This systematic review aimed to investigate the drugs used and their potential effect on noninvasive ventilation (NIV). NIV is used increasingly in acute respiratory failure (ARF). Sedation and analgesia are potentially beneficial in NIV, but they can have a deleterious impact. Proper guidelines to specifically address this issue and the recommendations for or against it are scarce in the literature. In the most recent guidelines published in 2017 by the European Respiratory Society/American Thoracic Society (ERS/ATS) relating to NIV use in patients having ARF, the well-defined recommendation on the selective use of sedation and analgesia is missing. Nevertheless, some national guidelines suggested using sedation for agitation. Electronic databases (PubMed/Medline, Google Scholar, and Cochrane library) from January 1999 to December 2019 were searched systematically for research articles related to sedation and analgosedation in NIV. A brief review of the existing literature related to sedation and analgesia was also done. Sixteen articles (five randomized trials) were analyzed. Other trials, guidelines, and reviews published over the last two decades were also discussed. The present review analysis suggests dexmedetomidine as the emerging sedative agent of choice based on the most recent trials because of better efficacy with an improved and predictable cardiorespiratory profile. Current evidence suggests that sedation has a potentially beneficial role in patients at risk of NIV failure due to interface intolerance, anxiety, and pain. However, more randomized controlled trials are needed to comment on this issue and formulate strong evidence-based recommendations. Karim HMR, Šarc I, Calandra C, Spadaro S, Mina B, Ciobanu LD, et al. Role of Sedation and Analgesia during Noninvasive Ventilation: Systematic Review of Recent Evidence and Recommendations. Indian J Crit Care Med 2022;26(8):938–948.

Background: Previous studies have suggested that the coronavirus disease 2019 (COVID-19) pandemic was associated with a decreased rate of acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Data on how the COVID-19 pandemic has influenced mortality, seasonality of, and susceptibility to AECOPD in the chronic obstructive pulmonary disease (COPD) population is scarce. Methods: We conducted a national population-based retrospective study using data from the Health Insurance Institute of Slovenia from 2015 to February 2021, with 2015–2019 as the reference. We extracted patient and healthcare data for AECOPD, dividing AECOPD into severe, resulting in hospitalisation, and moderate, requiring outpatient care. The national COPD population was generated based on dispensed prescriptions of inhalation therapies, and moderate AECOPD events were analysed based on dispensed AECOPD medications. We extracted data on all-cause and non-COVID mortality. Results: The numbers of severe and moderate AECOPD were reduced by 48% and 34%, respectively, in 2020. In the pandemic year, the seasonality of AECOPD was reversed, with a 1.5-fold higher number of severe AECOPD in summer compared to winter. The proportion of frequent exacerbators (⩾2 AECOPD hospitalisations per year) was reduced by 9% in 2020, with a 30% reduction in repeated severe AECOPD in frequent exacerbators and a 34% reduction in persistent frequent exacerbators (⩾2 AECOPD hospitalisations per year for 2 consecutive years) from 2019. The risk of two or more moderate AECOPD decreased by 43% in 2020. In the multivariate model, pandemic year follow-up was the only independent factor associated with a decreased risk for severe AECOPD (hazard ratio [HR]: 0.71; 95% confidence interval [CI]: 0.61–0.84; p < 0.0001). In 2020, non-COVID mortality decreased (−15%) and no excessive mortality was observed in the COPD population. Conclusion: In the pandemic year, we found decreased susceptibility to AECOPD across severity spectrum of COPD, reversed seasonal distribution of severe AECOPD and decreased non-COVID mortality in the COPD population.

Introduction: The immunopathogenesis of end-stage chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) remains poorly understood. Emerging evidence suggests that distinct T cell subpopulations may play critical roles in the progression of both diseases. A better understanding of these roles could provide important insights into underlying mechanisms and guide the development of targeted therapies.Methods: We performed flow cytometric analysis of explanted lung tissue from patients with advanced COPD (n = 9), IPF (n = 9), and idiopathic pulmonary arterial hypertension (IPAH, n = 3) undergoing lung transplantation. Healthy donor lung tissue (n = 7) served as controls.Results: Both COPD and IPF lungs demonstrated an increased frequency of Th1 (CXCR3⁺CCR4^-CCR6^-) lymphocytes compared to controls. In contrast, Tc17 cells were significantly reduced. No notable differences were observed in Th2, Th17, or Tc1 cell populations. Activated CD4⁺ T cells (CD69⁺CD25⁺HLA-DR^-/+) were significantly enriched in IPF compared to COPD and donor lungs. COPD lungs exhibited a marked expansion of terminally differentiated cytotoxic CD8⁺CD28^-CD27^- T cells. In double-negative (DN; CD3⁺CD4^-CD8^-) T cell compartment, CD25⁺ T cells were increased in COPD, whereas DN tissue-resident memory (TRM; CD69⁺CD25^-HLA-DR^-) cells were reduced in both COPD and IPF. Invariant natural killer T (iNKT; Vα24⁺Vβ11⁺) cell levels were uniformly low without intergroup differences.Discussion: Our findings identify disease-specific immune signatures in end-stage COPD and IPF. Th1 cell expansion together with a reduction in Tc17 and DN TRM subsets represented shared features of COPD and IPF, whereas accumulation of terminally differentiated cytotoxic CD8⁺ T cells and CD25⁺ DN T cells was specific to COPD. These findings enhance our understanding of adaptive immune dysregulation in COPD and IPF and may support the development of immunomodulatory strategies.

Turkthoracj, Turkish Thoracic Journal