Fig. 1. - Algorithm to correct hypoxaemia in an acutely ill chronic obstructive pulmonary disease patient. ABG: arterial blood gas; Pa,O2: arterial oxygen tension; O2: oxygen; Sa,O2: arterial oxygen saturation; Pa,CO2: arterial carbon dioxide tension; NPPV: noninvasive positive pressure ventilation.
Acute increases in FI,O2 may cause a ventilation/perfusion mismatch and lead to hypercarbia. Hence, it is recommended that the initial flow setting be adjusted to increase the Pa,O2 to just above 8 kPa (60 mmHg) [12, 13].
Following the initial setting, the oxygen flow should be adjusted via ABG to bring the oxygen pressure to >8 kPa (60 mmHg) or Sa,CO2 >90% (92-96%). If CO2 retention occurs, the pH should be observed. If it is nonacidemic, the high CO2 should be accepted as it is chronic. If the pH is acidemic, a Venturi mask should be considered, to closely control the FI,O2, or invasive or noninvasive mechanical ventilation. All other medical treatments, including bronchodilators, secretion clearance, steroids and treatment of infection, should be optimised. As the patient becomes ambulatory, pulse oximetry can be used to determine an exercise flow setting while walking in the hallway (fig. 1) .
Patients with Pa,CO2 <6 kPa (45 mmHg), receiving oxygen sufficient to raise Pa,O2 to 8 kPa (60 mmHg), will be unlikely to experience CO2 retention . If CO2 retention does occur, it is often minor and not usually accompanied by significant acidosis. It is a reasonable goal to adjust the oxygen setting to correct the hypoxaemia to a Pa,O2 slightly >8 kPa (60 mmHg), allowing 20-30 min to achieve steady state. The pH should be monitored for changes in acid-base status. If adequate oxygenation is unachievable without progressive respiratory acidosis, then noninvasive or invasive mechanical ventilation should be considered (see Exacebation: assisted ventilation) [15-18].
Patients may be started on oxygen for the first time during hospitalisation for an acute exacerbation and discharged before recovery is complete. Patients with hypoxaemia at discharge may require short-term oxygen therapy as the effects of the exacerbation are clearing. After 30-90 days, oxygen may no longer be required. Thus re-evaluation of the patient’s oxygen and medical status should be completed. If the patient no longer meets the prescribing criteria for long-term oxygen therapy (LTOT), oxygen should be discontinued, as there is no proven survival benefit for patients with mild hypoxaemia  (see Management of stable COPD: long-term oxygen therapy).
Some patients who needed oxygen prior to hospitalisation may, over time, increase their Pa,O2 to the point that they no longer qualify for oxygen. This phenomenon is thought to be due to a reparative effect of LTOT. Withdrawing oxygen from these patients may negate the reparative effect and cause the patient’s status to deteriorate to the point of meeting the physiological requirement for oxygen. Consequently, these patients should continue their oxygen therapy without interruption as withdrawing their oxygen might be detrimental [20, 21].
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