Oxygen therapy

All critically ill patients should receive additional inspired O2 on a ‘more not less is best’ philosophy.

Principles

• High flow, high concentration O2 should be given to any acutely dyspnoeicor hypoxaemic patient until accurate titration can be performed using arterial blood gas analysis.

• In general, maintain SaO2 between 92–98%. Compromises may need to be made during acute on chronic hypoxaemic respiratory failure, or prolonged severe ARDS, when lower values may suffice provided tissue O2 delivery is maintained.

• When starting mechanical ventilation use a high FIO2 until accurate titration is performed using arterial blood gas analysis.

• Apart from patients being treated for carbon monoxide poisoning or hyperbaric therapy, e.g. diving accidents, there is no need to maintain supranormal levels of PaO2. Indeed this may cause harm.

Type II respiratory failure

Patients in chronic type II (hypoxaemic, hypercapnic) respiratory failure may develop apnoea if their central hypoxic drive is removed by supplemental O2. This is seldom (if ever) abrupt; a period of deterioration and increasing drowsiness will prompt consideration of either (i) FIO2 reduction if overall condition allows; (ii) non-invasive or invasive mechanical ventilation if fatiguing; or (iii) use of respiratory stimulants such as doxepram. Close supervision and monitoring is necessary.

Oxygen toxicity

This is well described in animal models. Normal volunteers become symptomatic (chest pain, dyspnoea) after several hours of breathing pure O2. Washout of nitrogen can cause microatelectasis. O2 may induce direct oxidant damage to proteins, lipids, and DNA, and is a potent vasoconstrictor; high levels of PaO2 may paradoxically compromise regional O2 delivery. The relative importance of O2 toxicity to the lung compared to other forms of ventilator trauma in critically ill patients remains unclear. Efforts should be made to minimise FIO2 whenever possible. Debate continues as to whether FIO2 or other ventilator settings (e.g. PEEP, VT, inspiratory pressures) should be reduced fi rst. The authors’ present view is to minimise the risks of ventilator trauma and accept progressively lower values of SaO2/PaO2 rather than continue with a high FIO2.

Monitoring

• A normal pulse oximetry reading may obscure deteriorating gas exchange and progressive hypercapnia.

• An O2 analyser in the inspiratory limb of the ventilator or CPAP/BiPAP circuit confi rms the patient is receiving a known FIO2. Some ventilators have built-in calibration devices.

• Adequacy and any changes in arterial O2 saturation can be monitored continuously by pulse oximetry and intermittently with laboratory blood gas analysis.

Oxygen masks

• Hudson-type masks or nasal ‘spectacles’ give an imprecise FIO2 and should only be used when hypoxaemia is not a major concern. Hudsontype masks do allow delivery of humidifi ed gas (e.g. via an ‘Aquapak’). Valves fi tted to the Aquapak system do not deliver an accurate FIO2 unless gas fl ow is at the recommended level.

• Masks fitted with a Venturi valve deliver a reasonably accurate FIO2 (0.24 at 2L/min, 0.28 at 4L/min, 0.35 at 8L/min, 0.40 at 10L/min, 0.60 at 15L/min) except in patients with very high inspiratory fl ow rates. Pure O2 is delivered via a fi xed jet drawing in air from around the jet to give a known dilution of O2 to the desired concentration. These masks do not allow delivery of humidified gas but are preferable in the short term for dyspnoeic patients as they enable more precise monitoring of PaO2 /FIO2 ratios.

• A tight-fitting anaesthetic mask and reservoir bag allows 100% O2 to be delivered.