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P0.1, respiratory drive and inspiratory effort

June 27, 2021

Original post written on 27th June 2021 by Giuseppe Natalini


Many mechanical ventilators show us, among measured values, a variable called P0.1 (to be read as P-zero-one)*: what is P0.1? What is its physiological significance? What is its clinical use? Today we will try to reach a clear answer to these questions, which are far from simple.

Respiratory drive and inspiratory effort

Respiratory drive is the intensity of the activity of the respiratory centers located in the brain stem. In other words, it's the intensity of the stimulus to breathe, generated in the central nervous system (1).

Respiratory drive is increased with rising PaCO2, in presence of severe hypoxia (PaO2 lower than 50-60 mmHg, at least), with pulmonary parenchyma inflammation and/or congestion, or with stimuli originating from the brain (pain, delirium, fear, anxiety). On the contrary, respiratory drive can be decreased with hypocapnia, drugs, and cerebral lesions.

Since it’s impossible to measure the level of activity of the respiratory center neurons directly, respiratory drive is quantified by analyzing the physiological signals that depend directly from it.

An increase in respiratory drive translates in a more intense contraction of inspiratory muscles and thus in a greater pleural pressure fall. This is why the inspiratory reduction of esophageal pressure is also a measure of respiratory drive. This is true in the absence of neuro-muscular alterations or of chest wall lesions which could damp the effect of respiratory drive on pleural pressure.

The use of inspiratory effort to measure respiratory drive requires esophageal pressure monitoring. Is there a way to have information on inspiratory effort (and therefore on respiratory drive) using airway pressure  only? 


P0.1

P0.1 was born in 1975 precisely to estimate respiratory drive from airway pressure (2). Joseph Milic-Emili, one of the most important respiratory physiologists of the twentieth century -who became a star in the world of respiratory intensive care at the end of the past century (3)-, is among the “parents” of  P0.1.

During spontaneous inspiration, the airway pressure has an inspiratory variation which is clearly smaller than the simultaneous reduction in esophageal pressure, as you can see in Figure 1 (the inspiratory variation is identified by the distance between the dashed red lines).

Figure 1

This happens if the air enters the lungs during inspiration. In case of an inspiration against occluded airways (with an end expiratory occlusion in ventilated patients or by closing nose and mouth of non ventilated patients), the airway pressure variation is the same as the simultaneous fall in pleural pressure.

In Figure 2 you can see a first inspiration with open airways and a second one against occluded airways. The airway pressure variation is indicated by dashed red lines.

Figure 2


The reduction in airway pressure during occlusion becomes the same as the simultaneous reduction in pleural pressure and therefore permits to use the drop of pressure in occluded airways as a measure of inspiratory effort and hence of respiratory drive.

When airways are occluded, inspiratory effort stays the same as the one of non occluded breaths as long as the patient doesn't perceive the occlusion, and only at that point inspiratory effort starts to increase.

The occluded airways pressure reduction can be therefore used to have information on respiratory drive and inspiratory effort of non occluded breaths, up to the moment in which the patient perceives the occlusion.

It has been shown that the pressure reduction of occluded airways is linear and constant for the first 250 milliseconds (i.e. 0.25 seconds) from the start of inspiration, while after this time the pressure variations become chaotic (Figure 3). It has been therefore hypothesized that respiratory drive in the first 0.25 seconds of an occluded breath is similar to that of non occluded breaths.

Figure 3


Prudentially, a time of 0.1 seconds has been proposed as a safe limit in which the occlusion is not perceived by the patient, therefore the pressure reduction in occluded airways in the first 0.1 seconds of inspiration is considered as an estimate of inspiratory effort (and therefore of respiratory drive). This has been called  P0.1 or airway occlusion pressure.

To support this hypothesis, P0.1 at different PaCO2 levels was measured in healthy volunteers, by making them breath gas mixtures enriched with CO2. In all subjects,P0.1 increased with increasing PaCO2, as is expected for respiratory drive (Figure 4).

