Spontaneous breathing, assisted ventilation, and patient self-inflicted lung injury (P-SILI)


Spontaneous breathing can occur without ventilatory support (unassisted spontaneous breathing) or be integrated with mechanical ventilation with assisted ventilation modes (assisted spontaneous breathing).

  • ~30% of invasively ventilated patients with acute respiratory distress syndrome (ARDS) breath spontaneously at day 1 post-intubation, regardless of severity, and the proportion increases greatly over the following days (Bellani et al, 2016)
  • Patient self-inflicted lung injury (P-SILI) is a controversial, emerging concept, whereby intense inspiratory efforts by spontaneously breathing patients – whether assisted or unassisted – may exacerbate lung injury.
  • Concerns about P-SILI must be balanced against the harms from prolonged controlled ventilation, over-sedation, and paralysis, when allowing patients to breathe spontaneously.


Regardless of the ventilation strategy, ventilation occurs due to a pressure difference is across the respiratory system, in other words, between the mouth and the external surface of the chest wall (Mauri et al, 2017).

  • Unassisted spontaneous breathing
    • pressure gradient is generated only by the work of respiratory muscles
  • assisted spontaneous ventilation (invasive or non-invasive)
    • the ventilator acts as a pressure generator in series with the respiratory muscles and the work is shared by the muscles and the machine
  • controlled ventilation
    • all respiratory work is done by the ventilator in creating positive pressure to drive the tidal volume to the alveolar space; muscles remain passive

This pressure difference (regardless of the mode of ventilation) is determined at a given time (t) by this equation (Mauri et al, 2017):

  • Pao(t) + Pmus(t) = PEEP + [Ers × V(t)] + [Rrs × Flow(t)]
    • Pao = pressure at the airway opening
    • Pmus = pressure generated by respiratory muscles (difference between the pressure generated by the relaxed chest wall and the change in pleural pressure (Ppl) at given lung volume)
    • PEEP= positive end-expiratory pressure
    • Ers = respiratory system elastance
    • V = tidal volume
    • Rrs = resistance of the respiratory system
    • Flow = inspired gas flow
  • Differences in Pao and Pmus
    • Pmus = 0 in controlled ventilation
    • Pao = 0 in unassisted spontaneous ventilation
    • Both Pmus and Pao are >0 in assisted spontaneous ventilation
  • Pao—Palv gradient
    • This pressure gradient drives ventilation regardless of the mode
      • In controlled ventilation, Palv is always positive and greater than intravascular capillary pressure
      • In unassisted spontaneous ventilation, Palv decreases below PEEP throughout inspiration to generate positive Pao—Palv gradient
      • In assisted spontaneous ventilation (e.g. PSV or pressure support ventilation), Palv decreases below PEEP for only a portion of the inspiratory time that increases with Pmus (respiratory effort) (Bellani et al, 2016b)
    • Under similar conditions of flow and volume, plateau pressures and transpulmonary pressure change are similar between controlled ventilation and assisted spontaneous breathing (e.g. PSV).

Measurement of pressure generated by respiratory muscles (Pmus) (Mauri et al, 2017)

  • Uses
    • determine total pressure difference across the respiratory system (Pao + Pmus)
    • estimate of patient’s inspiratory effort, to set assisted ventilation and avoid under- and over-assistance
  • Pmus is the pressure difference between the pressure generated by the relaxed chest wall and the change in pleural pressure (Ppl) at given lung volume
  • esophageal pressure (Pes) can be used as a surrogate measure of Ppl
  • chest wall elastance (Ew) is the elastic recoil of the chest wall at a given volume
    • can be measured by switching the patient to controlled ventilation and dividing the change in Pes by Vt
    • I.e. Ew = ∆Pes/Vt
    • individual Ew can also be calculated as 4% of predicted vital capacity (VC)
  • Pmus can be calculated (and monitored) at the bedside, at any time t, using esophageal manometry in spontaneously breathing patients as:
    • Pmus = Vt(t) × Ew − ∆Pes(t)
      • V is the tidal volume
      • Ew is the chest wall elastance
      • ∆Pes is the inspiratory Pes change from baseline during controlled ventilation
  • pressure generated during the first 100 milliseconds against an occluded airway (P0.1) has been suggested as a surrogate to evaluate patient’s effort


