Secondary Logo

Journal Logo

Featured Articles: Narrative Review Article

Obesity and Obesity Hypoventilation, Sleep Hypoventilation, and Postoperative Respiratory Failure

Kaw, Roop MD*; Wong, Jean MD, FRCPC†,‡,§; Mokhlesi, Babak MD

Author Information
doi: 10.1213/ANE.0000000000005352
  • Free


Diagnosis of obesity hypoventilation syndrome (OHS) requires obesity defined by body mass index (BMI) ≥30 kg/m2, sleep-disordered breathing, and awake daytime hypercapnia (awake resting Paco2 ≥ 45 mm Hg), after other causes for hypoventilation have been excluded.1 Patients with OHS are more likely to have comorbidities like chronic heart failure (CHF) and pulmonary hypertension (PH) when compared to eucapnic obese patients. They are also more likely to require hospitalization due to acute-on-chronic hypercapnic respiratory failure and have higher mortality when compared to patients with obstructive sleep apnea (OSA).2

The prevalence of OHS has been estimated to be about 0.4% of the adult population3 and increases with higher BMI.4 Approximately 8%–20% of obese patients referred to sleep clinics are diagnosed with OHS.4,5 Patients with hypercapnia from definite or possible OHS are at higher risk for postoperative respiratory failure, postoperative heart failure, prolonged intubation, postoperative intensive care unit (ICU) transfer, and longer ICU and hospital stay when compared to patients with OSA.6

OSA as defined by an apnea-hypopnea index (AHI) ≥5 is seen in 90% of patients with OHS, and up to 70% have severe OSA (AHI ≥30 events/h).7 Nonobstructive hypoventilation that worsens during sleep can be seen in up to 10% patients with OHS.8 Sleep-related hypoventilation is suggested by the presence of persistent hypoxemia during sleep (mostly rapid eye movement [REM] sleep), not present during wakefulness. Its presence is confirmed by monitoring of carbon dioxide levels during sleep (an increase in Pco2 >55 mm Hg for >10 minutes or an increase in Pco2 >10 mm Hg during sleep in comparison to awake supine values to a value exceeding 50 mm Hg for >10 minutes, typically measured by transcutaneous Pco2 monitoring). Sleep-related hypoventilation can be attributed to OHS, medications that impair ventilatory drive, or an underlying pulmonary or neuromuscular disorder.

Polysomnography is required to diagnose OHS and to individualize therapy. Weight loss is the optimal treatment for OHS. However, because weight loss may be difficult to achieve, positive airway pressure (PAP) therapy is the mainstay of treatment of sleep-disordered breathing in these patients. In addition to improving sleep-disordered breathing during sleep, effective PAP therapy can improve awake hypoxemia and hypercapnia after 2–6 weeks of use. Continuous positive airway pressure (CPAP) or noninvasive ventilation (NIV) usually with bilevel PAP settings or volume-targeted pressure support are the most commonly prescribed PAP modalities for patients with OHS9 (Figure 1).

Figure 1.:
Treatment algorithm for ambulatory and hospitalized patients with suspected OHS. ABG indicates arterial blood gas; CPAP, continuous positive airway pressure; NIV, noninvasive ventilation; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnea; PAP, positive airway pressure; SDB, sleep disordered breathing.

Although most anesthesiologists are aware of practice guidelines for management of surgical patients with OSA, OHS may be underdiagnosed or underrecognized by anesthesiologists and surgeons. As the prevalence of obesity and morbid obesity increases worldwide, anesthesiologists are more likely to encounter patients with OHS for obesity- and nonobesity-related surgery. The objectives of this review are to discuss the preoperative assessment and intraoperative and postoperative management of patients with OHS.


A thorough history and physical examination can help identify comorbid conditions associated with OHS. The most common among these are severe OSA, hypersomnolence, and severe obesity (BMI ≥40 kg/m2).7 OSA may have been previously diagnosed on the basis of polysomnography or suspected on the basis of a validated screening questionnaire. OHS is more likely in patients with severe obesity, severe OSA, and restrictive thoracic defect on spirometry or pulmonary function testing.10 As Paco2 increases in patients with OHS, renal compensation leads to retention of serum bicarbonate to maintain a balanced pH in the arterial blood. As such, serum bicarbonate can be used as a screening tool. If a patient has a low or moderate probability of having OHS, and the serum bicarbonate is <27 mEq/L, the probability of OHS is extremely low. However, an elevated serum bicarbonate >27 mEq/L has a low specificity and, therefore, cannot be used as a diagnostic tool for OHS. The American Thoracic Society (ATS) recommends obtaining an arterial blood gas (ABG) in severely obese patients with signs and symptoms of OHS, if the serum bicarbonate >27 mEq/L not explained by another cause9 (Figure 2). Additional preoperative evaluation has also been recommended in patients with suspected or partially treated OSA, if they have evidence of hypoventilation, PH, and resting hypoxemia not attributable to other cardiopulmonary diseases.11

Figure 2.:
Perioperative decision tree in patients with suspected OHS. ABG indicates arterial blood gas; AHI, apnea-hypopnea index; BMI, body mass index; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnea; PSG, polysomnography; Spo 2, oxygen saturation.