Figure 4

Based on this data, P0.1 became a measure of respiratory drive.

In-depth analysis (optional). ΔPocc: differences and similarities with P0.1

A small in depth analysis for those of you who managed to follow all the reasoning up to now (those of you who had difficulties can jump to the next chapter, “P0.1 in practice”). 

Recently, it has been proposed that the whole difference in airway pressure during occlusion (and not only that of the first 0.1 seconds), defined as ΔPocc,  is an estimate of the inspiratory reduction of pleural pressure (4): airways are occluded at the end of exhalation and the entity of the inspiratory fall in pressure of the occluded breath is measured (Figure 5, black two-pointed arrow).

You can see that the reduction of esophageal pressure during the occluded breath is greater than the one during the previous non occluded breath (red two-pointed arrow), while ΔPocc is similar to the simultaneous fall in esophageal pressure (as it should be). It has been calculated that an approximately constant relationship exists  between ΔPocc  (which, we repeat, is the same as the esophageal pressure reduction in the occluded breath) and the esophageal pressure inspiratory variation in non occluded breaths: the esophageal pressure reduction during non occluded inhalation is 66% (i.e two thirds) of ΔPocc.

Now we can understand how P0.1 and ΔPocc estimate the entity of  the fall in pleural pressure using, in both cases, airway occlusion. The only difference between P0.1 e ΔPocc is the way in which the problem caused by the fact that the occluded breath (which we use to get to know pleural pressure variations) is deeper than non occluded breaths (of which we want to estimate inspiratory effort and respiratory drive) is solved.

P0.1 solves the problem by analyzing only the initial part of the occluded inhalation, because it is only with the progress of the occluded inhalation that this becomes greater than the non occluded one. In Figure 5, I have drawn dashed blue lines on the slope of the initial section of the inspiratory pressure reduction of the occluded breath. I have put lines parallel to them also on non occluded breaths, both on airway pressure and on esophageal pressure: you can see that the slope doesn’t change between occluded and non occluded breaths, further supporting the fact that P0.1 of occluded breaths follows the same variations of pressure in the first 0.1 seconds of non occluded breaths. 

Instead, ΔPocc  finds the solution by resizing occluded inspiratory effort to two thirds of the value measured on occluded airways, because this is the magnitude of the increase in esophageal pressure variation induced by the occlusion.

Figura 5


P0.1 in pratice

How can P0.1 be used in the care of subjects undergoing mechanical ventilation?

P0.1, since its origin, has been tested mainly with two objectives: during weaning from mechanical ventilation and to estimate the inspiratory workload of respiratory muscles during mechanical ventilation.

P0.1 has shown to be of little utility (5,6) as a predictor of weaning from mechanical ventilation, after an initial enthusiasm. 

On the contrary, P0.1 has repeatedly shown to be related to inspiratory workload during mechanical ventilation and to its variations due to the variations of inspiratory assistance and PEEP (7-11). 

In particular, it has shown a good ability in identifying patients whose respiratory muscles are maintained at excessive rest during assisted ventilation (when P0.1 is less than 1 cmH2O) or patients in which the workload is excessive  (when P0.1 is greater than 3-5 cmH2O) (7).

Limits of P0.1

P0.1 can be used in concert with the other evaluations used to set inspiratory assistance, but it cannot be followed acritically because it has some important limitations.

First of all, the P0.1 which is measured automatically by mechanical ventilators is really imprecise when compared to the effective value (about ± 2 cmH2O) (7,12). This approximation is anything but negligible, since the diagnosis of inappropriate respiratory muscle activity is made on a really small difference in cmH2O.

Moreover, in subjects with respiratory muscle weakness we could have a low P0.1 (≤ 1 cmH2O) in presence of insufficient inspiratory support. We would make the wrong choice if, in this case, we lowered the inspiratory support because of a low P0.1.

Lastly, we should consider that the threshold to identify an excessive inspiratory effort (between 3 ed i 5 cmH2O) is really wide compared to the accuracy of the measurement and does not permit us to identify this condition with certainty. 

