This had become a hot topic in 2016, to such an extent that it had merited an entire 10-mark SAQ (Question 25 from the first paper of 2017).
In terms of using literature and FOAM, as always LITFL does it better. For the time-poor candidate, the single most useful reference would have to be the "pros and cons" article by Talmor and Fessler (2010). An excellent review article by Sarge et al (2009) and another recent article (Sahetya et al, 2016) were used to generate this summary chapter. Specifically, Sahetya et al also have a nice list of advantages and disadvantages which is ideally suited to answering Question 25 from the first paper of 2017. If one reads the article carefully, one gets the impression that the examiners used this as their major resource as well. The points made in the (comprehensive) college answer closely resemble the points made by Sahetya et al, particularly at the end.
- Transpulmonary pressure = (Pplat -Pes), where Pes is oesophageal pressure, a reasonable surrogate for pleural pressure.
- TPP excludes the effects of chest wall compliance on respiratory mechanics
- Using TPP to guide PEEP and VT settings may reduce VILI
- TPP can also be used to perform smarter recruitment manoevres, set the ventilator in morbidly obese patients, measure auto-PEEP in awake patients, detect patient-ventilatory dyssynchrony and detect ineffective respiratory efforts.
- Howeve, oesophageal manometry is also affected by
- Elastic recoil of the oesophagus
- Oesophageal muscle tone
- Transmitted pressure from mediastinal structures
- Position relative to the lung
- Oesophageal balloon shape, size and filing volume
- It is prone to error:
- Various assumptions are made (eg. that pleural pressure is equal throughout the chest)
- There is little evidence that it has any effect on patient-centered outcomes
- There are alternatives (eg. derecruitment manoeuvres for finding the optimal PEEP) which can arrive at the same conclusions without oesophageal manometry
In apocryphal detail:
What is the TPP? Loring et al (2016) railed bitterly against the "inconsistent and mutually exclusive definitions" used by contemporary researchers. Apparently, these reprobates have been describing TPP as distending pressure across only lung tissue (a concept known to normal sane people as "elastic recoil pressure of the lung").
Loring et al list such physiology luminaries as John West’s Respiratory Physiology-the Essentials and Weinberger’s Principles of Pulmonary Medicine among the heretics who have taken "transpulmonary pressure" to mean "pressure gradient from lung parenchyma to pleura", negligently ignoring the pressure drop across the airway down to the alveoli. This is clearly madness; use or non-use of airway pressure has all sorts of important implications which we require to make correct assumptions about the respiratory system. In brief:
However, in their answer to Question 25 from the first paper of 2017, the college defined TPP as "the difference between the alveolar pressure (Palv) and pleural pressure (Ppl)", or as "the net distending pressure applied to the lung". If we take the college model answers as canon, then this definition is gospel law, equivalent in its legitimacy to the official Scrabble dictionary. For some reason which pedants might find maddening the college have decided to re-brand this physiological concept as TPP, where others might call it "elastic recoil pressure of the lung". Practically speaking (and no matter what you call it) it is important for the intensivist to make management decisions on the basis of the pressure which affects lung parenchyma, because this pressure is what leads to Ventilator-Associated Lung Injury (VALI). The airway resistance pressure in ARDS is practically useless for all our intents and purposes; it is only there to generate annoying ventilator alarm sounds.
We can escape from academic debates about physiological definitions by taking refuge in the classical ICU tradition of measuring stuff by inserting things into people. You need to measure the pleural pressure somehow. There are several possible means of doing this:
Of the direct measurment methods, the only one which does not involve actually penetrating the chest wall is the oesophageal balloon method. Thoracocentesis purely for the purpose of taking measurements seems a bit excessive in a fragile ARDS patient. Fortunately the lower third of the oesophagus offers a convenient window on the state of pleural pressure, because the oesophagus is usually a highly compliant easily deformable tube and one might be able to measure this pressure (Pes)by means of a thin-walled latex balloon catheter (such as this Carefusion product).
The balloon is then filled with about 0.5ml of air (Akoumaniaki et al, 2014). Obviously, the accuracy of the techniqe depends on how much air you inject, and how fat the balloon. Big fat balloon will give erroneously high pressure readings.
Using the faulty definition of TPP which is favoured by CICM and West of West's we conclude that we are interested in the difference between the pressure inside the alveoli and pressure inside the pleural cavity. The alveolar pressure can be measured using an inspiratory hold manoeuvre: it corresponds to Pplat, the pressure across the airway when flow has ceased and all the alveoli (presumably) equilibrate pressure among themselves.
In this manner, we can calculate TPP as (Pplat - Pes).
Is lower oesophageal balloon pressure really equal to pleural pressure?
Several variables affect Pes:
How do you know it is in the correct position? According to LITFL,
Let's just assume the pressure you managed to measure is the true transpulmonary pressure. What is the point of using it?
An excellent article by Akoumaniaki et al (2014) explores the various possible uses of TPP. In summary:
What is the meaning of this variable? How do you use it? Well. In brief, one needs to regularly perform expiratory and inspiratory hold manoeuvres to use the TPP. A low (or even negative) expiratory TPP will lead to derecruitment and atelectasis, whereas a high end-inspiratory TPP will lead to VILI.
How do you actually measure and use this variable?
For instance, in a patient with a massively obese chest wall the pleural pressure may be highly positive. Let's say it is 15 cmH2O. At a Pplat of 30 cmH2O, the TPP is still only 15. With an expiratory hold at a PEEP of 10, the Pplat ends up being 12 cmH2O, giving a TPP of -3 cmH2O. In this scenario, the fat patient develops atelectasis - clearly more PEEP is required. This is supported by Eichler et al (2017) who explored the use of TPP in ventilation of morbidly obese patients undergoing bariatric surgery. To maintain a TPP of at least 0, on average PEEP levels of 16.7 cm H2O before and 23.8 cm H2O during capnoperitoneum were necessary.
Here is a real-life example from a paper by Mauri et al (2016):
Here, the patient's Pplat is around 17 cm H2O; the inspiratory Pes is around 20, which is a safe level unlilely to cause VILI. However at the end of expiration Pes seems to be around 18, and the PEEP is 5. The patient's TPP is therefore -13 cmH2O, a recipe for atelectasis.
There are several situations in which the Pes does not correlate with pleural pressure:
The practical limitations of the technique
There has been surprisingly little research on the use of this therapy in the ICU. The college answer quotes Talmor et al (2008): "Mechanical ventilation guided by esophageal pressure in acute lung injury." This was a randomised controlled study of 61 ARDS patients, of whom the TPP-guided group has better survival. The primary endpoint was oxygenation, and this too was better when PEEP was guided by TPP. Unfortunately the study sample was too small for the results to reach statistical significance. Fortunately, we have an updated EPVent 2 trial (Beitler et al, 2019) which had a much better sample size (200) and which also did not find any benefit (looking at a composite outcome). True believers will point out that the real population of people who would benefit from TPP has never been studied in either of these papers.
Perhaps for whatever reason you don't want to shove any more tubes into your patient. Is there some way of getting the benefit from TPP-guided therapy without actually having to measure the TPP? Well;