For the following partial pressures of oxygen the limits are: 45 minutes at 1.6 bar (160 kPa), 120 minutes at 1.5 bar (150 kPa), 150 minutes at 1.4 bar (140 kPa), 180 minutes at 1.3 bar (130 kPa) and 210 minutes at 1.2 bar (120 kPa), but it is impossible to predict with any reliability whether or when toxicity symptoms will occur. Many nitrox-capable dive computers calculate an oxygen loading and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the partial pressure of oxygen in the breathing gas or by reducing the time spent breathing gas of greater oxygen partial pressure. As the partial pressure of oxygen increases with the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas, or by shortening the duration of exposure to oxygen-rich gases. This function is provided by some technical diving decompression computers and rebreather control and monitoring hardware.Diving below 56 m (184 ft) on air would expose a diver to increasing danger of oxygen toxicity as the partial pressure of oxygen exceeds 1.4 bar (140 kPa), so a gas mixture must be used which contains less than 21% oxygen (a hypoxic mixture). Increasing the proportion of nitrogen is not viable, since it would produce a strongly narcotic mixture.
Using a slit lamp, a posterior embryotoxon characterized by a prominent anteriorly displaced Schwalbes ring near the temporal corneal limbus can be revealed. The unexpected finding of a posterior embryotoxon as a single whitish irregular arcuate ridge, on routine examination, is not necessarily a diagnosis of ARS, as this occurs in a percentage estimated in the literature from 8% to 15% of the normal population. In the case of gonioscopy, we can observe that the extension of the posterior embryotoxon can be greater and be present in the 360○, with a variable thickness of the annulus and unusually detached and hanging within the anterior chamber. Regarding the iris, we can observe peripheral extensions to Schwalbes line, which can be thin or thick and extend over the trabecular meshwork, obscuring the scleral spur and even pulling the iris and producing corectopia in iris tissue that can range from atrophy mild stromal to the presence of uveal ectropion, pseudopolycoria or even absence of iris. These chamber sinus anomalies predispose half of the cases to open-angle glaucoma, which can manifest throughout life and therefore require regular ophthalmological check-ups. Other related anomalies are strabismus due to alteration in the insertions of the extraocular muscles or secondary to amblyopia, and with a predisposition to exotropia and retinal detachment.Systemic manifestations:
In the case of pathologies that affect the extraocular organs, greater attention must be paid to anomalies in the cardiovascular system, since they represent the most worrying associations due to their repercussions at the systemic level.