Acute hypoxemic respiratory failure is the principal cause of hospitalization, invasive mechanical ventilation and death in severe COVID-19 infection. Nearly half of intubated patients with COVID-19 eventually die. High-Flow Nasal Oxygen (HFNO) and Noninvasive Ventilation (NIV) constitute valuable tools to avert endotracheal intubation in patients with severe COVID-19 pneumonia who do not respond to conventional oxygen treatment. Sparing Intensive Care Unit beds and reducing intubation-related complications may save lives in the pandemic era. The main drawback of HFNO and/or NIV is intubation delay. Cautious selection of patients with severe hypoxemia due to COVID-19 disease, close monitoring and appropriate employment and titration of HFNO and/or NIV can increase the rate of success and eliminate the risk of intubation delay. At the same time, all precautions to protect the healthcare personnel from viral transmission should be taken. In this review, we summarize the evidence supporting the application of HFNO and NIV in severe COVID-19 hypoxemic respiratory failure, analyse the risks associated with their use and provide a path for their proper implementation.

Sarcoidosis is characterized by reduced quality of life (QoL), yet QoL is poorly correlated to conventional spirometric lung function tests. What is the relationship of a QoL measure with comprehensive lung function assessment using oscillometry in sarcoidosis?. Sixty-two patients with pulmonary sarcoidosis completed the St George Respiratory Questionnaire (SGRQ), a respiratory QoL measure, and underwent lung function assessment including oscillometry, spirometry, diffusion capacity, fractional exhaled nitric oxide (FE_NO) and body plethysmography. Relationships of lung function parameters with SGRQ were determined with Spearman's rank coefficient (rho), and receiver-operating characteristic curves plotted. Logistic regression and hierarchy cluster analysis of parameters from multiple lung function techniques were performed RESULTS: Oscillometric indices describing peripheral lung dysfunction, showed significant associations with SGRQ (R5, rho=0.43, p<0.01, R5-R20, rho=0.35, p<0.01, X5, rho=-0.42, p<0.01, Ax, rho=0.44 <0.01), whereas FVC% and RV/TLC ratio, were weakly related to SGRQ (rho=-0.30, p=0.02, rho=0.30, p=0.02). Oscillometry reactance, measuring elastic properties of the lung, predicted an impaired QoL (AUC, Ax, 0.80, p<0.001 and X5, 0.78, p<0.001), even in patients with absence of an obstructive or restrictive spirometry pattern. Ax remained significantly associated with SGRQ even after adjustment for FVC and Scadding stage on multivariable analysis (p=0.005). FE_NO was not associated with SGRQ. Peripheral airway function parameters (R5-R20, Ax, RV/TLC) were grouped in an independent cluster, whereas X5 constituted a single cluster INTERPRETATION: Oscillometric lung function parameters, especially those of peripheral airway dysfunction, are more strongly correlated to a QoL measure than spirometry in patients with sarcoidosis.

Defective tissue repair and remodeling are main aspects of Chronic Obstructive Pulmonary Disease (COPD) pathophysiology. Bone marrow mesenchymal stem cells (BM-MSCs) have been implicated in this direction, as their functional impairment and recruitment could possibly contribute to disease development and progression. The present study characterizes for the first time the expression of migration related chemokine receptors and their ligands in BM-MSCs from COPD patients. CXCR4/SDF1a and CCR7/CCL19-CCL21 mRNA levels were evaluated in BM-MSCs obtained from twelve COPD patients and seven healthy donors. SDF1a protein levels in sera and BM-MSCs’ conditioned media were also evaluated. CXCR4, SDF1a, CCL19, and CCL21 mRNA levels were significantly reduced in COPD BM-MSCs while CCR7 levels were undetectable. Notably, SDF1a protein levels were marginally elevated in both patient sera and BM-MSCs’ conditioned media while the increase in SDF1a serum levels significantly correlated with disease severity in COPD. Our findings show posttranscriptional regulation of SDF1a levels in BM-MSCs of COPD patients and significant downregulation of SDF1a and CXCR4 mRNA indicating an involvement of the SDF1a signaling pathway in the disease pathophysiology.