Secondary Logo

Journal Logo

Review Articles

Protective mechanical ventilation in the obese patient

Falcão, Luiz F.d.R. MD, MBA, PhD, TSAa; Pelosi, Paolo MD, FERSb,c; de Abreu, Marcelo Gama MD, MSc, PhD, DESAd

Author Information
International Anesthesiology Clinics: Summer 2020 - Volume 58 - Issue 3 - p 53-57
doi: 10.1097/AIA.0000000000000284
  • Free

On a global scale, obesity has increased in the past few decades,1 affecting >700 million individuals. Since the 1980s, the prevalence of obesity has doubled in many countries and continues to increase in most regions of the world.2 If current trends continue, by 2025, ∼2.7 billion adults will be overweight, with an additional 1 billion affected by obesity [body mass index (BMI) ≥30 kg/m2] and 177 million affected by morbid obesity3 (BMI ≥40 kg/m2). The obesity epidemic and the development of laparoscopic and robotic surgery have resulted in an exponential increase in bariatric procedures during the past decade, making them one of the more commonly performed gastrointestinal operations.4

Anesthesiologists play an important role in the success of these procedures, especially considering enhanced recovery protocols. For the obese population, the goal of the enhanced recovery after bariatric surgery pathway is to maintain physiological function and reduce perioperative surgical stress.5 In addition, there is a strong recommendation to perform lung-protective ventilation5 to avoid postoperative pulmonary complications (PPC). Enhanced recovery after bariatric surgery pathways improve outcomes and reduce morbidity and length of hospital stay.6 By protectively ventilating the lungs intraoperatively, PPC might be avoided and further improvement in outcome achieved.

Patients with obesity are under increased risk of PPC.7,8 Ball et al,9 in a study including only patients with obesity from the LAS VEGAS study,8 demonstrated that patients with morbid obesity had a higher incidence of PPC compared with nonobese patients (18.5% vs. 11.7%, respectively). Also, the incidence of severe PPC, excluding the cases of unplanned O2 therapy, was higher in morbidly obese compared with nonobese patients (7.3% vs. 2.8%, respectively). For this reason, the interest in strategies to improve protective mechanical ventilation in surgical patients with obesity has increased, as pointed out in the 2016 SIAARTI Consensus.10 Therefore, anesthesiologists must possess an updated knowledge on lung-protective ventilation to safely manage these patients.

In this review, we summarize the current state of knowledge about the respiratory physiology in obesity, the importance of intraoperative protective mechanical ventilation, and aspects of different ventilation settings to achieve the best intraoperative ventilation strategy.

Background of lung function in obesity, anesthesia, and surgery

Patients with obesity have unique respiratory physiology and ventilatory mechanics characteristics (Fig. 1). In addition, they more frequently present with respiratory comorbidities, which increases the risk of developing PPC. Excessive adipose tissue in the chest wall poses a major burden to the respiratory system. Atelectasis formation is usually increased due to reduction of transpulmonary pressure in dependent lung zones. The latter is directly related to a loss of respiratory system compliance that increases the intrapleural pressure, and ultimately leads to decreased end expiratory lung volume (EELV), a surrogate for functional residual capacity, and arterial oxygenation. Such changes are particularly important when the obese patient is anesthetized and adequate pressure to counteract decreased compliance is missing.

Figure 1
Figure 1:
Pulmonary function abnormalities resulting from obesity during spontaneous breathing and mechanical ventilation, followed by a summary of protective mechanical ventilation to avoid postoperative pulmonary complications. FiO2 indicates fraction of inspired oxygen; PBW, predicted body weight; PCV, pressure-controlled ventilation; PCV-VG, pressure control ventilation-volume guaranteed; PEEP, positive end expiratory pressure; SpO2, oxygen saturation; VCV, volume-controlled ventilation; VT: tidal volume.

