Acta Anaesthesiol Scand 2014; ••: ••–•• Printed in Singapore. All rights reserved
© 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd ACTA ANAESTHESIOLOGICA SCANDINAVICA
doi: 10.1111/aas.12317
Continuous positive airway pressure/pressure support pre-oxygenation of morbidly obese patients P. Harbut1, W. Gozdzik2, E. Stjernfält1, R. Marsk3 and J. F. Hesselvik1
Departments of 1Anesthesiology and Intensive Care, 3Surgery, Danderyd Hospital, Stockholm, Sweden and 2Department of Anesthesiology and Intensive Care, Wroclaw University Hospital, Wrocław, Poland Background: Morbidly obese patients are more prone to desaturation of arterial blood during apnea with induction of anesthesia than are non-obese. This study aimed to assess the effect of low-pressure continuous positive airway pressure (CPAP) with pressure support ventilation (PSV) during preoxygenation on partial oxygen pressure in arterial blood (PaO2) immediately after tracheal intubation (post-intubation PaO2). Methods: Forty-four adult patients scheduled for laparoscopic gastric bypass surgery were pre-oxygenated with 80% O2 for 2 min, randomized either to CPAP 5 cm H2O + PSV 5 cm H2O (CPAP/PSV, n = 22) or neutral-pressure breathing without CPAP/PSV (control, n = 22). Anesthesia was induced in a rapidsequence protocol and the trachea was intubated without prior mask ventilation. Arterial blood gases were measured before pre-oxygenation, before induction of anesthesia, and immediately following intubation, before the first positive pressure breath. Results: After pre-oxygenation, partial carbondioxide pressure
was significantly lower in the CPAP/PSV group (4.9 ± 0.5 kPa), (mean ± standard deviation) than in the control group (5.2 ± 0.7 kPa) (P = 0.025). Post-preoxygenation PaO2 did not differ between the groups, but post-intubation PaO2 was significantly higher in the CPAP/PSV group (32.2 ± 4.1 kPa) than in the control group (23.8 ± 8.8 kPa) (P < 0.001). In the control group, nadir oxygen saturation was lower (median 98%, range 83–99%) than in the CPAP/PSV group (median 99%, range 97–99%, P = 0.011). Conclusions: In morbidly obese patients, low-pressure CPAP combined with low-pressure PSV during pre-oxygenation resulted in better oxygenation, compared with neutral-pressure breathing, and prevented desaturation episodes.
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obese patients using arterial blood gas and respiratory gas measurements. Our primary end point was partial oxygen pressure in arterial blood (PaO2) on completion of intubation following a standardized rapid-sequence induction. Because the mode of preoxygenation conceivably could have effects on the lung that would be more long lasting, we in addition studied gas exchange parameters at intervals throughout the remainder of the anesthetic; these were secondary end points. The hypothesis of our study was that low-pressure CPAP/PSV applied during induction of anesthesia could result in higher PaO2 immediately after tracheal intubation (post-intubation PaO2).
ace mask pre-oxygenation with 100% oxygen before intravenous induction of anesthesia increases the time to oxygen desaturation of arterial blood with apnea1,2 and different techniques for this procedure have been described.3–6 It is clear that the duration of apnea tolerated before desaturation occurs is largely influenced by atelectasis formation and the volume of oxygen in the functional residual capacity (FRC) at onset of apnea.7 Several factors such as metabolic rate, blood hemoglobin concentration, supine position, general anesthesia, as well as obesity also contribute.7–9 Suggested strategies to maintain oxygenation during induction of anesthesia of the severely obese include a 25 degree head-up position10 and continuous positive airway pressure (CPAP).11 In this study, we planned to assess the feasibility of non-invasive respiratory support, being low-pressure CPAP with pressure support ventilation (PSV) during pre-oxygenation, at pressures lower than previously reported, and its efficacy during induction of anesthesia in morbidly
Accepted for publication 28 February 2014 © 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd
Methods Patients The investigation was approved by the Regional Human Ethics Committee in Stockholm, Nobels väg 12 A, 17177 Stockholm, Sweden, Protocol number
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P. Harbut et al.
2008/4:4, approval date 02 April 2008. Written informed consent was obtained from each subject. The trial is registered at http://www.clinicaltrials .gov (registration number NCT01780571). Inclusion criteria were (1) body mass index (BMI) > 35 kg/m2, (2) scheduled to undergo elective gastric bypass surgery, (3) age ≥ 18 years, and (4) American Society of Anesthesiologists Physical Status Classification II-III. Exclusion criteria were (1) significant cardiopulmonary disease, (2) previous abdominal or thoracic surgery, or (3) inability to comprehend the protocol.
Groups Included patients were prospectively randomized by sealed envelope to either the CPAP/PSV group: Pre-induction of anesthesia, noninvasive CPAP/ PSV (5 + 5 cm H2O) was given for 2 min in the PSV-Pro mode of an Aisys anesthesia care station (GE Healthcare, Helsinki, Finland); or the control group: Pre-oxygenation was given without positive pressure, neither in the inspiratory nor the expiratory phase.
Power analysis and sample size Based on our previous experience in the bariatric population, it was expected that the CPAP/PSV group would have a PaO2 that was 25% higher than controls. We expected a PaO2 of 30 kPa in the control group and a standard deviation (SD) around 9 kPa. Assuming alpha = 0.05, 22 patients in each group were needed to achieve a statistical power of 80%.
