Abstract
This review describes the current understanding of the lungs’ response to deforming stress under conditions of both normal physiology and acute lung injury. Several limiting assumptions are needed to infer lung parenchymal stress and strain from airway pressure, volume, and flow data from mechanically ventilated patients with injured lungs. These assumptions include the effects of the chest wall on lung-surface pressure, its topographical distribution, and the effects of non-uniform tissue properties on local parenchymal stresses. In addition, there is a spectrum of biophysical lung injury mechanisms that involves normal as well as tangential alveolar wall stresses. To these are added important secondary effects on pulmonary vascular resistance and right heart function. Understanding both the assumptions of lung mechanics and the scope of injury mechanisms operating during ARDS is necessary to interpret the results of clinical trials that inform prevailing ventilator-management guidelines. The implications issuing from these 3 topics inform a safer approach to setting and adjusting the ventilator to minimize the risk of ventilator-induced lung injury. This is enumerated in a 5-step approach that can be used to guide ventilator management of unstable patients with severe lung injury.
Key Points
- Stress and Strain in the Respiratory System: Pulmonary stress is defined as the force per unit area exerted on lung tissue, while strain is the lung deformation in response to stress. Non-uniform lung expansion in ARDS complicates the estimation of lung stress using standard ventilator parameters.
- Hooke’s Law in Respiratory Mechanics: The relationship between lung stress and strain follows Hooke’s law, but measuring true lung strain is challenging due to the lung’s pre-stressed state in vivo. Conventional definitions of strain in engineering cannot be directly applied to respiratory physiology.
- Clinical Trials and Ventilator-Induced Lung Injury (VILI): The ARMA trial demonstrated the benefits of low tidal volume (VT) ventilation in ARDS, though later analyses suggest that driving pressure (ΔP) may be a better predictor of lung injury risk than VT alone.
- Biotrauma and the Role of PEEP: High ventilatory pressures not only contribute to direct mechanical injury but also activate inflammatory pathways (biotrauma). Proper PEEP titration is crucial for preventing alveolar collapse (atelectrauma) while avoiding excessive stress on the lung.
- Strategies for Lung-Protective Ventilation: Common approaches to setting PEEP include FiO2-guided titration and ΔP minimization. Emerging tools such as esophageal manometry and electrical impedance tomography may offer better PEEP optimization strategies.
- Challenges in PEEP Selection and Right Heart Dysfunction: While PEEP helps prevent atelectrauma, excessive PEEP can cause right heart strain, leading to hemodynamic instability. Balancing oxygenation with cardiovascular stability remains a challenge.
- Maximal Lung Stress and Plateau Pressure (Pplat): While keeping Pplat ≤30 cm H2O is a common guideline, this assumption does not always hold in patients with high abdominal pressure, where higher PEEP may be necessary to maintain alveolar recruitment.
- Uncertainties in VILI Prevention: Despite improvements in mechanical ventilation strategies, individualizing treatment remains difficult due to variations in lung mechanics and patient-specific risk factors. Spontaneous breathing efforts and hyperoxia also contribute to lung injury.
- Five-Step Approach to Safer Ventilator Management: The authors propose a structured method for setting ventilator parameters, starting with volume-controlled ventilation, assessing hemodynamics, titrating PEEP based on ΔP, optimizing gas exchange, and considering rescue therapies when needed.
- Future Directions and Research Needs: Further studies are required to refine individualized ventilation strategies, better understand the impact of oxygen therapy, and explore new methods for monitoring lung mechanics and injury risk.