During general anesthesia and mechanical ventilation, development of atelectasis can be relevant in patients with obesity and become a challenge. This is due to neuromuscular blockade, sedation, and supine and steep Trendelenburg positioning.11,12 The EELV of anesthetized patients decreases in part because of the reduction in respiratory muscle tone.13 During muscle relaxation for general anesthesia, the muscle tone of the diaphragm is lost, increasing abdominal pressure over the dependent regions of the lung, resulting in preferential ventilation of nondependent regions, and ventilation-perfusion mismatch. This is worst in the supine position during general anesthesia due to cephalic shift of the diaphragm contributing further to atelectasis formation.11 The amount of atelectasis formation has been shown to correlate with body weight.14 Accordingly, atelectasis is most pronounced in patients with morbid obesity, and might be present even in the postoperative period.15

During anesthesia and immediately after surgery, it is important to avoid atelectasis to preserve the integrity of the lung parenchyma. The formation of atelectasis can increase physiological shunt, ventilation-perfusion mismatch, and work of breathing.16 Once the lungs are less compliant at lower volumes, atelectasis can also impair respiratory mechanics.13 This effect can be reduced when the patient is in the sitting position during the postoperative period, with an increase in forced vital capacity ranging from 4.6% to 20%.17

The position of the patient for anesthesia and surgery plays an important role. In the supine position, cephalic displacement of the diaphragm occurs and the increased effect of the abdominal contents upon the diaphragm and the thoracic cavity decreases lung volumes.18 During laparoscopic surgery, the beach chair or reverse Trendelenburg position can promote higher lung compliance and a greater EELV.19 Prone positioning leads to a rise in EELV, reduces lung elastance, and improves gas exchange in mechanically ventilated obese patients compared with supine positioning.

Laparoscopic procedures can produce several challenges for intraoperative ventilatory support due to the respiratory physiological changes in obesity. Laparoscopic surgery requires the creation of pneumoperitoneum, achieved by insufflation of CO2 into the abdomen. Pneumoperitoneum is a well-tolerated state characterized by an increase in intra-abdominal pressure with important respiratory effects. The changes in mechanical ventilation are associated with compression of the lung bases by cephalic displacement of the diaphragm with ensuing reduction of the EELV, increased peak and mean airway pressures, and increased risk of pneumothorax.20 For this reason, pneumoperitoneum during general anesthesia can cause a reduction in blood oxygenation due to atelectasis,21 mainly in dependent regions.22 In addition, opening and closing of atelectatic regions can increase the mechanical stress on lung parenchyma.23 Thus, low lung volume can add to preoperative or intraoperative alterations in lung structure and homeostasis to produce significant perioperative lung dysfunction.

Therefore, the patient with obesity under general anesthesia and mechanical ventilation for laparoscopic surgery poses a major challenge to the anesthesiologist because there is a need to limit the consequences of mechanical ventilation on the lung parenchyma, and thereby reduce the risk of PPC. Although different strategies may play a role in protective ventilation, settings suggested to protect lungs from ventilator-induced lung injury (VILI) include low tidal volumes (VT) and a low positive end expiratory pressure (PEEP) level without recruitment maneuvers (RM),24,25 despite the higher incidence of atelectasis in obese patients.

Low tidal volume to protect lungs

In patients with obesity, low VT is recommended irrespective of the risk of atelectasis. Despite this recommendation, patients with obesity are still ventilated in the perioperative period with VT that are too high.26 In the late 1970s, the improvement of intraoperative gas exchange was associated with higher VT.27 Arterial oxygen tension values were comparable to that observed at PEEP of 10 cm H2O, but the potential of ventilation induced injurious effects from high VT was ignored. It is reasonable to believe that lung volume increases proportionally to body weight,28 but this does not hold not true in patients with obesity in whom the increase in body fat does not affect lung volume. Mammals in general have a normal VT of ∼6.3 mL/kg of ideal body weight,28 which has been termed “low” VT. There is now consensus that low VT is lung protective in patients with acute respiratory distress syndrome (ARDS).29 This cut-off has also been considered for patients under general anesthesia, where the general practice includes larger VT in patients with healthy lungs, leading to a vivid debate.30,31

In 2006, Fernandez-Perez et al32 showed that postoperative respiratory failure was more common in patients who were ventilated with larger VT [8.3 vs. 6.7 mL/kg predicted body weight (PBW)]. In cardiac surgery patients, VT >10 mL/kg PBW was a risk factor for postoperative complications, such as organ failure and prolonged stay in the intensive care unit.33 In abdominal surgery, the IMPROVE trial34 showed that in patients who were ventilated with 2 different VT and PEEP strategies (10 to 12 mL/kg and no PEEP vs. 6 to 8 mL/kg and PEEP of 6 to 8 cm H2O combined with periodic RM), the higher VT group had a greater risk of postoperative respiratory failure and longer in-hospital stay. Serpa Neto et al35 published a meta-analysis including surgical patients under general surgery and found a positive dose-response relationship between the incidence of PPC and VT.

