Oxygen toxicity
Pathophysiology
The oxygen molecule has 2 unpaired electrons in its outer shell which gives it its properties of stability (indefinite half life) and paramagnetism.
It can easily be transformed into a variety of free radicals and other toxic substances.
Many physiological processes and exogenous compounds (bleomycin, paraquat) reduce oxygen by receiving one of its electrons to form a superoxide anion.
This decays to hydrogen peroxide and then water.
Superoxide and hydrogen peroxide are toxic but combine to produce even more toxic free radicals.
These attack DNA, enzymes, lipids and collagen.
Adverse effects
Dose related
100% max of 12h, 80% 24h, 60% 36h, 50% indefinitely.
Effects more profound in hyperbaric conditions.
Lungs
ARDS effects - release of inflammatory mediators, impairment of surfactant production, pulmonary oedema and then development of fibrosis.
Absorption atelectasis as more soluble than nitrogen (diffuses out of alveoli into blood faster than nitrogen in blood diffuses into alveoli).
Hypoventilation if hypoxic respiratory drive.
CNS
Hyperoxaemia causes oxidative stress and harms post ischaemic neurones (in animal studies). Post resuscitation hyperoxaemia associated with worse outcome in one study.
Eyes - Retrolental fibroplasia in infants.
Symptoms
Respiratory
Retrosternal discomfort, coughing, SOB
CNS
Nausea, facial twitching and numbness, convulsions, narrowing of visual fields, myopia