PEEP Strategies in the Morbidly Obese

by Thomas J. Krall, MD
Cardiac Anesthesia Fellow UCSF School of Medicine, San Francisco, CA

Volume 28 | Issue 2 | Summer 2017

The care of morbidly obese patients presents many challenges to the intensivist. Notable among them is the optimization of mechanical ventilation. Obesity is associated with prolonged mechanical ventilation and increased ICU length of stay.¹ The optimal strategy for mechanical ventilation of obese patients is still a matter of debate.² Decreased compliance of the chest and abdominal walls lead to atelectasis, low end-expiratory lung volumes, and hypoxemia.^3-6 Despite this knowledge, we continue to provide inadequate PEEP to morbidly obese patients.⁷ Recent literature describing the use of esophageal manometry and decremental PEEP trials in obese patients provides a potential solution.

Obesity significantly decreases FRC and ERV in both awake¹ and sedated^4,8,9 patients. If the FRC falls below closing capacity, small airway closure and atelectasis will result. This leads to the potential for a negative transpulmonary pressure (P_TP = P_{airway opening (AO)} – P_pleura(pl)) at end expiration, despite the absence of flow. Behazin et al. recorded esophageal pressure (P_es) and airway pressure at which lung inflation begins (threshold pressure, P_AO-thr) in 50 sedated and paralyzed morbidly obese patients at FRC.¹⁰ They found marked elevations in both values compared to lean controls, suggesting elevated pleural pressures and small airway collapse at end expiration.  Notably, neither P_es nor P_AO-thr correlated with BMI, suggesting that obesity per se does not predict elevated pleural pressures and a mechanism for customized PEEP determination may be needed to mitigate end-expiratory chest wall force.  The measurement of intra-esophageal pressure as a proxy for pleural pressure allows one to set PEEP to maintain a positive transpulmonary pressure at end-expiration.

In their 2016 article, Pirrone and colleagues demonstrated that 1) we are setting PEEP too low for our obese patients and 2) PEEP guided by P_es and decremental PEEP trials can remedy that. ⁷ The study examined 14 mechanically ventilated obese patients without ARDS.  Their end-expiratory lung volumes, airway pressures, and esophageal pressures were measured at baseline PEEP, zero PEEP, PEEP set to maintain positive end-expiratory transpulmonary pressure (P_TPe) without a recruitment maneuver (RM), PEEP set to maintain a positive P_TPe after a RM, best decremental PEEP with a RM,¹¹ and best decremental PEEP with the head of the bed at 30 degrees.  They found that the PEEP set by the ICU team (11.6±2.9 cmH2O) was on average 9.1 cmH₂0 less than the PEEP required to keep a positive P_TPe.  End expiratory lung volumes, lung elastance, and oxygenation improved markedly and similarly in the RM+P_TPe and RM+best decremental PEEP groups.  Similar to prior publications,⁶ they showed that recruitment maneuvers were necessary to see the benefits of increased PEEP levels. They also found that higher PEEP levels did not lead to changes in hemodynamics, vasopressor usage, or fluid administration. 

That higher PEEP levels improved oxygenation is not surprising; the more notable conclusions are the improvement in lung compliance and lack of hemodynamic effects with higher PEEP.  This parallels the findings of Talmor et al. in ARDS patients, who also found better compliance and unchanged V_d/V_t in a positive P_TP strategy.¹² Together they suggest that higher PEEP in P_es-guided ventilation strategy is not merely over-distending normal lung.

While a measurement of the chest wall’s effect on respiratory mechanics is very appealing, questions remain about the utility of esophageal manometry. Patient position, compression from mediastinal contents, consolidated lung, pleural fluid, gravitational gradients in pleural pressure, and esophageal wall tension have the potential to introduce error into P_es as a surrogate of pleural pressure (P_pl).^13,14 Potential errors like these are arguably the largest barrier to widespread adoption of this technique. As opposed to using absolute value of P_es, one calculation technique uses the change in P_es to estimate end-inspiratory P_TP, but this method assumes that end-expiratory P_TP is zero and provides no information about the lung at end-expiration.^15,16 Unfortunately, concerns about the ability of the absolute value of P_es to reflect the pleural pressure are unlikely to be completely resolved because esophageal manometry remains the only method currently suitable for estimating pleural pressure in humans.¹⁷ A study in a dog model of ARDS, however, showed excellent correlation in absolute P_es and P_pl in the middle lung field across a wide range of pleural and esophageal pressures.¹⁸ The degree to which measurement error is small compared to the wide range of P_es in ARDS patients (0-34 cmH₂0)¹⁹ and obese patients without ARDS (3-26 cmH₂0)¹⁰ allows the esophageal pressure to provide useful information about the contribution of the chest wall to pulmonary mechanics.^20,21

It may be possible to set optimal PEEP without placing the esophageal balloon.  However, the Pirrone study started their decremental PEEP trial 4 cmH₂0 above the P_TPe, which was determined by esophageal manometry.  Finding the best PEEP may be more difficult without the pleural pressure estimate because pleural pressures in obese patients vary widely and do not correlate with BMI.^10,19 Placement of an esophageal balloon also allows monitoring of respiratory muscle and ventilator synchrony, calculation of work of breathing, and quantification of intrinsic PEEP in spontaneously breathing patients.^13,22 The marginal utility of this additional information is hard to assess because most physicians’ daily practice does not currently include esophageal manometry.

