Stress & strain in mechanically nonuniform alveoli using clinical input variables: a simple conceptual model.

Clinicians currently monitor pressure and volume at the airway opening, assuming that these observations relate closely to stresses and strains at the micro level. Indeed, this assumption forms the basis of current approaches to lung protective ventilation. Nonetheless, although the airway pressure applied under static conditions may be the same everywhere in healthy lungs, the stresses within a mechanically non-uniform ARDS lung are not. Estimating actual tissue stresses and strains that occur in a mechanically non-uniform environment must account for factors beyond the measurements from the ventilator circuit of airway pressures, tidal volume, and total mechanical power. A first conceptual step for the clinician to better define the VILI hazard requires consideration of lung unit tension, stress focusing, and intracycle power concentration. With reasonable approximations, better understanding of the value and limitations of presently used general guidelines for lung protection may eventually be developed from clinical inputs measured by the caregiver. The primary purpose of the present thought exercise is to extend our published model of a uniform, spherical lung unit to characterize the amplifications of stress (tension) and strain (area change) that occur under static conditions at interface boundaries between a sphere's surface segments having differing compliances. Together with measurable ventilating power, these are incorporated into our perspective of VILI risk. This conceptual exercise brings to light how variables that are seldom considered by the clinician but are both recognizable and measurable might help gauge the hazard for VILI of applied pressure and power.

Effects of mechanical ventilation on the interstitial extracellular matrix in healthy lungs and lungs affected by acute respiratory distress syndrome: a narrative review.

BACKGROUND: Mechanical ventilation, a lifesaving intervention in critical care, can lead to damage in the extracellular matrix (ECM), triggering inflammation and ventilator-induced lung injury (VILI), particularly in conditions such as acute respiratory distress syndrome (ARDS). This review discusses the detailed structure of the ECM in healthy and ARDS-affected lungs under mechanical ventilation, aiming to bridge the gap between experimental insights and clinical practice by offering a thorough understanding of lung ECM organization and the dynamics of its alteration during mechanical ventilation. MAIN TEXT: Focusing on the clinical implications, we explore the potential of precise interventions targeting the ECM and cellular signaling pathways to mitigate lung damage, reduce inflammation, and ultimately improve outcomes for critically ill patients. By analyzing a range of experimental studies and clinical papers, particular attention is paid to the roles of matrix metalloproteinases (MMPs), integrins, and other molecules in ECM damage and VILI. This synthesis not only sheds light on the structural changes induced by mechanical stress but also underscores the importance of cellular responses such as inflammation, fibrosis, and excessive activation of MMPs. CONCLUSIONS: This review emphasizes the significance of mechanical cues transduced by integrins and their impact on cellular behavior during ventilation, offering insights into the complex interactions between mechanical ventilation, ECM damage, and cellular signaling. By understanding these mechanisms, healthcare professionals in critical care can anticipate the consequences of mechanical ventilation and use targeted strategies to prevent or minimize ECM damage, ultimately leading to better patient management and outcomes in critical care settings.

The Respiratory Mechanics of COVID-19 Acute Respiratory Distress Syndrome-Lessons Learned?

Acute respiratory distress syndrome (ARDS) is a well-defined clinical entity characterized by the acute onset of diffuse pulmonary injury and hypoxemia not explained by fluid overload. The COVID-19 pandemic brought about an unprecedented volume of patients with ARDS and challenged our understanding and clinical approach to treatment of this clinical syndrome. Unique to COVID-19 ARDS is the disruption and dysregulation of the pulmonary vascular compartment caused by the SARS-CoV-2 virus, which is a significant cause of hypoxemia in these patients. As a result, gas exchange does not necessarily correlate with respiratory system compliance and mechanics in COVID-19 ARDS as it does with other etiologies. The purpose of this review is to relate the mechanics of COVID-19 ARDS to its underlying pathophysiologic mechanisms and outline the lessons we have learned in the management of this clinic syndrome.

Does 'sub-threshold' ventilatory stress promote healing after lung injury?