Anesthesia and study protocol Patients were pre-medicated with oral acetaminophen 1.5 g (Alvedon®, GlaxoSmithKline, Bröndby, Danmark), celecoxib 200 mg (Celebra®, Pfizer AB, Sollentuna, Sweden) and slow-release oxycodone 20 mg (Oxycontin®, Mundipharma AB, Göteborg, Sweden) 1 h before surgery. After 1% lignocaine infiltration (Xylocain®, AstraZeneca AB, Södertälje, Sweden), a radial arterial catheter was inserted during preparation for anesthesia. Patients were positioned in a 25–30 degree head-up position, and pre-oxygenation was given for 2 min with a 15 l/min fresh gas flow of 80% oxygen in a circle system using a tight-fitting face mask, according to either the study or control protocol. Anesthesia was then induced in intravenous rapid sequence with propofol 2–2.5 mg/kg (Propofol-®Lipuro, B. Braun Medical AB, Danderyd, Sweden) of ideal body weight, and remifentanil (Ultiva®, GlaxoSmithKline
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AB, Solna, Sweden) according to Minto’s target controlled infusion model12 with a target concentration of 3 ng/ml, followed immediately by succinylcholine (Celocurin®, Meda AB, Solna, Sweden) 0.6 mg/kg of actual body weight. The first intubation attempt was made by an experienced anesthesia consultant 60 s after succinylcholine. After verification of the tube position by lung auscultation and capnography, a recruitment maneuver (30 cm H2O for 5 s) was performed in all patients. Ventilation was continued by pressure control ventilation– volume guaranteed (the pressure control/volume guarantee mode of the Aisys anesthesia delivery unit) using 7 cm H2O positive end-expiratory pressure (PEEP) and an initial-tidal volume of 500 ml at 12 breaths/min, adjusted to maintain an end-tidal CO2 concentration (EtCO2) of 4,5–5,5 kPa, with a fresh gas flow of 1 l/min of a mixture of sevoflurane in oxygen and air, and a target end-tidal oxygen (EtO2) of 40%. Anesthesia was maintained with sevoflurane (0.8–1 MAC) and remifentanil targetcontrolled infusion (5–10 ng/ml). Neuromuscular blockade was maintained with bolus increments of atracurium (Atracurium-hameln®, Algol Pharma AB, Kista, Sweden) calculated for ideal body weight. Toward the end of the anesthesia, morphine 5–10 mg (Morfin Meda®, Meda AB) was given i.v. Following reversal of blockade with neostigmine 25 mcg/kg (Neostigmin®, PharmaCoDane ApS, Herlev, Danmark) and glycopyrrolate 4 mcg/kg (Robinul®, Meda AB), all patients were extubated and brought to the recovery room where they were cared for in a 25–30 degree head-up position and received oxygen 2 l/min by nasal cannula.
Measurements Arterial blood samples for measurement of PaO2 and partial carbondioxide pressure in arterial blood (PaCO2) were collected at the following time points and processed on an ABL 725 blood gas analyzer (Radiometer, Copenhagen, Copenhagen, Denmark): 1. Before beginning of pre-oxygenation (breathing air) 2. After 2 min of pre-oxygenation 3. Directly after intubation, before any respiratory support was given 4. At the beginning of insufflation 5. On exsufflation 6. 30 min after admission to post-anesthesia care unit. Inspiratory and end-tidal (Et) concentrations (%) of O2 and CO2 were recorded every 5 min from the
Pre-oxygenation in obese patients Table 1 Demographic variables (mean ± SD). CPAP/PSV Control
Age (years)
Weight (kg)
Height (cm)
BMI
46.9 (± 12.9) 42.1 (± 12.4)
119.4 (± 16.6) 127.7 (± 17.2)
166.8 (± 8.3) 170.4 (± 8.6)
43 (± 6.3) 44.1 (± 6.0)
BMI, body mass index; CPAP, continuous positive airway pressure; PSV, pressure support ventilation; SD, standard deviation.
onset of pre-oxygenation until extubation. Pulse oximeter saturation (SpO2) was measured continuously during the anesthetic, and the minimum value during the induction process was noted. The apnea time (from onset of apnea with anesthetic induction until the first breath after endotracheal intubation) was recorded.
Statistics Repeated measurements analysis of variance (ANOVA) was used for comparison between groups for all variables except SpO2, where the Kruskall– Wallis test for nonparametric variables was used, because a normal distribution was not expected. The Sidak multiple comparison test for ANOVA was performed for confirmation. Data are presented as mean ± SD, or median ± range, respectively. A P value of less than 0.05 was considered statistically significant.
Results Forty-eight patients were recruited from 10 January 2009 to 31 March 2009 to the study (CPAP/PSV group, n = 24; control group, n = 24). Two patients in each group were excluded because of conversion to open surgery (two patients), undiagnosed liver cirrhosis (one patient) and technical failure causing a 3 min delay in intubation (one patient). The remaining 22 patients in each group were similar regarding age, gender, height, weight, BMI (Table 1); and for baseline PaO2, baseline PaCO2 and baseline SpO2 (Table 2). The apnea time was 89 ± 10 s in the CPAP/PSV group and 91 ± 6 s in the control group; this difference was not statistically significant. The median nadir SpO2 was significantly (P = 0.011) lower in the control group (98%, range 83–99%) than in the CPAP/PSV group (99%, range 97–99%). We noted three cases of moderate hypoxia in control group – 88%, 84%, and 83% and none in CPAP/PSV group. After pre-oxygenation, PaCO2 was significantly lower in the CPAP/PSV group (4.8 ± 0.5 kPa) than in the control group (5.2 ± 0.7 kPa) (P = 0.025). Postpre-oxygenation PaO2 did not differ between the
groups, but post-intubation PaO2 was significantly higher in the CPAP/PSV group (32.2 ± 4.1 kPa) than the control group (23.8 ± 8.8 kPa) (P < 0.001). This difference was no longer present at the onset of capnoperitoneum nor at the subsequent measurement points (Fig. 1). Statistical significance was confirmed by the Sidak test. The calculated oxygen content of arterial blood (CaO2), although higher in CPAP/PSV group, did not differ significantly (20.6 ± 2.5 and 19.9 ± 2.4 vol%, respectively, P = 0.33).
