Mechanical Ventilation in Patients with Morbid Obesity

| November 20, 2012

This ongoing column is authored by members of the International Society for the Perioperative Care of the Obese Patient (ISPCOP), an organization dedicated to the bariatric patient.

Column Editor: Stephanie B. Jones, MD
Dr. Jones is Vice Chair for Education, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts.

This month’s column by Adrian Alvarez, MD. Dr. Alvarez is the Founder President of ISPCOP. He is Professor of Anesthesia, Anesthesia Department, Hospital Italiano de Buenos Aires, Argentina.

Bariatric Times. 2012;9(11):20–22
Extracted with permission from: Sprung J, Weingarten TN, Warner DO. Ventilatory strategies during anesthesia. In: Alvarez A, Brodsky BB, Lemmens HJM, Morton JM, eds. Morbid Obesity Peri-operative Management. 2nd Edition. Cambridge, United Kingdom: Cambridge University Press; 2010:124–137.

Funding: No funding was provided.

Disclosures: The author reports no conflicts of interest relevant to the content of this article.

Morbid obesity results in physiologic derangement of the respiratory system, which presents a challenge to achieving safe mechanical ventilation. The development of atelectasis (i.e., collapse of part of a lung) after induction of anesthesia is exaggerated in patients with morbid obesity, and it is the main contributor to respiratory dysfunction.[1,2]

In an attempt to improve intraoperative ventilation, anesthesiologists often increase tidal volume (VT). However, this maneuver increases airway pressure, which may induce ventilator-associated lung injury (VALI).[3]

In this installment of “Anesthetic Aspects of Bariatric Surgery,” we will discuss the physiologic basics of respiratory mechanics and current strategies proposed to improve oxygenation while ideally avoiding development of lung injury.

Factors affecting mechanical ventilation
Position and anesthesia. Supine position reduces lung volumes and decreases respiratory system compliance. This is exaggerated in patients with obesity.[4–6]

Chest wall compliance decreases because the increased weight of the abdomen presses against the diaphragm. As a result, lung volume decreases and atelectasis develops, causing respiratory system compliance to decrease.[4–6]

Anesthesia reduces functional residual capacity (FRC) to approximately 50 percent of the preinduction value[7] in patients with obesity promoting atelectasis as both the FRC and VT fall below the closing volume. This atelectasis contributes to reduce respiratory system compliance.[2]

The reduced lung volume of patients with obesity diminishes airway diameter, increasing airway resistance and decreasing expiratory flow.[8] Consequently, airway pressure must be increased to achieve adequate VT during positive pressure ventilation.

Pneumoperitoneum is the presence of air within the peritoneal cavity. Increased intra-abdominal pressure associated with pneumoperitoneum shifts the diaphragm cephalad. This negatively affects lung expansion during inspiration.

Pneumoperitoneum in patients with morbid obesity decreases static compliance of the respiratory system.[9–11] Additionally, pneumoperitoneum increases intra-abdominal pressure, and, because the abdominal compartment is mechanically coupled to the chest wall, chest wall compliance further decreases.[12–14]

All of these changes result in a large increase in end-inspiratory pressure (PEI). Peak inspiratory pressure (PIP) also increases 50 percent with pneumoperitoneum.[15]

Mechanical ventilation and lung injury
Several factors, including reduced compliance, increased resistance, and pneumoperitoneum, increase the airway pressure required during positive pressure ventilation in anesthetized patients with obesity. High-pressure ventilation may cause parenchymal stress and disrupt lung structures. Lungs may get injured from alveolar overdistension and repetitive opening and closing of collapsed lung units. Mechanical ventilation with high pressure can induce acute VALI.[16–17]

It is important to note that the use of high VT and a high respiratory rate are independent predictors of lung injury.[18]

Ventilatory strategies
Intra-operative oxygenation in patients with morbid obesity is largely determined by the magnitude of post-induction atelectasis. Thus, increasing intra-operative PaO2 (i.e., partial pressure of oxygen in arterial blood) depends on recruiting atelectatic lung and maintaining the expansion. This should ideally be done while avoiding mechanical lung injury.

Different strategies have been recommended for patients with obesity to achieve this goal.
High tidal volume. Large VT (up to 20mL/kg) does not improve PaO2 in patients with morbid obesity.[15,16] This maneuver may promote lung injury due to overdistension. To reduce the risk of overdistension, PEI limit values of 30 to 35cm H2O have been recommended,[19,20] which is difficult to achieve in the patient with obesity.

Take-home points:
1.    High tidal volume does not improve oxygenation
2.    High tidal volume increases risk of lung injury.

Positive end expiratory pressure. Application of high positive end expiratory pressure (PEEP) theoretically is beneficial for some patients with areas of atelectatic parenchyma.[21] Because atelectasis is especially prominent during anesthesia of patients with morbid obesity, PEEP is an attractive treatment method. Two studies showed that PEEP may be modestly beneficial;[22,23] however, the effects on PaO2 attributed to isolated application of PEEP in patients with obesity are inconsistent.

Take-home point:
1.    Isolated use of PEEP is not effective in improving oxygenation in patients with morbid obesity.

Alveolar recruitment maneuvers. An alveolar recruitment maneuver is the use of high, sustained, positive airway pressure to increase end-expiratory lung volume and re-expand atelectatic lung areas. In nonobese patients during anesthesia, an initial pressure of at least 40cm H2O is needed.[24] This sustained pressure is termed critical opening pressure (P crit).[25]

To re-expand atelectatic lungs and maintain expansion, the following three conditions are required: 1) insufflation pressure must exceed P crit (pressure needed to open collapsed alveoli), 2) inspiratory pressure must be sustained because considerable time is required for alveoli to open, and 3) to maintain open alveoli, recruitment needs to be followed by adequate levels of PEEP.[24]

The recruitment maneuver efficiently improves intraoperative PaO2 in patients with obesity.[26,27]

Take-home points:
1.    Alveolar recruitment maneuvers are the most effective method of improving PaO2
2.    To maintain open alveoli, recruitment needs to be followed by adequate levels of PEEP.

