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Intensive Care Medicine
Published in Elizabeth Combeer, The Final FRCA Short Answer Questions, 2019
Overinflation may directly damage (volutrauma and barotrauma) remaining healthy areas of lung (as their compliance is greater than diseased areas). Resulting cytokine release mediates “biotrauma” to lungs and distant organs.
Acute respiratory distress syndrome (ARDS) caused by the novel coronavirus disease (COVID-19): a practical comprehensive literature review
Published in Expert Review of Respiratory Medicine, 2021
Francisco Montenegro, Luis Unigarro, Gustavo Paredes, Tatiana Moya, Ana Romero, Liliana Torres, Juan Carlos López, Fernando Esteban Jara González, Gustavo Del Pozo, Andrés López-Cortés, Ana M Diaz, Eduardo Vasconez, Doménica Cevallos-Robalino, Alex Lister, Esteban Ortiz-Prado
The third cause is an injury caused by invasive mechanical ventilation (VILI), which can lead to new damage to already affected lungs or worsen current injuries. Injuries generated by mechanical ventilation lead to what is known as biotrauma, where the tissue injury generate a local and sometimes systemic inflammatory response that will cause more damage. Laceration of the lung endothelium and epithelium results in a flooding of the air space with protein-rich lung edema, macrophages, and activated neutrophils, with loss of aeration, increased concentrations of hydroxyproline, β-growth factor, and interleukin-8 and release of proinflammatory mediators IL-1b, TNF-α, IL-8 and IL-6 at the pulmonary and systemic level. Translocation of inflammatory mediators, lipopolysaccharides, and bacteria into the systemic circulation can lead to multiple organ dysfunction and possibly death [22,23]
The acute respiratory distress syndrome
Published in Baylor University Medical Center Proceedings, 2020
Christopher Wood, Vivek Kataria, Ariel M. Modrykamien
In a normal healthy lung, fluid movement is regulated to keep the alveoli dry and hold on to a small amount of interstitial fluid. Lung injury, such as ARDS, disrupts this regulatory process, resulting in diffuse alveolar damage.17 One form of ventilator-induced injury, referred to as “biotrauma,” can happen in both healthy and injured lungs.18 It causes a systemic inflammatory response releasing a cascade of cytokines.18 Three general regions of the lung have been described in ARDS: normal lung tissue, densely consolidated lung, and a collapsible region during expiration that is recruitable during inspiration.19 In the absence of optimal PEEP, this collapsible/recruitable region of the lung can form an injury known as “atelectrauma” due to the repeated opening and closing of the airway and alveoli.20 Proposed methods to determine optimal PEEP will be discussed further.
Extracorporeal membrane oxygenation support in adult patients with acute respiratory distress syndrome
Published in Expert Review of Respiratory Medicine, 2020
Evidence-based guidelines for optimal mechanical ventilation during ECMO have not been established, but existing strategies minimize ventilator stress when ECMO adopts the role of the native lung because it allows the lung to rest and potentially reduces the risk of further injury by ventilator while waiting for the lung to recover. The ELSO guidelines recommend ‘rest settings’ with a plateau inspiratory pressure <25 cmH2O and FiO2 < 40%, and the majority of international ECMO centers has reported that they prefer the lung-protective mechanical ventilation strategy with ‘lung rest’ as the primary goal, although the range of ventilator settings used varies [18,27,28]. In recent years, further reductions in tidal volume beyond the current standard of 6 mL/kg of predicted body weight have been suggested because the current standard may not completely prevent VILI in patients with ARDS [29,30]. Recently, the Ventilation Management of Patients with ECMO for Acute Respiratory Distress Syndrome (LIFEGARDS) study described that moderate to high case-volume ECMO centers typically adopt an ultraprotective lung ventilation approach, defined as driving pressure ≤15 cm H2O and tidal volume ≤4 mL/kg of predicted body weight during ECMO [31]. In addition, a recent randomized clinical trial showed that the use of an ultraprotective lung ventilation strategy led to significantly reduced pulmonary biotrauma compared with the standard protective-lung ventilation strategy [32]. However, the clinical impact of ultraprotective lung ventilation is controversial. A systematic review aiming to describe mechanical ventilation practices in ARDS patients treated with ECMO showed the lowest mortality in studies with a combined tidal volume ≤4 mL/kg and a plateau pressure ≤26 cmH2O [17], whereas mechanical ventilation settings during the first 2 days of ECMO were not associated with survival in the LIFEGARDS study [31]. In addition, lung collapse induced by ultraprotective lung ventilation might lead to worsening hypoxemia due to gravitation and reabsorption atelectasis [33]. Moreover, diffuse alveolar collapse might lead to increased pulmonary vascular resistance and acute cor pulmonale [34]. It is important to be aware that, despite the use of ECMO, decreasing tidal volume to <4 mL/kg of predicted body weight may increase atelectasis and result in severe ventilation/perfusion mismatch unless the PEEP is appropriately increased [35]. Therefore, considering all the aspects mentioned above, the PEEP level should be adjusted according to individual respiratory condition while considering potential side effects. A recent review that provided consensus expert opinions of clinicians and researchers with expertise in mechanical ventilation, ARDS, and ECMO suggested that a PEEP of at least 10 cmH2O is reasonable in patients with ARDS receiving ECMO [36].