The STOP-Bang (Snoring, Tiredness, Observed apnea, high blood Pressure, Body mass index, Age, Neck circumference and Gender) questionnaire is a commonly used screening tool for OSA in surgical patients with high sensitivity at scores >3 but with lower specificity for moderate OSA (47%) and severe OSA (37%).12 The specificity for predicting OSA can be increased to 85% with a measured serum bicarbonate >27 mEq/L and, in the case of severe OSA, to 79% with serum bicarbonate >27 mEq/L.13 When possible, consideration should be given to obtaining polysomnography preoperatively (Figure 2), but there is no evidence to support cancelling or delaying elective surgery to formally diagnose patients with suspected OSA unless there is associated uncontrolled systemic disease or evidence of hypoventilation.11

Ambulatory Versus Inpatient Surgery

Patients with OHS are generally not suitable candidates for surgery at office-based practices or ambulatory surgical centers that are not attached to a hospital.11 These facilities usually do not have adequate PAP equipment, staffing, postoperative monitoring, and the ability to admit patients for intraoperative or postoperative complications. Consideration can however be given to those compliant with PAP, optimized comorbid conditions, and minimal anticipated postoperative opioid requirements.


Airway Management

Presence of OSA and obesity in patients with OHS together places patients at risk of airway management problems in the perioperative period. Obesity, thick neck, and OSA are all independent predictors of difficult mask ventilation.14 Awake fiberoptic intubation under local anesthesia may be required if difficult mask ventilation is suspected. In such situations, videolaryngoscopy should also be readily available and supraglottic airway devices can be used as a rescue device and conduit for intubation (Table).

Table. - Recommendations for Perioperative Management of OHS
- In patients with known or suspected OSA, consider additional preoperative evaluation when there is evidence of hypoventilation, pulmonary hypertension, and or resting hypoxemia not attributable to other cardiopulmonary diseases.
- Patients with severe OSA should be screened for OHS preoperatively.
- Serum bicarbonate should be part of routine screening for OHS. A relatively recent serum bicarbonate (in the last 2–3 mo) ≤27 mEq/L is very useful to exclude OHS.
- If in a severely obese patient, the clinical suspicion for OHS is high, consider getting an ABG preoperatively if the serum bicarbonate is >27 mEq/L.
- Although there is a paucity of literature on OHS patients, local or regional anesthesia techniques wherever possible avoid airway complications and respiratory depression due to residual neuromuscular blockade and sedation associated with general anesthesia.
- Ramped position is preferred for induction and intubation.
- Avoid sedatives as premedication as much as possible.
- Apneic oxygenation with high-flow nasal oxygen during laryngoscopy may help prevent desaturation, increase safe apnea time during induction of general anesthesia, and can be used in conjunction with/or as an alternative to conventional preoperative oxygenation with a facemask.
- Extubation should be done when the patient is close to fully awake and without residual sedation or neuromuscular weakness.
- Monitoring the patient in the PACU for recurrent respiratory events, including apnea, bradypnea, pain-sedation mismatch, CO2 retention, or oxygen desaturation can identify patients at high risk for postoperative respiratory complications and need for increased postoperative monitoring.
- Opioid analgesia, if possible, should be avoided, otherwise titrated slowly with careful monitoring.
- Caution should be advised in using high-flow supplemental oxygen in postoperative obese patients with known or suspected OHS especially when they are sedated and on intravenous opioids.
Abbreviations: ABG, arterial blood gas; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnea; PACU, postanesthesia care unit.