Conducting the alveolar recruitment maneuver.
Manually. Close the anesthetic circuit and use the anesthesia bag to apply continuous pressure above the P crit (40cm H2O in normal weight patients).[25] Patients with morbid obesity usually need higher pressures.
Mechanically. To conduct the alveolar recruitment maneuver mechanically, use a conventional mechanical ventilator with a selected VT based on ideal body weight.[27] While maintaining ventilation in a volume-controlled mode, increase PEEP in a gradual, stepwise manner up to 20cm H2O.[26,27] Starting at 5cm H2O increase an additional 2 to 5cm H2O every 5 ventilations. To allow reopening of atelectatic lung areas, a larger number of breaths should be performed at the highest levels of PEEP.[5,6,9]

After the recruitment manuever, mechanical ventilation should be continued with low VT (6–8mL/kg of ideal body weight) and higher PEEP (10–12cm H2O).[26,27]

1.    Atelectasis should be re-expanded with recruitment maneuvers.
2.    Adequate PEEP should be used to keep parenchyma open.
3.    VT should be maintained between and 6 and 8mL/kg of ideal body weight.
4.    PEI should be below 30cm H2O.

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2.    Eichenberger A, Proietti S, Wicky S, et al. Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Anesth Analg. 2002;95:1788–1792.
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7.    Damia G, Mascheroni D, Croci M, et al. Perioperative changes in functional residual capacity in morbidly obese patients. Br J Anaesth. 1988;60:574–578.
8.    Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol. 1997;82:811–818.
9.    Sprung J, Whalley DG, Falcone T, et al. The impact of morbid obesity, pneumoperitoneum, and posture on respiratory system mechanics and oxygenation during laparoscopy. Anesth Analg. 2002;94:1345–1350.
10.    Dumont L, Mardirosoff C. Effects of a pneumoperitoneum in the obese patient. Eur J Anaesthesiol. 2000; 17:786–787.
11.    Nguyen NT, Anderson JT, Budd M, et al. Effects of pneumoperitoneum on intraoperative pulmonary mechanics and gas exchange during laparoscopic gastric bypass . Surg Endosc. 2004;18:64–71.
12.    Ranieri VM , Brienza N , Santostasi S , et al . Impairment of lung and chest wall mechanics in patients with acute respiratory distress syndrome: role of abdominal distension. Am J Respir Crit Care Med. 1997;156:1082–1091.
13.    Mutoh T, Lamm WJ, Embree LJ, et al. Volume infusion produces abdominal distension, lung compression, and chest wall stiff ening in pigs. J Appl Physiol. 1992;72:575–582.
14.    Fahy BG, Barnas GM, Flowers JL, et al. The effects of increased abdominal pressure on lung and chest wall mechanics during laparoscopic surgery. Anesth Analg. 1995;81:744–750.
15.    Bardoczky GI, Yernault JC, Houben JJ, et al. Large tidal volume ventilation does not improve oxygenation in morbidly obese patients during anesthesia. Anesth Analg. 1995; 81:385–388.
16.    Carlton DP, Cummings JJ, Scheerer RG, et al . Lung overexpansion increases pulmonary microvascular protein permeability in young lambs. J Appl Physiol. 1990;69:577–583.
17.    Tsuno K, Prato P, Kolobow T. Acute lung injury from mechanical ventilation at moderately high airway pressures. J Appl Physiol. 1990;69:956–961.
18.    Mascia L, Zavala E, Bosma K, et al. Brain IT group. High tidal volume is associated with the development of acute lung injury aft er severe brain injury: an international observational study. Crit Care Med. 2007;35:1815–1820.
19.    Slutsky AS. Consensus conference on mechanical ventilation—January 28–30, 1993 at Northbrook, Illinois, USA. Part I. European Society of Intensive Care Medicine, the ACCP and the SCCM. Intensive Care Med. 1994;20:64–79. Erratum in: Intensive Care Med. 1994;20:378.
20.    Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock. Crit Care Med. 2008;36:296–327. Erratum in: Crit Care Med. 2008;36:1394–1396.
21.    Caironi P , Gattinoni L. [Use of positive end-expiratory pressure in acute respiratory distress syndrome: current views]. Recenti Prog Med. 2007;98:509–517. [Article In Italian].
22.    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.
23.    Perilli V, Sollazzi L, Modesti C, et al. Comparison of positive end-expiratory pressure with reverse Trendelenburg position in morbidly obese patients undergoing bariatric surgery: eff ects on hemodynamics and pulmonary gas exchange. Obes Surg. 2003;13:605–609.
24.    Lachmann B. Open up the lung and keep the lung open. Intensive Care Med. 1992;18:319–321.
25.    Rothen HU, Sporre B, Engberg G, et al . Re-expansion of atelectasis during general anaesthesia: a computed tomography study. Br J Anaesth. 1993;71:788–795.
26.    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. Erratum in: Anesth Analg. 2006;102:881.
27.    Sprung J, Whalen FX, Comfere T, et al. Alveolar recruitment and arterial desfl urane concentration during bariatric surgery. Anesth Analg. 2009;108:120–127.

Category: Anesthetic Aspects of Bariatric Surgery, Past Articles

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