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A 59-year-old man with a body mass index of 47 kg/m2 was admitted to the ICU with septic shock. After intubation, positive end-expiratory pressure (PEEP) was titrated to 16 cm H2O after measuring the transpulmonary pressure gradient, as previously described (1). On Day 4, a standard 30-minute spontaneous breathing trial (SBT) with pressure support of 3 cm H2O and PEEP of 5 cm H2O (2) failed, owing to the development of tachycardia and dyspnea. An esophageal pressure tracing obtained during the SBT demonstrated inspiratory pressure swings of more than 30 cm H2O (Figure 1A), suggesting increased work of breathing (3). Electrical impedance tomography (EIT) during the SBT showed a “pendelluft effect” (4), with air flowing within the lungs, from the most dependent to nondependent areas (Video 1A).
Figure 1. Esophageal (red) and airway (blue) pressure traces during spontaneous breathing trials (SBTs) (A) with a positive end-expiratory pressure (PEEP) of 5 cm H2O (failed SBT) and (B) with a PEEP of 16 cm H2O (successful SBT).
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Video 1. Tomographic representation of ventilation distribution with electrical impedance tomography during spontaneous breathing trials. (A) At the transition between inspiration and expiration at positive end-expiratory pressure (PEEP) of 5 cm H2O, exhalation begins in the dependent lung regions, then a pendelluft phenomenon appears with gas flowing from the dependent to nondependent lung regions. The mechanical load of obesity increases pleural pressure, causing reduced lung volumes with air trapping as a result of airway closure and increased airway resistance. An increase in respiratory drive caused by the elevated pleural pressure is then observed, stimulated by low lung volumes and ineffective ventilation, in the attempt to overcome the increased mechanical load. The pendelluft phenomenon, as shown in this video, suggests a pronounced diaphragmatic contraction resulting in concentration of force within dependent areas of the lung. This concentration of force generates a pendular movement of air from dependent to nondependent lung regions, likely resulting in ineffective ventilation. (B) When PEEP is increased to 16 cm H2O, a more homogeneous distribution of ventilation is observed with a significantly reduced pendelluft.
A second SBT was performed minutes later at pressure support of 3 cm H2O and PEEP of 16 cm H2O. The higher PEEP resulted in an approximately threefold reduction in inspiratory esophageal pressure swings (Figure 1B), and EIT showed a regular breathing pattern and reduced pendelluft (Video 1B). Offline analysis of the EIT traces showed a gain in compliance of about 41% by increasing PEEP from 5 cm H2O to 16 cm H2O, suggesting improved homogeneous ventilation and decreased atelectasis. The patient was successfully extubated to 16 cm H2O continuous positive airway pressure, discharged from the ICU, and eventually discharged from the hospital without the need for reintubation.
In critically ill obese patients, SBTs at low PEEP levels often fail, leading to ventilator dependency (5). The elevated pleural pressure in these patients works as a mechanical load, reducing lung volumes and causing airway closure, increased airway resistance, and development of atelectasis, especially within dependent lung regions. This case illustrates the importance of a physiology-based approach to PEEP titration in this obese patient.
An SBT at high PEEP showed a similar mechanism of work of breathing unloading to that described previously by Vitacca and colleagues (6). In addition, we showed a reduced pendelluft, resulting in more homogeneous ventilation. Future studies should address the safety of extubation at high PEEP levels in obese patients.
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The uncompressed video is accessible from this article’s supplementary material page.
Originally Published in Press as DOI: 10.1164/rccm.201712-2411IM on April 27, 2018
Author disclosures are available with the text of this article at www.atsjournals.org.
