = 0.51, P = 0.003) but not in the PEEP group (R2 = 0.14, P = 0.25) (Fig. 2).



View larger version (14K):
[in this window]
[in a new window]
  		Figure 2. Correlation between duration of nonhypoxic apnea and body mass index (BMI) in control (A) and positive end-expiratory pressure (PEEP) patients (B).

 

There was no correlation between BMI and Pao2 before apnea in the control group (R2 = 0.21, P = 0.16) or in the PEEP group (R2 = 0.18, P = 0.20).


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The main finding of this study is that application of positive airway pressure (10 cm H2O) during induction of general anesthesia in morbidly obese patients increases nonhypoxic apnea duration by 50% or 1 minute. This is an important clinical benefit, because difficult airway management is frequently encountered in morbidly obese patients. Indeed, it has been shown that difficult tracheal intubation is more frequent in obese than in lean patients (15.5% versus 2.2%) (15).

The increase of the duration of nonhypoxic apnea that we have demonstrated may be explained by two mechanisms. First, PEEP decreases the amount of atelectasis as previously shown (17), and this increases the functional residual capacity (FRC) which is the main oxygen store of the body (18). Second, decreasing atelectasis also decreases intrapulmonary shunt (3,4). Indeed, the higher Pao2 seen in the PEEP group may reflect a lower level of intrapulmonary shunt. Therefore, increasing the oxygen store of the body and decreasing the intrapulmonary shunt may prolong the duration of nonhypoxic apnea and the margin of safety during anesthesia induction.

We have previously shown that application of PEEP of only 6 cm H2O in nonobese patients prolongs the duration of nonhypoxic apnea by >2 minutes (13). In this study, the duration of nonhypoxic apnea in the control group, without any PEEP or CPAP, was 8 minutes. In our study, we found that in morbidly obese patients, when PEEP was applied, this duration of nonhypoxic apnea was only 3 min. This difference may be explained by the fact that even without any atelectasis, FRC is markedly decreased in morbidly obese patients compared with nonobese patients (19). Therefore, the oxygen store of morbidly obese patients is less than in nonobese patients. Indeed, it has been shown that when FRC is decreased, as can be seen in women compared with men (20), the duration of nonhypoxic apnea is also decreased (13). Moreover, during apnea, the lungs are open to the atmosphere and atelectasis may arise very quickly in these circumstances when 100% O2 has been used (21). One of the mechanisms of atelectasis formation is compression (6), particularly in the lower dorsal part of the lungs where the diaphragm compresses the lungs. In morbidly obese patients, the abdominal pressure is much higher than in nonobese patients (22,23) and therefore this mechanism of compression is increased, hastening atelectasis formation and increasing intrapulmonary shunt during apnea. These two mechanisms may therefore explain the shorter duration of nonhypoxic apnea seen in morbidly obese compared with nonobese patients.

Another finding of the present study is that there is a negative correlation between BMI and the nonhypoxic apnea duration when no CPAP or PEEP is applied (Fig. 2). For the obese patients with the highest BMI, the time of desaturation may be <1 minute. However, when PEEP is applied, no such correlation is seen. Therefore, this technique may be useful even without difficult airway management.

One limitation of the study is that it is not possible to evaluate whether CPAP during the administration of O2 is useful in the procedure or if PEEP during mechanical ventilation is sufficient for increasing the duration of nonhypoxic apnea. In a previous study, Cressey et al. (24) did not find that application of CPAP during administration of O2 could prolong the time of desaturation in morbidly obese women. However, the administration of O2 was limited to 3 minutes with only 7 cm H2O of CPAP and the induction was a rapid sequence with the use of succinylcholine without ventilation until tracheal intubation. This may explain why they did not find a beneficial effect of application of CPAP. It is possible that application of a higher level of CPAP might also be useful for rapid sequence induction with succinylcholine. Indeed, FRC is lower in supine morbidly obese patients and therefore during normal sleep they may develop atelectasis without high Fio2 or general anesthesia. Therefore, application of CPAP may increase FRC and decrease the amount of atelectasis in awake patients but this remains to be demonstrated.

A potential risk of mechanical ventilation by mask with PEEP is to expose a sedated, paralyzed patient to insufflation of the stomach and, as a result, increase the risk of regurgitation and bronchoaspiration. This risk exists with an insufflation pressure >25 mm Hg, which can be obtained with manual ventilation (25,26). To avoid this complication, we used the pressure-controlled mode to ventilate the patients, which prevents the use of higher pressure. In addition, alarm limits of the ventilator can be set at 25 mm Hg, which will prevent the use of higher pressure via the facemask. Therefore, with this precaution, mechanical ventilation via facemask may even be safer than manual ventilation.

In conclusion, application of CPAP (10 cm H2O) for 5 minutes in conscious morbidly obese patients followed by 5 minutes of mechanical ventilation with PEEP (10 cm H2O) during anesthesia induction is safe, simple, and well tolerated (no patients refused to participate and all patients of the PEEP group tolerated CPAP for 5 min). This technique completely prevents atelectasis formation during anesthesia induction in morbidly obese patients (17) and increases nonhypoxic apnea duration by 50% (1 minute). Therefore, application of CPAP and PEEP throughout anesthesia induction might be applied in all morbidly obese patients, particularly when difficult airway management is anticipated or for extreme obesity.