Discussion There is a large body of literature supporting the volume recruiting maneuver and PEEP during anesthesia in obese individuals to prevent atelectasis and improve oxygenation. By contrast, the technique for pre-oxygenation has received relatively little attention. Obese patients are commonly anesthetized using the rapid-sequence technique because they may be at increased risk for gastroesophageal reflux and pulmonary aspiration.13,14 Effective preoxygenation is also important in severely obese patients since they may be more difficult to mask ventilate15,16 and desaturate more rapidly in apnea than do normal-weight individuals.17 Some authors have found that difficulty in tracheal intubation is more frequent in this population,18 while others have not.19 Adding patient-triggered, positive pressure inspiratory support to CPAP during pre-oxygenation could theoretically be valuable because morbidly obese patients have an increased work of breathing,20 and breathing at low lung volumes promotes peripheral airway closure in the dependent lung zones.21,22 Our data demonstrate that in a group of morbidly obese patients, application of low levels of CPAP/ PSV during pre-oxygenation significantly improved PaO2 at the end of a standardized rapid-sequence induction. One can reasonably infer that these patients had a higher margin of safety and would tolerate apnea better than patients who had been pre-oxygenated at neutral airway pressure, before hypoxemia would ensue. The probable mechanism for this improvement is a faster increase in end
3
4
42 (± 2.6) 47 (± 3.1) 46 (± 2.5) 5.4 (± 0.5) 20.0 (± 4.5) 21.6 (± 4.8)
5.4 (± 0.6)
6.4 (± 1.0) 6.1 (± 0.6) 23.8 (± 8.8) 32.2 (± 4.1)***
*P = 0.049, **P = 0.013, ***P < 0.001. CPAP, continuous positive airway pressure; EtO2, end-tidal oxygen; Insp, inspiratory; PSV, pressure support ventilation; SD, standard deviation.
42 (± 3.4)
1 min 67.6 (± 3.9) 1 min 72.4** (± 3.9) 21 80 21 80 5.3 (± 0.6) 5.2 (± 0.7) 5.4 (± 0.5) 4.9 (± 0.5)* 15.0 (± 3.1) 38.8 (± 4.0) 14.5 (± 2.8) 40.2 (± 6.9)
Baseline After preoxygenation After intubation (before ventilation) Before insufflation
EtO2 (%)
CPAP PSV Control
PaCO2 (kPa)
CPAP PSV Control
PaO2 (kPa)
CPAP PSV
Gasometric and spirometric variables compared between study groups, mean (± SD).
Table 2
Control Insp O2 (%)
CPAP PSV
2 min 74.6** (± 2.0)
Control
2 min 71.3 (± 2.0)
P. Harbut et al.
Fig. 1. PaO2 values (mean ± standard deviation, n = 22 in each group) at measurement points: (1) baseline, breathing air; (2) following 2 min of pre-oxygenation, immediately before induction of anesthesia; (3) directly after endotracheal intubation, before the first positive pressure breath; (4) before capnoperitoneum; (5) after capnoperitoneum; (6) in post-anesthesia care unit. The treatment [continuous positive airway pressure/ pressure support ventilation (CPAP/PSV), triangles] and control (circles) groups differ significantly (P < 0.001, two-way repeated measurements analysis of variance).
expiratory lung volume and diminished airway closure during the induction process; importantly, PaO2 did not differ between the treatment and control groups immediately post-preoxygenation, yet the control patients displayed a more rapid decline in PaO2 post-induction, indicating that their oxygen reserve was lower than that of the CPAP/ PSV group. Our study differed in several ways from earlier published work. Cressey et al.11 were unable to demonstrate benefit (in terms of post-induction time to pulse oximeter desaturation) in obese women receiving CPAP alone (without PSV) during preoxygenation before a rapid-sequence induction. Coussa et al.23 used CPAP 10 cm H2O for 5 min, induced anesthesia in conventional intravenous fashion with nondepolarizing neuromuscular blockade, and then mechanically ventilated by face mask for 5 min using 10 cm PEEP before intubation. The combination resulted in significantly better oxygenation and less atelectasis than with no CPAP or PEEP, as measured at a time point 3 min after intubation. Gander et al.,24 in the similarly designed study protocol, demonstrated significantly longer duration of non-hypoxic apnea in a CPAP/PEEP group. Delay et al.,25 in a model more similar to the present study, pre-oxygenated with 100% O2 for 5 min using either CPAP/PSV (6 + 8 cm H2O) or neutral pressure. A significantly higher proportion of patients reached the target EtO2 concentration of 95%, the rate of increase in EtO2 was significantly greater, and
Pre-oxygenation in obese patients
average post-pre-oxygenation EtO2 was significantly higher in the CPAP/PSV group vs. control. PaO2 was higher and PaCO2 was lower in the CPAP/PSV group than the control group after pre-oxygenation, but these differences did not achieve statistical significance. However, blood gas data were only available from a minority of the patients. After intubation, patients were left apneic until decrease of SaO2 to 95%; the time to desaturation did not differ between the groups, but the authors concluded that the target level might have been set too high to detect a difference. In accordance with the above investigation, we found a modestly increased EtO2 during and after pre-oxygenation in the CPAP/PSV group. However, a higher EtO2 value alone does not necessarily imply a higher oxygen reserve, particularly in patients with a diminished FRC. In our view, a higher level of PaO2 immediately after the intubation attempt (as was found in our study) more clearly demonstrates the value of CPAP/PSV during anesthetic induction in obese patients consistent with less hypoxic events detected by pulse oximetry. By its impact on the alveolar gas equation, PaCO2 can affect PaO2. In the present study, the difference in PaCO2 after intubation reached statistical significance, but the difference was not large enough to influence our results. We chose, contrary to previous studies, low expiratory pressure (CPAP 5 cm H2O) but with the addition of flow-triggered positive inspiratory pressure (PSV 5 cm H2O). The administration of using low bi-level pressures is in our clinical experience better tolerated by ‘untrained patients’ than sole CPAP (unpublished observations from our bariatric anesthesia division and obstructive sleep apnea division). This finding is supported by the results of Baral’s healthy-volunteer study.26
our study is that we did not measure apnea times to desaturation, but rather attempted to restore optimal lung function by a volume recruitment maneuver and application of PEEP directly after intubation, so as not to subject the patients to unnecessary risk of atelectasis and hypoxia. The patients received detailed instruction of the experience of CPAP/PSV and the need for a tight mask fit, both during the consent process and directly before pre-oxygenation. The pressure levels were relatively low because there is a certain risk of gastric distension, as seen in a few patients both in our study and that of Delay et al.25 It is also important to recognize that different models of anesthesia ventilators differ significantly in their performance regarding trigger sensitivity and ability to meet inspiratory flow requirements.29 Only the most recent models approach the capacity of ICU ventilators, and the results of our study would only apply to a high-performance ventilator. In accordance with what is probably the current standard of practice for general anesthesia involving muscle paralysis in obese patients, we performed a volume recruiting maneuver directly after intubation in all subjects and continued positive pressure ventilation with PEEP, at an FiO2 adequate for oxygenation yet unlikely to contribute to resorption atelectasis (40%).30 We saw no differences in oxygenation parameters between the groups at any of the subsequent time points after anesthesia induction phase. In summary, this study has shown that CPAP/PSV during pre-oxygenation of obese patients resulted in significantly higher PaO2 and no oxygen desaturations after a 60 s apnea period with a rapid-sequence induction, compared with preoxygenation with neutral pressure.