P-SILI may occur in spontaneously breathing patients receiving:

  • assisted ventilation via an endotracheal tube
  • non-invasive ventilation (NIV)
  • no ventilatory support

P-SILI may result from intense inspiratory effort, resulting in:

  • swings in transpulmonary pressure (i.e. lung stress) causing the inflation of big volumes in an aerated compartment markedly reduced by the disease-induced aeration loss
  • abnormal increases in transvascular pressure, favouring negative-pressure pulmonary edema
  • an intra-tidal shift of gas between different lung zones, generated by different transmission of muscular force (i.e. pendelluft)
  • diaphragm injury
  • increased lung inflammation

P-SILI may be more likely if:

  • vigorous spontaneous breathing efforts
  • severe lung disease (e.g. ARDS patients with a PaO2/FiO2 ratio below 200 mmHg may be an “at risk’ group)

More research is needed to determine:

  • mechanisms of P-SILI
  • identification of patients, and phases of lung disease, at risk of P-SILI
  • Strategies for monitoring and management of P-SILI


Advantages of spontaneous breathing during mechanical ventilation (Mauri et al, 2017) include:

  • Active diaphragmatic contraction and reduced diaphragmatic atrophy
  • avoids neuromuscular blockers and their adverse effects
  • Decreased sedation and their adverse effects
  • Improved ventilation/perfusion matching
  • Improvement of dorsal ventilation (dorsal diaphragm moves preferentially in spontaneous breathing)
  • Improvement of gas-exchange
  • associated with improved hemodynamics (increased venous return)
  • Potentially reduction of pneumonia (better secretions clearance) in extubated patients
  • Intact respiratory muscle tone promotes expansion of chest-wall and lungs at end expiration (recruits lung and improves functional residual capacity)
  • The diaphragm may actually contract during expiration, maintaining distal airway patency and reducing expiratory atelectasis

Disadvantages of spontaneous breathing during mechanical ventilation (Mauri et al, 2017) include:

  • uncontrolled inspiratory efforts may worsen lung injury (P-SILI):
    • high tidal volumes (volutrauma)
    • high transpulmonary pressures (barotrauma)
  • increased ventilation heterogeneity leading to “occult pendelluft”
    • transpulmonary pressures become regionally elevated despite a safe mean value
    • due to movement of air from non-dependent to dependent lung areas during inspiration) and cyclic opening and closing of small airways (regional atelectrauma in the dorsal lung) (Yoshida et al, 2013)
  • increased inspiratory resistance
  • Patient-ventilator dyssynchrony and patient distress
    • “double triggering” and “reverse triggering” can also worsen lung injury
  • Interstitial and alveolar edema
    • increased gradient between intravascular capillary pressure and alveolar pressure during inspiration
  • diaphragm dysfunction may lead to atrophy, muscle exhaustion, and prolonged weaning
  • Haemodynamic instability
    • increase filling of the right heart and dysfunction of left heart
  • Difficult to ensure protective ventilation unless using esophageal manometry (to measure Pes)
    • Usually, only airway pressure (Pao) is measured (zero pressure), not Pmus, so the pressure gradient across the respiratory system is unquantified if there is spontaneous breathing – Pmus = V(t) × Ew − ∆Pes(t) (see above)
    • Driving pressure (∆Pao = Pplat – PEEP) measurement is not feasible during spontaneous breathing, Transpulmonary pressure (TPP = Pao – Pes at the end of inspiration) can be used instead
  • Not possible if neuromuscular blockers (NMBs) are used
    • Immediately after intubation if NMBs are used to optimise intubation conditions
    • NMBs associated with benefits in animal studies and in the first 48h of ARDS in the ACURASYS trial (2010), despite no difference in the primary outcome of 90-day mortality . However, there was no benefit from NMBs in the subsequent ROSE trial (2019).

