Central retinal artery occlusion (CRAO) is an uncommon eye disorder, but one that typically produces severe and irreversible vision loss in the affected eye. The retina has a dual blood supply, with the retinal circulation supplying the inner layers and the choroidal circulation supplying the outer layers. In CRAO, vision loss results from cell death in the inner retinal layers despite relative sparing of the outer layers. If supplemental oxygen is provided, however, oxygen from the choroidal circulation may diffuse in adequate quantity to the inner layers of the retina to maintain retinal function and restore vision. In some patients this can be achieved with normobaric hyperoxia; in others, hyperbaric oxygen (HBO2) may be required. The challenge is to provide the supplemental oxygen early enough after the onset of vision loss to prevent irreversible damage to the retina. In experimental models of complete CRAO, the ischemic time window before permanent retinal damage occurs is just over 90 minutes; in the clinical setting where occlusion may be incomplete, return of vision may be achieved even after delays of eight to 24 hours. In patients with a clinical picture of CRAO who present within 24 hours of vision loss, supplemental oxygen should be started immediately at the highest possible fraction of inspired oxygen (FiO2). If vision is not quickly restored, emergent HBO2 should be undertaken if feasible. If the patient responds to HBO2, follow-up treatment with supplemental oxygen should be customized to maintain retinal viability until the obstructed retinal artery recanalizes, which typically occurs within the first 72 hours. This paper reviews the pertinent literature on CRAO and HBO2 and provides a treatment algorithm.