High airway and alveolar pressures

Reviewed and revised 22 December 2015

OVERVIEW

High airway pressures are important because they may:

  • have adverse effects on the patient
  • indicate a deterioration of the patient’s condition
  • indicate an equipment problem that needs to be addressed

It is important to distinguish between airway pressure and alveolar pressure

AIRWAY PRESSURE AND ALVEOLAR PRESSURE

Airway pressure

airway pressure = flow x resistance + alveolar pressure

  • Thus if flow or resistance is markedly altered, a change in airway pressure will not be indicative of a change in the alveolar pressure
  • Airway pressure is more conveniently measured than alveolar pressure
  • Peak inspiratory pressure (PIP) is displayed on most ventilators
  • A maximum acceptable PIP of <35 cmH20 is widely used

Alveolar pressure

  • Alveolar pressure is estimated by determining the inspiratory pause pressure, which corresponds to the plateau pressure
  • The inspiratory pause pressure is determined by observing the plateau pressure in an apneic ventilated patient when when the ‘inspiratory pause hold‘ control is activated
  • Because flow is reduced to zero, airway pressure and alveolar pressures will equalise and the airway pressure will correspond to the alveolar pressure at full inspiration

airway pressure = 0 x resistance + alveolar pressure = alveolar pressure

  • To prevent lung injury, alveolar pressure (aka the plateau pressure) should be kept <30 cmH2O
  • High alveolar pressures can be due to excessive tidal volume, gas trapping, PEEP or low compliance as shown by this relationship:

alveolar pressure = (volume/ compliance) + PEEP

PRESSURE-TIME CURVES SHOWING PIP AND PLATEAU PRESSURES IN VOLUME CONTROL VENTILATION

PIP vs Pplat

Normal curve – demonstrates normal PIP , Pplat , PTA (transairway pressure), and Ti (inspiratory time). High Raw curve – A significant increase in the PTA is associated with increased airway resistance. High Flow curve – the inspiratory time is shorter than normal, indicating a higher inspiratory gas flow rate. Decreased Lung Compliance curve – An increase in the plateau pressure and a corresponding increase in the PIP is consistent with decreased lung compliance.

EFFECTS OF HIGH PRESSURES

High airway pressure is not necessarily harmful, unless it reflects high alveolar pressure which can have these effects:

  • barotrauma may result in acute lung injury (leading to ARDS) or air leaks (e.g. pneumothorax, pneumomediastinum)
  • Excessive intrathoracic pressure may also result, with potential hemodynamic consequences (particularly decreased venous return, leading to hypotension and potentially cardiac arrest)
  • High airway pressures may result in inadequate ventilation

Ventilator response to high airway pressures:

  • Inadequate ventilation can occur because many ventilators are set to terminate the inspiratory flow if the upper pressure limit setting is reached. When this occurs inspiratory volumes are markedly reduced, resulting in low tidal volumes and minute ventilation
  • Other ventilators do not do this but will simply hold the airway pressure at the pressure limit, resulting in a smaller reduction in tidal volume

There many also be other consequences of the underlying cause

CAUSES OF HIGH PRESSURES

  • Think “Man versus machine”

First, let’s consider the machine:

  • Ventilator
    • inappropriate settings
    • ventilator malfunction
  • Circuit
    • kinking
    • pooling of condensed water vapour
    • wet filters causing increased resistance
  • Endotracheal tube
    • displacement, e.g. endobronchial intubation
    • kinking
    • obstruction with foreign material

And now the man:

  • bronchospasm (e.g. asthma)
  • decreased compliance
  • lung  (e.g. collapse, consolidation, pulmonary edema, ARDS)
  • pleural  (e.g. pneumothorax, pleural effusion)
  • chest wall (e.g. abdominal distention, kyhposcoliosis, obesity)
  • patient-ventilator dysynchrony, coughing

APPROACH TO PATIENT WITH HIGH AIRWAY PRESSURES

  • Disconnect the patient from the ventilator and manually bag the patient using high-flow oxygen and bag-valve-mask
  • While the patient is disconnected from the ventilator assess the “feel” of the lungs while bagging:
    • If the patient is not difficult to ventilate then the problem is with the ventilator or the circuit
    • If the patient is difficult to ventilate it is a problem with the endotracheal tube or the respiratory system
  • For ventilator and circuit problems:
    • check the ventilator settings that it is functioning correctly (e.g. on a test lung)
    • check the circuit for obstruction or kinking
  • For patient or ETT problems:
    • examine the patient looking for:
      • wheeze
      • asymmetrical chest expansion
      • evidence of collapse
      • evidence of dyssynchrony
    • Pass a suction catheter through the ETT to check its patency
    • Use ETCO2 and perform a CXR to check ETT position and look for potential causes of decreased compliance

If the cause is still not clear measure inspiratory pause pressure to estimate alveolar pressure, in addition to the peak inspiratory pressure that reflects airway pressure.

  • If both airway and alveolar pressure are high the problem is due to poor compliance (e.g. pulmonary edema)
  • If only the airway pressure is high the problem is one of high resistance (e.g. bronchospasm)

Seek and treat underlying causes


References and Links

LITFL

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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