Preoxygenation with 100% oxygen in a 25° head-up position using a tight-fitting mask can prolong the time to desaturation.15 During apnea, more oxygen is absorbed from the lungs compared to the amount of carbon dioxide produced, leading to net negative pressure which can augment ventilation, providing that the airway is patent. Adding CPAP up to 10 cm H2O to oxygen for 5 minutes until the moment of intubation can also reduce the drop in functional residual capacity (FRC) due to change in body position, paralysis, and absorptive atelectasis from high concentration of oxygen and thereby help prolong nonhypoxic apnea up to a minute.16 Apneic oxygenation with high-flow nasal oxygen during laryngoscopy may help prevent desaturation in patients with OHS and anticipated difficult intubation.17

Positioning for Induction of Anesthesia

The head elevation laryngoscopy position (HELP) provides a better laryngeal view by aligning the pharyngeal and laryngeal axis when the angle of neck flexion over the chest is about 35°.18 In the morbidly obese, this can only be achieved by a 35° flexion of lower cervical spine on the chest and a 90° extension of the head on the neck at the atlanto-occipital joint also known as the ramp position.19 Elevation pillows such as the Troop Elevation Pillow place obese patients in optimal position for both preoxygenation and intubation.20

Preoxygenation with the patient in the 25° back-up position compared to the supine position resulted in higher Pao2 and longer time to desaturate to 92% during an apnea.15 For upper abdominal laparoscopic procedures, a beach chair position with the table in 20° reverse Trendelenburg and legs elevated at 45° provides a larger abdominal working space and increases end-expiratory lung volumes during upper abdominal surgery. For lower abdominal laparoscopic procedures, the Trendelenburg is ideal.21 Skilled staff such as anesthesiology assistants or respiratory therapists should be available to assist with airway management.

Choice of Anesthesia

In patients with OSA, local or regional anesthesia techniques such as peripheral nerve blocks rather than general anesthesia where appropriate are strongly recommended by both the American Society of Anesthesiologists and Society of Anesthesia and Sleep Medicine.22,23 Although there is a paucity of literature on OHS patients undergoing surgery, local or regional anesthesia techniques avoid airway complications and respiratory depression (RD) due to residual neuromuscular blockade and sedation associated with general anesthesia; therefore, similar recommendations are likely prudent. Patients with OHS have an already blunted respiratory drive, therefore central neuraxial anesthesia is preferred over general anesthesia and airway instrumentation.24 In morbidly obese patients with minimal landmarks, these techniques, however, can be technically more difficult, requiring specialized equipment (eg, longer spinal or epidural needles), and likely ultrasound or even fluoroscopic guidance.25 Obese patients also often cannot tolerate supine or Trendelenburg positions, so hypotension can be a big concern during neuraxial anesthesia.

Epidural anesthesia is preferred over spinal anesthesia, if PH is suspected, because the latter has a rapid onset and profound sympatholytic effect. Hypotension can precipitate right ventricular ischemia and is best avoided in patients with PH. In patients with PH, etomidate is preferred for induction over propofol because of minimal effect on myocardial contractility and systemic vascular resistance.26 Nitrous oxide can also worsen right ventricular ischemia by increasing pulmonary resistance and causing an obligatory decrease in the fraction of inspired oxygen (Fio2).27 During local or regional anesthesia techniques, minimal sedation should be given to avoid airway obstruction, hypoventilation, and hypercapnia. Continuous capnography is recommended to detect airway obstruction when moderate sedation is used. Consideration should be given to bringing the patient’s PAP device into the operating room to use intraoperatively.28

Dosing of anesthetic agents is challenging since morbidly obese patients have often been

excluded from clinical trials during the drug development process.29 While dosing general anesthetic agents, lipophilicity and volume of distribution need to be taken into consideration. Loading dose should be calculated based on lean body weight (LBW) for drugs that are mainly distributed to lean tissues and based on total body weight (TBW) for drugs equally distributed in adipose and lean tissues. Propofol, for example, is highly lipophilic and its pharmacokinetics are cardiac output dependent; thus, a high volume of distribution in obese patients should be dosed based on TBW.30 Hydrophilic compounds like neuromuscular blockers should be dosed based on LBW, with the exception of succinylcholine. Obese patients have higher levels of plasma cholinesterase and metabolize succinylcholine, so it should be dosed based on TBW.31 Rocuronium, a good alternative for rapid induction when succinylcholine is contraindicated, is dosed by LBW.32 For maintenance, a drug with similar clearance in both obese and nonobese patients should be based on LBW, while drugs whose clearance increases with obesity should have the maintenance dose calculated according to TBW.29,33 Neostigmine should be based on TBW and half-life of neuromuscular blocking agents being reversed and should be titrated for desired effect.34

Intraoperative Ventilation Strategies

Tidal volumes used on the basis of TBW instead of ideal body weight may be overestimated by 20%–50%,35 and potentially increase postoperative pulmonary complications.36 In patients undergoing laparoscopic surgery, pressure control ventilation has been shown to result in better intraoperative oxygenation when compared to volume-controlled ventilation.37 Positive end-expiratory pressure (PEEP) carefully titrated up to 10 cm H2O can mitigate atelectasis after laparoscopic bariatric surgery.36

