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A similar observation was made by Torres et al.;[24] they stated that mMRC dyspnea score negatively correlated with PaO2 (r =-0.59, P ATPase possibility of exercise desaturation. The causes for EID in patients with COPD are multifactorial with ventilation-perfusion mismatching, diffusion-type limitation, shunting, and reduced oxygen content of mixed venous blood, all of which contribute to some degree.[4] The increasing severity of COPD and consequently decreasing lung functions contribute to the worsening of SpO2 levels that is further worsened with exercise. Hence, oxygen supplementation has been documented to improve the functional capacity and quality of life of COPD patients.[8] However, continuous oxygen supplementation is advocated for patients of COPD with resting nonhypoxemia having oxygen saturation ��88% by the Centers for Medicare and Medicaid Services.[25] Therefore, identifying those nonhypoxemic COPD patients who will be desaturated on exertion is important click here to prevent the potential adverse effects of hypoxemia. Therefore, several researchers have tried to determine various predictors of EID, including FEV1, diffusing capacity of the lung for carbon monoxide (DLCO), and baseline-SpO2.[12,13,16,18] Owen et al.[15] evaluated that a DLCO cutoff of >55% of predicted had 82% sensitivity and 100% specificity for excluding EID. They reported that FEV1 had 82% specificity MG-132 chemical structure for FEV1, above 55% of predicted. The sensitivity of diffusing capacity with this cutoff point was 68% as compared to 46% for FEV1. Van Gestel et al. observed that the only independent predictor of EID was FEV1 and the optimal cutoff of FEV1 was 50% or lower for predicting EID in patients with COPD. Crisafulli et al.[26] indicated FEV1