In all patients (obese and nonobese) with healthy lungs, the optimal VT is in the range of 6 to 8 mL/kg of PBW. VT settings must be guided by the patient’s predicted body weight, considering sex and height, rather than the actual body weight. There are many formulas for the calculation of PBW.36 It is appropriate to use the ARDS Network PBW equation37 (50+[0.91×(cm height−152.4)] for males and 45.5+[0.91×(cm height−152.4)] for females) because it is associated with studies that identified 6 mL/kg PBW as an appropriate target for ARDS patients36 and is the equation used by several publications on mechanical ventilation, such as LAS VEGAS.8

PEEP and recruitment maneuvers—the open lung controversy

Patients with obesity are predisposed to develop atelectasis mainly in dependent lung regions, making RM and PEEP a strategy to improve gas exchange and lung mechanics38,39 through reopening collapsed alveoli and maintaining the aeration of lungs.38,40 Application of PEEP may also eliminate auto-PEEP without increasing plateau pressure.18 Whereas PEEP alone does not reduce atelectasis in patients with morbid obesity after anesthetic induction,41 a meta-analysis from Barbosa et al42 suggested that an open lung approach with PEEP improves postoperative oxygenation and decreases atelectasis after surgery without adverse events. However, Whalen et al43 suggested that, although intraoperative RM followed by PEEP of 12 cm H2O improved gas exchange, this effect disappeared 30 minutes after extubation. For PEEP, a large meta-analysis from Serpa Neto et al35 showed that PPC was not different for high or low PEEP levels. In-hospital mortality and length of stay were also similar. There was no association between higher cut-offs of PEEP and the incidence of PPC compared with 0 to 2 cm H2O. Similarly, the incidence of PPC was not different for patients receiving RM (adjusted relative risk, 0.84; 95% confidence interval, 0.54-1.29; P=0.84). Interestingly, Ball et al9 showed that RM by bag squeezing and “rescue” RM were associated with the development of PPC.

There is much uncertainty in terms of the optimal level of PEEP for patients with obesity and healthy lungs. Recently, the results of the largest study on mechanical ventilation ever, namely, the “Protective Intraoperative Ventilation with Higher Versus Lower Levels of Positive End-Expiratory Pressure in Obese Patients (PROBESE)” trial,24 were published. PROBESE24 enrolled 1976 patients with obesity under general anesthesia with the goal of testing whether a higher level of PEEP (12 cm H2O) and RM reduced the incidence of PPC during the initial 5 postoperative days compared with a lower level of PEEP (4 cm H2O) without alveolar RM. The rate of PPC was 21.3% among those randomized to alveolar RM and higher PEEP compared with 23.6% among those with lower PEEP without alveolar RM; there was no statistically significant difference. Patients in the higher PEEP group showed lower driving pressure (12 vs. 17.9 cm H2O for the lower PEEP group), but this did not result in improved clinical outcome. This result demonstrates that driving pressure usefulness as a therapeutic target is still unclear. Low PEEP was associated with an overall lower risk of adverse events (eg, pleural effusion, hypotension, bradycardia, and use of vasoactive drugs) compared with the high PEEP group; therefore, patients with obesity might be ventilated with low VT and PEEP equal to or below 4 cm H2O without RM. In case of desaturation, clinicians should increase FiO2. Therefore, the role of PEEP and RM in avoiding PPC is still unclear and anesthesiologists might choose PEEP to improve lung function or maintain hemodynamic stability, as indicated.