Excessive tidal stretching may initiate damage or retard healing after lung injury. However, it is seldom considered whether intracycle power and ventilatory forces of lesser magnitude than those required to cross an injury threshold might stimulate or accelerate beneficial adaptive responses. Acute lung injury is a dynamic process that may exhibit phase-dependent reparative responses to mechanical stress broadly similar to physical training, body trauma or sepsis. We propose that lower stress may not always be better through all phases of ARDS; moderately high tidal airway pressures that stay below the threshold of global injury may have potential to speed healing of the injured lung.

Mechanical power ratio threshold for ventilator-induced lung injury.

RATIONALE: Mechanical power (MP) is a summary variable incorporating all causes of ventilator-induced-lung-injury (VILI). We expressed MP as the ratio between observed and normal expected values (MPratio). OBJECTIVE: To define a threshold value of MPratio leading to the development of VILI. METHODS: In a population of 82 healthy pigs, a threshold of MPratio for VILI, as assessed by histological variables and confirmed by using unsupervised cluster analysis was 4.5. The population was divided into two groups with MPratio above or below the threshold. MEASUREMENTS AND MAIN RESULTS: We measured physiological variables every six hours. At the end of the experiment, we measured lung weight and wet-to-dry ratio to quantify edema. Histological samples were analyzed for alveolar ruptures, inflammation, alveolar edema, atelectasis. An MPratio threshold of 4.5 was associated with worse injury, lung weight, wet-to-dry ratio and fluid balance (all p < 0.001). After 48 h, in the two MPratio clusters (above or below 4.5), respiratory system elastance, mean pulmonary artery pressure and physiological dead space differed by 32%, 36% and 22%, respectively (all p < 0.001), being worse in the high MPratio group. Also, the changes in driving pressure, lung elastance, pulmonary artery occlusion pressure, central venous pressure differed by 17%, 64%, 8%, 25%, respectively (all p < 0.001). LIMITATIONS: The main limitation of this study is its retrospective design. In addition, the computation for the expected MP in pigs is based on arbitrary criteria. Different values of expected MP may change the absolute value of MP ratio but will not change the concept of the existence of an injury threshold. CONCLUSIONS: The concept of MPratio is a physiological and intuitive way to quantify the risk of ventilator-induced lung injury. Our results suggest that a mechanical power ratio > 4.5 MPratio in healthy lungs subjected to 48 h of mechanical ventilation appears to be a threshold for the development of ventilator-induced lung injury, as indicated by the convergence of histological, physiological, and anatomical alterations. In humans and in lungs that are already injured, this threshold is likely to be different.

Evaluating humidity recovery efficiency of currently available heat and moisture exchangers: a respiratory system model study

OBJECTIVES: To evaluate and compare the efficiency of humidification in available heat and moisture exchanger models under conditions of varying tidal volume, respiratory rate, and flow rate. INTRODUCTION: Inspired gases are routinely preconditioned by heat and moisture exchangers to provide a heat and water content similar to that provided normally by the nose and upper airways. The absolute humidity of air retrieved from and returned to the ventilated patient is an important measurable outcome of the heat and moisture exchangers' humidifying performance. METHODS: Eight different heat and moisture exchangers were studied using a respiratory system analog. The system included a heated chamber (acrylic glass, maintained at 37°C), a preserved swine lung, a hygrometer, circuitry and a ventilator. Humidity and temperature levels were measured using eight distinct interposed heat and moisture exchangers given different tidal volumes, respiratory frequencies and flow-rate conditions. Recovery of absolute humidity (%RAH) was calculated for each setting. RESULTS: Increasing tidal volumes led to a reduction in %RAH for all heat and moisture exchangers while no significant effect was demonstrated in the context of varying respiratory rate or inspiratory flow. CONCLUSIONS: Our data indicate that heat and moisture exchangers are more efficient when used with low tidal volume ventilation. The roles of flow and respiratory rate were of lesser importance, suggesting that their adjustment has a less significant effect on the performance of heat and moisture exchangers.