Is More Better?

Recently I was on a Trimix dive to 270 fsw. A diver, about 5 minutes after surfacing, complained of blurred vision, as well as left elbow and shoulder pain. After further confirmation of the symptoms, the diver was placed on 80% 02. After approximately 30 minutes, the blurred vision cleared up and the diver continued on 02. He had a benign motor/sensory exam at that point and was thus encouraged to seek treatment at a hyperbaric oxygen facility (HBO). He did so about 18 hours after the dive. This delay is in keeping with what DAN reports as, "being in the range of the typical delay after symptom onset with untreated DCS." While there are an abundance of experts who advocate 100% oxygen in this setting, I wonder if given the propensity for delay, less wouldn't be better? Acuity dictates the timeliness of intervention, but mild cases can be perplexing. On one hand, the application of 100% 02 is based on solid evidence. The 02 gradient set up between a bubble containing an inert gas (N2 or He) and the tissue favor collapse (implosion) of the bubble. Parenthetically, an analogous situation in the lung or alveoli (breathing sac) occurs and is called absorption alalectasis. This is a well-documented phenomenon and so it appears N2 "stents" or keeps open the alveoli under normal circumstances. As we get older, when we exhale and empty our lungs, the alveoli in the dependent or lower parts of the lungs, start to collapse. The amount of air in the lungs, when that occurs, is the closing capacity. We usually do not empty our lungs enough to be left with just the amount that equals the closing capacity. But with smoking, increases of mucus in the lungs, or obesity, we get closer to that volume and therefore collapse alveoli when we exhale. This can be attenuated by correcting the previously mentioned factors as well as deep breathing. Coupled with the increased 02 can be the complication of 02 toxicity. Using the UPTD (Unit Pulmonary Toxicity Dose) or OTU (Oxygen Toxicity Units) it becomes a factor in prolonged 02 utilization. As we have been taught, these parameters manifest themselves in several ways.

One way is subjective, i.e. substernal chest pain, shortness of breath and dry hacking cough. Objectively, one pulmonary function test (PFT) parameter that would show alveolar collapse is loss in vital capacity (which is the maximum amount of air that can be breathed in after forcefully exhaling). As divers, we know that with mold DCS and its treatment, we should not exceed a 2% drop in vital capacity (VC) and with more severe DCS, a 10% drop in VC is the upper limit. Given the likelihood of HBO treatment delay, is it wise to automatically place the diver on 100% 02 and anticipate that definitive treatment will begin soon. At least before the diver has been exposed to enough 02 to alter his vital capacity or has incurred a significant debt to the pulmonary clock. In fairness to DAN, their article does state that they feel that once divers enter the clinical "health care net," the delay will be less. Whether that holds up is yet to be seen. In essence and in practical terms, if 100% 02 is the only resuscitatable gas available, would I use it? Of course. If a variety of 02 concentrations are available, would I use less than 100%? That depends on the acuity of the situation and while this isn't a recipe for oxygen therapy, it should stimulate or encourage thoughts about oxygen, what we expect from it and what we can get from it.

Useful references: Physiology and Medicine of Diving by Bennett, et al, 1993; Hyperbaric 02 Therapy by Camporesi, et al, 1991; Diving and Sub Aquatic Medicine, 3rd Edition by Pennefather, et al, 1992; NOAA Diving Medicine Syllabus Course, XX, 1994; DAN Alert Diver, September/October Issue, 1994; Schwiz-Z-Sport Med by Wendling, et al, December 1992 (German).