Ventilatory Mechanics in the Patient With Obesity

Luigi Grassi, M.D.; Robert Kacmarek, Ph.D.; Lorenzo Berra, M.D.


Anesthesiology. 2020;132(5):1246-1256. 

In This Article

Mechanics During Artificial Ventilation Without Lung Injury

Sedation and use of neuromuscular blocking agents make it feasible to study the intrinsic mechanical characteristics of the respiratory system. By coupling the measurements of the airway pressure (Paw) with those given by esophageal pressure (a surrogate for pleural pressure), the transmural pressure distending the lung parenchyma is obtained (transpulmonary pressure = Paw – pleural pressure, approximated as transpulmonary pressure = Paw – esophageal pressure). Thus, one could explore the relative contribution of the lung and the chest wall to the global respiratory system alteration in the population with obesity. Obesity is characterized by an increased respiratory system elastance, and the major contributor to this increase is the lung, while the elastic properties of the chest wall are less affected or substantially unchanged.[35–38] The abdominal load is associated with an elevated esophageal pressure (pleural pressure), which in turn results in negative transpulmonary pressure, especially at the end of exhalation. Indeed, the subject with obesity might spend most of his respiratory cycle (inspiration and exhalation) below the threshold for positive transpulmonary pressure, even when mechanically ventilated with positive pressures, and this results in lung collapse and reduced volumes at FRC.[39] Lung collapse produces increased lung elastance and impacts gas exchange, with the development of hypoxemia. A direct consequence of this mechanism is that an artificially ventilated obese subject requires higher levels of airway pressure to keep the lung open, especially during exhalation. In subjects with high body mass index undergoing general anesthesia, a higher level of end-expiratory pressure is associated with positive transpulmonary pressure and higher compliance of the respiratory system, although PEEP alone is not able to restore oxygenation.[40] The best approach to restore both lung mechanics and gas exchange seems to be to associate a higher titrated level of PEEP with the performance of recruitment maneuvers.[41] In critically ill patients with obesity, recruitment maneuvers (performed through a stepwise increment of end-expiratory airway pressure) associated with PEEP tailored on the best compliance or a positive transpulmonary pressure at end expiration results in higher end-expiratory volumes and in an improved elastance of the lung, with a consequent positive impact on oxygenation.[37] By restoring a positive transpulmonary pressure, this approach ameliorates the gas distribution in the lung, without significant hemodynamic drawbacks.[38] Despite these strong physiologic premises, a recent large randomized control trial that compared a low level of PEEP (4 cm H2O) with a strategy providing regular recruitment maneuvers and a PEEP of 12 cm H2O to obese patients undergoing general anesthesia failed to demonstrate a benefit in terms of clinical outcomes (i.e., incidence of postoperative complications).[42] A possible explanation for such surprising results could be that obese patients require a PEEP titrated based on their specific respiratory characteristics rather than a fixed predetermined value of "high PEEP." Up to now, no level of body mass index predicts PEEP requirements.

The use of transpulmonary pressure to titrate lung mechanics has limitations. First, as stated above, esophageal pressure is a surrogate for the actual pressure in the pleural cavity, which is prohibitive to measure in a human being. As a surrogate, absolute values are different and generally overestimated by at least 3 cm H2O in the general population.[43] Second, esophageal pressure reflects better pleural pressure at the level of the esophagus or in the more dependent lung, while less can be inferred about nondependent pleural pressure.[44] Furthermore, as of today, there is no available knowledge about the distribution of pleural pressure in morbid obesity, and it is unknown if the gradient between the dependent and nondependent lung is small (as in a lean subject with healthy lungs), or if it is significantly higher (as in adult respiratory distress syndrome [ARDS]) due to atelectasis and changes in lung geometry (Figure 3). In the presence of this gradient, absolute values of a set transpulmonary pressure could be higher than those calculated with esophageal manometry, especially in the nondependent lung, thus resulting in overdistension. Figure 3 illustrates some aspects of transpulmonary pressure monitoring through esophageal manometry. Table 2 includes some experienced base recommendations on how to use esophageal manometry to set PEEP in the obese patient.

Figure 3.

Role of esophageal manometry in the assessment of transpulmonary pressure. (A) A supine model, as it could be seen in a chest computed tomography scan, is shown. The pleural space, in blue, is subdivided into three zones (nondependent space, in red; the midlung space, in green; and the dependent space, in yellow). The esophagus, with the esophageal balloon in place, is represented by the violet mark. From classic physiology, it is known that the pleural pressure in the dependent pleura is around 2 cm H2O higher than the one in the nondependent space so that a gradient exists (vertical black arrow). Theoretically, esophageal pressure (Pes) is directly exposed to the pleural space and reflects pleural pressure at its same gravitational level (dotted line), but the absolute value could be overestimated due to compression by the mediastinum (M) on the esophagus, intrinsic tone of the esophageal musculature, esophageal content, and intrinsic tone of the esophageal balloon. In conditions like adult respiratory distress syndrome, high superimposed pressure caused by inflammatory edema increases this gradient, so that Pes is likely to significantly overestimate nondependent pleural pressure. The entity of this gradient is unknown in morbid obesity. (B) An upright model is shown, during endotracheal intubation and positive pressure mechanical ventilation. Transpulmonary pressure is calculated as the difference between alveolar pressure and pleural pressure. A high abdominal load increases pleural pressure, thus resulting in lower transpulmonary pressure. Being exposed to the pleural space, esophageal manometry can be assumed to be a surrogate for pleural pressure, otherwise not measurable in a human being in the clinical setting.

The effects of pneumoperitoneum on the respiratory system mechanics differ from those of abdominal fat. Pneumoperitoneum induces an increase in the respiratory system elastance sustained mainly by an increased chest wall elastance, while the lung's elastic properties are mostly unaffected.[45] An acute increase in abdominal pressure deforms the chest wall cavity, whose change in geometry is protective for the lung, which is spared from squeezing and compression. Pneumoperitoneum and obesity have a negative additive interaction on the respiratory system during laparoscopic surgery.[46] An approach based on lung recruitment can improve lung mechanics and oxygenation and, when feasible, a beach chair position can be combined to an appropriate level of PEEP to counteract the combined effect of abdominal fat and pneumoperitoneum best.

Finally, the Trendelenburg position negatively impacts lung mechanics. As stated above, obesity is characterized by early airway closure, with a high threshold for airway opening pressure. When pneumoperitoneum is associated with the Trendelenburg position, lung collapse increases, and the airway opening pressure rises even further.[47] This mechanism has some clinical implications: for example, pressure control ventilation can result in hypoventilation and apnea in obese patients in the Trendelenburg position, since the critical opening threshold to generate flow may not be reached. In the same way, if one decides to assess lung mechanics, the level of intrinsic PEEP should be accounted for. For instance, driving pressure is defined as the difference between airway pressure during an inspiratory pause (plateau pressure) and total PEEP, which is the sum of applied and intrinsic PEEP. In this setting, the value of driving pressure would be overestimated if not corrected for the intrinsic PEEP.