In general, the disadvantages are likely to be greater and more detrimental in severe ARDS (“solid-like” lung), compared to mild and moderate ARDS (“fluid-like” lungs) where spontaneous breathing may be beneficial (Yoshida et al, 2015).


Controlled mechanical ventilation may be beneficial in early severe ARDS (Güldner et al, 2014), however, at some point, there must be a transition to spontaneous breathing in order to liberate from the ventilator.

  • in general, spontaneous breathing should be facilitated when when lung injury and patient effort are mild

For spontaneous breathing during mechanical ventilation optimising of patient-ventilator synchrony is required (Mauri et al, 2017):

  • Timing of assist
    • E.g. delayed inspiration common with auto-PEEP
    • E.g. early cycling and double triggering common if poor lung compliance
    • May be improved using diaphragmatic electromyography
  • Magnitude of assist
    • E.g. over-assistance contributes to diaphragmatic atrophy
    • E.g. under-assistance contributes to respiratory weakness
    • May be improved by monitoring Pmus (via esophageal manometry)

Severity of lung disease can be assessed:

  • P/F ratio or other oxygenation indices
  • Lung compliance (Cstat)
  • Imaging (e.g. chest radiograph, pulmonary CT)

Patient respiratory drive and work of breathing can be monitored using (Mauri et al, 2017):

  • diaphragmatic electromyography
  • Pmus (via esophageal manometry; Pmus = V(t) × Ew − ∆Pes(t))
  • P0.1 (airway pressure drop during the first 100 msec of an inspiratory effort against an occluded airway)

Patient respiratory drive can be decreased by (Mauri et al, 2017):

  • Targeting physiological PaO2 and PaCO2 (rather than permissive hypoxemia or hypercapnia)
  • Treat fever and pain (decreasing O2 consumption and CO2 production)
  • Extracorporeal CO2 removal (e.g. ECCO2R and VV ECMO)
    • in severe ARDS, CO2 removal may not be sufficient in preventing potentially harmful spontaneous breathing efforts (Crotti et al, 2017)

Despite these measures, and depending on the underlying lung pathology and other patient factors, harmful inspiratory efforts during spontaneously breathing, leading to P-SILI, may be difficult to avoid.

  • One experimental approach describes the use of “partial neuromuscular blockade” with subtherapeutic doses of rocuronium (!) (Doorduin et al, 2017)
  • high PEEP may also be beneficial in allowing safe spontaneous ventilation (e.g. Pressure support ventilation with high PEEP settings, Bi-level with conventional TH:TL (high PEEP time: low PEEP time) ratios, or Airway Pressure Release Ventilation (APRV)
  • in non-intubated patients, suggested strategies for mitigating P-SILI include (Greico et al, 2019):
    • use of high-flow nasal cannulae (HFNC) instead of NIV
    • use of high-PEEP helmet NIV 

See also Patient-ventilator dyssynchrony


Spontaneous breathing during mechanical ventilation is more physiologic but is associated with both advantages and disadvantages

  • Controlled ventilation is a preferred strategy for early severe ARDS
  • Transition to spontaneous breathing is necessary for weaning from the ventilator
  • Timing of the transition is complicated due to potential for P-SILI balanced against the harms from prolonged controlled ventilation, over-sedation, and paralysis
  • Optimisation of patient-ventilator synchrony is necessary for a safe transition to spontaneous breathing
  • Techniques that are not currently widely used in intensive care in Australia and New Zealand may be useful:
    • Esophageal manometry, to allow determination of transpulmonary pressure (TPP), may be useful to assess inspiratory effort (Pmus) and achieve safe ventilation
    • Diaphragm electromyography may help improve patient-ventilator synchrony by coordinating ventilatory support with diaphragmatic contraction

References and Links


Journal articles

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a 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 three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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