3. Hyperbaric oxygen and oxygen toxicity

young adult in good health and breathing room air therefore will have a PaO2 of 20.93  0.66 = 13.3 kPa (100 mmHg). hyperventilation can increase this to around 16 kPa (from the alveolar gas equation, the fall in PaCO2 allowing a rise in PaO2), but further rises are possible only by enriching the inspired oxygen concentration

13.3 kPa, haemoglobin is almost 100% saturated. Further increases in inspired oxygen (FiO2) can therefore increase the oxygen saturation (SpO2) only marginally, although the PaO2 will rise substantially the arterial oxygen content rises from around 19 ml dl1 to only 21 ml d if breathinf 100% @ room air

application of Henry’s Law, which states that the number of molecules (in this case oxygen) which dissolve in the solvent (plasma) is directly proportional to the partial pressure of the gas at the surface of the liquid very high arterial PaO2 values (greater than 80 kPa) can be obtained. Thus, at 2 atmospheres the PaO2 will be 175 kPa. Even at these levels, however, the venous content will only be of the order of 18 ml dl1, and it is not until the blood is exposed to oxygen at 3 atmospheres of pressure, at which the arterial content is 25.5 ml d Content is determined by the product of the [Hb]  [% saturation]  [1.31] (O2-carrying capacity of Hb) plus dissolved oxygen. Dissolved oxygen (0.003 ml dl1 mmHg1) is small and is usually ignored, except under these hyperbaric conditions when it assumes great importance.

depth, the tissues become supersaturated with nitrogen. If the diver ascends too rapidly, the partial pressure of nitrogen in tissues exceeds the ambient pressure, and so the gas forms bubbles in the circulation and elsewhere Hyperbaric treatment mimics controlled ascent from depth, and this allows the nitrogen to wash out exponentially without causing symptoms.

Infection: the evidence supports the use of hyperbaric oxygen therapy as part of the management of patients with bacterial infections. The main indications are for anaerobic bacterial infections, particularly with clostridia, osteomyelitis and necrotizing soft tissue infections. Oxygen-derived free radicals are bactericidal.

Carbon monoxide (CO) poisoning: the half-life of CO while breathing 100% oxygen is reduced to an hour. This is reduced further to about 20 minutes in a hyperbaric chamber, but, unless the chamber is on site, the transfer time alone will make this benefit negligible.

hyperbaric oxygen therapy may be of benefit to patients in whom wound healing is delayed by ischaemia

Anaemic hypoxia: Jehovah’s witnesses who have lost blood but whose religious beliefs prohibit transfusion, and others in whom very low haemoglobin concentrations have compromised oxygen delivery to tissues, have been managed successfully using hyperbaric oxygen.

pathological changes which begin with tracheobronchitis, neutrophil recruitment and the release of inflammatory mediators. Surfactant production is impaired, pulmonary interstitial oedema appears, followed, after around 1 week of exposure, by the development of pulmonary fibrosis.

: this is complex and not fully elucidated. Although oxygen is a stable molecule, it is readily transformed into substances that are potentially toxic. In various normal metabolic pathways and enzymatic reactions, oxygen becomes partially reduced to a superoxide anion (O2 –). Both H2O2 and O2 – are potentially toxic and in higher concentrations interact to produce highly reactive species of which the hydroxyl free radical is the most dangerous

: the major problem is dose-related direct toxicity. Dose–time curves have been constructed to allow the recommendation that 100% should be administered for no longer than 12 hours at atmospheric pressure, 80% for no longer than 24 hours and 60% for no longer than 36 hours. An FiO2 of 0.5 can be maintained indefinitely.

: up to a partial pressure of oxygen of about 60 kPa, a number of endogenous antioxidant enzymes are effective. These include catalase, superoxide dismutase and glutathione peroxidase

These are most marked in conscious patients who are breathing oxygen under hyperbaric conditions. include retrosternal discomfort, carinal irritation and coughing. This becomes more severe with time, with a burning pain that is accompanied by the urge to breathe deeply and to cough. As exposure continues, symptoms progress to severe dyspnoea with paroxysmal coughing. CNS symptoms may supervene, with nausea, facial twitching and numbness as well as disturbances of taste and smell. Convulsions may occur, preceded by a premonitory aura. long-term ventilated patients in whom high inspired oxygen concentrations tend to be the norm, the non-specific clinical signs will be those of progressively impaired gas exchange with decreased pulmonary compliance

An FiO2 as high as 0.6 is associated with only a small increase in umbilical venous oxygenation. However, what do rise are markers of oxygen free radical activity in both mother and baby. These radicals deplete intrinsic antioxidant systems Neonatal hyperoxia is known, moreover, to mediate tissue damage in conditions as diverse as retinopathy of prematurity, necrotizing enterocolitis, bronchopulmonary dysplasia and intracranial haemorrhage.

This toxicity presents the major limitation of hyperbaric oxygen therapy. It is dose dependent and affects not only the lung but also the CNS, the visual system and probably the myocardium, liver and renal tract. Pulmonary toxicity: oxygen at 2 atmospheres produces symptoms in healthy volunteers at 8–10 hours, together with a quantifiable decrease in vital capacity which starts as early as 4 hours. This persists after exposure ceases. CNS: oxygen at 2 atmospheres is associated with nausea, facial twitching and numbness, olfactory and gustatory disturbance. Tonic–clonic seizures may then supervene without any prodrome, although some subjects report a premonitory aura. Eyes: hyperoxia may be associated in adults with narrowing of the visual fields and myopia.

neonates and infants of post-conceptual age less than 44 weeks may develop retrolental fibroplasia if they are allowed to maintain a PaO2 greater than 10.6 kPa (80 mmHg) for longer than 3 hours. In practice, this means keeping the oxygen saturation (SpO2) in these babies at around 90%. The condition, however, is almost certainly multifactorial and not related to oxygen toxicity alone.

Absorption atelectasis: this is a predictable adverse effect of therapy.

Hypoventilation: oxygen concentrations higher than 24% may suppress respiration in patients who are reliant on hypoxaemic ventilatory drive. This is another adverse effect of therap