   Footnotes
 
This work is attributed to the Department of Anesthesiology, University Hospital, Lausanne, Switzerland.

Accepted for publication August 10, 2004.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Marshall BE, Wyche MQ. Hypoxemia during and after anesthesia. Anesthesiology 1972;37:178–209.[ISI][Medline]
  2. Moller JT, Johannessen NW, Berg H, et al. Hypoxaemia during anaesthesia: an observer study. Br J Anaesth 1991;66:437–44.[Abstract/Free Full Text]
  3. Hedenstierna G, Tokics L, Strandberg A, et al. Correlation of gas exchange impairment to development of atelectasis during anaesthesia and muscle paralysis. Acta Anaesthesiol Scand 1986;30:183–91.[ISI][Medline]
  4. Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth 2003;91:61–72.[Free Full Text]
  5. Neumann P, Rothen HU, Berglund JE, et al. Positive end-expiratory pressure prevents atelectasis during general anaesthesia even in the presence of a high inspired oxygen concentration. Acta Anaesthesiol Scand 1999;43:295–301.[ISI][Medline]
  6. Brismar B, Hedenstierna G, Lundquist H, et al. Pulmonary densities during anesthesia with muscular relaxation: a proposal of atelectasis. Anesthesiology 1985;62:422–8.[ISI][Medline]
  7. Lundquist H, Hedenstierna G, Strandberg A, et al. CT-assessment of dependent lung densities in man during general anaesthesia. Acta Radiol 1995;36:626–32.[ISI][Medline]
  8. Eichenberger A, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg 2002;95:1788–92.[Abstract/Free Full Text]
  9. Reber A, Englberg G, Wegenius G, Hedenstierna G. Lung aeration: the effect of pre-oxygenation and hyperoxygenation during total intravenous anaesthesia. Anaesthesia 1996;51:733–7.[ISI][Medline]
  10. Rothen HU, Sporre B, Englberg G, et al. Prevention of atelectasis during general anaesthesia. Lancet 1995;345:1387–91.[ISI][Medline]
  11. Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003;98:28–33.[ISI][Medline]
  12. Rusca M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during induction of general anesthesia. Anesth Analg 2003;97:1835–9.[Abstract/Free Full Text]
  13. Herriger A, Frascarolo P, Spahn DR, Magnusson L. The effect of positive airway pressure during pre-oxygenation and induction of anaesthesia upon duration of non-hypoxic apnoea. Anaesthesia 2004;59:243–7.[ISI][Medline]
  14. Hood DD, Dewan DM. Anesthetic and obstetric outcome in morbidly obese parturients. Anesthesiology 1993;79:1210–8.[ISI][Medline]
  15. Juvin P, Lavaut E, Dupont H, et al. Difficult tracheal intubation is more common in obese than in lean patients. Anesth Analg 2003;97:595–600.[Abstract/Free Full Text]
  16. Berthoud MC, Peacock JE, Reilly CS. Effectiveness of preoxygenation in morbidly obese patients. Br J Anaesth 1991;67:464–6.[Abstract/Free Full Text]
  17. Coussa M, Proietti S, Schnyder P, et al. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesth Analg 2004;98:1491–5.[Abstract/Free Full Text]
  18. Lumb AD. Oxygen. In: Nunn’s applied respiratory physiology. Oxford: Butterworth-Heinemann, 2000:288–90.
  19. Pelosi P, Croci M, Ravagnan I, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998;87:654–60.[Abstract/Free Full Text]
  20. Lumb AD. Elastic forces and lung volumes. In: Nunn’s applied respiratory physiology. Oxford: Butterworth-Heinemann, 2000:37–57.
  21. Rothen HU, Sporre B, Englberg G, et al. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995;82:832–42.[ISI][Medline]
  22. Pelosi P, Croci M, Ravagnan I, et al. Total respiratory system, lung, and chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest 1996;109:144–51.[Abstract/Free Full Text]
  23. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol 1997;82:811–8.[Abstract/Free Full Text]
  24. Cressey DM, Berthoud MC, Reilly CS. Effectiveness of continuous positive airway pressure to enhance pre-oxygenation in morbidly obese women. Anaesthesia 2001;56:680–4.[ISI][Medline]
  25. Ho-Tai LM, Devitt JH, Noel AG, O’Donnell MP. Gas leak and gastric insufflation during controlled ventilation: face mask versus laryngeal mask airway. Can J Anaesth 1998;45:206–11.[Abstract/Free Full Text]
  26. Vyas H, Milner AD, Hopkin IE. Face mask resuscitation: does it lead to gastric distension? Arch Dis Child 1983;58:373–5.[Abstract]



This article has been cited by other articles:


Home page
 Br J AnaesthHome page
P. Cadi, T. Guenoun, D. Journois, J.-M. Chevallier, J.-L. Diehl, and D. Safran
Pressure-controlled ventilation improves oxygenation during laparoscopic obesity surgery compared with volume-controlled ventilation
Br. J. Anaesth., May 1, 2008; 100(5): 709 - 716.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gander, S.
Right arrow Articles by Magnusson, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gander, S.
Right arrow Articles by Magnusson, L.

Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press