2013•Unpublished venueRequires access

Incidence of CNS Oxygen Toxicity with Mild Hyperoxia: A Literature and Data Review

BE Shykoff

Open publisher page 1 citations

Abstract

Abstract : Central nervous system (CNS) oxygen toxicity manifests in a number of ways, from mild symptoms to loss of consciousness and seizure. The available data were reviewed in 1986 and predictive models were proposed. However, the outcomes of many mildly hyperoxic dives (1.0PO21.7 atm) conducted since 1986 may be poorly predicted by the models. This report examines the correspondence of five published models to all available data, those with which the models were developed and those from more recent experiments. Differences within the data sets for mild hyperoxia are examined, and empirical probabilities of CNS oxygen toxicity are suggested. The published models overestimate experimental incidence of CNS oxygen toxicity at low PO2 where CNS oxygen toxicity is extremely rare. For training dives, adverse events are more common, probably as a result of CO2 retention by trainee divers, and data from experimental and training dives cannot be combined. During a MK 16 dive within the decompression tables, probability p 1.5% (95% confidence interval) of any symptom of CNS oxygen toxicity with N2O2, and p 0.4% with HeO2. For a 240-minute dive with PO2 = 1.4 atm, p 1.7% for a definite CNS oxygen toxicity event. However, if CO2 is poorly controlled, p 10%.

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What this paper is about

Abstract : Central nervous system (CNS) oxygen toxicity manifests in a number of ways, from mild symptoms to loss of consciousness and seizure. The available data were reviewed in 1986 and predictive models were proposed. However, the outcomes of many mildly hyperoxic dives (1.0PO21.7 atm) conducted since 1986 may be poorly predicted by the models. This report examines the correspondence of five published models to all available data, those with which the models were developed and those from more recent experiments. Differences within the data sets for mild hyperoxia are examined, and empirical probabilities of CNS oxygen toxicity are suggested. The published models overestimate experimental incidence of CNS oxygen toxicity at low PO2 where CNS oxygen toxicity is extremely rare. For training dives, adverse events are more common, probably as a result of CO2 retention by trainee divers, and data from experimental and training dives cannot be combined. During a MK 16 dive within the decompression tables, probability p 1.5% (95% confidence interval) of any symptom of CNS oxygen toxicity with N2O2, and p 0.4% with HeO2. For a 240-minute dive with PO2 = 1.4 atm, p 1.7% for a definite CNS oxygen toxicity event. However, if CO2 is poorly controlled, p 10%.

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Available abstract

Abstract : Central nervous system (CNS) oxygen toxicity manifests in a number of ways, from mild symptoms to loss of consciousness and seizure. The available data were reviewed in 1986 and predictive models were proposed. However, the outcomes of many mildly hyperoxic dives (1.0PO21.7 atm) conducted since 1986 may be poorly predicted by the models. This report examines the correspondence of five published models to all available data, those with which the models were developed and those from more recent experiments. Differences within the data sets for mild hyperoxia are examined, and empirical probabilities of CNS oxygen toxicity are suggested. The published models overestimate experimental incidence of CNS oxygen toxicity at low PO2 where CNS oxygen toxicity is extremely rare. For training dives, adverse events are more common, probably as a result of CO2 retention by trainee divers, and data from experimental and training dives cannot be combined. During a MK 16 dive within the decompression tables, probability p 1.5% (95% confidence interval) of any symptom of CNS oxygen toxicity with N2O2, and p 0.4% with HeO2. For a 240-minute dive with PO2 = 1.4 atm, p 1.7% for a definite CNS oxygen toxicity event. However, if CO2 is poorly controlled, p 10%.

Key concepts: Hyperoxia, Oxygen toxicity, Toxicity, Oxygen, Incidence (geometry), Hyperbaric oxygen, Central nervous system, Adverse Outcome Pathway

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