Virtual Naval Hospital: United States Naval Flight Surgeon Manual: Third Edition 1991: Chapter 1: Oxygen Toxicity

United States Naval Flight Surgeon's Manual: Third Edition 1991: Chapter 1: Physiology of Flight

Oxygen Toxicity

Naval Aerospace Medical Institute
Peer Review Status: Internally Peer Reviewed

The need for oxygen to sustain life at any altitude is indisputable. However, excessive amounts of oxygen or excessively high oxygen partial pressures can be detrimental or even fatal. The amounts of oxygen and oxygen partial pressures breathed by aviation personnel are usually not great enough to cause significant harm to the body. However, the problem of oxygen toxicity is more significant in underwater and hyperbaric operations where the partial pressures of the breathing gases are excessive.

The harmful effects of elevated partial pressures of oxygen are directly related to the level of elevation of partial pressures and the duration of exposure. There are several types of oxygen toxic effects known to occur in man.

Pulmonary Oxygen Toxicity
There is a risk of pulmonary oxygen toxicity whenever there is prolonged exposure (in excess of 12 to 15 hours) to inspired partial pressures of oxygen of 0.5 ATA or more. It is sometimes called the Lorraine Smith Effect after the researcher who first described it. Pulmonary oxygen toxicity begins with a progressive hydration or fluid accumulation of the lungs under hyperoxic conditions. The pulmonary edema leads to greater mechanical difficulties in ventilation together with impaired gas transfer. The individual finds it harder to breath; he may feel a deep substernal pain and if not returned to a subtoxic breathing mix he may become hypoxic as the alveolar walls swell and the edema further impairs oxygen diffusion. Thus a paradoxical situation is reached in which elevation of the oxygen level in the gas ventilating the lungs actually decreases blood oxygenation in the pulmonary capillaries.

Pulmonary oxygen toxicity can progress to a point where hypoxia can result in death unless the alveolar oxygen pressure is elevated to increase the oxygen diffusion gradient to elevate the arterial oxygen pressure. This does provide temporary relief but also causes further edema, a further reduction in the oxygen diffusion capacity and an eventual return to hypoxia until a still higher inspired oxygen pressure is required and so the subject enters a vicious cycle which can only terminate in death. The only known treatment for pulmonary oxygen poisoning is reduction of the inspired oxygen partial pressure to less than 0.5 ATA. Endotracheal intubation and positive end-expiratory pressure ventilation (PEEP) may be necessary in severe cases to allow adequate oxygenation with oxygen partial pressure of less than 0.5 ATA.

Central Nervous System Oxygen Toxicity
The onset of neurological oxygen toxicity can be quite sudden and dramatic. It is manifested by generalized convulsions, indistinguishable from the convulsions of grand mal epileptic seizure. Central nervous system oxygen toxicity usually occurs when an individual is exposed to inspired oxygen partial pressures above 1.5 to 2.0 ATA. Other manifestations of CNS oxygen toxicity include dizziness, nausea, tunnel vision, blindness, unusual fatigue, anxiety, confusion, and a lack of coordination in movement.

Muscular twitching - particularly lip twitching - can precede a convulsion but no reliance can be placed on this as an early warning. If one displays any signs of CNS oxygen toxicity, the first and most important step in treatment is to quickly switch the victim to air breathing. Chamber depth should not be altered until the victim's signs or symptoms have cleared.

Acceleration Atelectasis
Another oxygen effect which may be loosely grouped under the general heading of oxygen toxicity is atelectasis while breathing 100 percent oxygen during +G_z acceleration, although the term "oxygen toxicity" in this context is a misnomer. Acceleration atelectasis is included in this section only because it occurs when an aviator is breathing 100 percent oxygen. The primary factor responsible for the atelectasis is probably the complete cessation of basilar alveolar ventilation under acceleration. There is also markedly increased blood flow to the basilar alveoli as opposed to the apical ones, along with a reduction in basilar alveolar volumes as the weight of the lung under acceleration compresses the bases against the diaphragm. With these factors acting in concert, and when the alveoli in question contain only oxygen, water vapor, and carbon dioxide, oxygen absorption (the main cause of acceleration atelectasis) leads to alveolar collapse, and atelectasis can occur very rapidly.

