Airway occlusion pressure (P0.1)

Case vignette

56 yo gentleman recovering from severe ARDS, muscle paralysis was discontinued 24hrs ago. Still on continuous sedation with Propofol and Midazolam. Clear “asynchrony” on the ventilator with frequent double cycling. Oxygenation has worsened in the last 6 hours. You go to the bedside and find:

What maneuver can help you understand the underlying status of patient´s respiratory drive and take therapeutic decisions?


The average P0.1 is 6 cmH2O. Based on the high respiratory drive and effort, together with worsening oxygenation, you consider the possibility of increasing sedation or restarting paralysis.

An alternative scenario would’ve been a patient with the same clinical presentation but:

In which case, you activate the P0.1 maneuver and find:

In this case, double cycling are most likely due to reverse triggering in the context of low respiratory drive and high sedative doses. Depending on the degree of worsening oxygenation you can decide a) to stop sedation (if oxygenation is improving) in order to increase the drive for the patient to start triggering the ventilator or b) add paralysis (if oxygenation is significantly worse). Interestingly, increasing sedation in this condition is very unlikely to solve the problem.

Airway occlusion pressure (P0.1)

–an old friend that came back to help us-

Why monitoring respiratory drive and inspiratory effort is relevant during assisted ventilation?

As mentioned in previous posts, patients are at risk of lung (VILI and P-SILI) and respiratory muscle injury (MYOTRAUMA) during assisted mechanical ventilation. Excessive respiratory drive can result in strong inspiratory efforts in the context of under-assistance leading to excessive stress and strain to the lung (P-SILI) and load induce diaphragm injury (MYOTRAUMA). Low drive, in the context of over-assistance or excessive sedation, results in weak or absent efforts leading to diaphragm atrophy, a well described mechanism of MYOTRAUMA. Additionally, patients with breathing efforts within an intermediate range during assisted ventilation have better outcomes, suggesting that low and high respiratory drive and effort might be injurious.

Frequent asynchronies are also associated with adverse clinical outcomes, however mechanisms and consequences of each type of asynchrony are completely different. Different types of asynchronies occur in the context of:

  • high respiratory drive: flow starvation, short cycling, and double triggering
  • low respiratory drive: prolonged cycling, ineffective efforts, reverse triggering (with and without double cycling)

Management of these asynchronies depend on the status of respiratory drive.

Given the influence of respiratory drive and inspiratory effort on the risk of lung, diaphragm injury, and asynchronies, monitoring these parameters is crucial in patients under assisted ventilation.

Why monitoring respiratory drive and inspiratory effort is challenging?

Respiratory drive is the intensity of the neural stimulus to breath. Currently, there is no method to directly measure the activity of the respiratory centers, therefore respiratory drive is inferred based on their output. Each measure of output entails limitations as an estimate of drive:

  • breathing pattern (tidal volume and respiratory rate): influenced by respiratory mechanics independently of the status of respiratory drive.
  • electrical activity of the diaphragm: requires catheter insertion, there is no reference value to follow, and represents the activity of only one muscle
  • inspiratory effort (esophageal pressure and diaphragm ultrasound): in patients with respiratory muscle weakness, despite a high respiratory drive inspiratory effort might be low (risk of underestimation of repiratory drive)
  • airway occlusion pressure (P0.1) will be discussed later

The gold standard to measure inspiratory effort requires the insertion of an esophageal catheter, which is not routinely performed in patients under assisted ventilation.

What is P0.1?

Airway occlusion pressure is the pressure generated at the airways during the first 100 msec of an inspiratory effort against an occluded airway (Figure 1).

Why is P0.1 a good measure of respiratory drive?

P0.1 increases proportionally to an increase in pCO2, the main determinant of respiratory drive, even during respiratory muscle weakness.

During the occlusion, airway pressure follows the pressure generated by the respiratory muscles and, since there is no volume displacement, respiratory mechanics do not influence the measurement. The occlusion itself does not modify the effort because during the first 100 because there is no conscious or unconscious reaction to the occlusion.

How can we measure P0.1 in modern ventilators?

Most modern ventilators provide the measurement of P0.1. Some ventilators (Servo ventilators, Gettinge) estimate the value based on the drop in airway pressure during the trigger phase on a breath-by-breath basis (Figure 2). In others, activation of a single key generates a short end-expiratory occlusion, subsequent measurement of the drop in airway pressure providing a value for P0.1 (Figure 3). However, accuracy of the P0.1 displayed by modern ventilators needs to be tested.

