Transpulmonary pressure (TPP)

OVERVIEW

Transpulmonary pressure (TPP) is the net distending pressure applied to the lung by contraction of the inspiratory muscles or by positive-pressure ventilation

  • TPP is the difference between alveolar pressure (Palv) and pleural pressure (Ppl); i.e. TPP = Palv – Ppl
  • Oesophageal pressure [Pes] is used as a surrogate for Ppl, so TPP can be measured by performing oesophageal manometry during an end-inspiratory or end-expiratory occlusion; i.e. TPP = Palv – Pes

PHYSIOLOGY

  • in a normal spontaneously breathing person TPP is always positive; this keeps the lung expanded
    • Ppl is always negative, and may be large during inspiration
    • Palv changes from slightly positive to slightly negative
  •  If ‘transpulmonary pressure’ = 0 (alveolar pressure = intrapleural pressure), as occurs during a pneumothorax, the lung will collapse due to elastic recoil of the lung parenchyma

RATIONALE FOR TPP MEASUREMENT

  • Airway pressure is a poor surrogate of lung stress because it ignores the effect of chest recoil
  • chest recoil is affected by impaired chest wall mechanics in the critically ill
  • TPP is the true distending pressure of the lungs
  • TPP measurement allows partitioning of lung compliance from chest wall compliance

USES OF TPP AND Pes

  • Assessing lung recruitability using low flow pressure-volume curve
    • Lung recruitability is indicated by a lung pressure-volume curve with a well defined lower inflection point and a large hysteresis
    • In the absence of lung recruitability recruitment manoeuvres may cause VILI
  •  Titrating recruitment manoeuvres
    • aim to fully recruit the lung but avoid excessive overdistension
    • target TPP of 25 cmH2O during recruitment
  • Setting PEEP
    • aim to maintain oxygenation while preventing lung injury from alveolar collapse (atelectrauma) or overdistension
    • set PEEP to maintain TPP of 0 to 10 cmH2O at end expiration using an end-expiration occlusion
  • Setting tidal volume and inspiratory pressures
    • aim to to limit stress applied to the lung
    • keep TPP at end-inspiration below 25 cmH2O
  • Determination of respiratory muscle effort in spontaneously breathing patients
    • by assessment of work of breathing or the esophageal pressure time product
  • Assessment of patient-ventilator synchrony (e.g. auto-triggering, inspiratory trigger delay and ineffective inspiratory effort)

INTERPRETATION OF INCREASED Pes

Increased Pes means extra-pulmonary/ chest wall compliance is decreased, causes include:

  • pleural effusion
  • thoracic trauma
  • oedematous intrathoracic viscera
  • intraabdominal hypertension
  • massive ascites
  • oedematous intra-abdominal viscera

MEASUREMENT OF Pes

  • Pes is usually measured via an esophageal catheter with an air-filled thin-walled latex balloon inserted nasally or orally
  • Pes is used as a surrogate of pleural pressure
  • Tidal changes in Pes correlate with changes in pleural pressure applied to the surface of the lung
  • Validation of Pes measurement (Baydur’s technique)
    • a dynamic occlusion test is performed
    • airway is occluded at end-expiration
    • the ratio of change in Pes to change in Paw is measured during spontaneous inspiratory efforts against a closed airway
    • A ratio close to unity (e.g. 0.8 to 1.2) indicates that the system provides a valid measurement
    • Baydur’s technique is valid in spontaneously breathing subjects in sitting, supine, and lateral positions
  • Measurement in passively ventilated patients
    • catheter is advanced into the stomach and is verified by transiently increasing balloon pressure with abdominal compression
    • catheter is withdrawn into the esophagus and is verified by obvious cardiac oscillations
    • changes in PTP during tidal ventilation are used to adjust the esophageal balloon catheter to the correct position

PROBLEMS

  • erroneous Pes results if malpositioned balloon catheter
  • a single local pressure measurement cannot represent global pressure
    • Pleural surface pressure distributions are not uniform, especially in ARDS
    • titration of ventilation to global TPP measurements may lead to hetergoenous regional overdistention and under-recruitment, resulting in VILI
  • Pes is subject to various artefacts and assumptions — the correlation between Pes and Ppl is affected by many factors:
    • mediastinal artefact in the supine position: the pressure vector generated by the weight of the mediastinum may increase Pes
    • in the upright position Pes represents the least positive local pressure along its own horizontal (gravitational) plane
    • Pes has limited ability to track globalaverage changes in pleural pressure when supine and if there is heterogenous lung disease
    • elevation of intra-abdominal pressure
    • position-related lung volume changes
    • obesity
  • TPP is not equivalent to transalveolar pressure (the stress generated in the lung parenchyma) (Loring et al, 2016)
    • TPP includes the pressure drop across the airways
    • static TPP may often approximate transalveolar pressure, but may not when the airways are obstructed or closed, as ioccurs at very low lung volumes or in severe lung disease

EVIDENCE

Talmor et al, NEJM 2008

  • SCRCT
  • n = 61 patients with ALI/ARDS
  • Intervention: TTP-targeted mechanical ventilation (targeting end-inspiratory Pes to < 25 cmH20 and end-expiratory Pes to <10 cmH2O) versus ARDSNet protocol
  • Outcomes:
    • higher PEEP and better oxygenation (primary outcome) in the intervention group (mean increase in Pao2 of 88 mmHg at 72h )
    • higher Pplat in the intervention group, but no difference in end-inspiratory TTP
    • non-significant trends towards improved respiratory-system compliance and favourable clinical outcomes such as mortality (secondary outcomes)
  • trial stopped early as met stopping criterion

References and Links

Journal articles

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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