Patient self-inflicted lung injury
11.05.2020 n
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
dExperimental 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.
dThe 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).
dRecent 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 effortdependent 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 endexpiratory 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).
Conclusion
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 PSILI.
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
References
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Date of Printing: 07.06.2022
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