It is paradoxical that oxygen is vital to life, but may become a poison to the central nervous system CNS, lungs, and eyes when present at high levels and for a long duration. Yet, the harmful biochemical effects of oxygen toxicity on cell membranes, enzymatic reactions, and metabolism are well known. The increased pressure due to great depth Boyle’s law is probably the most common way that oxygen toxicity occurs. For example, if a mixture is breathed at an ocean depth of, external hydrostatic pressure increases the density and decreases the volume of this gas, making it equivalent to breathing at a depth of only. It is unusual, however, to breathe air at depths below because of problems with CO toxicity and nitrogen narcosis see paragraphs below. Obviously, breathing pure oxygen for a prolonged time is a second way to induce oxygen toxicity. Because closed-circuit scuba systems utilize a pure oxygen canister, the potential for oxygen poisoning exists; except in extraordinary circumstances, a closed-circuit scuba apparatus should not be used at a depth of more than ft. Selected symptoms of oxygen toxicity, categorized by the organs affected, are presented in table ..< The lungs experience the highest concentrations of any organ in the body; pulmonary symptoms of oxygen toxicity usually begin with either coughing, a mild irritation under the sternum, or a burning sensation in the trachea and bronchial tubes. If the brain and the CNS are affected,
You will recall that nitrogen gas N, which constitutes approximately of air, is an inert gas that is not utilized biochemically in respiration. Nevertheless, N in the lungs moves across the alveolar membrane into the blood, and dissolves in the intracellular fluid. Y ou also should recall that the total pressure of each gas in a diver's lungs increases in direct proportion to the depth of the dive. Thus, at a depth of, when lung air equilibrates with intracellular fluid, the tissue N is about three times greater than at the surface. This increased level of N causes many exotic physical and mental symptoms that are similar to alcohol intoxication. Known as nitrogen narcosis, this condition generates anesthetic-like euphoria, over-confidence, poor judgment, and a slower reaction time. Many divers have died from nitrogen narcosis because of serious errors in diving techniques and accidents. The greatest hazard may be that it keeps a diver from caring about the task at hand or his or her own safety. Because this condition usually becomes a major problem below, authorities recommend that sport divers not descend below this depth. Interestingly, breathing other inert gases creates a similar euphoric state, known as inert gas narcosis. The order of potency of the inert gases, from least to most narcotic, is helium, neon, hydrogen, nitrogen, argon, krypton, and xenon. Because this list is identical to the relative solubility of these gases in lipids, a mechanism for inert gas action has been advanced. This theory proposes that the lipid component of cell membranes is altered by absorption of inert gases into the membrane's molecular structure.
Tissue nitrogen also plays an important role in decompression sickness DCS, known for years as the bends. The term bends originated at the turn of the th century among workers who were building the Brooklyn Bridge in New York City. Hobbled by severe pain, these laborers walked by bending forward at the hips because ofjoint stiffness. DCS typically begins at depths below ft; atm, when a diver's tissues are loaded with increased quantities of and N, as described in the previous two paragraphs. Usually the diver returns to the surface too rapidly swift decompression, causing the gas pressure within the tissue to exceed the external hydrostatic pressure. This establishes a state of supersaturation and liberates N bubbles within cells, similar to the bubbles that form in a can of carbonated beverage the air pressure above the soda decreases rapidly when the can is opened. Interestingly, experiments have shown that N bubbles are common in the bloodstream of recreational divers immediately after underwater excursions, and are presumed to be harmless in small volumes because they are filtered by the lung's capillary network and subsequently exhaled. In contrast, excessive N gas bubbles can disturb organ and cell function by a blocking arteries, veins, and lymph vessels; b causing compartment syndrome in a muscle bounded by fascia; andrupturing cell membranes. Signs and symptoms of DCS tableoccur when decompression is inadequate, within of completing a dive. When symptoms appear in the CNS, respiratory system, or circulatory system, the required medical treatment is more extensive than if only joint
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Recent research in our laboratory evaluated individual perception of CO in gas mixtures to determine if scuba divers could sense small elevations in the CO content of inspired air, and to provide cues that scuba divers might use to warn themselves of hypercapnia elevated blood CO levels before it reaches injurious levels. Resting college-aged males could sense that inhaling room air was different from both a and CO gas mixture, and that their responses respiratory rate, headache, restlessness, faintness, and breathlessness during the experiment were greater than during the trial. We concluded that military, technical, and labor personnel should avoid tasks that require mental acuity air traffic control for at least after breathing an CO gas mixture. Further, we suggested that divers use headache as a warning signal of hypercapnia because it occurred more often than any other symptom.
One final physiological effect of CO deserves consideration. A low carbon dioxide level in blood has been implicated in breath-hold diving blackout via hypoxia; this life-threatening syndrome was described above, in the section titled Predive Hyperventilation: Useful but Risky, page .