Recommendations for rescue of a submerged unresponsive compressed-gas diver
Department of Anesthesiology, University of Auckland, New Zealand.Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc (Impact Factor: 0.77). 01/2013; 39(6):1099-108.
The Diving Committee of the Undersea and Hyperbaric Medical Society has reviewed available evidence in relation to the medical aspects of rescuing a submerged unresponsive compressed-gas diver. The rescue process has been subdivided into three phases, and relevant questions have been addressed as follows. Phase 1, preparation for ascent: If the regulator is out of the mouth, should it be replaced? If the diver is in the tonic or clonic phase of a seizure, should the ascent be delayed until the clonic phase has subsided? Are there any special considerations for rescuing rebreather divers? Phase 2, retrieval to the surface: What is a "safe" ascent rate? If the rescuer has a decompression obligation, should they take the victim to the surface? If the regulator is in the mouth and the victim is breathing, does this change the ascent procedures? If the regulator is in the mouth, the victim is breathing, and the victim has a decompression obligation, does this change the ascent procedures? Is it necessary to hold the victim's head in a particular position? Is it necessary to press on the victim's chest to ensure exhalation? Are there any special considerations for rescuing rebreather divers? Phase 3, procedure at the surface: Is it possible to make an assessment of breathing in the water? Can effective rescue breaths be delivered in the water? What is the likelihood of persistent circulation after respiratory arrest? Does the recent advocacy for "compression-only resuscitation" suggest that rescue breaths should not be administered to a non-breathing diver? What rules should guide the relative priority of in-water rescue breaths over accessing surface support where definitive CPR can be started? A "best practice" decision tree for submerged diver rescue has been proposed.
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ABSTRACT: Oxygen is by its chemical nature a toxic molecule and organisms that survive in its presence have evolved potent antioxidant defenses. Through basic and clinical research we have come to understand many of the mechanisms of oxygen (O2) toxicity as well as measures that mitigate its risks. When the partial pressure of oxygen (PO2) is increased in the cell, the formation of reactive oxygen species (ROS) is enhanced at multiple locations, such as in the mitochondria. ROS attack biological macromolecules, which disrupts homeostasis and causes tissue and organ system dysfunction that will ultimately be lethal. An oxygen partial pressure (PO2) of 0.21 to 1.0 atm absolute (ATA) is in the normobaric range while a PO2 above 1.0 ATA is termed hyperbaric hyperoxia. As the PO2 in the normobaric range increases, specific physiological disturbances, such as disordered pulmonary gas exchange and retinopathy of prematurity appear, while others occur exclusively at hyperbaric pressures such as peripheral visual loss, seizures, and neurogenic pulmonary injury. Ultimately, the utility of O2 is limited by this toxicity and its therapeutic applications in medicine, aeronautics, and diving must be counterbalanced by the risk of harm.
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