Patient-Self Inflicted Lung Injury: A Practical Review

Guillaume Carteaux, Mélodie Parfait, Margot Combet, Anne-Fleur Haudebourg, Samuel Tuffet, Armand Mekontso Dessap, Guillaume Carteaux, Mélodie Parfait, Margot Combet, Anne-Fleur Haudebourg, Samuel Tuffet, Armand Mekontso Dessap

Abstract

Patients with severe lung injury usually have a high respiratory drive, resulting in intense inspiratory effort that may even worsen lung damage by several mechanisms gathered under the name "patient-self inflicted lung injury" (P-SILI). Even though no clinical study has yet demonstrated that a ventilatory strategy to limit the risk of P-SILI can improve the outcome, the concept of P-SILI relies on sound physiological reasoning, an accumulation of clinical observations and some consistent experimental data. In this review, we detail the main pathophysiological mechanisms by which the patient's respiratory effort could become deleterious: excessive transpulmonary pressure resulting in over-distension; inhomogeneous distribution of transpulmonary pressure variations across the lung leading to cyclic opening/closing of nondependent regions and pendelluft phenomenon; increase in the transvascular pressure favoring the aggravation of pulmonary edema. We also describe potentially harmful patient-ventilator interactions. Finally, we discuss in a practical way how to detect in the clinical setting situations at risk for P-SILI and to what extent this recognition can help personalize the treatment strategy.

Keywords: acute respiratory distress syndrome; acute respiratory failure; artificial ventilation; patient-self inflicted lung injury; ventilator induced lung injury.

Conflict of interest statement

G.C. reports personal fees from Air Liquide Medical System, Medtronic and Löwenstein, outside the submitted work. A.M.D. reports grants from Fischer Paykel, Baxter, Philips, Ferring and GSK, personal fees from Air Liquide, Baxter, Amomed, Getingue and Addmedica, outside the submitted work. M.P., M.C., A.-F.H. and S.T. declare no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic illustration of the pendelluft phenomenon. Pendelluft corresponds to an intrapulmonary shift of gas from the non-dependent anterior regions to the dependent posterior regions at the very onset of the inspiratory effort (just after the onset of the deflection on the esophageal pressure curve (Pes), blue dashed line), even before the beginning of the ventilator’s insufflation (red dashed line). Thus, with no change in overall volume, there is an abrupt loss of aeration in the anterior regions, and a concomitant increase in aeration in the posterior ones. Definition of abbreviations: Paw: airway pressure; Flow: airway flow; Pes: esophageal pressure.
Figure 2
Figure 2
Combined effects of inspiratory effort and respiratory mechanics on tidal volume and alveolar pressure during pressure support ventilation. A ventilator set in pressure support ventilation with a PEEP level of 5 cm H2O and a pressure support level of 10 cm H2O was connected to an active lung simulator that simulated various respiratory system compliance (C), resistance (R) and muscle pressure (Pmus). Note that Pmus of 5 and 20 cm H2O correspond to esophageal pressure swings (∆Pes) around 3 and 18 cm H2O. When simulating normal respiratory mechanics and low inspiratory effort (A), the tidal volume was within usual clinical range and alveolar pressure (Palv, red line) remained above the PEEP. Marked increases in inspiratory effort (B) resulted in important increase in tidal volume and decrease in alveolar pressure below the PEEP. Thus, the decrease in respiratory system compliance with the same strong simulated inspiratory effort (C) yielded a decrease in tidal volume without changing that much the alveolar pressure. Finally increasing the resistance (D) led to an important decrease in tidal volume and a dramatic drop in alveolar pressure far below 0 cm H2O. Note that of these four conditions, the one that represented the lowest risk of P-SILI (A: normal respiratory mechanics, low inspiratory effort, alveolar pressure above the PEEP) and the one that represented the highest risk of P-SILI (D: impaired respiratory mechanics, intense inspiratory effort, fall in alveolar pressure far below zero) led to similar tidal volumes and comparable flow and airway pressure waveforms. Thus, the detection of a situation at high risk of P-SILI can be particularly difficult during pressure support ventilation and may be facilitated by esophageal pressure monitoring and careful clinical assessment. Definition of abbreviations: Paw: airway pressure; Flow: airway flow.
Figure 3
Figure 3
Effect of inspiratory effort on the airway pressure waveform during volume assist-control ventilation. A ventilator set in volume assist-control ventilation was connected to an active lung simulator. Passive conditions were simulated (A), followed by increasing inspiratory effort with a simulated muscle pressure of 5 (B), 10 (C), and 20 (D) cm H2O. As inspiratory effort increased, the airway pressure decreased and the waveform became “deeper”. This phenomenon makes it possible to detect intense inspiratory efforts by analyzing the ventilator’s waveforms at the bedside. Note that a Pmus of 5, 10 and 20 cm H2O correspond to an esophageal pressure swings (∆Pes) around 3, 8 and 18 cm H2O. Definition of abbreviations: Paw: airway pressure; Flow: airway flow; Pmus: muscle pressure of the inspiratory muscles.

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Source: PubMed

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