Conclusions

At the end of this post we can summarize the main concepts:

- inspiratory effort is an expression of respiratory drive  and can be therefore used to estimate it;

- P0.1, measured on airway pressure, is an estimation the entity of the first part of the inspiratory reduction of esophageal pressure, which is proportional to the pressure developed by the respiratory muscles. For this reason,  P0.1 is an indicator of inspiratory effort and respiratory drive;

- P0.1 values equal or less than 1 cmH2O can suggest that the activity of respiratory muscles is a lot reduced, and therefore that a reduction in inspiratory support can be considered. This should not be taken into consideration if the patients seems to have respiratory muscle weakness or fatigue. 

 - a P0.1 greater than about 3-4 cmH2O could be a sign of excessive respiratory muscle workload, inducing us to evaluate the possibility of increasing inspiratory support or pharmacologically reducing respiratory drive;

- P0.1 is not particularly accurate, and as such always needs to be integrated with other available data in order to evaluate the appropriateness of respiratory muscle workload (respiratory rate, tidal volume, dyspnea, use of accessory muscles, shape of the inspiratory flow, ...).

And to end, as always, a smile for all of ventilab’s friends.

Note:

* I think that it can be useful to state, for those who are less expert on the subjects, how to read P0.1. I have had this habit since the Nineties when, during an important congress, the moderator of a session on mechanical ventilation presented a speech on P0.1  by reading it as P-O (as the alphabet letter)-one, as if it were similar to PO2... (TRANSLATOR'S NOTE: this is not so relevant in American English, where zero can be pronounced O, as the letter of the alphabet)

References

1) Jonkman AH, de Vries HJ, Heunks LMA: Physiology of the respiratory drive in ICU patients: implications for diagnosis and treatment. Crit Care 2020; 24:104

2) Whitelaw WA, Derenne J-P, Milic-Emili J: Occlusion pressure as a measure of respiratory center output cm conscious man. Respir Physiol 1975; 23:181–199

3) Milic-Emili J: A Respiratory Physiologist by Hook or by Crook. Am J Respir Crit Care Med 2003; 167:1167–1168

4) Bertoni M, Telias I, Urner M, et al.: A novel non-invasive method to detect excessively high respiratory effort and dynamic transpulmonary driving pressure during mechanical ventilation. Crit Care 2019; 23:346

5) Sassoon CSH, Mahutte CK: Airway occlusion pressure and breathing pattern as predictors of weaning outcome. Am Rev Respir Dis 1993; 148:860–866

6) Fernandez R, Raurich JM, Mut T, et al.: Extubation failure: diagnostic value of occlusion pressure (P0.1) and P0.1-derived parameters. Intensive Care Med 2004; 30:234–240

7) Telias I, Junhasavasdikul D, Rittayamai N, et al.: Airway occlusion pressure as an estimate of respiratory drive and inspiratory effort during assisted ventilation. Am J Respir Crit Care Med 2020; 201:1086–1098

8) Alberti A, Gallo F, Fongaro A, et al.: P0.1 is a useful parameter in setting the level of pressure support ventilation. Intensive Care Med 1995; 21:547–553

9) Rittayamai N, Beloncle F, Goligher EC, et al.: Effect of inspiratory synchronization during pressure-controlled ventilation on lung distension and inspiratory effort. Ann Intensive Care 2017; 7:100

10) Perrigault P-FO, Pouzeratte YH, Jaber S, et al.: Changes in occlusion pressure (P0.1) and breathing pattern during pressure support ventilation. Thorax 1999; 54:119–123

11) Mancebo J, Albaladejo P, Touchard D, et al.: Airway occlusion pressure to titrate Positive End-expiratory Pressure in patients with dynamic hyperinflation. Anesthesiology 2000; 93:81–90

12) Beloncle F, Piquilloud L, Olivier P-Y, et al.: Accuracy of P0.1 measurements performed by ICU ventilators: a bench study. Ann Intensive Care 2019; 9:104

 




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