Patient self-inflicted lung injury

Author: Munir Karjaghli, Reviewer: David Grooms, Branka Cupic

Facilitating spontaneous efforts in those patients under light sedation is an important part of mechanical ventilation in the ICU.

Takeaway messages

  • Experimental and clinical data show that spontaneous effort is difficult to control within a safe range when lung injury is more severe, and strong spontaneous effort may worsen lung injury.
  • The concept of “ventilation”-induced lung injury covers lung injury occuring from overdistension caused either by the mechanical ventilator (VILI) or the patient’s own breathing (P-SILI).
  • Recent experimental and clinical studies indicate that higher levels of PEEP may result in less injurious spontaneous efforts in patients with moderate to severe ARDS.

On the one hand, assisting these efforts can bring various benefits to the patients, such as better gas exchange, maintenance of peripheral muscles, and diaphragm function.  On the other hand, it may also be associated with a deterioration in oxygenation (1) as well as cause lung injury (2). This conflict has led to extensive discussions about the potential risk of spontaneous effort during mechanical ventilation and how this risk may be avoided (3, 4).  In 2017, the term “patient self-inflicted lung injury” (P-SILI) was coined to describe effort-dependent lung injury. Although the concept of P-SILI is relatively new, the underlying mechanism of P-SILI is similar to that of VILI (4, 5). In the case of P-SILI, the patient’s own spontaneous effort (i.e., negative pleural pressure) causes global and local overdistension, which is then exacerbated to a degree by the ventilator. A recent publication by Yoshida et al. (6) looked more closely at the causes of P-SILI, as well as the use of higher PEEP for safe spontaneous breathing.

Mechanisms of patient self-inflicted lung injury (P-SILI)

There are three mechanisms by which spontaneous effort may potentially cause lung injury: global and local overdistension, increased lung perfusion, and patient–ventilator asynchrony.

1. Overdistension

During pressure assist-control or pressure support ventilation, spontaneous breathing reduces pleural pressure (Ppl), while transpulmonary pressure (PL) and tidal volume (VT) will be increased. Global overdistension reflected by high PL, can then exacerbate lung injury, caused by either the mechanical ventilator or the patient’s effort, or both. A result of strong efforts are negative local ‘swings’ in Ppl; these are observed more in the dependent lung than in the rest of the lung (7). The higher local (dependent) lung stress then leads to local overdistension. In addition, it also causes considerable tidal recruitment and decruitment at expiration in the dependent lung, by drawing gas from other lung regions (e.g., the nondependent lung). Recent data has confirmed that the majority of effort-dependent lung injury occurs in the dependent lung, that is, the same region in which strong effort caused greater inspiratory stress and stretch (8).

2. Increased lung perfusion

The more negative Ppl, generated by spontaneous effort leads to increased transmural vascular pressure, the net pressure distending the intrathoracic vessels. In fact, strong spontaneous effort during volume-controlled low VT ventilation can generate such negative Ppl that ARDS patients may suffer from pulmonary edema (9). Recently, strong spontaneous effort has also been shown to increase lung perfusion and a tendency to edema, as well as have a negative impact on outcomes in children with acute exacerbations of asthma (10).

3. Patient–ventilator asynchrony

Asynchrony can potentially worsen lung injury, and data from 50 ventilated patients suggests an association with higher mortality (11). Double triggering, for example, is potentially injurious because of the high VT delivered to the patient. This form of asynchrony is more common in patients with a higher respiratory drive, which is easy to detect and widely recognized to be harmful. Reverse triggering, on the other hand, can occur in heavily sedated patients where the risk of asynchrony is considered to be low. Reverse triggering can result in increased PL and/or VT, and through pendelluft may also increase dependent-lung stress and stretch.

PEEP for safe spontaneous breathing

Higher PEEP may be effective in reducing lung injury from spontaneous efforts. Earlier publications showed that ∆Pes or Ppl following phrenic nerve stimulation is minimized, as the end-expiratory lung volume is increased. This is a phenomenon observed consistently in both normal animal and human lungs (12). More recently, the same observation has been confirmed in an ARDS model (rabbits and pigs). Higher PEEP - and thus higher end-expiratory lung volume - was associated with less spontaneous effort (estimated by ∆Pes or ∆Ppl), and reduced P-SILI (13). The most recent randomized clinical trial to re-evaluate systemic early neuromuscular blockade in moderate to severe ARDS (ROSE trial) provides indirect support for the argument that higher PEEP may render spontaneous effort less injurious (14).

