Podcast: Play in new window | Download
Subscribe: Apple Podcasts | Spotify | Android | Pandora | iHeartRadio | TuneIn | RSS
We talk about the phenomenon of airway closure during mechanical ventilation, with Thomas Piraino, RRT, FCSRT, FAARC, adjunct lecturer for the Department of Anesthesia at McMaster University, editor of The Centre of Excellence in Mechanical Ventilation Blog, and a member of the editorial board of Respiratory Care.
Learn more at the Intensive Care Academy!
Takeaway lessons
- Airway closure occurs when airways, probably smaller ones (ie bronchioles) completely collapse at some point during expiration, causing flow to cease.
- This creates a false understanding of the “PEEP,” which may actually be higher than the set PEEP (effectively an autoPEEP), and hence an incorrect understanding of the driving pressure and compliance. (This autoPEEP may or may not be effective, as at higher FiO2s, this trapped volume may rapidly absorp, causing absorption atelectasis.)
- It may cause lung injury at the airway level from cyclic opening/closing, separate from more-discussed alveolar injury.
- ARDS, pulmonary edema, and obesity are all risk factors. Post-cardiac arrest is a particularly common substrate. Obstructive diseases like asthma/COPD can probably see this as well, although the recent discourse has focused on the hypoxic conditions; the phenotype is probably different, caused by intrathoracic pressure, not by air-fluid interfaces and surfactant issues.
- Probably 40% of at-risk patients may see this phenomenon occur. Its presence and the pressure where it occurs may be labile and dependent on the clinical condition. It should probably be checked at least daily in such patients.
- It may cause hypercarbia by terminating expiration early, leading to air trapping. Prolonging the expiratory time will not help, as flow has ceased.
- Plateau pressure may be elevated. Expiratory holds will not reveal this, however. A visible inflection point in continuous-flow VC breaths that has a different height (higher) than the gap between the peak and plateau pressure may be a rough suggestion of this as well.
- Plateau pressures will be accurate, as the airways should be open at peak inspiration (or no breath would be delivered). Thus, increasing PEEP and seeing no change in plateau pressure may be a sign of airway closure, although it can also be due to alveolar recruitment.
- Active patient effort during exhalation may worsen this phenomenon, particularly in the obstructive patient, due to increasing intrathoracic pressure.
- The best test is a slow-flow inflation curve. Draeger and Hamilton should have this built in (Hamilton does this incrementally, not continuously, which may make it a little harder to identify the exact inflection point). It can be done manually as such (patient must be passive):
- Set VC mode
- Square wave flow
- Flow 5L/min
- Rate 5/min
- PEEP 5 (or higher if needed for oxygenation)
- Freeze the screen and inspect the pressure scalar during inspiration. The upramp should be steady and continuous. If there is a change in slope or inflection point, this suggests a change in compliance, probably due to airway opening. Use the vent to measure pressure at this point.
- A clever time to do this might be shortly after intubation, while patients are deeply sedated and paralyzed.
- That this inflection represents airway opening can be proven by measuring the compliance up to that point (volume delivered vs pressure), which will usually be <3 cmH2O/ml, roughly the compliance of the ventilator circuit.
- Inflection can occur from alveolar recruitment as well, but this is usually a less abrupt, steady change in slope. If present, it will occur above the airway closing pressure inflection.
- In general, set the vent PEEP at the same level as the measured closing pressure. This will normalize your understanding of the driving pressure and probably limit cyclic collapse and lung injury. It may also facilitate expiration and hence ventilation.