In nonobese patients undergoing laparoscopic or open abdominal surgery, tidal volumes of 6–8 mL/kg of predicted body weight, PEEP of 6–8 cm H2O, and lung recruitment in the form of 30 seconds of CPAP at 30 cm H2O improved the incidence of postoperative pulmonary and extrapulmonary complications.38 More recently, however, high levels of PEEP (12 cm H2O) and alveolar recruitment maneuvers during intraoperative mechanical ventilation did not reduce postoperative pulmonary complications in obese patients, when compared to low levels of PEEP (4 cm H2O) although hypoxia was more frequent in the latter.39 It is important to mention here that this randomized controlled study did not specifically include patients with OHS or report its prevalence.


Postoperative Complications in OHS

Patients with OHS have higher prevalence of CHF, CAD, cor pulmonale, PH when compared to patients with OSA and obese eucapnic patients.6,40,41 Consequently, patients with hypercapnia from definite or possible OHS or from overlap syndrome (OSA with concomitant chronic obstructive pulmonary disease [COPD]) are more likely to have postoperative respiratory failure, heart failure, prolonged intubation, postoperative ICU transfer, and longer ICU and hospital stay, when compared to those with OSA6 (Table).

In patients undergoing bariatric surgery, higher surgical mortality (2.4%) has been reported in patients with a higher Obesity Surgery Mortality Risk Score (OS-MRS: 4–5) compared to 0.2% in low-risk patients (OS-MRS: 0–1). OS-MRS assigns 1 point to each of the 5 preoperative variables: arterial hypertension, male sex, BMI >50 kg/m2, age >45 years, and risk factors for pulmonary thromboembolism (prior venous thromboembolism, hypoventilation, PH, presence of inferior vena cava filter).42 In obese patients, when postoperative respiratory failure is not explained by other predisposing risk factors, OHS should be strongly considered.

Extubation and PAP Therapy After Anesthesia

Obese patients should be extubated only after they have regained consciousness, preferably in the semisitting or in the sitting position. Sevoflurane and desflurane are preferred as maintenance anesthesia during tracheal extubation to allow rapid recovery. Even with their rapid recovery profile, subanesthetic concentrations of these anesthetics can impair the already blunted hypoxic and hypercapnic drives causing postoperative hypoxemia.43 Adding short-acting adjuvants like remifentanil or combining general and regional anesthetics can help reduce the dose of volatile anesthetics and washout time from muscle and fat.44 Complete reversal of muscle relaxant effect should be emphasized.22 Even minor reduction in train-of-four fade ratio (<0.9) from a residual anesthetic effect may worsen the hypercapnia in patients with OHS. Acute respiratory acidosis augments the activity of some neuromuscular blocking agents and interferes with their reversal. Therefore, a low tidal volume will result in a vicious cycle of worsening respiratory acidosis and blunting of respiratory drive that ultimately leads to worsening hypercapnia and hypoxemia when supplemental oxygen is used.45,46

NIV initiation immediately after extubation has been shown to reduce postextubation respiratory failure and prevent reintubation in obese ICU patients, especially those who develop signs of airway obstruction.47 In patients with OHS, inspiratory PAP ranging from 18 to 20 cm H2O and an expiratory PAP of 8 to 10 cm H2O can be tried empirically, based on typical requirements in patients with known OHS. Ventilation can be increased by a combination of increasing tidal volume, decreasing dead space ventilation, and increasing respiratory rate. Increasing pressure support (pressure support = inspiratory positive airway pressure [IPAP] − expiratory positive airway pressure [EPAP]) will increase tidal volumes. There are 2 ways to increase pressure support: increasing IPAP or decreasing EPAP. Patients will require lower EPAP in the sitting position because it can improve upper airway collapsibility. By lowering EPAP and keeping the same IPAP, the patient will effectively receive a higher level of pressure support leading to larger tidal volumes. It is important to note that, in the immediate postoperative setting, bilevel PAP ventilation should ideally include a backup respiratory rate (bilevel PAP spontaneous/timed or ST). The backup respiratory rate should be set 2–3 breaths per minute below the patient’s spontaneous rate before surgery keeping in mind that the respiratory rate may be low in the immediate postoperative period as the patient is recovering from anesthetics and sedatives. Volume-assisted pressure devices can adjust inspiratory PAP and provide optimal pressure support targeted to expiratory tidal volume or alveolar ventilation averaged over several breaths, but their use is not currently supported in the perioperative setting.48

Monitoring the patient in the postanesthesia care unit (PACU) for recurrent respiratory events, including apnea, bradypnea, pain-sedation mismatch, CO2 retention, or oxygen desaturation can identify patients at high risk for postoperative respiratory complications and need for increased postoperative monitoring.49 Maintaining patients with OHS in a semisitting or sitting position in the PACU and on the ward may be advantageous because it can improve upper airway collapsibility leading to improved OSA and may decrease atelectasis and dead space ventilation.

