2024/08/30 by Solano, Gustavo, Patiño, Jhonny, Bonilla-Llanos, Maria +6
#Critical Care #Life Sciences #Medical Specialties #Medicine and Health Sciences #Pulmonology
paper · doi:10.17605/osf.io/wv85t
Acute Lung Injury, clinically exemplified as Acute Respiratory Distress Syndrome (ARDS), stands as a condition causing substantial mortality annually. Implementing "protective" ventilatory strategies for ARDS mitigation has been instrumental in reducing the incidence of Ventilator-Induced Lung Injury (VILI), and curtailing mortality rates. Nonetheless, these strategies may inadvertently result in alveolar carbon dioxide (CO2) elevation and subsequent pH decline over protracted periods. Recent investigations have underscored the clinical ramifications of hypercapnia, demonstrating its significance as an autonomous predictor of mortality and implying a heightened ARDS severity among patients exhibiting sustained hypercapnia. However, current evidence of hypercapnia's clinical impact remains scant, with contradictory perspectives on its underlying pathophysiological mechanisms. The overarching objective of this scoping review is to present extant literature on hypercapnia's effects within experimental models, encompassing acute lung injury scenarios, to characterize the immunomediated pulmonary tissue damage.