Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

Abstract

Patients undergoing mechanical ventilation in intensive care units (ICUs) may develop ventilator-induced lung injury (VILI). Beside the high tidal volume (Vt) and plateau pressure (Pplat), hyperoxia is supposed to precipitate lung injury. Oxygen toxicity is presumed to occur at levels of fraction of inspired oxygen (FiO 2 ) exceeding 0.40. The exposure time to hyperoxia is certainly very important and patients who spend extended time on mechanical ventilation (MV) are probably more exposed to severe hyperoxic acute lung injury (HALI). Together, hyperoxia and biotrauma (release of cytokines) have a synergistic effect and can induce VILI. In the clinical practice, the reduction of FiO 2 to safe levels through the appropriate use of the positive end expiratory pressure (PEEP) and the alignment of mean airway pressure is an appropriate goal. The strategy for lung protective ventilation must include setting up FiO 2 to a safe level that is accomplished by using PaO 2 /FiO 2 ratio with a lower limit of FiO 2 to achieve acceptable levels of PaO 2 , which will be safe for the patient without local (lungs) or systemic inflammatory response. The protocol from the ARDS-net study is used for ventilator setup and adjustment. Cytokines (IL-1, IL-6, TNFα and MIP-2) that are involved in the inflammatory response are determined in order to help the therapeutic approach in counteracting HALI. Computed tomography findings reflect the pathological phases of the diffuse alveolar damage. At least preferably the lowest level of FiO 2 should be used in order to provide full lung protection against the damage induced by MV.

Electrical remodeling and cardiotoxicity precedes structural and functional remodeling of mouse hearts under hyperoxia treatment

“…Mechanical ventilation with hyperoxia (>90% oxygen) is frequently implemented to relieve respiratory distress or failure in patients with post‐cardiac stress, sepsis, stroke, and traumatic brain injury (Vincent et al, 2017). However, studies demonstrate that exposure to hyperoxia leads to hyperoxemia and subsequent development of lung complications (Elmer et al, 2015; Gole et al, 2011; Shosholcheva et al, 2017; Vincent et al, 2017; Visser et al, 2010; Waring et al, 2003). Furthermore, its usage in ICU patients has been linked to astounding in‐hospital mortality rates of up to 34.5% (Couper & Yeung, 2014; Damiani et al, 2014; Helmerhorst et al, 2014; Janz et al, 2012; Kilgannon et al, 2010; Nelskyla et al, 2013; Rincon et al, 2013; Shen & Zhang, 2015; Wunsch et al, 2010).…”

Hepatic artery flow, inspired oxygen, and hemoglobin determine liver tissue saturation measured with visible diffuse reflectance spectroscopy (vis‐DRS) in an in vivo swine model

“…[7][8][9] FiO 2 is usually maintained at the minimum level to achieve normoxia in order to protect the lungs from oxygen toxicity. [10][11][12][13] In our model, during unimpeded hepatic artery flow liver tissue saturation did not change over a wide range of hemoglobin (4.5-11 g/dl) (Figure 2), suggesting that permissive anemia alone is well tolerated. In contrast, Figure 1 shows that when hepatic artery flow was reduced to 25%, lower hemoglobin values were associated with lower liver tissue saturations.…”

“…Postoperative patient management after liver transplantation routinely includes permissive anemia to improve the rheology of blood, combined with anticoagulation and antiplatelet therapy 7–9 . FiO 2 is usually maintained at the minimum level to achieve normoxia in order to protect the lungs from oxygen toxicity 10–13 …”

Impact of hyperoxia on cardiac pathophysiology

“…The negative impact associated with ventilation is collectively referred to as ventilator‐induced lung injury (VILI; Cipulli et al, ). VILI has been shown to develop in both healthy and diseased lungs (Shosholcheva, capital Je, Kartalov, Kuzmanovska, & Miladinova, ). Many factors have also been reported to contribute to VILI, including duration and intensity of mechanical ventilation, factors involving pulmonary volume and pressure, and the use of high oxygen levels (hyperoxia) (Curley, Laffey, Zhang, & Slutsky, ; Dreyfuss & Saumon, ; Shosholcheva et al, ).…”

“…VILI has been shown to develop in both healthy and diseased lungs (Shosholcheva, capital Je, Kartalov, Kuzmanovska, & Miladinova, ). Many factors have also been reported to contribute to VILI, including duration and intensity of mechanical ventilation, factors involving pulmonary volume and pressure, and the use of high oxygen levels (hyperoxia) (Curley, Laffey, Zhang, & Slutsky, ; Dreyfuss & Saumon, ; Shosholcheva et al, ). Although, currently, there are practical methods to reduce the risk of VILI, such as by adjustment of tidal volume, positive‐end‐expiratory pressure, and oxygen titration (Cipulli et al, ), these methods are not sufficient to eradicate VILI in a clinical setting.…”