Study limitations
Clinical implication
We pre-oxygenated with 80% O2 at a high flow rate in a circle system. One-hundred-percent oxygen is commonly used for pre-oxygenation, yet it is associated with increased atelectasis.27 However, in that study, it was also demonstrated that the safe apneic time until desaturation to SpO2 90% was significantly shorter than when 100% oxygen was used. This may be a point of criticism in regard to our protocol. Also, the time of pre-oxygenation was fixed at 2 min, which is shorter than the more commonly used 3 min period. Still, the study of Berry and Myles28 demonstrated a relatively flat part of the oxygen wash-in graph between 120 and 180 s, indicating that our choice of a 2 min pre-oxygenation period probably was adequate. Another limitation of
Our study suggests that pre-oxygenation with lowpressure CPAP/PSV applied during induction of anesthesia of morbidly obese patients may improve oxygenation of arterial blood when compared with conventional management without any respiratory support. Of note, however, this effect was only of short duration.
Acknowledgment The authors would like to express their deep gratitude to Professor Göran Hedenstierna for his encouragement and useful critiques during manuscript work. Conflict of interest: None Funding: Funding received from Department of Anesthesiology, Danderyd Hospital.
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References 1. Nolan RT. Pre-oxygenation and thiopentonesuxamethonium induction. Br J Anesth 1967; 39: 794–7. 2. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology 2003; 98: 1269–77. 3. Baraka AS, Taha SK, Aouad MT, El-Khatib MF, Kawkabani NI. Preoxygenation: comparison of maximal breathing and tidal volume breathing techniques. Anesthesiology 1999; 91: 612–6. 4. Goldberg ME, Norris MC, Larijani GE, Marr AT, Seltzer JL. Preoxygenation in the morbidly obese: a comparison of two techniques. Anesth Analg 1989; 68: 520–2. 5. Valentine SJ, Marjot R, Monk CR. Preoxygenation in the elderly: a comparison of the four-maximal-breath and threeminute techniques. Anesth Analg 1990; 71: 516–9. 6. Benumof JL. Preoxygenation: best method for both efficacy and efficiency. Anesthesiology 1999; 91: 603–5. 7. Farmery AD, Roe PG. A model to describe the rate of oxyhaemoglobin desaturation during apnoea. Br J Anesth 1996; 76: 284–91. 8. Don HF, Wahba M, Cuadrado L, Kelkar K. The effects of anesthesia and 100 per cent oxygen on the functional residual capacity of the lungs. Anesthesiology 1970; 32: 521–9. 9. Froese AB, Bryan AC. Effects of anesthesia and paralysis on diaphragmatic mechanics in man. Anesthesiology 1974; 41: 242–55. 10. Dixon BJ, Dixon JB, Carden JR, Burn AJ, Schachter LM, Playfair JM, Laurie CP, O’Brien PE. Preoxygenation is more effective in the 25 degrees head-up position than in the supine position in severely obese patients: a randomized controlled study. Anesthesiology 2005; 102: 1110–5, discussion 5A. 11. Cressey DM, Berthoud MC, Reilly CS. Effectiveness of continuous positive airway pressure to enhance preoxygenation in morbidly obese women. Anesthesia 2001; 56: 680–4. 12. Minto CF, Schnider TW, Egan TD, Youngs E, Lemmens HJ, Gambus PL, Billard V, Hoke JF, Moore KH, Hermann DJ, Muir KT, Mandema JW, Shafer SL. Influence of age and gender on the pharmacokinetics and pharmacodynamics of remifentanil. I. Model development. Anesthesiology 1997; 86: 10–23. 13. Freid EB. The rapid sequence induction revisited: obesity and sleep apnea syndrome. Anesthesiol Clin North America 2005; 23: 551–64, viii. 14. Hampel H, Abraham NS, El-Serag HB. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med 2005; 143: 199–211. 15. Kheterpal S, Han R, Tremper KK, Shanks A, Tait AR, O’Reilly M, Ludwig TA. Incidence and predictors of difficult and impossible mask ventilation. Anesthesiology 2006; 105: 885–91. 16. Yildiz TS, Solak M, Toker K. The incidence and risk factors of difficult mask ventilation. J Anesth 2005; 19: 7–11. 17. Jense HG, Dubin SA, Silverstein PI, O’Leary-Escolas U. Effect of obesity on safe duration of apnea in anesthetized humans. Anesth Analg 1991; 72: 89–93. 18. el Ganzouri AR, McCarthy RJ, Tuman KJ, Tanck EN, Ivankovich AD. Preoperative airway assessment: predictive value of a multivariate risk index. Anesth Analg 1996; 82: 1197–204. 19. Juvin P, Lavaut E, Dupont H, Dupont H, Lefevre P, Demetriou M, Dumoulin JL, Desmonts JM. Difficult tracheal
