Clinical Deployment of the Esophageal Balloon Catheter—Making the Case*
In this issue of Critical Care Medicine, Fumagalli et al (5) demonstrate that decremental PEEP titration with TPP following a recruitment maneuver to total lung capacity can be used to identify the minimum end-expiratory airway pressure that avoids atelectasis in obese patients without acute respiratory distress syndrome (ARDS), as validated in animals with obesity modeled by raising intra-abdominal pressure. Of themselves, such results are hardly surprising (6), but they do add to the growing literature supporting the indications for (and potential utility of) inserting an esophageal catheter in the clinical setting. What is eye opening about this particular dataset, however, is the very high level of PEEP (approximating 20 cm H2O) needed to maintain TPP positive under these “non-ARDS” conditions. Furthermore, this elevated level of PEEP was accompanied clinically by optimized lung compliance, and in a pig model of obesity, similar benefits were attained without impairing pulmonary vascular resistance or adversely affecting pulmonary gas exchange. In combination, such data suggest that the TPP-determined decremental approach strikes a favorable balance between regional overdistention and lung recruitment, despite nominally high values of PEEP. Doing so may be important, given the logic of avoiding amplified parenchymal stress and the recent concern to assure lung-protective ventilation, even in patients “without” overt lung disease (7).
If extrapolating from a single alveolus model to the mechanically complex lungs were valid, few would contest the logic of maintaining positive transpulmonary pressure or the desirability of measuring it. More opposition has been leveled against the idea that Pes, currently our only reasonable option for estimating Ppl, is needed or should be used in TPP calculations intended to determine the best airway pressure settings (8). Opponents might reasonably argue that Pes reflects its own immediate intraluminal environment and therefore is susceptible to local artifacts, especially in the presence of the abnormal chest wall of obesity and abdominal hypertension (4). Such concerns are treading on familiar ground; physiologists have long understood that esophageal pressure (or indeed any local pressure measured at a single site) cannot reflect the absolute values of pleural pressures on remote lung surfaces or even the true average pressure that surrounds the lung (9). They also agree, however, that Pes does much better in tracking changes in pressure that occur during the respiratory cycle.
The thoracic mechanics of obese patients have been reasonably well defined. Mild to moderate obesity displaces the pressure volume curve of the chest wall rightward, similar to adding an unchanging weight to the body surface. However, as its severity advances, obesity eventually impairs the elastance slope of the chest wall (10), largely because the abdominal cavity has a generous but limited capacity to accommodate distention of its content. (In the study under discussion, e.g., severe obesity increased chest wall elastance by approximately 80% over the expected value .