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:
Definition of transpulmonary pressure
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:
- Transpulmonary pressure is continuously measurable, while elastic recoil pressure of the lung requires hold manoeuvres (because alveolar pressure can only be recorded when there is no flow in the circuit)
- Elastic recoil pressure of the lung depends only on lung volume and elastance, whereas TPP is also influenced by airway resistance
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.
Measurement of transpulmonary pressure
Measuring pleural pressure
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:
- Connect a hand-held digital manometer to a pleural drain, which is the gold standard (Lee et al, 2014)
- Use a water-filled U-tube and a pleural drain
- Use an electronic transducer and a pleural drain (essentially, this means connecting a Wheatstone bridge transducer to it)
- Use an oesophageal balloon manometer
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.
Measuring alveolar pressure
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).
Variables which affect the validity of oesophageal manometry
Is lower oesophageal balloon pressure really equal to pleural pressure?
Several variables affect Pes:
- Elastic recoil of the oesophagus which should be close to zero, as it is usually a compliant floppy tube
- Oesophageal muscle tone which should be fairly flaccid, unless the patient is swallowing or vomiting
- Transmitted pressure from surrounding structures:
- Pleural pressure (what you are interested in)
- Mediastinal pressure
- Posture, which creates a vertical pressure gradient and changes the extent to which mediastinal content affects the oesophageal balloon. Classically, the patient needs to be upright for the measurement. In the supine position the oesophageal measurement is falsely elevated, by as much as 7cm H2O (Ferris et al, 1958).
- Position relative to the lung: the balloon is supposed to sit at approximately the midpoint of the lung’s gravitational plane, and therefore reflects pleural pressure at that height. This means it underestimates the pleural pressure around the lower zones of the lung, and overestimates it for the apical regions. In ARDS the lung is heavier, so this becomes more of a problem.
- Balloon shape and size: There seems to be no standard for this, and each device may give highly idosyncratic readings.
How do you know it is in the correct position? According to LITFL,
- Insert the thing into the patient up to around 60cm
- Inflate the balloon
- Transduce the pressure
- Ballot the stomach: a properly positioned transduced catheter will "feel" your abdominal poking
- Withdraw the catheter into the oesophagus (to a depth of around 40cm)
- Confirm placement with "cardiac oscillations".
Rationale for the use of transpulmonary pressure
Let's just assume the pressure you managed to measure is the true transpulmonary pressure. What is the point of using it?
- Airway pressure alone may be misleading
- TPP offers a more accurate asssement of stress upon the lung parenchyma
- TPP has the advantage of separating chest wall compliance from lung compliance.
- Customisation of PEEP and VT settings is possible, particularly for the morbidly obese and patients with high abdominal compartment pressure.
- The measurement of TPP by oesophageal manometry is fairly non-invasive
An excellent article by Akoumaniaki et al (2014) explores the various possible uses of TPP. In summary:
- Perform smarter recruitment manoevres, eg. using TPP of 25
- Set the PEEP in ARDS to prevent atelectasis (TPP 0-10)
- Set the VT in ARDS to prevent volutrauma (TPP <25)
- Set the ventilator in morbidly obese patients, those with abdominal compartment syndrome or with some sort of rapidly changing abdominal pressure (pregnant, undergoing laparsocopy, etc).
- Detect "respiratory entrainment" or reverse triggering, a form of patient-ventilator dyssynchrony where the mandatory inspiration causes the patient's respiratory muscles to contract, as if in protest.
- Detect ineffective respiratory efforts
- Improve the synchrony of SIMV with weak patient efforts
- Improve the cohesion between ventilator inspiratory time and the patients respiratory time
- Auto-PEEP can be measured using this method
- It may provide a simple measure of patient effort in weaning from mechanical ventilation
Practical use of transpulmonary pressure to guide therapy
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?
- To measure Pplat, perform an inspiratory hold manoeuvre.
- At the same time, record your Pes reading.
- Calculate TPP (Pplat - Pes )
- This is your end-inspiratory TPP; keep this no greater than 25 cmH2O
- Now, perform an expiratory hold and record your Pes at end-expiration (i.e. just on PEEP and iPEEP)
- Calculate your end-expiratory TPP.
- Your end-expiratory TPP should be higher than 0 to prevent atelectasis, but brobably no higher than 10.
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.
Limitations of oesophageal manometry as a guide to therapy
There are several situations in which the Pes does not correlate with pleural pressure:
- Gravitational pressure gradient (when the patient is not supine)
- Local variations (eg. pressure from consolidated lung)
- The oesophageal balloon is closes to the left lower lobe; therefore it may not reflect pleural pressure in other (better aerated) regions.
The practical limitations of the technique
- Relies on correct balloon position
- Heterogeneity of ARDS means the pressure determined by oesophageal manometry does not represent the TPP in much of the lung
- Nobody knows how to interpret it in the prone patient
- Pes overestimates pleural pressure in the well-aerated regions of lung and underestimates it in dependent regions of lung. Thus, it relocates the VILI without reducing its severity.
Evidence for the use of TPP in mechanical ventilation
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. Apart from this study, the EpVent Trial (Fish et al, 2014) is under way and plans to enrol 200 patients. There seems to be little else.
Alternatives to the use of TPP
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;
- Rodriguez et al (2013) found that the decremental titration of PEEP in ARDS patients eventually achieved the same PEEP level as would have been recommended by the TPP. From this, one might surmise that one may continue to do the same derecuitment manoeuvres we have been doing for years, and forget about oesophageal manomery.
- Terragni et al (2013) found that using the "Stress Index", an index derived from the shape of the airway pressure over time curve during constant flow, was even better than TPP for preventing "injurious ventilation".