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intubation is more common in obese than in lean patients. Anesth Analg 2003; 97: 595–600, table of contents. Pelosi P, Croci M, Ravagnan I, Tredici S, Pedoto A, Lissoni A, Gattinoni L. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesth Analg 1998; 87: 654–60. Holley HS, Milic-Emili J, Becklake MR, Bates DV. Regional distribution of pulmonary ventilation and perfusion in obesity. J Clin Invest 1967; 46: 475–81. Salome CM, King GG, Berend N. Physiology of obesity and effects on lung function. J Appl Physiol 2010; 108: 206–11. Coussa M, Proietti S, Schnyder P, Frascarolo P, Suter M, Spahn DR, Magnusson L. Prevention of atelectasis formation during the induction of general anesthesia in morbidly obese patients. Anesth Analg 2004; 98: 1491–5, table of contents. Gander S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Positive end-expiratory pressure during induction of general anesthesia increases duration of nonhypoxic apnea in morbidly obese patients. Anesth Analg 2005; 100: 580–4. Delay JM, Sebbane M, Jung B, Nocca D, Verzilli D, Pouzeratte Y, Kamel ME, Fabre JM, Eledjam JJ, Jaber S. The effectiveness of noninvasive positive pressure ventilation to enhance preoxygenation in morbidly obese patients: a randomized controlled study. Anesth Analg 2008; 107: 1707– 13. Baral PR, Bhattarai B, Pande R, Bhadani U, Bhattacharya A, Tripathi M. Breathing comfort associated with different modes of ventilation: a comparative study in non-intubated healthy Nepalese volunteers. Kathmandu Univ Med J 2007; 19: 302–6. Edmark L, Kostova-Aherdan K, Enlund M, Hedenstierna G. Optimal oxygen concentration during induction of general anesthesia. Anesthesiology 2003; 98: 28–33. Berry CB, Myles PS. Preoxygenation in healthy volunteers: a graph of oxygen ‘washin’ using end-tidal oxygraphy. Br J Anesth 1994; 72: 116–8. Jaber S, Tassaux D, Sebbane M, Pouzeratte Y, Battisti A, Capdevila X, Eledjam JJ, Jolliet P. Performance characteristics of five new anesthesia ventilators and four intensive care ventilators in pressure-support mode: a comparative bench study. Anesthesiology 2006; 105: 944–52. Rothen HU, Sporre B, Engberg G, Wegenius G, Högman M, Hedenstierna G. Influence of gas composition on recurrence of atelectasis after a reexpansion maneuver during general anesthesia. Anesthesiology 1995; 82: 832–42.
Address: Piotr Harbut Department of Anesthesiology and Intensive Care Danderyd Hospital SE-182 88 Stockholm Sweden e-mail: [email protected]
Appendix CONSORT 2010 Flow Diagram In our institution, a total number of 113 patients have been scheduled for the elective gastric by-pass surgery during the randomization period. Ninety of them have been assessed for eligibility.
© 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd ACTA ANAESTHESIOLOGICA SCANDINAVICA
doi: 10.1111/aas.12317
Continuous positive airway pressure/pressure support pre-oxygenation of morbidly obese patients P. Harbut1, W. Gozdzik2, E. Stjernfält1, R. Marsk3 and J. F. Hesselvik1
Departments of 1Anesthesiology and Intensive Care, 3Surgery, Danderyd Hospital, Stockholm, Sweden and 2Department of Anesthesiology and Intensive Care, Wroclaw University Hospital, Wrocław, Poland Background: Morbidly obese patients are more prone to desaturation of arterial blood during apnea with induction of anesthesia than are non-obese. This study aimed to assess the effect of low-pressure continuous positive airway pressure (CPAP) with pressure support ventilation (PSV) during preoxygenation on partial oxygen pressure in arterial blood (PaO2) immediately after tracheal intubation (post-intubation PaO2). Methods: Forty-four adult patients scheduled for laparoscopic gastric bypass surgery were pre-oxygenated with 80% O2 for 2 min, randomized either to CPAP 5 cm H2O + PSV 5 cm H2O (CPAP/PSV, n = 22) or neutral-pressure breathing without CPAP/PSV (control, n = 22). Anesthesia was induced in a rapidsequence protocol and the trachea was intubated without prior mask ventilation. Arterial blood gases were measured before pre-oxygenation, before induction of anesthesia, and immediately following intubation, before the first positive pressure breath. Results: After pre-oxygenation, partial carbondioxide pressure
was significantly lower in the CPAP/PSV group (4.9 ± 0.5 kPa), (mean ± standard deviation) than in the control group (5.2 ± 0.7 kPa) (P = 0.025). Post-preoxygenation PaO2 did not differ between the groups, but post-intubation PaO2 was significantly higher in the CPAP/PSV group (32.2 ± 4.1 kPa) than in the control group (23.8 ± 8.8 kPa) (P < 0.001). In the control group, nadir oxygen saturation was lower (median 98%, range 83–99%) than in the CPAP/PSV group (median 99%, range 97–99%, P = 0.011). Conclusions: In morbidly obese patients, low-pressure CPAP combined with low-pressure PSV during pre-oxygenation resulted in better oxygenation, compared with neutral-pressure breathing, and prevented desaturation episodes.
