ICU Physiology in 1000 Words: Patient Self-Inflicted Lung Injury – Part 2

Jon-Emile S. Kenny MD [@heart_lung]

In part 1, evidence for and against spontaneous breathing effort in acute respiratory distress syndrome [ARDS] was briefly outlined.  The mechanisms of patient self-inflicted lung injury [P-SILI] are touched upon herein with reconciliation of the clinical and experimental data.

Mechanisms: basics

A handful great reviews on spontaneous breathing in ARDS and P-SILI are authored by pioneers in this space [1-4].  Simply, the foundation of P-SILI is distilled into three, non-mutually exclusive mechanisms: heightened lung stress and blood flow and patient-ventilator asynchrony [1, 2, 4].  This cursory composition focuses on the former two, within the milieu of the ‘stress raiser’ hypothesis.

As discussed previously, lung stress is the pressure between the airway and the pleural compartments.  Clinically, lung stress is approximated by the transpulmonary pressure [Ptp] which is the airway pressure [Paw] less the esophageal pressure – as surrogate of pleural pressure.  Importantly, lung stress [i.e. pressure, or barotrauma] is related to lung strain [i.e. volume, or volutrauma] via the specific elastance, k.  In humans, k is roughly 12 cm H2O such that increasing lung strain by 1.0 elevates the trans-pulmonary stress to 12 cm H2O.  Even in severe ARDS, the specific elastance remains unchanged [5], however, ‘stress raisers’ amplify local stress.

A stress raiser [or riser] is any area of two, adjacent materials of differing elasticity.  In a classic, theoretical analysis, Mead et al. found that stress raisers amplified local stress by a factor of over 4.5 [6]; clinically, the amplification factor is closer to 2.0 [7].

Mechanisms: P-SILI

How does the above relate to elevated lung stress and blood flow in P-SILI?  In pressure-targeted modes of mechanical ventilation, airway pressure provides the ‘break’ for the ventilator.  If there is superimposed patient effort [i.e. diminished pleural pressure], then lung stress and strain can become quite large because volume is a dependent variable in this mode.  In the setting of abundant stress raisers, patient effort may be injurious.

In volume-targeted modes of mechanical ventilation, patient effort can still augment both stress and strain.  How can strain rise if the ventilator limits volume?  In elegant works [8, 9], Yoshida and colleagues established two key insights in severe lung injury: 1. The lung behaves more like a ‘solid’ than ‘liquid’ and 2. Pendelluft, or the ‘swinging air’ phenomenon.

That the lung behaves more ‘solid-like’ in severe lung injury, to my eye, is a gross extension of the stress raiser hypothesis.  Normally, the lung is ‘liquid’ in that falling pleural pressure distributes homogenously across the lung surface [1, 2, 4, 9].  By contrast, solid consolidations in severe lung injury locally amplify the pleural pressure in the dependent, caudal lung.  When the diaphragm contracts, pleural pressure falls significantly around the solid-like, injured lung and less so around the non-dependent region.  Consequently, stress is magnified near the diaphragm and this pulls air away from the ventral, non-dependent regions; pendelluft augments dependent strain [see figure 1].

Figure 1: Left panel shows normal, homogeneous, fluid like behaviour of pleural pressure when diaphragm contracts. Right panel shows solid-like behaviour and inhomogeneous pleural pressure distribution when diaphragm contracts. Red arrow represents pendelluft and local strain augmentation. Ppl is pleural pressure. See text and reference [8].

While stress and strain amplify around injured lung, hazard is not limited to the airways.  Disparate radial traction forces also damage blood vessels.  As illustrated previously, ‘corner vessels’ [10] may be particularly susceptible to injury when adjacent to stress raisers and when effort is high.  Trans-mural vascular pressure could reach nearly 100 mmHg based on the Mead model [6]!  This siphoning of blood towards areas of high stress might be termed ‘pendelblut.’

The Conjoined Triangle of Distress

While heightened lung stress and strain, perfusion and ventilator asynchrony are underlying mediators of P-SILI, these are somewhat abstract concepts at the bedside.  Therefore, the proposed ‘conjoined triangle of distress’ of P-SILI helps predict risk, plan therapy and also explain disparate evidence outlined in part 1.

The 3 vertices of the triangle are elevated stress raisers, high effort and low positive end-expiratory pressure [PEEP].  Each of these features are physiologically linked.  For example, lungs with significant stress raisers are often typified by a small ‘baby lung.’  The diminished baby lung is characterized by a high ‘superimposed pressure’ [11] and rostral diaphragm displacement magnified by low PEEP.  This environment stimulates strong effort by activating juxta-capillary receptors [12] which can cause a self-perpetuating cycle [3] [see figure 2].

Figure 2: The conjoined triangle of distress for patient self-inflicted lung injury [P-SILI]. PEEP is positive end-expiratory pressure. See text.

How is this triangle evoked at the bedside?  Without lung imaging, ARDS severity [e.g. P/F ratio] and dead space fraction [e.g. PaCO2] have been directly associated with stress raiser burden [7].  Thus, severe ARDS [e.g. P/F ratio less than 100-150] suggests a high proportion of dependent inhomogeneity.  Gas exchange data is supplemented by CT imaging and lung ultrasound to help detect dependent opacities that raise the risk for P-SILI.  Patient effort is largely a bedside examination: accessory muscle use, nasal flaring [4], ventilator asynchrony, but also an elevated P0.1 if the patient is ventilated [13].  While esophageal pressure monitoring can also help, this modality is rarely used [14].  Lung ultrasound is a novel approach to assessing patient effort [15].

As well, this triangle helps explain conflicting data regarding patient effort.  Many of the investigations that demonstrated benefit of spontaneous effort were carried out in milder disease [i.e. less lung inhomogeneity] with higher PEEP [e.g. APRV].  Indeed, severe disease augments the hazard of spontaneous breathing as compared to mild disease [16].  Further, because PEEP homogenizes stress raisers [7], PEEP protects against P-SILI.  This too has been demonstrated by Yoshida and colleagues [17].  PEEP ablates the ‘solid like’ behaviour of the lung, and changes the geometry of the diaphragm such that it is less able to generate large swings in pleural pressure [1-4].  Further, even in milder ARDS, spontaneous breathing increases lung inflammation in low PEEP ventilation [18].

Lastly, the triangle explains the seemingly disparate results in neuromuscular blockade [19-22] described in part one.  Papazian and colleagues used a lower PEEP strategy while the ROSE Trial used a higher PEEP approach.  Thus, the benefit of attenuating spontaneous effort may have been magnified in patients with lower PEEP and, in theory, greater lung inhomogeneity and more negative pleural pressure swings in dependent lung regions [1, 2].

Implications for Management

Briefly, management focuses on the triangle’s vertices.  Both higher PEEP and prone position attenuate stress raisers.  Higher PEEP may be challenging to accomplish with non-invasive ventilation and high flow nasal cannula; thus, in more severe disease, consideration is given to helmet ventilation to ensure higher PEEP if non-invasive ventilation is used [23, 24].  Close attention must be paid to signs of high respiratory effort; in moderate to severe disease [e.g. P/F ratio < 150], P-SILI may be hard to mitigate without invasive mechanical ventilation and, potentially, pharmacological control of effort [25].

Please see other posts in this series,

JE

Dr. Kenny is the cofounder and Chief Medical Officer of Flosonics Medical; he is also the creator and author of a free hemodynamic curriculum at heart-lung.org

References

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