Monitoring of Opioid-Induced Respiratory Depression

Opioids tend to raise the apneic threshold (rightward shift of CO2 response curve) and reduce the minute ventilation response to increasing Paco2 (decrease the slope of the CO2 response curve).50,51 Patients with OHS are known to have a decreased hypoxic ventilatory drive.28

Central neuraxial blocks, peripheral nerve blocks, peripheral nerve catheters, local anesthetic infiltration, and other multimodal opioid-sparing regimens like acetaminophen and nonsteroidal anti-inflammatory drugs can help minimize opioid-induced respiratory depression (OIRD).52 Dexmedetomidine, clonidine, intravenous lidocaine, low-dose ketamine, and low-dose magnesium have also been reported but await high-quality supportive evidence.53 Centralized continuous pulse oximetry monitoring as recommended by the American Patient Safety Foundation (APSF) can help in early detection of OIRD.54 Low respiratory rate is not a reliable sign of OIRD; therefore, implementation of sedation scoring systems can also help better detect OIRD.55,56 It has been reported that standard spot checks of pulse oximetry every 4–6 hours can miss more than 90% of prolonged hypoxemic episodes on the general surgical floors.57 OIRD in postoperative patients receiving intravenous opioids can evolve very rapidly as reported by a closed claims analysis and most events can be prevented. RD was discovered within 2 hours of the last nursing check in 42% claims and within 15 minutes in 16% of the claims.58 More recently, an international prospective trial (PRediction of Opioid-induced Respiratory Depression In Patients monitored by capnoGraphY [PRODIGY]) developed a risk prediction tool designed to predict OIRD in 1335 hospitalized patients on general medical/surgical floors, using continuous capnography and oximetry, of which 614 (46%) developed one or more episodes of RD. Patients with a high PRODIGY score >15 were more likely to develop OIRD compared to those with a PRODIGY score <8 (odds ratio [OR] = 6.07, 95% confidence interval [CI] 4.44-8.30).59

Supplemental Oxygen in OHS

Patients with known OHS should resumed on their PAP device postoperatively, regardless, up to 40% of patients with OHS are prescribed nocturnal home oxygen in addition.60 Supplemental oxygen therapy can hamper early detection of OIRD using pulse oximetry.61 Extreme caution is particularly advised against prolonged use of high concentration (50%) of supplemental oxygen in patients with OHS because it can worsen hypoventilation.62,63 In patients with OHS, receiving high-flow oxygen postoperatively for any reason after surgery, while on intravenous patient-controlled analgesia capnographic monitoring of ventilation, is advisable.64


OHS is distinct from OSA and may be unrecognized by anesthesiologists. Patients with OHS are at higher risk for perioperative complications and anesthesiologists should have a high index of suspicion in morbidly obese patients who have signs or symptoms of OHS. Screening questionnaires and a serum bicarbonate can be used to screen for OHS. Preoperative referral to sleep medicine should be considered before major surgery for diagnosis and initiation of treatment with PAP therapy and treatment of comorbidities. Regional anesthetic techniques and opioid-sparing multimodal analgesics should be utilized when possible, and a difficult airway should be anticipated. PAP therapy should be used postoperatively, care should be taken with oxygen therapy, and careful monitoring of ventilation should be arranged for these high-risk patients.


Name: Roop Kaw, MD.

Contribution: This author was responsible for helping with the concept; drafting the manuscript preparation; critical revisions, assuring accuracy and integrity and final approval.

Conflicts of Interest: R. Kaw is involved in speaking engagements with Medtronic.

Name: Jean Wong, MD, FRCPC.

Contribution: This author helped with drafting the assigned sections of the manuscript; critical revisions, assuring accuracy and integrity and final approval.

Conflicts of Interest: J. Wong received grants from the Ontario Ministry of Health and Long-Term Care, Anesthesia Patient Safety Foundation and Merck Inc outside of the submitted work. J. Wong is supported by a Merit Research Award from the Department of Anesthesia, University of Toronto.

Name: Babak Mokhlesi, MD.