Some researchers speculate that the strategy to protect the lungs should include individualized levels of PEEP targeted to physiological goals, as excessive or suboptimal PEEP may fail to prevent PPC. It is already known that PEEP requirements vary extensively among patients44 receiving low VT during anesthesia and individualized PEEP settings can reduce postoperative atelectasis while improving intraoperative gas exchange and driving pressures. A major challenge is that PEEP titration must be simple enough to make it feasible in routine anesthesia.30,45 Another concern is that the “best” PEEP may vary according to the physiological goal. Furthermore, physiological goals are not necessarily translated into maximal lung protection. In fact, PEEP represents a compromise between hyperdistention and atelectasis,46 and volutrauma was shown to produce more lung inflammation than atelectrauma.47

Mechanical ventilation mode

There is no strong evidence for superior lung protection with either volume or pressure-controlled mechanical ventilation.40 The preferred ventilatory mode for patients with obesity is pressure-controlled ventilation (PCV) because it can promote more homogeneous ventilation within different lung compartments, which in turn mitigates alveolar overdistention and improves oxygenation.48,49 In patients with obesity undergoing laparoscopic surgery in the Trendelenburg position, PCV with an inverse respiratory ratio (1.5:1) can improve ventilation, promote gas exchange and oxygenation, and is associated with decreased levels of surfactant protein A and TNF-alpha.50 However, volume-controlled ventilation allows better control of VT during procedures intermittently affecting chest wall compliance. A recent large retrospective study51 found an association between the use of volume-controlled ventilation and lower incidence of PPC. However, to our knowledge, there is no evidence suggesting superior clinical outcomes with use of different intraoperative ventilatory modes in patients with obesity.40

Pressure control ventilation-volume guaranteed (PCV-VG) has been gaining popularity among anesthetists. It is a mode with a variable inspiratory flow to achieve a preset VT. PCV-VG may have some advantages in the obese patient by assuring a low VT with lower peak inspiratory pressures,52 even during laparoscopic surgery in the Trendelenburg position.53 It is likely not the mode of mechanical ventilation that is key,54 but rather intraoperative vigilance of VT and driving pressure, particularly when respiratory compliance changes frequently.

Airway pressure, driving pressure, and transpulmonary pressure

Ball et al9 demonstrated that high peak airway pressures during anesthesia are associated with PPC. However, the airway pressure is not sufficient to quantify the real forces acting on the lung tissue that are supposed to cause VILI.55 The components of the whole respiratory system (lung and wall) define the respiratory system compliance. Therefore, ventilating patients with lower chest wall compliance, as in patients with obesity, with a limited plateau pressure (30 cm H2O) may lead to atelectasis and hypoxemia. In other words, during mechanical ventilation in patients with obesity, the lungs and predominantly the chest wall become “stiffer,” which can require higher pressure to insufflate the lungs. Thus, it seems to make sense to monitor the mechanical ventilation via the driving pressure, which represents the VT adjusted for the respiratory system compliance.

Driving pressure is calculated as the difference between plateau pressure and PEEP. Recently, higher driving pressures were associated with mortality in ARDS,56 and in a large retrospective study,57 intraoperative driving pressure above 13 cm H2O was associated with a 2-fold increase in the incidence of PPC. A recent meta-analysis observed a dose-response effect between driving pressure and the development of PPC.31 In patients with obesity, keeping driving pressure below a desired threshold is not always achievable, as a patient might be objectively difficult to ventilate due to low lung compliance or surgical conditions.

The cut-off value of protective driving pressure in patients with obesity is likely higher than that in nonobese patients. It should ideally be limited to a maximum value of 17 cm H2O in ARDS and 15 cm H2O in non-ARDS patients with obesity.58 Notably, the PROBESE trial24 could not detect a beneficial effect of reducing the driving pressure by 5 cm H2O, on average, on PPC. This result is in line with the meta-analysis from Serpa Neto et al,31 where an increase in the level of PEEP that results in an increase in driving pressure is associated with a greater risk of PPC than in patients ventilated with low PEEP. Therefore, appropriate use of driving pressure might be helpful to (1) avoid excessive levels of PEEP and to (2) optimize tidal volume.

