Hypoxia Signatures in Closed-Circuit Rebreather Divers

Daniel Popa, UCSD, Hamilton Award Recipient 2018

Malfunctions in closed circuit rebreathers (CCRs) can cause hypoxia if oxygen is not added to the breathing loop and the diver remains unaware of decreasing oxygen levels. Hypoxia, dangerously low oxygen levels, can lead to confusion, loss of consciousness underwater and drowning. Pilots in a low-pressure (hypobaric) exposure have shown a “hypoxia signature” with the same constellation of hypoxia symptoms each time they are exposed to hypobaric hypoxia. This study examines CCR divers’ ability to recognize their hypoxia signature and perform self-rescue.

Closed circuit rebreather (CCR) diving has proliferated recently but carries a significantly higher mortality risk than open-circuit scuba diving. Hypoxia is one of the leading causes of rebreather diving injuries and fatalities, particularly since symptoms come on gradually as the diver consumes oxygen in the breathing circuit.

Among aviators, acute hypobaric hypoxia can present with a variety of symptoms with substantial differences between individuals. Interestingly, each pilot’s hypobaric hypoxia symptoms with repeated exposures appears reproducible and serves as a “hypoxia signature.”

This study investigates these hypoxic signatures in an equal number of CCR and scuba divers. They are asked to identify a hypoxic trial while blinded to the gas mix they are breathing from a CCR after a non-blinded trial of hypoxia. Each subject undergoes an experimental day of four trials with the first trial non-blinded and stimulating hypoxia. We prevent the CCR from adding oxygen to the breathing loop so the subject consumes the oxygen in the loop and gradually becomes hypoxic, mimicking a real world CCR failure. After this episode of known hypoxia, each subject undergoes three additional randomized, blinded trials with one hypoxic trial and two sham trials (i.e., the CCR functions correctly and maintains room air). While breathing from a CCR, each subject pedals a cycle ergometer at low wattage to simulate swimming underwater. While the subject breathes and cycles, they perform a validated computer-based neurocognitive test, “Go/No-Go,” to track decision-making capacity, reaction time and cognitive inhibition. This test further mimics underwater distractions. In addition, each subject points to common hypoxia symptoms listed on a board as they appear in real time during each trial to record each subject’s hypoxic signature. During each trial, we monitor the subject’s pulse oximetry, breath-by-breath end tidal CO2 and O2, and inspired O2 from the CCR. If at any point the subject’s O2 saturation drops to 75%, we terminate the trial.

If at any time the subject feels that they are experiencing a dive emergency from which they would normally perform a self-rescue procedure, the subject turns a ball valve to simulate switching to a bail-out gas mixture to demonstrate the cognitive ability to perform self-rescue. Upon completion of each trial, we ask the subject if they thought the blinded trial was a sham or hypoxia and why. After completion of each of the four trials, we debrief further in order to educate the subject on which of the blinded trials was hypoxic versus sham.

Twenty of a proposed 30 subjects have undergone the study protocol. Data analysis is ongoing with preliminary data accepted as two abstracts at the Undersea and Hyperbaric Medical Society’s Annual Scientific Meeting.

This study was partially funded through the DAN/R.W. Hamilton Dive Medicine Research Grantin 2018.