Assessment of Airway Closure and Expiratory Airflow Limitation to Set Positive End-Expiratory Pressure in Morbidly Obese Patients with Acute Respiratory Distress Syndrome.

To the Editor:

We read the study by De Santis Santiago and colleagues with great interest (1). They demonstrated, in a very elegant crossover study that included morbidly obese patients with acute respiratory distress syndrome (ARDS) (mean body mass index of 57 kg/m2), physiological respiratory and hemodynamics benefits of a ventilator strategy including a high positive end-expiratory pressure (PEEP) as compared with a strategy with a low PEEP–FiO table. The high PEEP strategy was determined with a lung recruitment maneuver with increased stepwise of PEEP until 50 cm H2O of plateau pressure while keeping constant driving pressure of 10 cm H2O, followed by a decreasing stepwise of 2 cm H2O of PEEP until 5 cm H2O allowing the determination of optimal PEEP (PEEP level for best compliance of the respiratory system + 2 cm H2O). This strategy was associated with improvement of respiratory mechanics (decrease of driving pressure, increase of respiratory system compliance) and oxygenation through reduction of atelectasis. Interestingly, this was not accompanied by impairment in right and left ventricular functions. Moreover, a very similar swine model confirmed these results.

Besides these findings, we are surprised that some important points of respiratory mechanics in morbidly obese patients are not discussed. First, complete airway closure is a very frequent phenomena in those patients (up to 65% for class III obesity) (2). It can be easily identified as the inflection point on the initial portion of a low-flow inflation pressure–volume when volume started to increase. The lack of consideration of complete airway pressure (by using a PEEP lower than the opening airway pressure) induces an overestimation of driving pressure, respiratory system, and lung elastances (2). Second, the association of low Vt and supine position in obesity may induce consequent expiratory airflow limitation, which can be easily visualized and measured as intrinsic PEEP (3). Therefore, if intrinsic PEEP is not considered, it could mislead correct values of expiratory transpulmonary pressure (total PEEP minus expiratory esophageal pressure). Regarding electrical impedance tomography results, we are surprised that the authors reported regional compliance only for 10 patients, whereas electrical impedance tomography measurements were made on 18 patients.

Furthermore, the authors report good hemodynamic tolerance of high levels of PEEP in class III obese patients. We are then surprised that the authors did not report variations, easily measured during transthoracic echocardiography, which was performed on 17 patients. Lack of variation of vasoactive-inotropic score or mean arterial pressure does not exclude that high PEEP did not decrease . To support this comment, in the ARDS swine study, the authors report a trend to lower (−13%, P = 0.053) and higher venous O2 saturation (SvO) with higher PEEP, despite similar mean arterial pressure and vasoactive-inotropic score. The authors conclude that higher SvO reflects adequate systemic perfusion. However, because tends to be lower and VO stable, it is more likely that higher SvO is explained by the rise of SaO due to higher PEEP.

In patients with class III obesity, we advocate that the strategy of high pleural pressures should be compared with 1) complete evaluation of respiratory mechanics, which include checking for possible airway closure and expiratory airflow limitation, and 2) complete evaluation of hemodynamics, including , to set a sufficient level of PEEP.