Oxygen therapy and acute respiratory failure

Oxygen is the commonest drug given in the emergency department, and it is also one of the most often misused. It is a treatment for hypoxaemia, not a panacea, and like any drug it has a target, a dose and adverse effects. The aim of emergency oxygen therapy is to correct tissue hypoxia by restoring arterial oxygen content while the underlying cause is diagnosed and treated; it is always an adjunct to, never a substitute for, definitive care. Used well it is life-saving; used carelessly it causes carbon-dioxide retention in the susceptible and lung injury at the extremes. The Fellowship-level understanding rests on three things: the physiology of oxygenation, the mechanisms by which it fails, and the devices, targets and hazards of the therapy. [1]

The physiology of oxygenation

Oxygen moves from the inspired gas to the mitochondrion down a cascade of partial pressures: from the dry inspired oxygen (around 21 kPa or 160 mmHg at sea level), through the humidified tracheal gas, the alveolar gas (around 13 kPa), the arterial blood (around 10 to 13 kPa), and on to the tissues. The alveolar gas equation defines the gap between the inspired and the arterial oxygen, and a widened alveolar-to-arterial gradient is the signature of a lung problem rather than a low inspired fraction or hypoventilation. Arterial oxygen content is carried almost entirely by haemoglobin — CaO2 = (1.34 x haemoglobin x saturation) plus a negligible dissolved term — which is why anaemia and saturation, not PaO2, dominate content, and why oxygen alone cannot rescue the profoundly anaemic or the carbon-monoxide-poisoned patient. The oxyhaemoglobin dissociation curve is sigmoid: above a saturation of about 90 per cent (a PaO2 of about 8 kPa) the curve is flat, so additional oxygen raises saturation little; below 90 per cent the curve is steep, so a small fall in PaO2 causes a large fall in saturation and oxygen delivery. This is why a saturation in the low 90s is a warning, not a reassurance. [1]

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