Oxygen is administered at greater than atmospheric pressure for a number of conditions when 100% oxygen at 1 atm is insufficient.
Hyperbaric oxygen therapy has two components: increased hydrostatic pressure and increased oxygen pressure. Both factors are necessary for the treatment of decompression sickness and air embolism. The hydrostatic pressure reduces bubble volume, and the absence of inspired nitrogen increases the gradient for elimination of nitrogen and reduces hypoxia in downstream tissues. Increased oxygen pressure at the tissue level is the primary therapeutic goal for most of the other indications for hyperbaric oxygen. For example, even a small increase in Po2 in previously ischemic areas may enhance the bactericidal activity of leukocytes and increase angio-genesis. Thus, repetitive brief exposures to hyperbaric oxygen are a useful adjunct in the treatment of chronic refractory osteomyelitis, osteoradionecrosis, or crush injury or for the recovery of compromised skin, tissue grafts, or flaps. Furthermore, increased oxygen tension itself can be bacte-riostatic; the spread of infection with Clostridium perfringens and production of toxin by the bacteria are slowed when oxygen tensions exceed 33 kPa (250 mm Hg), justifying the early use of hyperbaric oxygen in clostridial myonecrosis (gas gangrene).
Hyperbaric oxygen also is useful in selected instances of generalized hypoxia. In CO poisoning, hemoglobin (Hb) and myoglobin become unavailable for O2 binding because of the high affinity of these proteins for CO. This affinity is -250 times greater than the affinity for O2; thus, an alveolar concentration of CO = 0.4 mm Hg (1/250th that of alveolar O2, which is -100 mm Hg), will compete equally with O2for binding sites on Hb. A high Po2 facilitates competition of O2for Hb binding sites as CO is exchanged in the alveoli; i.e., the high Po2 increases the probability that O2 rather than CO will bind to Hb once CO dissociates. In addition, hyperbaric O2 will increase the availability of dissolved O2 in the blood (see Table 15-1). The occasional use of hyperbaric oxygen in cyanide poisoning has a similar rationale.
Oxygen toxicity probably results from increased production of hydrogen peroxide and reactive agents such as superoxide anion, singlet oxygen, and hydroxyl radicals that attack and damage lipids, proteins, and other macromolecules, especially those in biological membranes. A number of factors limit the toxicity of oxygen-derived reactive agents, including enzymes such as superoxide dismu-tase, glutathione peroxidase, and catalase, which scavenge toxic oxygen by-products, and reducing agents such as iron, glutathione, and ascorbate. These factors, however, are insufficient to limit the destructive actions of oxygen when patients are exposed to high concentrations over an extended time period. Tissues show differential sensitivity to oxygen toxicity, which is likely the result of differences in both their production of reactive compounds and their protective mechanisms. Decreases of inspired oxygen concentrations remain the cornerstone of therapy for oxygen toxicity.
The pulmonary system, continuously exposed to the highest O2 tensions in the body, is usually the first to exhibit toxicity; subtle changes in pulmonary function can occur within 8-12 hours of exposure to 100% oxygen. Increases in capillary permeability and decreased pulmonary function can be seen after only 18 hours of exposure. Serious injury and death require much longer exposures. Pulmonary damage is directly related to the inspired oxygen tension, and concentrations of >0.5 atm appear to be safe over long time periods. The capillary endothelium is the most sensitive tissue of the lung.
Retrolental fibroplasia can occur when neonates are exposed to increased oxygen tensions; these changes can progress to blindness. The incidence of this disorder has decreased with an improved appreciation of the issues and avoidance of excessive inspired oxygen concentrations. Adults do not seem to develop the disease.
CNS problems are rare, and toxicity occurs only under hyperbaric conditions >200 kPa (2 atm). Symptoms include seizures and visual changes, which resolve when oxygen tension is returned to normal. These problems are a further reason to replace oxygen with helium under hyperbaric conditions (see below).
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