F
obese patients using arterial blood gas and respiratory gas measurements. Our primary end point was partial oxygen pressure in arterial blood (PaO2) on completion of intubation following a standardized rapid-sequence induction. Because the mode of preoxygenation conceivably could have effects on the lung that would be more long lasting, we in addition studied gas exchange parameters at intervals throughout the remainder of the anesthetic; these were secondary end points. The hypothesis of our study was that low-pressure CPAP/PSV applied during induction of anesthesia could result in higher PaO2 immediately after tracheal intubation (post-intubation PaO2).
ace mask pre-oxygenation with 100% oxygen before intravenous induction of anesthesia increases the time to oxygen desaturation of arterial blood with apnea1,2 and different techniques for this procedure have been described.3–6 It is clear that the duration of apnea tolerated before desaturation occurs is largely influenced by atelectasis formation and the volume of oxygen in the functional residual capacity (FRC) at onset of apnea.7 Several factors such as metabolic rate, blood hemoglobin concentration, supine position, general anesthesia, as well as obesity also contribute.7–9 Suggested strategies to maintain oxygenation during induction of anesthesia of the severely obese include a 25 degree head-up position10 and continuous positive airway pressure (CPAP).11 In this study, we planned to assess the feasibility of non-invasive respiratory support, being low-pressure CPAP with pressure support ventilation (PSV) during pre-oxygenation, at pressures lower than previously reported, and its efficacy during induction of anesthesia in morbidly
Accepted for publication 28 February 2014 © 2014 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd
Methods Patients The investigation was approved by the Regional Human Ethics Committee in Stockholm, Nobels väg 12 A, 17177 Stockholm, Sweden, Protocol number
1 bs_bs_banner
P. Harbut et al.
2008/4:4, approval date 02 April 2008. Written informed consent was obtained from each subject. The trial is registered at http://www.clinicaltrials .gov (registration number NCT01780571). Inclusion criteria were (1) body mass index (BMI) > 35 kg/m2, (2) scheduled to undergo elective gastric bypass surgery, (3) age ≥ 18 years, and (4) American Society of Anesthesiologists Physical Status Classification II-III. Exclusion criteria were (1) significant cardiopulmonary disease, (2) previous abdominal or thoracic surgery, or (3) inability to comprehend the protocol.
Groups Included patients were prospectively randomized by sealed envelope to either the CPAP/PSV group: Pre-induction of anesthesia, noninvasive CPAP/ PSV (5 + 5 cm H2O) was given for 2 min in the PSV-Pro mode of an Aisys anesthesia care station (GE Healthcare, Helsinki, Finland); or the control group: Pre-oxygenation was given without positive pressure, neither in the inspiratory nor the expiratory phase.
Power analysis and sample size Based on our previous experience in the bariatric population, it was expected that the CPAP/PSV group would have a PaO2 that was 25% higher than controls. We expected a PaO2 of 30 kPa in the control group and a standard deviation (SD) around 9 kPa. Assuming alpha = 0.05, 22 patients in each group were needed to achieve a statistical power of 80%.
Anesthesia and study protocol Patients were pre-medicated with oral acetaminophen 1.5 g (Alvedon®, GlaxoSmithKline, Bröndby, Danmark), celecoxib 200 mg (Celebra®, Pfizer AB, Sollentuna, Sweden) and slow-release oxycodone 20 mg (Oxycontin®, Mundipharma AB, Göteborg, Sweden) 1 h before surgery. After 1% lignocaine infiltration (Xylocain®, AstraZeneca AB, Södertälje, Sweden), a radial arterial catheter was inserted during preparation for anesthesia. Patients were positioned in a 25–30 degree head-up position, and pre-oxygenation was given for 2 min with a 15 l/min fresh gas flow of 80% oxygen in a circle system using a tight-fitting face mask, according to either the study or control protocol. Anesthesia was then induced in intravenous rapid sequence with propofol 2–2.5 mg/kg (Propofol-®Lipuro, B. Braun Medical AB, Danderyd, Sweden) of ideal body weight, and remifentanil (Ultiva®, GlaxoSmithKline
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AB, Solna, Sweden) according to Minto’s target controlled infusion model12 with a target concentration of 3 ng/ml, followed immediately by succinylcholine (Celocurin®, Meda AB, Solna, Sweden) 0.6 mg/kg of actual body weight. The first intubation attempt was made by an experienced anesthesia consultant 60 s after succinylcholine. After verification of the tube position by lung auscultation and capnography, a recruitment maneuver (30 cm H2O for 5 s) was performed in all patients. Ventilation was continued by pressure control ventilation– volume guaranteed (the pressure control/volume guarantee mode of the Aisys anesthesia delivery unit) using 7 cm H2O positive end-expiratory pressure (PEEP) and an initial-tidal volume of 500 ml at 12 breaths/min, adjusted to maintain an end-tidal CO2 concentration (EtCO2) of 4,5–5,5 kPa, with a fresh gas flow of 1 l/min of a mixture of sevoflurane in oxygen and air, and a target end-tidal oxygen (EtO2) of 40%. Anesthesia was maintained with sevoflurane (0.8–1 MAC) and remifentanil targetcontrolled infusion (5–10 ng/ml). Neuromuscular blockade was maintained with bolus increments of atracurium (Atracurium-hameln®, Algol Pharma AB, Kista, Sweden) calculated for ideal body weight. Toward the end of the anesthesia, morphine 5–10 mg (Morfin Meda®, Meda AB) was given i.v. Following reversal of blockade with neostigmine 25 mcg/kg (Neostigmin®, PharmaCoDane ApS, Herlev, Danmark) and glycopyrrolate 4 mcg/kg (Robinul®, Meda AB), all patients were extubated and brought to the recovery room where they were cared for in a 25–30 degree head-up position and received oxygen 2 l/min by nasal cannula.
