Reply to Chalkias and Xanthos: Airway Pressure Monitoring May Improve Small Airway Flow, Hemodynamics, and Tissue Oxygenation.

To the Editor:

We are very grateful to Dr. Chalkias and Dr. Xanthos for their thoughtful comments regarding the description of the phenomenon of intrathoracic airway closure reported in the Journal (1).

These authors recently reported an impressive series of 300 out-of-hospital patients with cardiac arrest who were resuscitated with a strategy combining rapid intubation, continuous chest compression (CC), and positive pressure ventilation delivered via a ventilator (2). The unexpectedly high percentage of return of spontaneous circulation reported in this study was significantly associated with highest mean airway pressure (Paw) measured after 3 minutes of resuscitation via an external monitor. CO2 measured via a mainstream monitor was similar between survivors and nonsurvivors. The authors concluded that a mean Paw above 42.5 mbar was associated with a higher chance of return of spontaneous circulation.

Interestingly, the apparent negative effect of a low mean Paw during CC could be related to (or associated with) the intrathoracic airway closure we recently reported (1). In fact, the transmission of pressure generated by CC at the airway opening is limited or absent in the case of intrathoracic airway closure. Conversely, the expected beneficial effect of positive pressure delivered by the ventilator (which refers to the thoracic pump effect) can be effective only if the positive airway pressure applied at the airway opening is transmitted to the intrathoracic compartment, although this transmission will be limited by intrathoracic airway closure. The methodological difficulty of capturing the highest value of CO2 that seems the best surrogate of alveolar CO2 during resuscitation limits the interpretation of the lack of difference reported in their study.

Therefore, if we accept that the association between a mean Paw below 42.5 mbar and a worse prognosis reported in the study of Chalkias and colleagues might be explained by intrathoracic airway closure, several different mechanisms could still be at play. First, intrathoracic airway closure could simply be a marker of poor prognosis that also limits transmission of pressure generated by CC at the airway opening, making the calculated mean airway pressure at the mouth lower. Second, intrathoracic airway closure may have impaired the transmission of positive pressure generated by ventilation to the intrathoracic compartment, thus limiting its expected beneficial effect on the thoracic pump effect. By overcoming intrathoracic airway closure, higher mean airway pressure could be beneficial on both circulation and ventilation. Finally, one cannot exclude that the lower mean Paw associated with the lower chance of return of spontaneous circulation in the abovementioned study could be simply the reflection of less effective CC, independent of intrathoracic airway closure. These fascinating physiological discussions deserve additional observations to better understand the mechanisms at play and the evolution of airway closure along the time of resuscitation. The use of the capnogram during CC, based on the description of Grieco and colleagues, may permit us to adapt ventilator settings according to intrathoracic airway closure to balance both the beneficial and potential harmful effects of positive airway pressure during resuscitation.