Airway pressure cannot quantify the real forces acting on the lung tissue. Transpulmonary pressure can reflect the actual lung distending pressure, which represents the pressure difference between the airway pressure and pleural pressure. In this respect, the most physiological approach to set protective mechanical ventilation and to prevent VILI should be targeting transpulmonary pressure instead of plateau pressure or driving pressure. The main challenge is to simplify the transpulmonary pressure measurement in clinical practice.

New researchers are attempting to interpret VILI as the result of energy transfer from ventilation to the respiratory system.59 This theory was considered for the injured lung, but can be extrapolated for protective ventilation in healthy lungs because the energy is transferred to the lungs through mechanical power, triggering inflammation.


Protective mechanical ventilation is strongly recommended to avoid PPC. In the light of current evidence, this can be achieved with low VT (6 to 8 mL/kg ideal body weight) and low PEEP (<5 cm H2O) without RM. For rescue from intraoperative hypoxemia, an increase of PEEP and RM can be considered whenever the adjustment of FiO2 alone is not sufficient, or contraindicated. The role of driving pressure for guiding mechanical ventilation in surgical patients with obesity remains to be determined, but adjustments of PEEP that lead to an increase of driving pressure should ideally be avoided.

Conflicts of interest disclosure

The authors declare that they have nothing to disclose.