Although sometimes leading to alarmingly high PEEP levels, combining esophageal manometry and decremental PEEP trials has shown great promise in ventilating challenging patients.²³ There is compelling physiologic data to show that obesity causes an increase in expiratory pleural pressures, the effects of which can be offset by first recruiting atelectatic lung units and then setting a PEEP level specifically to counteract the increased mass of the chest wall.  Esophageal pressure monitoring may prove to be a valuable tool is this regard. 

Resources

1. Akinnusi ME, Pineda LA, El Solh AA, Mph. Effect of obesity on intensive care morbidity and mortality: A meta-analysis *. Crit Care Med. 2008;36(1):151-158.
2. Shah U, Wong J, Wong DT, Chung F. Preoxygenation and intraoperative ventilation strategies in obese patients: A comprehensive review. Current Opinion in Anaesthesiology. 2016;29(1):109-118.
3. Parameswaran K, Todd DC, Soth M. Altered respiratory physiology in obesity. Canadian Respiratory Journal : Journal of the Canadian Thoracic Society. 2006;13:203-210.
4. Pelosi, Paolo C, Massimo R, et al. The effects of body mass on lung volumes, respiratory mechanics, and gas exchange during general anesthesia. Anesthesia & Analgesia. 1998;87(3):654-660.
5. Strandberg Å, Tokics L, Brismar B, Lundquist H, Hedenstierna G. Constitutional factors promoting development of atelectasis during anaesthesia. Acta Anaesthesiol Scand. 1987;31(1):21-24.
6. Reinius MD,H, Jonsson MD,L, Gustafsson MD, P., et al. Prevention of atelectasis in morbidly obese patients during general anesthesia and ParalysisA computerized tomography study. Anesthesiology. 2009;111(5):979-987.
7. Pirrone M, Fisher DRRT, Chipman DRRT, et al. Recruitment maneuvers and positive end-expiratory pressure titration in morbidly obese ICU patients. Crit Care Med. 2016;44(2):300-307.
8. Pelosi P, Croci M, Ravagnan I, Vicardi P, Gattinoni L. Total respiratory system, lung, and chest wall mechanics in sedated-paralyzed postoperative morbidly obese patients. Chest. 1996;109(1):144-151.
9. Pelosi P, Croci M, Ravagnan I, et al. Respiratory system mechanics in sedated, paralyzed, morbidly obese patients. J Appl Physiol. 1997;82(3):811.
10. Behazin N, Jones SB, Cohen RI, Loring SH. Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity. J Appl Physiol. 2010;108:212.
11. Kacmarek RM, Villar J. Management of refractory hypoxemia in ARDS. Minerva Anestesiol. 2013;79(11):1173.
12. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation guided by esophageal pressure in acute lung injury. N Engl J Med. 2008;359(20):2095-2104.
13. Akoumianaki E, Maggiore SM, Valenza F, et al. The application of esophageal pressure measurement in patients with respiratory failure. Am J Respir Crit Care Med. 2014;189(5):520-531.
14. Sahetya SK, Brower RG. The promises and problems of transpulmonary pressure measurements in acute respiratory distress syndrome. Curr Opin Crit Care. 2016;22(1):7-13.
15. Gattinoni L, Carlesso E, Cressoni M. Selecting the 'right' positive end-expiratory pressure level. Curr Opin Crit Care. 2015;21(1):50-57.
16. Gulati GAB, Novero A, Loring SH, Talmor D. Pleural pressure and optimal positive end-expiratory pressure based on esophageal pressure versus chest wall elastance: Incompatible results*. Crit Care Med. 2013;41(8):1951-1957.
17. Lai-Fook S. Mechanics of the pleural space: Fundamental concepts. Lung. 1987;165(1):249-267.
18. PELOSI P, GOLDNER M, McKIBBEN A, et al. Recruitment and derecruitment during acute respiratory failure. Am J Respir Crit Care Med. 2001;164(1):122-130.
19. Talmor D, Sarge T, O'Donnell CR, et al. Esophageal and transpulmonary pressures in acute respiratory failure *. Crit Care Med. 2006;34(5):1389-1394.
20. Washko GR, O'Donnell CR, Loring SH. Volume-related and volume-independent effects of posture on esophageal and transpulmonary pressures in healthy subjects. J Appl Physiol. 2006;100(3):753-758. doi: 10.1152/japplphysiol.00697.2005.
21. Owens RL, Campana LM, Hess L, Eckert DJ, Loring SH, Malhotra A. Sitting and supine esophageal pressures in overweight and obese subjects. Obesity. 2012;20(12):2354-2360.
22. Brochard L. Measurement of esophageal pressure at bedside: Pros and cons. Curr Opin Crit Care. 2014;20(1):39-46.
23. Zhang C, Pirrone M, Imber DAE, et al. Optimization of mechanical ventilation in a 31-year-old morbidly obese man with refractory hypoxemia. A&A Case Reports. 2017;8(1):7-10.