Introduction
Mechanics of Spontaneous Breathing
Lung Injury During Spontaneous Breathing: Patient Self-Inflicted Lung Injury
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Excessive global lung stress. As already discussed, patient respiratory efforts can increase tidal volume and PL above safe limits when respiratory drive is elevated.
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Excessive regional lung stress. In the injured lung, collapsed and consolidated lung introduces parenchymal mechanical heterogeneities [9], increasing the risk of volutrauma through regional stress amplification. Mechanical stress and strain is not evenly redistributed during inflation. Consequently, inspiratory efforts generate large PL swings in dorsal consolidated regions, resulting in the movement of air from nondependent to dependent regions (pendelluft). While this recruits collapsed lung and improves ventilation-perfusion mismatch, this phenomenon increases the overstretch of dependent lung area. In this case, the rise in PL detected by esophageal manometry may not be a reliable measure of the local stress [10].
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Transvascular pressure and pulmonary edema. During spontaneous breathing, the negative Ppl generated by respiratory effort raises transvascular pressure (the pressure gradient driving fluid migration across pulmonary vessels), increasing total lung water and pulmonary edema [9, 10] and further impairing respiratory function.
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Asynchronies. Ventilator asynchronies, including double triggering (double mechanical breaths from a single inspiratory effort) and reverse triggering (diaphragm contractions induced by passive thoracic insufflation in passively ventilated patients) [11] can increase tidal volume and PL and generate pendelluft, leading to lung injury.
Diaphragm Injury During Spontaneous Breathing: Myotrauma
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Excessive unloading. Over-assistance from mechanical ventilation and suppression of respiratory drive from sedation leads to acute disuse atrophy and diaphragm weakness [12]. Diaphragmatic unloading caused by over-assisted ventilation (both in control or assisted mode) is frequent during mechanical ventilation, in particular during the first 48 h. Of note, the low level of respiratory effort required to trigger the ventilator is not sufficient to avoid disuse atrophy [3], such that diaphragm atrophy can occur under pressure support ventilation.
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Excessive concentric loading. The diaphragm is sensitive to excessive respiratory load. Higher inspiratory patient effort, dyssynchronies, and under-assistance due to an insufficient level of support are frequent in assisted mechanical ventilation. Vigorous concentric contractions provoke high muscular tension resulting in muscle inflammation, proteolysis, myofibrillar damage, and sarcolemma disarray [13, 14]. In critically ill patients, systemic inflammation renders muscle myofibrils more vulnerable to mechanical injury ([10, 15].
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Eccentric loading. Eccentric contractions occur when a muscle generates contractile tension while it is lengthening (rather than shortening); such contractions are much more injurious than concentric (shortening) contractions [16]. When a low positive end-expiratory pressure (PEEP) and excessive reduction in end-expiratory lung volume are present, the diaphragm contracts even as it lengthens during the expiratory (“post-inspiratory”) phase to avoid atelectasis (“expiratory braking” phenomenon) [17]. Specific forms of dyssynchrony (reverse triggering, short cycling, ineffective effort) can generate eccentric contractions because the diaphragm is activated during the expiratory phase.
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Excessive PEEP. Preliminary experimental evidence suggests that maintaining the diaphragm at a shorter length with the use of excessive PEEP may cause sarcomeres to “drop out” of the muscle and shorten its length (longitudinal atrophy) [18]. This could theoretically disadvantage the length-tension characteristics of the muscle once PEEP is reduced, impairing diaphragm performance.
Monitoring Spontaneous Breathing Using Esophageal Pressure
Transpulmonary Pressure
Respiratory Muscle Pressure
Transdiaphragmatic Pressure
Monitoring Spontaneous Breathing by Occlusion Maneuvers
Inspiratory Occlusion Maneuver
Expiratory Occlusion Maneuver
Airway Occlusion Pressure
Monitoring Spontaneous Breathing by Diaphragm Electrical Activity
Monitoring Spontaneous Breathing by Diaphragm Ultrasound
Conclusion
Targets for Lung and Diaphragm-Protective Ventilation
Technique | Parameter | Possible target range of values for safe spontaneous breathing |
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Esophageal pressure | Peak end-inspiratory transpulmonary pressure (PL) | ≤20 cmH2O |
Swing in transpulmonary pressure (ΔPL) | ≤15 cmH2O | |
Peak inspiratory muscle pressure (Pmus) | 5–10 cmH2O | |
Esophageal pressure swing (ΔPes) | 3–8 cmH2O | |
Transdiaphragmatic pressure swing (ΔPdi) | 5–10 cmH2O | |
Pressure time product (PTP) | 50–100 cmH2O/s/min | |
Occlusion maneuvers | Inspiratory occlusion for plateau airway pressure (Pplat) | ≤30 cmH2O |
Inspiratory occlusion for driving pressure (ΔPaw = Pplat − PEEP) | ≤15 cmH2O | |
Expiratory occlusion for estimated Pmus | 5–10 cmH2O | |
Airway occlusion pressure (P0.1) | 1.5–3.5 cmH2O | |
Electromyography | Diaphragm electrical activity (EAdi) | Uncertain |