1. Piche ME, Poirier P, Lemieux I, et al. Overview of epidemiology and contribution of obesity and body fat distribution to cardiovascular disease: an update. Prog Cardiovasc Dis. 2018;61:103–113.
2. Ng M, Fleming T, Robinson M, et al. Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013. Lancet. 2014;384:766–781.
3. World Obesity Federation. About obesity. 2017. Available at: Accessed September 23, 2018.
4. Smith BR, Schauer P, Nguyen NT. Surgical approaches to the treatment of obesity: bariatric surgery. Endocrinol Metab Clin North Am. 2008;37:943–964.
5. Thorell A, MacCormick AD, Awad S, et al. Guidelines for perioperative care in bariatric surgery: Enhanced Recovery After Surgery (ERAS) Society recommendations. World J Surg. 2016;40:2065–2083.
6. Ahmed OS, Rogers AC, Bolger JC, et al. Meta-analysis of enhanced recovery protocols in bariatric surgery. J Gastrointest Surg. 2018;22:964–972.
7. Bamgbade OA, Rutter TW, Nafiu OO, et al. Postoperative complications in obese and nonobese patients. World J Surg. 2007;31:556–560; discussion 561.
8. LAS VEGAS Investigators. Epidemiology, practice of ventilation and outcome for patients at increased risk of postoperative pulmonary complications: LAS VEGAS—an observational study in 29 countries. Eur J Anaesthesiol. 2017;34:492–507.
9. Ball L, Hemmes SNT, Serpa Neto A, et al. Intraoperative ventilation settings and their associations with postoperative pulmonary complications in obese patients. Br J Anaesth. 2018;121:899–908.
10. Petrini F, Di Giacinto I, Cataldo R, et al. Perioperative and periprocedural airway management and respiratory safety for the obese patient: 2016 SIAARTI Consensus. Minerva Anestesiol. 2016;82:1314–1335.
11. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol. 1997;82:811–818.
12. Wahba RW. Perioperative functional residual capacity. Can J Anaesth. 1991;38:384–400.
13. Hedenstierna G, Rothen HU. Respiratory function during anesthesia: effects on gas exchange. Compr Physiol. 2012;2:69–96.
14. Strandberg A, Tokics L, Brismar B, et al. Constitutional factors promoting development of atelectasis during anaesthesia. Acta Anaesthesiol Scand. 1987;31:21–24.
15. Eichenberger A, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg. 2002;95:1788–1792.
16. Tokics L, Hedenstierna G, Svensson L, et al. V/Q distribution and correlation to atelectasis in anesthetized paralyzed humans. J Appl Physiol. 1996;81:1822–1833.
17. Martinez BP, Silva JR, Silva VS, et al. Influence of different body positions in vital capacity in patients on postoperative upper abdominal. Braz J Anesthesiol. 2015;65:217–221.
18. Lemyze M, Mallat J, Duhamel A, et al. Effects of sitting position and applied positive end-expiratory pressure on respiratory mechanics of critically ill obese patients receiving mechanical ventilation. Crit Care Med. 2013;41:2592–2599.
19. Valenza F, Vagginelli F, Tiby A, et al. Effects of the beach chair position, positive end-expiratory pressure, and pneumoperitoneum on respiratory function in morbidly obese patients during anesthesia and paralysis. Anesthesiology. 2007;107:725–732.
20. Mutoh T, Lamm WJ, Embree LJ, et al. Volume infusion produces abdominal distension, lung compression, and chest wall stiffening in pigs. J Appl Physiol. 1992;72:575–582.
21. Duggan M, Kavanagh BP. Pulmonary atelectasis: a pathogenic perioperative entity. Anesthesiology. 2005;102:838–854.
22. Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth. 2003;91:61–72.
23. Grasso S, Terragni P, Mascia L, et al. Airway pressure-time curve profile (stress index) detects tidal recruitment/hyperinflation in experimental acute lung injury. Crit Care Med. 2004;32:1018–1027.
24. Writing Committee for the PROBESE Collaborative Group of the PROtective Ventilation Netwotk of the Europeas Society of Anaesthesiology, Bluth T, Serpa Neto A, Schultz MJ, et al. 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;321:2292–2305.
25. Young CC, Harris EM, Vacchiano C, et al. Lung-protective ventilation for the surgical patient: international expert panel-based consensus recommendations. Br J Anaesth. 2019;123:898–913.
26. Jaber S, Coisel Y, Chanques G, et al. A multicentre observational study of intraoperative ventilatory management during general anaesthesia: tidal volumes and relation to body weight. Anaesthesia. 2012;67:999–1008.
27. Eriksen J, Andersen J, Rasmussen JP, et al. Effects of ventilation with large tidal volumes or positive end-expiratory pressure on cardiorespiratory function in anesthetized obese patients. Acta Anaesthesiol Scand. 1978;22:241–248.
28. Villar J, Kacmarek RM, Hedenstierna G. From ventilator-induced lung injury to physician-induced lung injury: why the reluctance to use small tidal volumes? Acta Anaesthesiol Scand. 2004;48:267–271.
29. Rackley CR, MacIntyre NR. Low tidal volumes for everyone? Chest. 2019;156:783–791.
30. Borges JB, Amato MBP, Hedenstierna G. The increasing call for protective ventilation during anesthesia. JAMA Surg. 2017;152:893–894.
31. Neto AS, Hemmes SN, Barbas CS, et al. Association between driving pressure and development of postoperative pulmonary complications in patients undergoing mechanical ventilation for general anaesthesia: a meta-analysis of individual patient data. Lancet Respir Med. 2016;4:272–280.