If nitrogen is present in the inspired gas, the gas absorption and consequent alveolar collapse are greatly slowed. The time required for complete absorption of gas contained in the lower quarter of the unventilated lung, with normal blood flow distribution, is increased from five minutes on 100 percent oxygen to about 25 minutes on 50 percent oxygen, 50 percent nitrogen. In addition, there is evidence that nitrogen in the lung acts as a "spring" by preventing alveolar collapse when all the oxygen is absorbed.

Pulmonary atelectasis during flight may result in several performance-degrading effects, including distracting or perhaps even incapacitating cough and chest pain and arterial hypoxia due to the shunt of venous blood through the nonaerated alveoli. The Flight Surgeon should remain aware that coughing, substernal pain, and decreased altitude tolerance may indicate the development of this condition. In any event, acceleration atelectasis usually resolves itself in a few days with little or no treatment.

Oxygen Paradox
Restoration of normal alveolar oxygen tension in a hypoxic individual may be accompanied by a temporary increase in severity of symptoms, a phenomenon known as "oxygen paradox. " Like atelectasis, oxygen paradox may be loosely grouped under the heading of oxygen toxicity only because it also occurs when an aviator is breathing 100 percent oxygen. The paradox occurs when reoxygenation is brought about suddenly and in severe cases it can result in muscle spasms and unconsciousness which may last from a few seconds up to a minute. Usually this condition is transient and may pass unnoticed. Accompanying effects are decreased vision, mental confusion, dizziness and nausea. The mechanism responsible for this condition is uncertain, but is thought to be due to a combination of factors which include the effects of hypocapnia, the loss of the PO₂ dependent simulation of the aortic and carotid peripheral chemoreceptors, and hypotension.

A decrease in arterial PO₂ is a potent stimulus to the carotid and aortic chemoreceptors to cause hyperventilation. The hyperventilation response due to decreased PO₂ as a result of aortic and carotid stimulation results in hypocapnia. The ensuing hypocapnia leads to cerebral vasoconstriction and systemic vasodilation. In addition the hyperventilation results in a respiratory alkalosis shifting the oxyhemoglobin dissociation curve upward and to the left (Bohr Effect). This shift increases the capacity of the blood to onload oxygen in the lungs but restricts offloading of oxygen at the tissue level. The combined effects of vasodilation of blood vessels in the extremities, vasoconstriction of cerebral blood vessels, and the shift of the oxyhemoglobin curve to the left reduces blood flow and oxygen supply to the brain (stagnant hypoxia).

Upon restoration of oxygen, there is a reduction or cessation of breathing and a hypotension. The reduction or cessation of ventilation (apnea) results from the loss of the PO₂ dependent simulation of the carotid and aortic peripheral chemoreceptors. With the administration of 100 percent oxygen following hypoxia, arterial PO₂ increases, removing or reducing the one and only stimulus to respiration. The result is a reduction in breathing or a sudden onset of apnea. The hypotension produced by the restoration of oxygen is probably due to vasodilation, which occurs by the direct action of oxygen on the pulmonary vascular bed.

The hypocapneic effects of hypoxia and the apnea or reduction of ventilation and hypotension which follow reoxygenation, combine to further reduce cerebral blood flow. This further reduction in blood flow in all probability intensifies an already existing cerebral hypoxia for a short period of time until the cardiovascular effects have passed and carbon dioxide tension returns to normal. Once arterial carbon dioxide tension returns to normal, it will stimulate the central respiratory chemoreceptors to resume ventilation and resolve the cerebral hypoxia.

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