Understanding Oxygen Toxicity in Hyperbaric Medicine

Oxygen toxicity is a known risk during hyperbaric oxygen therapy (HBOT). While its more severe forms — like seizures — can be prevented, oxidative stress at the cellular level remains a complex challenge.

Why Oxygen Toxicity Occurs in HBOT

Preventing oxygen toxicity is a primary goal in hyperbaric oxygen therapy (HBOT). However, complete prevention of the direct, intracellular enzymatic effects of oxygen toxicity is not possible in the presence of high cellular oxygen tensions¹. While seizures can be prevented using anticonvulsants, these do not block the cellular-level toxicity caused by hyperoxia¹.

Many preventive strategies aim to prolong the latent period before oxygen seizures begin — but they don’t stop other toxic effects occurring within the cell².

The Body’s Natural Antioxidant Defenses

Within the body, enzymes like superoxide dismutase, which degrades superoxide radicals, as well as catalase and glutathione peroxidase, which break down hydrogen peroxide, help detoxify reactive oxygen species³. These antioxidant enzymes are found naturally, and convert harmful free radicals into harmless compounds such as water.

Additional defenses include Vitamin E, which is found in lipid membranes; cytoplasmic antioxidants like ascorbate; and sulfhydryl-containing compounds such as glutathione, cysteine, and cysteamine⁴.

Hyperoxic environments can stimulate increased production of these protective enzymes over time, leading to some degree of tolerance⁴. However, acute exposures can overwhelm the body’s defenses.

The Role of Vitamin E and Other Protective Agents

Some researchers have proposed that prophylactic Vitamin E may reduce cellular-level toxicity due to its influence on glutathione production⁵. While empirically used in some hyperbaric centers, definitive clinical proof is lacking⁵.

These approaches aim to support the body’s antioxidant response, but no pharmacologic intervention has matched the reliability of oxygen scheduling itself.

Air Breaks: The Most Reliable Prevention Strategy

The most effective and time-tested preventive method is the use of intermittent “air breaks.” These short breaks during HBOT allow the body’s enzymatic defenses to catch up and help detoxify the cellular environment⁶.

The use of air breaks in hyperbaric therapy was first observed in 1939 by Soulie⁷ and later expanded upon during World War II by Donald⁸. In 1955, Lambertsen detailed their formal application in HBOT protocols, leading to widespread adoption by the U.S. Navy in the 1960s⁸. Today, air breaks remain the global standard for preventing central nervous system oxygen toxicity.

By alternating oxygen exposure with room air, this method helps delay toxicity across all organ systems — without the limitations of drug-based protection⁶. The success of air breaks lies in the periodic fluctuation of oxygen tension, which gives the body a chance to reset without needing to cross cell membrane barriers⁶.

SHS Spotlight

With more than 25 years of experience in wound care and hyperbaric program development, Shared Health Services equips hospitals and physician practices with the resources, tools, and peer-to-peer expertise needed to build successful, sustainable HBOT programs. We work directly with center staff—serving as trusted liaisons—to provide clinical guidance, compliance support, and ongoing education aligned with the highest standards of care. When it comes to safety concerns like oxygen toxicity, our role is to help teams implement proven protocols, such as air breaks, to promote consistency and protect patient well-being. Our goal is to empower your clinicians, strengthen operations, and support a safer, more effective hyperbaric environment—one treatment at a time.

References

1. Clark JM. Oxygen toxicity. In: Neuman TS, Thom SR, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. Philadelphia, PA: Saunders Elsevier; 2008:527–563.

   
   

2. Clark JM, Fisher AB. Oxygen toxicity and extension of tolerance in oxygen therapy. In: Davis JC, Hunt TK, eds. Hyperbaric Oxygen Therapy. Bethesda, MD: Undersea Medical Society; 1977.

   
   

3. Donald K. Oxygen and the Diver. Worcs, UK: The SPA Ltd; 1992.

   
   

4. Hammarlund C. The physiologic effects of hyperbaric oxygen. In: Kindwall EP, ed. Hyperbaric Medicine Practice. Flagstaff, AZ: Best Publishing Co.; 1994:17–32.

   
   

5. Hart GB, Strauss MB. Central nervous system oxygen toxicity in a clinical setting. In: Bove AA, Bachrach N, Greenbaum U, eds. Undersea and Hyperbaric Physiology IX: Proceedings of the Ninth International Symposium on Underwater and Hyperbaric Physiology. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1987:695–699.

   
   

6. Lambertsen CJ. Respiratory and circulatory actions of high oxygen pressure. In: Goff LG, ed. Proceedings of the Underwater Physiology Symposium. Washington, DC: National Academy of Sciences, National Research Council; 1955:25–38. Publication 377.

   
   

7. Neuman TS, Thom SR, eds. Physiology and Medicine of Hyperbaric Oxygen Therapy. Philadelphia, PA: Saunders Elsevier; 2008.

   
   

8. Soulie P. Modifications expérimentales de la résistance individuelle de certains animaux à l’action toxique de l’oxygène. CR Seances Soc Biol. 1939;130:541–542.

   
   

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