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