32. Fernandez-Perez ER, Keegan MT, Brown DR, et al. Intraoperative tidal volume as a risk factor for respiratory failure after pneumonectomy. Anesthesiology. 2006;105:14–18.
33. Lellouche F, Dionne S, Simard S, et al. High tidal volumes in mechanically ventilated patients increase organ dysfunction after cardiac surgery. Anesthesiology. 2012;116:1072–1082.
34. Futier E, Constantin JM, Paugam-Burtz C, et al. A trial of intraoperative low-tidal volume ventilation in abdominal surgery. N Engl J Med. 2013;369:428–437.
35. Serpa Neto A, Hemmes SN, Barbas CS, et al. Protective versus conventional ventilation for surgery: a systematic review and individual patient data meta-analysis. Anesthesiology. 2015;123:66–78.
36. Linares-Perdomo O, East TD, Brower R, et al. Standardizing predicted body weight equations for mechanical ventilation tidal volume settings. Chest. 2015;148:73–78.
37. Acute Respiratory Distress Syndrome Network, Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;342:1301–1308.
38. Pelosi P, Ravagnan I, Giurati G, et al. Positive end-expiratory pressure improves respiratory function in obese but not in normal subjects during anesthesia and paralysis. Anesthesiology. 1999;91:1221–1231.
39. 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.
40. Aldenkortt M, Lysakowski C, Elia N, et al. Ventilation strategies in obese patients undergoing surgery: a quantitative systematic review and meta-analysis. Br J Anaesth. 2012;109:493–502.
41. Reinius H, Jonsson L, Gustafsson S, et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and paralysis: a computerized tomography study. Anesthesiology. 2009;111:979–987.
42. Barbosa FT, Castro AA, de Sousa-Rodrigues CF. Positive end-expiratory pressure (PEEP) during anaesthesia for prevention of mortality and postoperative pulmonary complications. Cochrane Database Syst Rev. 2014:CD007922.
43. Whalen FX, Gajic O, Thompson GB, et al. The effects of the alveolar recruitment maneuver and positive end-expiratory pressure on arterial oxygenation during laparoscopic bariatric surgery. Anesth Analg. 2006;102:298–305.
44. Pereira SM, Tucci MR, Morais CCA, et al. Individual positive end-expiratory pressure settings optimize intraoperative mechanical ventilation and reduce postoperative atelectasis. Anesthesiology. 2018;129:1070–1081.
45. Fernandez-Bustamante A, Vidal Melo MF. The increasing call for protective ventilation during anesthesia-reply. JAMA Surg. 2017;152:894.
46. Carvalho AR, Spieth PM, Pelosi P, et al. Ability of dynamic airway pressure curve profile and elastance for positive end-expiratory pressure titration. Intensive Care Med. 2008;34:2291–2299.
47. Guldner A, Braune A, Ball L, et al. Comparative effects of volutrauma and atelectrauma on lung inflammation in experimental acute respiratory distress syndrome. Crit Care Med. 2016;44:e854–e865.
48. Cadi P, Guenoun T, Journois D, et al. Pressure-controlled ventilation improves oxygenation during laparoscopic obesity surgery compared with volume-controlled ventilation. Br J Anaesth. 2008;100:709–716.
49. Fernandez-Bustamante A, Hashimoto S, Serpa Neto A, et al. Perioperative lung protective ventilation in obese patients. BMC Anesthesiol. 2015;15:56.
50. Xu L, Shen J, Yan M. The effect of pressure-controlled inverse ratio ventilation on lung protection in obese patients undergoing gynecological laparoscopic surgery. J Anesth. 2017;31:651–656.
51. Bagchi A, Rudolph MI, Ng PY, et al. The association of postoperative pulmonary complications in 109,360 patients with pressure-controlled or volume-controlled ventilation. Anaesthesia. 2017;72:1334–1343.
52. Dion JM, McKee C, Tobias JD, et al. Ventilation during laparoscopic-assisted bariatric surgery: volume-controlled, pressure-controlled or volume-guaranteed pressure regulated modes. Int J Clin Exp Med. 2014;7:2242–2247.
53. Gad M, Gaballa K, Abdallah A, et al. Pressure-controlled ventilation with volume guarantee compared to volume-controlled ventilation with equal ratio in obese patients undergoing laparoscopic hysterectomy. Anesth Essays Res. 2019;13:347–353.
54. Jiang J, Li B, Kang N, et al. Pressure-controlled versus volume-controlled ventilation for surgical patients: a systematic review and meta-analysis. J Cardiothorac Vasc Anesth. 2016;30:501–514.
55. Gattinoni L, Carlesso E, Cadringher P, et al. Physical and biological triggers of ventilator-induced lung injury and its prevention. Eur Respir J Suppl. 2003;47:15s–25s.
56. Amato MB, Meade MO, Slutsky AS, et al. Driving pressure and survival in the acute respiratory distress syndrome. N Engl J Med. 2015;372:747–755.
57. Ladha K, Vidal Melo MF, McLean DJ, et al. Intraoperative protective mechanical ventilation and risk of postoperative respiratory complications: hospital-based registry study. BMJ. 2015;351:h364610.1136/bmj.h3646
58. Ball L, Pelosi P. How I ventilate an obese patient. Crit Care. 2019;23:176.
59. Ball L, Battaglini D, Pelosi P. Postoperative respiratory disorders. Curr Opin Crit Care. 2016;22:379–385.
Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.