Contribution: This author helped with drafting the assigned sections of the manuscript; critical revisions, assuring accuracy and integrity and final approval.

Conflicts of Interest: None.

This manuscript was handled by: Toby N. Weingarten, MD.


    1. Mokhlesi B, Tulaimat A, Faibussowitsch I, Wang Y, Evans AT. Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea. Sleep Breath. 2007;11:117–124.
    2. Castro-Añón O, Pérez de Llano LA, De la Fuente Sánchez S, et al. Obesity-hypoventilation syndrome: increased risk of death over sleep apnea syndrome. PLoS One. 2015;10:e0117808.
    3. Masa JF, Pepin J-L, Borel J-C, Mokhlesi B, Murphy PB, Sanchez-Quiroga MA. Obesity hypoventilation syndrome. Eur Respir Rev. 2019;28:180097.
    4. Balachandran JS, Masa JF, Mokhlesi B. Obesity hypoventilation syndrome epidemiology and diagnosis. Sleep Med Clin. 2014;9:341–347.
    5. Harada Y, Chihara Y, Azuma M, et al.; Japan Respiratory Failure Group. Obesity hypoventilation syndrome in Japan and independent determinants of arterial carbon dioxide levels. Respirology. 2014;19:1233–1240.
    6. Kaw R, Bhateja P, Paz Y Mar H, et al. Postoperative complications in patients with unrecognized obesity hypoventilation syndrome undergoing elective noncardiac surgery. Chest. 2016;149:84–91.
    7. Masa JF, Corral J, Alonso ML, et al.; Spanish Sleep Network. Efficacy of different treatment alternatives for obesity hypoventilation syndrome. Pickwick study. Am J Respir Crit Care Med. 2015;192:86–95.
    8. Mokhlesi B. Obesity hypoventilation syndrome: a state-of-the-art review. Respir Care. 2010;55:1347–1362.
    9. Mokhlesi B, Masa JF, Brozek JL, et al. Evaluation and management of obesity hypoventilation syndrome. an official American Thoracic Society Clinical Practice Guideline. Am J Respir Crit Care Med. 2019;200:e6–e24.
    10. Kaw R, Hernandez AV, Walker E, Aboussouan L, Mokhlesi B. Determinants of hypercapnia in obese patients with obstructive sleep apnea: a systematic review and metaanalysis of cohort studies. Chest. 2009;136:787–796.
    11. Chung F, Memtsoudis SG, Ramachandran SK, et al. Society of anesthesia and sleep medicine guidelines on preoperative screening and assessment of adult patients with obstructive sleep apnea. Anesth Analg. 2016;123:452–473.
    12. Chung F, Subramanyam R, Liao P, Sasaki E, Shapiro C, Sun Y. High STOP-Bang score indicates a high probability of obstructive sleep apnoea. Br J Anaesth. 2012;108:768–775.
    13. Chung F, Chau E, Yang Y, Liao P, Hall R, Mokhlesi B. Serum bicarbonate level improves specificity of STOP-Bang screening for obstructive sleep apnea. Chest. 2013;143:1284–1293.
    14. Kheterpal S, Han R, Tremper KK, et al. Incidence and predictors of difficult and impossible mask ventilation. Anesthesiology. 2006;105:885–891.
    15. Dixon BJ, Dixon JB, Carden JR, et al. 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;102:1110–1115.
    16. 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;100:580–584.
    17. Wong DT, Dallaire A, Singh KP, et al. High-flow nasal oxygen improves safe apnea time in morbidly obese patients undergoing general anesthesia: a randomized controlled trial. Anesth Analg. 2019;129:1130–1136.
    18. Isono S. Optimal combination of head, mandible and body positions for pharyngeal airway maintenance during perioperative period: lesson from pharyngeal closing pressures. Semin Anesth. 2007;26:83–93.
    19. Collins JS, Lemmens HJ, Brodsky JB, Brock-Utne JG, Levitan RM. Laryngoscopy and morbid obesity: a comparison of the “sniff” and “ramped” positions. Obes Surg. 2004;14:1171–1175.
    20. Lee BJ, Kang JM, Kim DO. Laryngeal exposure during laryngoscopy is better in the 25 degrees back-up position than in the supine position. Br J Anaesth. 2007;99:581–586.
    21. Mulier JP, Dillemans B, Van Cauwenberge S. Impact of the patient’s body position on the intraabdominal workspace during laparoscopic surgery. Surg Endosc. 2010;24:1398–1402.
    22. American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Management of Patients With Obstructive Sleep Apnea. Anesthesiology. 2014;120:268–286.
