The oxygen flow rate administered is not important, the (alveolar) PAO2 (and, indirectly, the SaO2) achieved is. the targeted approach is associated with decreased mortality in COPD patients and less respiratory acidosis. in patients with severe COPD who cannot increase minute ventilation, the Haldane effect accounts for about 25% of the total PaCO2 increase due to O2 administration. hence oxygen induces a rightward shift of the CO2 dissociation curve, which is called the Haldane effect. deoxygenated hemoglobin (Hb) binds CO2 with greater affinity than oxygenated hemoglobin (HbO2). this increase in Va/Q mismatch occurs in both CO2 retainers and non-retainers, the difference is presumably one of degree. Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological deadspace. 
In COPD, patients optimise their gas exchange by hypoxic vasoconstriction leading to altered alveolar ventilation-perfusion (Va/Q) ratios. increased V/Q mismatch (most important). Patients suffering from COPD exacerbation, regardless of whether they have CO2 retention, generally have supra-normal respiratory drive (unless there is impending hypercapnic coma). the traditional theory is that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure. 
The same phenomenon has also been described in severe asthma, community-acquired pneumonia and obesity hypoventilation syndrome and any patient with chronic respiratory failure may be at risk.COPD patients with more severe hypoxemia are at higher risk of CO2 retention from uncontrolled O2 administration.Excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients.
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