Measurements Arterial blood samples for measurement of PaO2 and partial carbondioxide pressure in arterial blood (PaCO2) were collected at the following time points and processed on an ABL 725 blood gas analyzer (Radiometer, Copenhagen, Copenhagen, Denmark): 1. Before beginning of pre-oxygenation (breathing air) 2. After 2 min of pre-oxygenation 3. Directly after intubation, before any respiratory support was given 4. At the beginning of insufflation 5. On exsufflation 6. 30 min after admission to post-anesthesia care unit. Inspiratory and end-tidal (Et) concentrations (%) of O2 and CO2 were recorded every 5 min from the
Pre-oxygenation in obese patients Table 1 Demographic variables (mean ± SD). CPAP/PSV Control
Age (years)
Weight (kg)
Height (cm)
BMI
46.9 (± 12.9) 42.1 (± 12.4)
119.4 (± 16.6) 127.7 (± 17.2)
166.8 (± 8.3) 170.4 (± 8.6)
43 (± 6.3) 44.1 (± 6.0)
BMI, body mass index; CPAP, continuous positive airway pressure; PSV, pressure support ventilation; SD, standard deviation.
onset of pre-oxygenation until extubation. Pulse oximeter saturation (SpO2) was measured continuously during the anesthetic, and the minimum value during the induction process was noted. The apnea time (from onset of apnea with anesthetic induction until the first breath after endotracheal intubation) was recorded.
Statistics Repeated measurements analysis of variance (ANOVA) was used for comparison between groups for all variables except SpO2, where the Kruskall– Wallis test for nonparametric variables was used, because a normal distribution was not expected. The Sidak multiple comparison test for ANOVA was performed for confirmation. Data are presented as mean ± SD, or median ± range, respectively. A P value of less than 0.05 was considered statistically significant.
Results Forty-eight patients were recruited from 10 January 2009 to 31 March 2009 to the study (CPAP/PSV group, n = 24; control group, n = 24). Two patients in each group were excluded because of conversion to open surgery (two patients), undiagnosed liver cirrhosis (one patient) and technical failure causing a 3 min delay in intubation (one patient). The remaining 22 patients in each group were similar regarding age, gender, height, weight, BMI (Table 1); and for baseline PaO2, baseline PaCO2 and baseline SpO2 (Table 2). The apnea time was 89 ± 10 s in the CPAP/PSV group and 91 ± 6 s in the control group; this difference was not statistically significant. The median nadir SpO2 was significantly (P = 0.011) lower in the control group (98%, range 83–99%) than in the CPAP/PSV group (99%, range 97–99%). We noted three cases of moderate hypoxia in control group – 88%, 84%, and 83% and none in CPAP/PSV group. After pre-oxygenation, PaCO2 was significantly lower in the CPAP/PSV group (4.8 ± 0.5 kPa) than in the control group (5.2 ± 0.7 kPa) (P = 0.025). Postpre-oxygenation PaO2 did not differ between the
groups, but post-intubation PaO2 was significantly higher in the CPAP/PSV group (32.2 ± 4.1 kPa) than the control group (23.8 ± 8.8 kPa) (P < 0.001). This difference was no longer present at the onset of capnoperitoneum nor at the subsequent measurement points (Fig. 1). Statistical significance was confirmed by the Sidak test. The calculated oxygen content of arterial blood (CaO2), although higher in CPAP/PSV group, did not differ significantly (20.6 ± 2.5 and 19.9 ± 2.4 vol%, respectively, P = 0.33).
Discussion There is a large body of literature supporting the volume recruiting maneuver and PEEP during anesthesia in obese individuals to prevent atelectasis and improve oxygenation. By contrast, the technique for pre-oxygenation has received relatively little attention. Obese patients are commonly anesthetized using the rapid-sequence technique because they may be at increased risk for gastroesophageal reflux and pulmonary aspiration.13,14 Effective preoxygenation is also important in severely obese patients since they may be more difficult to mask ventilate15,16 and desaturate more rapidly in apnea than do normal-weight individuals.17 Some authors have found that difficulty in tracheal intubation is more frequent in this population,18 while others have not.19 Adding patient-triggered, positive pressure inspiratory support to CPAP during pre-oxygenation could theoretically be valuable because morbidly obese patients have an increased work of breathing,20 and breathing at low lung volumes promotes peripheral airway closure in the dependent lung zones.21,22 Our data demonstrate that in a group of morbidly obese patients, application of low levels of CPAP/ PSV during pre-oxygenation significantly improved PaO2 at the end of a standardized rapid-sequence induction. One can reasonably infer that these patients had a higher margin of safety and would tolerate apnea better than patients who had been pre-oxygenated at neutral airway pressure, before hypoxemia would ensue. The probable mechanism for this improvement is a faster increase in end
3
4
42 (± 2.6) 47 (± 3.1) 46 (± 2.5) 5.4 (± 0.5) 20.0 (± 4.5) 21.6 (± 4.8)
5.4 (± 0.6)
6.4 (± 1.0) 6.1 (± 0.6) 23.8 (± 8.8) 32.2 (± 4.1)***
*P = 0.049, **P = 0.013, ***P < 0.001. CPAP, continuous positive airway pressure; EtO2, end-tidal oxygen; Insp, inspiratory; PSV, pressure support ventilation; SD, standard deviation.
42 (± 3.4)
1 min 67.6 (± 3.9) 1 min 72.4** (± 3.9) 21 80 21 80 5.3 (± 0.6) 5.2 (± 0.7) 5.4 (± 0.5) 4.9 (± 0.5)* 15.0 (± 3.1) 38.8 (± 4.0) 14.5 (± 2.8) 40.2 (± 6.9)
Baseline After preoxygenation After intubation (before ventilation) Before insufflation
EtO2 (%)
CPAP PSV Control
PaCO2 (kPa)
CPAP PSV Control
PaO2 (kPa)
CPAP PSV
Gasometric and spirometric variables compared between study groups, mean (± SD).