    23. Memtsoudis SG, Cozowicz C, Nagappa M, et al. Society of Anesthesia and Sleep Medicine guideline on intraoperative management of adult patients with obstructive sleep apnea. Anesth Analg. 2018;127:967–987.
    24. Shimura R, Tatsumi K, Nakamura A, et al. Fat accumulation, leptin, and hypercapnia in obstructive sleep apnea-hypopnea syndrome. Chest. 2005;127:543–549.
    25. Chin KJ, Tse C, Chan V. Ultrasonographic identification of an anomalous femoral nerve: the fascia iliaca as a key landmark. Anesthesiology. 2011;115:1104.
    26. Ebert TJ, Muzi M, Berens R, Goff D, Kampine JP. Sympathetic responses to induction of anesthesia in humans with propofol or etomidate. Anesthesiology. 1992;76:725–733.
    27. Schulte-Sasse U, Hess W, Tarnow J. Pulmonary vascular responses to nitrous oxide in patients with normal and high pulmonary vascular resistance. Anesthesiology. 1982;57:9–13.
    28. Zwillich CW, Sutton FD, Pierson DJ, Greagh EM, Weil JV. Decreased hypoxic ventilatory drive in the obesity-hypoventilation syndrome. Am J Med. 1975;59:343–348.
    29. Ingrande J, Lemmens HJM. Dose adjustment of anaesthetics in the morbidly obese. Br J Anaesth. 2010;105(suppl 1):i16–i23.
    30. Cortínez LI, Anderson BJ, Penna A, et al. Influence of obesity on propofol pharmacokinetics: derivation of a pharmacokinetic model. Br J Anaesth. 2010;105:448–456.
    31. Lemmens HJ, Brodsky JB. The dose of succinylcholine in morbid obesity. Anesth Analg. 2006;102:438–442.
    32. Pösö T, Kesek D, Winsö O, Andersson S. Volatile rapid sequence induction in morbidly obese patients. Eur J Anaesthesiol. 2011;28:781–787.
    33. Leykin Y, Miotto L, Pellis T. Pharmacokinetic considerations in the obese. Best Pract Res Clin Anaesthesiol. 2011;25:27–36.
    34. Naguib M, Brull SJ, Kopman AF, et al. Consensus statement on perioperative use of neuromuscular monitoring. Anesth Analg. 2018;127:71–80.
    35. Jaber S, Coisel Y, Chanques G, et al. A multicentre observational study of intra-operative ventilatory management during general anaesthesia: tidal volumes and relation to body weight. Anaesthesia. 2012;67:999–1008.
    36. Talab HF, Zabani IA, Abdelrahman HS, et al. Intraoperative ventilatory strategies for prevention of pulmonary atelectasis in obese patients undergoing laparoscopic bariatric surgery. Anesth Analg. 2009;109:1511–1516.
    37. Cadi P, Guenoun T, Journois D, Chevallier J-M, Diehl J-L, Safran D. Pressure-controlled ventilation improves oxygenation during laparoscopic obesity surgery compared with volume-controlled ventilation. Br J Anaesth. 2008;100:709–716.
    38. Futier E, Constantin J-M, Paugam-Burtz C, et al. A trial of intraoperative low-tidal-volume ventilation in abdominal surgery. N Engl J Med. 2013;369:428–437.
    39. Bluth T, Serpa Neto A, Schultz MJ, Pelosi P, Gama de Abreu M. Writing Committee for the PROBESE Collaborative Group of the PROtective VEntilation Network (PROVEnet) for the Clinical Trial Network of the European Society of Anaesthesiology; Effect of intraoperative high positive end-expiratory pressure (PEEP) with recruitment maneuvers vs low PEEP on postoperative pulmonary complications in obese patients: a randomized clinical trial. JAMA. 2019;321:2292.
    40. Berg G, Delaive K, Manfreda J, Walld R, Kryger MH. The use of health-care resources in obesity-hypoventilation syndrome. Chest. 2001;120:377–383.
    41. Nowbar S, Burkart KM, Gonzales R, et al. Obesity-associated hypoventilation in hospitalized patients: prevalence, effects, and outcome. Am J Med. 2004;116:1–7.
    42. DeMaria EJ, Murr M, Byrne TK, et al. Validation of the obesity surgery mortality risk score in a multicenter study proves it stratifies mortality risk in patients undergoing gastric bypass for morbid obesity. Ann Surg. 2007;246:578–582.
    43. Gupta A, Stierer T, Zuckerman R, Sakima N, Parker SD, Fleisher LA. Comparison of recovery profile after ambulatory anesthesia with propofol, isoflurane, sevoflurane and desflurane: a systematic review. Anesth Analg. 2004;98:632–641.