Mechanism for higher positive end-expiratory pressure

  • Higher PEEP can reduce the amount of atelectatic lung, which can lead to a more homogeneous distribution of ∆Ppl over the whole lung surface. This helps avoid local overdistension in dependent lung regions.
  • Higher PEEP may help to decrease those forces generated by spontaneous efforts (reflected by ∆Pes or ∆Ppl) in ARDS patients.
  • Higher PEEP often improves gas exchange, which in turn may help to reduce respiratory drive.
  • External PEEP may act as a counterbalancing force and minimize the pressure differences across the small airways, reducing the effort to trigger the ventilator and the increased load of inspiratory muscles (15).


Lung injury in mechanically ventilated patients occurs due to overdistension caused by either the ventilator or the patient’s own breathing, or both. In moderate to severe ARDS, higher levels of PEEP may allow “safe” spontanous breathing and therefore help prevent P-SILI.

Ventilators from Hamilton Medical offer a range of tools and features that not only enable clinicians to monitor the patient’s effort, but to customize ventilation therapy to each individual patient. You are able to measure and display esophageal and transpulmonary pressures in spontaneously breathing patients, monitor lung protection, and assess patient-ventilator interaction. IntelliSync+* allows continuous monitoring of ventilated patients and/or improved breath triggering and cycling.

* Not available in all markets



  1. Coggeshall JW, Marini JJ, Newman JH. Improved oxygenation after muscle relaxation in adult respiratory distress syndrome. Arch Intern Med 1985; 145:1718–1720. 
  2. Mascheroni D, Kolobow T, Fumagalli R, et al. Acute respiratory failure following pharmacologically induced hyperventilation: an experimental animal study. Intensive Care Med 1988; 15:8–14.
  3. Guldner A, Pelosi P, Gama de Abreu M. Spontaneous breathing in mild and moderate versus severe acute respiratory distress syndrome. Curr Opin Crit Care 2014; 20:69–76. 
  4. Yoshida T, Fujino Y, Amato MB, Kavanagh BP. Fifty years of research in ARDS: spontaneous breathing during mechanical ventilation: risks, mechanisms, and management. Am J Respir Crit Care Med 2017; 195:985–992.
  5. Bellani G, Grasselli G, Teggia-Droghi M, et al. Do spontaneous and mechanical breathing have similar effects on average transpulmonary and alveolar pressure? A clinical crossover study. Crit Care 2016; 20:142.
  6. Yoshida T, Grieco DL, Brochard L, Fujino Y. Patient self-inflicted lung injury and positive end-expiratory pressure for safe spontaneous breathing. Curr Opin Crit Care. 2020 Feb;26(1):59-65.
  7. Yoshida T, Torsani V, Gomes S, et al. Spontaneous effort causes occult pendelluft during mechanical ventilation. Am J Respir Crit Care Med 2013; 188:1420–1427.
  8. Morais CC, Koyama Y, Yoshida T, et al. High positive end-expiratory pressure renders spontaneous effort noninjurious. Am J Respir Crit Care Med 2018; 197:1285–1296.
  9. Kallet RH, Alonso JA, Luce JM, Matthay MA. Exacerbation of acute pulmonary edema during assisted mechanical ventilation using a low-tidal volume, lungprotective ventilator strategy. Chest 1999; 116:1826–1832.
  10. Kantor DB, Hirshberg EL, McDonald MC, et al. Fluid balance is associated with clinical outcomes an extravascular lung water in children with acute asthma exacerbation. Am J Respir Crit Care Med 2018; 197:1128–1135.
  11. Blanch L, Villagra A, Sales B, et al. Asynchronies during mechanical ventilation are associated with mortality. Intensive Care Med 2015; 41:633–641.
  12. Laghi F, Harrison MJ, Tobin MJ. Comparison of magnetic and electrical phrenic nerve stimulation in assessment of diaphragmatic contractility. J Appl Physiol (1985) 1996; 80:1731–1742.
  13. Kiss T, Bluth T, Braune A, et al. Effects of positive end-expiratory pressure and spontaneous breathing activity on regional lung inflammation in experimental acute respiratory distress syndrome. Crit Care Med 2019; 47:e358–e365.
  14. Moss M, Huang DT, Brower RG, et al. Early neuromuscular blockade in the acute respiratory distress syndrome. N Engl J Med 2019; 380:1997–2008.
  15. Rossi A, Brandolese R, Milic-Emili J, Gottfried SB. The role of PEEP in patients with chronic obstructive pulmonary disease during assisted ventilation. Eur Respir J 1990; 3:818–822.
P-SILI, patient self-inflicted lung injury, VILI, venilator induced lung injury, higher peep, spontaneous breathing, safe breathing, moderate ARDS, severe ARDS

Date of Printing: 21.04.2021
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