Review of Medical Physiology - William F. Ganong 2002

Respiration
Adaptive respiratory changes in health and disease
Oxygen therapy

Significance

Administering oxygen-enriched gas mixtures has limited efficacy in congestive, anemic, and histotoxic Hypoxia, as it merely increases The amount of dissolved O₂ in arterial Blood. This is also true for Hypoxic hypoxia, where shunted deoxygenated venous blood bypasses the Lungs. In Other forms of hypoxemic hypoxia, O₂ therapy is beneficial. Treatment regimens delivering up to 100% O₂ are valuable in acute and chronic forms of hypoxemic hypoxia; administering O₂ 24 hours a day for two years helps reduce mortality from chronic obstructive pulmonary disease.

Upon the initial inhalation of O₂, a slight suppression of breathing may occur in normal individuals due to the normal influence of certain hypoxic chemoreceptors. However, this effect is minor and can only be detected using specialized techniques. Additionally, There is a positive effect from a slight accumulation of H⁺ ions starting from the moment when the concentration of deoxygenated Hemoglobin in the blood decreases and Hb becomes a more powerful buffer than HbO₂ (see Chapter 35).

It is important to remember that in hypercapnic patients with severe pulmonary insufficiency, the CO₂ level can be high, and therefore it depresses rather than stimulates Respiration. Some such patients maintain breathing solely because carotid and aortic chemoreceptors influence the respiratory center. If the hypoxic drive is removed by administering O₂, respiration may cease. During apnea, arterial P_O2 decreases, but breathing does not resume because the subsequent rise in P_CO2 will suppress the respiratory center. Therefore, O₂ therapy in such situations must be initiated with caution.

Oxygen Toxicity

It is an interesting question why oxygen, which is so essential for the life of aerobic organisms, is also toxic. In fact, 100% oxygen has a toxic effect not only on animals but also on Bacteria, Fungi, and cultures of animal and plant Cells. Toxicity arises from The formation of the superoxide anion radical (O₂) and H₂O₂. When 80–100% O₂ is administered to humans for eight hours or more, the Airways become affected, causing substernal pain, nasal congestion, a dry throat, and coughing.

Some newborns treated with O₂ for respiratory distress syndrome develop a chronic condition characterized by pulmonary cysts and opacities (bronchopulmonary Dysplasia). Cases like this syndrome serve as evidence of O₂ toxicity. Another complication in such newborns is retinopathy of prematurity (retrolental fibroplasia)—the formation of opaque vascular tissue in the eyes, which can lead to severe visual impairment. Retinal receptors mature from the center toward the periphery of the retina and consume a significant amount of O₂. This facilitates the vascularization of the retina, similar to adults. Oxygen treatment prior to full maturation completely satisfies the metabolic demands of photoreceptors, and consequently, normal vascularization does not occur. There is evidence that this condition can be prevented or ameliorated with vitamin E treatment, which provides an antioxidant effect, and in animals, with Growth Hormone inhibitors.

Hyperbaric Oxygen Therapy

Administering 100% O₂ under increased pressure accelerates the onset of O₂ toxicity, leading not only to tracheobronchial irritation but also to Muscle twitching, tinnitus, dizziness, convulsions, and coma. The rate at which these symptoms appear is proportional to the pressure at which O₂ is administered; for example, at a pressure of 4 atmospheres, symptoms occur in half of individuals after 30 minutes, whereas at 6 atmospheres, convulsions occur within a few minutes. The administration of other gases under increased pressure also causes Central Nervous system symptoms (see below). Administering O₂ at elevated pressures in rats increases the levels of GABA (see Chapter 4) and ATP in the Brain, Liver, and Kidneys.

On the other hand, exposure to 100% O₂ at 2–3 atmospheres can increase the solubility of O₂ in arterial blood to the extent that arterial partial pressure exceeds 2000 mm Hg, and tissue O₂ pressure reaches 400 mm Hg. If exposure is limited to 5 hours or less at such pressures, O₂ toxicity does not occur. Therefore, hyperbaric oxygen chamber therapy is used for diseases where enhanced tissue oxygenation is required and cannot be achieved by other means. Such treatment is effective in Carbon monoxide poisoning, radiation tissue injury, gas gangrene, severe post-hemorrhagic anemias, Diabetic FOOT ulcers and other slow-healing wounds, lacerations, and Skin grafts where Circulation is marginal. Hyperbaric Oxygenation is the mainstay of treatment for decompression sickness and air embolism (see below).