    44. Hillman DR, Chung F. Anaesthetic management of sleep-disordered breathing in adults. Respirology. 2017;22:230–239.
    45. Kaw R, Argalious M, Aboussouan LS, Chung F. Obesity hypoventilation syndrome and anesthesia considerations. Sleep Med Clin. 2014;9:399–407.
    46. Chau EH, Lam D, Wong J, Mokhlesi B, Chung F. Obesity hypoventilation syndrome: a review of epidemiology, pathophysiology, and perioperative considerations. Anesthesiology. 2012;117:188–205.
    47. El-Solh AA, Aquilina A, Pineda L, Dhanvantri V, Grant B, Bouquin P. Noninvasive ventilation for prevention of post-extubation respiratory failure in obese patients. Eur Respir J. 2006;28:588–595.
    48. Selim BJ, Wolfe L, Coleman JM III, Dewan NA. Initiation of noninvasive ventilation for sleep related hypoventilation disorders: advanced modes and devices. Chest. 2018;153:251–265.
    49. Gali B, Whalen FX, Schroeder DR, Gay PC, Plevak DJ. Identification of patients at risk for postoperative respiratory complications using a preoperative obstructive sleep apnea screening tool and postanesthesia care assessment. Anesthesiology. 2009;110:869–877.
    50. Rowsell L, Wong KKH, Yee BJ, et al. The effect of acute morphine on obstructive sleep apnoea: a randomised double-blind placebo-controlled crossover trial. Thorax. 2019;74:177–184.
    51. Martins RT, Carberry JC, Wang D, Rowsell L, Grunstein R, Eckert DJ. Morphine alters respiratory control but not other key obstructive sleep apnoea phenotypes: a randomised trial. Eur Resp J. 2020;55:1901344.
    52. Apfelbaum JL, Hagberg CA, Caplan RA, et al. 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. 2013;118:251–270.
    53. de Raaff CAL, Gorter-Stam MAW, de Vries N, et al. Perioperative management of obstructive sleep apnea in bariatric surgery: a consensus guideline. Surg Obes Relat Dis. 2017;13:1095–1109.
    54. Taenzer AH, Pyke JB, McGrath SP, Blike GT. Impact of pulse oximetry surveillance on rescue events and intensive care unit transfers: a before-and-after concurrence study. Anesthesiology. 2010;112:282–287.
    55. Macintyre PE, Loadsman JA, Scott DA. Opioids, ventilation and acute pain management. Anaesth Intensive Care. 2011;39:545–558.
    56. Vila H Jr, Smith RA, Augustyniak MJ, et al. The efficacy and safety of pain management before and after implementation of hospital-wide pain management standards: is patient safety compromised by treatment based solely on numerical pain ratings? Anesth Analg. 2005;101:474–480.
    57. Sun Z, Sessler DI, Dalton JE, et al. Postoperative hypoxemia is common and persistent: a prospective blinded observational study. Anesth Analg. 2015;121:709–715.
    58. Lee LA, Caplan RA, Stephens LS, et al. Postoperative opioid-induced respiratory depression: a closed claims analysis. Anesthesiology. 2015;122:659–665.
    59. Khanna AK, Bergese SD, Jungquist CR, et al. Prediction of opioid-induced respiratory depression on inpatient wards using continuous capnography and oximetry: an international prospective observational trial. Anesth Analg. 2020;131:1012–1024.
    60. Banerjee D, Yee BJ, Piper AJ, Zwillich CW, Grunstein RR. Obesity hypoventilation syndrome: hypoxemia during continuous positive airway pressure. Chest. 2007;131:1678–1684.
    61. Fu ES, Downs JB, Schweiger JW, Miguel RV, Smith RA. Supplemental oxygen impairs detection of hypoventilation by pulse oximetry. Chest. 2004;126:1552–1558.
    62. Hollier CA, Harmer AR, Maxwell LJ, et al. Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study. Thorax. 2014;69:346–353.
    63. Liao P, Wong J, Singh M, et al. Postoperative oxygen therapy in patients with OSA: a randomized controlled trial. Chest. 2017;151:597–611.
    64. Chung F, Wong J, Mestek ML, Niebel KH, Lichtenthal P. Characterization of respiratory compromise and the potential clinical utility of capnography in the post-anesthesia care unit: a blinded observational trial. J Clin Monit Comput. 2020;34:541–551.
    Copyright © 2021 International Anesthesia Research Society