Hyperbaric files: oxygen toxicity.

Too much of good thing can be bad for you--including oxygen. Ask an anaerobe bacteria. I first heard of problems associated with oxygen when I was learning about COPD patients and oxygen-induced hypercarbia. High blood levels of oxygen in chronically hypercapnic patients can suppress the action of carotid and aortic bodies and suppress sensitivity to CO2 and eliminating hypoxia left these patients without an adequate stimulus to breathe. Later in my experience in the special care nursery I learned about premature babies and retrolental fibroplasia, now called (ROP) retinopathy of prematurity. ROP in these babies was demonstrated as complete obliteration and retinal detachment (blindness). This occurred due to the vasoconstriction effect of high oxygen levels and free radical production combined with a developing retinal tissue among other factors. Free radical production causes oxidant damage to the cell membranes. Shortly after that I learned of a problem called absorption atelectasis due to nitrogen washout associated with the administration of high levels oxygen. While trying to maintain life-sustaining pO2 values in patients with ARDS we see pulmonary changes occur on the cellular level including alteration of ciliary and leukocyte function. It was becoming clear that a high concentration of oxygen for too long could result in many disastrous effects. So, you can imagine my concern when I learned that I would be treating patients in a hyperbaric chamber who would have a pO2 of 2059 mmHg at 2.8 atmospheres absolute (ATA). In addition, treatment protocols require patients to stay at those pressures from 90 minutes to 5 or more hours depending upon indication. It was time to look into this toxicity issue closer.

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There are two ways oxygen toxicity occurs as a result from over exposure; pulmonary oxygen toxicity and cerebral oxygen toxicity. Pulmonary oxygen toxicity, also referred to as the Lorrain-Smith effect, is seen with 40% or higher oxygen concentrations or pressures greater than 0.5 ATA in a hyperbaric chamber for extended periods of time. Onset of symptoms for pulmonary oxygen toxicity usually begins with burning upon inspiration and progressing to pleural chest pain, substernal burning, cough and shortness of breath. Decreased vital capacity and tidal volume is seen along with atelectasis, which in time can progress, to ARDS. These effects can return quickly (within 12 hours) to normal once the oxygen levels are returned to normal, but there can be a cumulative effect when a large number of hyperbaric treatments are performed. One such effect is Myopia (nearsightedness), seen more often in diabetic and elderly patients, is typically a temporary occurrence and rarely permanent. We must inform patients that their vision will probably return to normal within about 6 weeks, so don't buy new glasses. Cerebral oxygen toxicity, also referred to as the Paul Bert effect, can occur anytime 100% oxygen is breathed at pressures over 2 ATA (atmospheres absolute) or at a water depth over 33 feet. Many of these symptoms can be identified and memorized by using an anacronym I borrowed from the dive industry; "CON-VENTID". It represents; CONvulsions, Visional changes, Ears (ringing or volume change), Nausea, Twitching, Irritability, and Dizziness. Other signs may include; facial pallor, sweating, bradycardia, palpitations, depression, apprehension, hiccups, weakness, amnesia, headache, vertigo and eventually the least desirable of these effects, grand mal seizure. Additional factors that increase the risk of seizure during hyperbaric oxygen therapy include an increase in carbon dioxide inhalation, (watch for hypoventilation) hyperthermia, insulin, adrenocortical hormones, and amphetamines. A reduction in the risk of seizures can be achieved with adrenergic blocking agents, antioxidants, vitamin E, and hypothermia. The good news is that a seizure in a hyperbaric chamber is a rare event, (1 in 10,000 cases) and there are no residual effects to these seizures, ruling out physical injury. All these effects can manifest sooner with increased exposure to oxygen but can be remedied by removal of the patient from the high oxygen environment. We can accomplish this by giving the patient what is called an "air-break". An air break is a procedure the patient is taught to perform during their treatment whereby they breathe on a positive pressure mask within the chamber that supplies 21% oxygen. This is typically done for 10 minutes and may be repeated several times during the treatment. An air-break will minimize the possibility of experiencing the unwanted effects of toxicity. Susceptibility to oxygen toxicity varies from person to person and can occur from anytime from the 1st to the 51st treatment. Other steps that can be taken to minimize the risk of oxygen toxicity are reduction in treatment pressures and/or treatment times and also the use of Diazepam.

My first experience witnessing the signs of oxygen toxicity was with a patient receiving hyperbaric oxygen therapy a few years ago. We always monitor patients visually throughout their treatment but we also have the ability to listen to patients via a microphone/speaker system in the door. This particular patient said to me, "something's wrong, I don't feel right". When a patient makes this statement always take notice. I asked what specifically was he experiencing? He then said, "The sound of the TV is getting louder and softer, louder and softer". As soon as he finished that statement he started to have twitching in his shoulders. I asked him to breathe on the air-break mask and ended the treatment. As I lowered the pressure for a quick removal (within a couple minutes) his symptoms disappeared and he never reached the point of a grand mal seizure. A year later we had a patient who did in fact seize in the chamber and the therapist managed it correctly. Despite ones natural tendency to get the patient out immediately, this would be a mistake. The appropriate initial response is call the physician and only start to reduce pressure when the tonic phase (seizure) ends and breathing resumes. As a scuba diver can tell you, the number one rule in diving is never stop breathing. The reason is Boyle's Law; decrease pressure and you increase volume. In a closed-off lung you have a recipe for barotrauma, pneumothorax and air embolism as you ascend (lower pressure) and do not exhale. Another application of Boyle's Law in the hyperbaric chamber is found when an intubated patient is treated. As the patient is pressurized, air in an endotracheal tube cuff gets smaller resulting in a major leak. Actually the diameter of the cuff will be one half its original size if pressure is doubled, and one third its size at 3 ATA. This problem is corrected quite simply by replacing air in the cuff with water in order to maintain an airtight seal (water balloon). Another example is when a patient brings a water bottle into the chamber and does not leave the vent open during ascent, it can be a hydrating experience.

Oxygen toxicity can also be seen outside the healthcare environment. "Nitrox" scuba diving is diving with a compressed gas mixture that contains more than 21% oxygen. When I took this Nitrox course I was trained to use an oxygen analyzer and test the gas concentration in my cylinder prior to using it to dive. There are safety protocols and tables employed to determine safe levels of depth and time when using each particular oxygen concentration. These gas mixtures are used to extend the length and depth of a dive and can add a measure of safety against decompression sickness. Unfortunately, when under water if oxygen toxicity does strike, it can be fatal.

Now that we know the downside of too much oxygen, my recommendation is to stay away from those oxygen bars or you could get caught DWO (driving while oxygenated).

by Kenneth Capek RRT, CHT, MPA