Table 2
Control Insp O2 (%)
CPAP PSV
2 min 74.6** (± 2.0)
Control
2 min 71.3 (± 2.0)
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Fig. 1. PaO2 values (mean ± standard deviation, n = 22 in each group) at measurement points: (1) baseline, breathing air; (2) following 2 min of pre-oxygenation, immediately before induction of anesthesia; (3) directly after endotracheal intubation, before the first positive pressure breath; (4) before capnoperitoneum; (5) after capnoperitoneum; (6) in post-anesthesia care unit. The treatment [continuous positive airway pressure/ pressure support ventilation (CPAP/PSV), triangles] and control (circles) groups differ significantly (P < 0.001, two-way repeated measurements analysis of variance).
expiratory lung volume and diminished airway closure during the induction process; importantly, PaO2 did not differ between the treatment and control groups immediately post-preoxygenation, yet the control patients displayed a more rapid decline in PaO2 post-induction, indicating that their oxygen reserve was lower than that of the CPAP/ PSV group. Our study differed in several ways from earlier published work. Cressey et al.11 were unable to demonstrate benefit (in terms of post-induction time to pulse oximeter desaturation) in obese women receiving CPAP alone (without PSV) during preoxygenation before a rapid-sequence induction. Coussa et al.23 used CPAP 10 cm H2O for 5 min, induced anesthesia in conventional intravenous fashion with nondepolarizing neuromuscular blockade, and then mechanically ventilated by face mask for 5 min using 10 cm PEEP before intubation. The combination resulted in significantly better oxygenation and less atelectasis than with no CPAP or PEEP, as measured at a time point 3 min after intubation. Gander et al.,24 in the similarly designed study protocol, demonstrated significantly longer duration of non-hypoxic apnea in a CPAP/PEEP group. Delay et al.,25 in a model more similar to the present study, pre-oxygenated with 100% O2 for 5 min using either CPAP/PSV (6 + 8 cm H2O) or neutral pressure. A significantly higher proportion of patients reached the target EtO2 concentration of 95%, the rate of increase in EtO2 was significantly greater, and
Pre-oxygenation in obese patients
average post-pre-oxygenation EtO2 was significantly higher in the CPAP/PSV group vs. control. PaO2 was higher and PaCO2 was lower in the CPAP/PSV group than the control group after pre-oxygenation, but these differences did not achieve statistical significance. However, blood gas data were only available from a minority of the patients. After intubation, patients were left apneic until decrease of SaO2 to 95%; the time to desaturation did not differ between the groups, but the authors concluded that the target level might have been set too high to detect a difference. In accordance with the above investigation, we found a modestly increased EtO2 during and after pre-oxygenation in the CPAP/PSV group. However, a higher EtO2 value alone does not necessarily imply a higher oxygen reserve, particularly in patients with a diminished FRC. In our view, a higher level of PaO2 immediately after the intubation attempt (as was found in our study) more clearly demonstrates the value of CPAP/PSV during anesthetic induction in obese patients consistent with less hypoxic events detected by pulse oximetry. By its impact on the alveolar gas equation, PaCO2 can affect PaO2. In the present study, the difference in PaCO2 after intubation reached statistical significance, but the difference was not large enough to influence our results. We chose, contrary to previous studies, low expiratory pressure (CPAP 5 cm H2O) but with the addition of flow-triggered positive inspiratory pressure (PSV 5 cm H2O). The administration of using low bi-level pressures is in our clinical experience better tolerated by ‘untrained patients’ than sole CPAP (unpublished observations from our bariatric anesthesia division and obstructive sleep apnea division). This finding is supported by the results of Baral’s healthy-volunteer study.26
our study is that we did not measure apnea times to desaturation, but rather attempted to restore optimal lung function by a volume recruitment maneuver and application of PEEP directly after intubation, so as not to subject the patients to unnecessary risk of atelectasis and hypoxia. The patients received detailed instruction of the experience of CPAP/PSV and the need for a tight mask fit, both during the consent process and directly before pre-oxygenation. The pressure levels were relatively low because there is a certain risk of gastric distension, as seen in a few patients both in our study and that of Delay et al.25 It is also important to recognize that different models of anesthesia ventilators differ significantly in their performance regarding trigger sensitivity and ability to meet inspiratory flow requirements.29 Only the most recent models approach the capacity of ICU ventilators, and the results of our study would only apply to a high-performance ventilator. In accordance with what is probably the current standard of practice for general anesthesia involving muscle paralysis in obese patients, we performed a volume recruiting maneuver directly after intubation in all subjects and continued positive pressure ventilation with PEEP, at an FiO2 adequate for oxygenation yet unlikely to contribute to resorption atelectasis (40%).30 We saw no differences in oxygenation parameters between the groups at any of the subsequent time points after anesthesia induction phase. In summary, this study has shown that CPAP/PSV during pre-oxygenation of obese patients resulted in significantly higher PaO2 and no oxygen desaturations after a 60 s apnea period with a rapid-sequence induction, compared with preoxygenation with neutral pressure.
Study limitations
Clinical implication
We pre-oxygenated with 80% O2 at a high flow rate in a circle system. One-hundred-percent oxygen is commonly used for pre-oxygenation, yet it is associated with increased atelectasis.27 However, in that study, it was also demonstrated that the safe apneic time until desaturation to SpO2 90% was significantly shorter than when 100% oxygen was used. This may be a point of criticism in regard to our protocol. Also, the time of pre-oxygenation was fixed at 2 min, which is shorter than the more commonly used 3 min period. Still, the study of Berry and Myles28 demonstrated a relatively flat part of the oxygen wash-in graph between 120 and 180 s, indicating that our choice of a 2 min pre-oxygenation period probably was adequate. Another limitation of
Our study suggests that pre-oxygenation with lowpressure CPAP/PSV applied during induction of anesthesia of morbidly obese patients may improve oxygenation of arterial blood when compared with conventional management without any respiratory support. Of note, however, this effect was only of short duration.
Acknowledgment The authors would like to express their deep gratitude to Professor Göran Hedenstierna for his encouragement and useful critiques during manuscript work. Conflict of interest: None Funding: Funding received from Department of Anesthesiology, Danderyd Hospital.
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Address: Piotr Harbut Department of Anesthesiology and Intensive Care Danderyd Hospital SE-182 88 Stockholm Sweden e-mail: [email protected]
Appendix CONSORT 2010 Flow Diagram In our institution, a total number of 113 patients have been scheduled for the elective gastric by-pass surgery during the randomization period. Ninety of them have been assessed for eligibility.
