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A recent study of applied respiratory physiology in the mechanically-ventilated, obese patient was published. The ubiquitous focus on lung protective ventilation with “low” [physiological] lung volumes, and low plateau pressure may leave the obese patient susceptible to respiratory embarrassment. Excess abdominal and chest wall weight affect each of the following: reduction in lung volume, increased expiratory flow limitation, increased gas-trapping and augmentation of auto-PEEP. Cephalad displacement of the diaphragm from increased intra-abdominal pressure may explain why obese patients have been found to have a negative transpulmonary pressure [Ptp = alveolar pressure minus pleural pressure]. Note that a negative Ptp designates a pleural pressure greater than alveolar pressure which suggests lung volume loss [collapse]. Because the pressure within the alveolus at end-expiration [or inspiration for that matter] reflects the elastance of both the lungs, and chest wall, it is possible that PEEP – in the obese – is ‘under-dosed.’
Given the aforeknown, an investigation of 14 mechanically-ventilated, paralyzed patients with a mean body mass index [BMI] of 51 was conducted. The majority of the patient  were intubated for sepsis. The patients were evaluated at baseline and following 2 methods of augmenting PEEP. All patients had an esophageal pressure monitor placed as a surrogate for pleural pressure.
One method used to titrate PEEP was to obtain ‘the lowest PEEP with a positive Ptp;’ the second method was to determine the ‘best decremental PEEP.’ The first method involved progressively increasing PEEP until the value of the trans-pulmonary pressure [estimated as PEEP minus esophageal pressure at end-expiration] became zero to +2 cm H2O [recall that a positive Ptp indicates that lung is no longer collapsed]. Best decremental PEEP builds upon the trans-pulmonary approach above. Firstly, PEEP is set to a level 4 cm H2O above the PEEP required to generate a positive Ptp, as above. Then, the driving pressure [Pplat – PEEP] is calculated and done so iteratively following 2 cm H2O reductions in PEEP for at least 5 decrements. The PEEP at which the driving pressure is the lowest is termed the ‘best decremental PEEP;’ 2 cm H2O was added to this value and kept in the patient. The physiological rationale for using driving pressure to calculate the best decremental PEEP can be found here [diagram 2, curve B].
As expected, the baseline PEEP chosen by the ICU team [12 cm H2O, mean] was much less than the amount of PEEP determined by the Ptp and best decremental PEEP methods [21 cm H2O, mean for both]. Additionally, the authors used nitrogen-wash out to measure end-expiratory lung volume and found that PEEP titration in the obese significantly increased lung volume, reduced lung elastance [increased compliance – made lung ‘less stiff’], increased oxygen tension and did not impair hemodynamics. Importantly, the effects of PEEP were most meaningful following a recruitment maneuver [RM]. They performed the RM by briefly transitioning the patient to pressure control at 15 cm H2O above a PEEP of 15 cm H2O. Every 30 seconds, PEEP was increased by 5 cm H2O until the patient was at a PEEP of 30 cm H2O plus 15 cm H2O pressure control. Thus the entire RM lasted about 2 minutes. A somewhat surprising finding was that the chest wall elastance of the obese was not found to be increased [i.e. stiffer].
This is a fantastic study of applied physiology in the ICU. As previously noted in the acute respiratory distress syndrome [ARDS] population, esophageal pressure [as a surrogate for pleural pressure] provides a rationale for allowing higher plateau pressures. Because the estimated pleural pressure in those patients was around 15 cm H2O at baseline, an end-inspiratory alveolar pressure [Pplat] could theoretically be allowed to reach 45 cm H2O as the stress across the alveolus would still be 30 cm H2O. A similar reasoning can be applied to the trial at hand; in the obese, one should not be afraid of PEEP in the high teens or even low 20s!
What I find a bit surprising is that chest wall elastance was not found to be increased [i.e. stiffer] in the obese. This is certainly not a universal finding, and I suspect that it arises from measurement error. Most importantly, the use of an esophageal pressure balloon as a surrogate for pleural pressure is exceptionally flawed. This was first realized decades ago when trying to truly measure pericardial surface pressure. The surface pressure formed between two elastic surfaces [e.g. the myocardium and pericardium or the visceral and parietal pleura] is the summation of both: 1. a liquid pressure and 2. a contact stress between the two structures. The liquid pressure is well-known to clinicians as it can be measured by a fluid-filled catheter like an esophageal balloon; the liquid pressure represents a hydrostatic pressure acting in all directions. To the liquid pressure, however, must be added the contact stress – a perpendicular force generated by the deformation of two surfaces pressing against each other. When atelectatic lung is recruited, a contact stress is generated between the expanded lung and chest wall that cannot be measured by a fluid-filled esophageal pressure balloon. Thus, a measurement artifact is introduced which underestimates the true surface [pleural] pressure thereby rendering a lower calculated elastance.
Lastly, the author’s anticipated a greater hemodynamic consequence in response to higher PEEP. While the obese do have higher pleural pressure and while the pleural pressure is integrally transmitted to the pericardial space, there are multiple variables at play. Firstly, the obese tend to have higher blood volume which maintains mean systemic pressure and venous return. Presumably, many of these patients were also fluid loaded; further, many were on vasoactive agents which augment venous tone and also maintain venous return – all said effects would blunt the preload reduction anticipated with high pleural pressure. Additionally, and perhaps more importantly given the study’s findings, is that alveolar recruitment and improved oxygenation will reduce right ventricular afterload. Thus, even if there is preload reduction with high intrathoracic pressure, this may be offset by greatly augmented RV forward flow!