Oxygen Toxicity: Introduction

Oxygen toxicity is not encountered in routine scuba diving using compressed air. It is a consideration when higher partial pressures of oxygen are used in the inspired gas. Increased oxygen concentration and increased ambient pressure lead to higher partial pressures of oxygen. Divers may use high-oxygen gas compositions to reduce inert gas narcosis, reduce decompression obligations or prolong underwater time.

Central nervous system toxicity, manifested by convulsions, is potentially lethal in the diver.

Pulmonary toxicity is more likely in the longer exposures of saturation chamber diving or hyperbaric oxygen therapy.

Oxygen also has a major role in therapy of many diving disorders.

Toxicity can be avoided by controlling the inspired partial pressure of oxygen and/or the duration of exposure. It can be delayed by intermittent exposure.

The normal partial pressure of oxygen (PO2) in air is approximately 0.2 ATA. Although essential for survival, oxygen may become toxic at an elevated PO2, and the complex systems we have for defending ourselves from oxygen toxicity are a testament to the evolutionary pressure to use this highly reactive molecule. A rise in the inspired oxygen fraction (FIO2), an increase in the environmental pressure or a combination of both will elevate the inspired PO2 (PIO2).

High PIO2 has several physiological effects on the body. Although increased PIO2 has no direct effect on ventilation, there is a decrease in alveolar and arterial carbon dioxide (CO2) buffering tension caused by the reduction in CO2-carrying capacity of haemoglobin. Other physiological responses to high oxygen include vagally mediated bradycardia and vasoconstriction of intracranial and peripheral vessels. There is a small rate-dependent fall in cardiac output.

High PIO2 is known to be associated with retinopathy of prematurity in pre-term infants and lung damage, convulsions, red blood cell suppression, visual defects, myopia and cataracts in adults. In vitro, toxic effects on cells of many other organs have also been demonstrated.

In diving, toxic effects on the central nervous system (CNS) and lungs are of prime importance, and only these are discussed in detail. The CNS threshold is above 1.5 ATA, and the pulmonary threshold is 0.55 ATA. At 1.6 ATA oxygen, pulmonary toxicity is the limiting factor regarding duration of exposure, whereas at higher pressures neurological toxicity is of prime concern.

In both the CNS and lungs there is a latent period before the onset of detectable toxicity. This delay enables high PO2 to be used for increasingly short periods as the PIO2 rises (Figure 17.1).

Predicted human pulmonary and central nervous system (CNS) tolerance to high-pressure oxygen
Figure 17.1 Predicted human pulmonary and central nervous system (CNS) tolerance to high-pressure oxygen.

In diving and diving medicine, oxygen toxicity is possible in the following situations:

  1. Closed-circuit and semi-closed-circuit rebreathing equipment.
  2. Use of high FIO2 mixtures.
  3. Saturation diving.
  4. Situations in which oxygen is used to shorten decompression times.
  5. Oxygen therapy for diving disorders (pulmonary only, and with prolonged use).
  6. Therapeutic recompression.
  7. Respiratory failure (e.g. near drowning).