Figure 2: Servo i ventilator with breath-by-breath P 0.1 estimate.
Figure 3: P 0.1 maneuver on the Drager V500 ventilator. This also can be set to perform the maneuver in timed intervals.

What are the potential pitfalls of P0.1 in patients under assisted ventilation?

Breath-by-breath variability of P0.1 in one patient within a clinical condition is substantial, therefore the average of 3 to 5 values should be considered. Intrinsic PEEP can introduce an error in the measurement, but this error may be less than 1cmH2O (Figure 4).

Figure 4: Two breaths are displayed in a patient under assisted mechanical with intrinsic PEEP (PEEPi). Flow, airway pressure (Paw) and esophageal pressure (Peso) are displayed. An end-expiratory occlusion is performed and the delay in drop in Paw during the occlusion compared to the drop in Peso can be seen. In this case, if P0.1 is measured since flow reaches zero, drop in Paw and Peso are superimposed and error in the measurement is minimized.

What reference values of P0.1 should be considered?

In healthy adults breathing spontaneously, P0.1 is about 1 cmH2O (0.5-1.5 cmH2O). In mechanically ventilated patients values above 3.5 cmH2O were associated with increased effort. However, further studies are needed to validate that values below 1.5 and above 3.5 cmH2O might be low or excessive in patient under assisted ventilation.

P0.1, an old friend that came back to help us

P0.1, first described by Whitelaw in 1975, is now available in most modern ventilators and can help us titrating ventilatory support and sedation to achieve a ventilatory strategy protective for the lung and diaphragm. As described, P0.1 might help us detecting an excessive or low respiratory drive and inspiratory effort. It can also help us understand what´s the status of respiratory drive in a patient with asynchronies (high or low) to guide further management.

Irene Telias MD
Critical Care Fellow
St. Michael’s Hospital and University Health Network
Interdepartmental Division of Critical Care Medicine
University of Toronto

Further Reading

Telias I, Damiani F, Brochard L. The airway occlusion pressure (P0.1) to monitor respiratory drive during mechanical ventilation: increasing awareness of a not-so-new problem. Intensive Care Med 2018;44:1532–1535

Pham T, Telias I, Piraino T, Yoshida T, Brochard LJ. Asynchrony Consequences and Management. Crit Care Clin 2018;34:325–341.

8 thoughts on “Airway occlusion pressure (P0.1)”

  1. Thank you for these educational cases. I’m curious about the first case you showed with a P0.1 of -6cmH2O which suggested a high respiratory drive. If you determined the plateau pressure in this patient to be safe (<25 or <30 or whatever you would deem to be acceptable) how would this change your management assuming that you do not have access to an esophageal manometer?

    Would you be reassured by the safe plateau pressure and accept this "high ventilatory drive" and thus maintain the patient on the current level of sedation?

    Or would you suspect that the high respiratory drive translates to more negative pleural pressure and thus increased transpulmonary pressure to a potentially dangerous level?…thereby prompting you to increase sedation/consider neuromuscular blockade… This seems like too far of a stretch given the unknown effects of respiratory system compliance and other factors without the esophageal pressure.

    1. Respiratory drive levels like this are associated with weaning failure. To have this type of drive while a patient is receiving full ventilation we feel should be concerning based on the clinical context (ie. patients course in ICU, the presence of ARDS, oxygen and PEEP requirements), and the risk of patient self-inflicted lung injury (P-SILI). Esophageal pressure is always valuable, but currently, we know P0.1 is a validated representation of respiratory drive, and levels of ~6 cmH2O are associated with weaning failure. If they have no underlying reason (chronic lung disease) for a high respiratory drive such as this, you have to weigh the potential injury risks (including oxygen consumption) with benefits of allowing patients to continue making spontaneous efforts. One method for reducing drive without affecting rate is careful titration of propofol, this may be considered rather than paralysis depending on the clinical condition. As for plateau, consider that patients in volume control can maintain transpulmonary pressure (PL) because airway pressure drops with increased effort. However, pendelluft can occur causing regional lung stress that is independent of PL

    1. Generally, yes. But if increasing PSV cannot reduce the P0.1 to an acceptable value we consider risk of self-inflicted injury.

      1. Do you find important titrate PS in PSV by P01 value, between -1,5 to -3,5 to protect diafragm and avoiding over ir under assist of the parient.

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