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Hypoxic drive - fact or fiction?

  • 24-11-2009 12:38am
    #1
    SomeDose
    Registered Users, Registered Users 2 Posts: 252 ✭✭


    I occasionally do some work with our local survive sepsis group, and during a recent seminar an interesting point came up. When discussing initial resus therapy (high-flow O2 being one of the first interventions), one of the nurses questioned the management of COPD-type patients and the risk of causing respiratory depression if high [O2] is given to such patients. The speaker countered this by pointing out that (a) minimising any tissue/organ hypoxia is more important in these situations and besides, resp depression can be managed if necessary, and (b) hypoxic drive doesn't actually exist anyway.

    Now, I've always bought into the "be careful with O2 therapy in COPD due to hypoxic drive" theory, and my (rudimentary) understanding of respiratory physiology supports this i.e. as they chronically retain CO2, peripheral O2 chemoreceptors become the dominant regulators of resp rate. I'm also fairly certain hypoxic drive could be easily demonstrated under experimental conditions. So I was tempted to call shenanigans on this guy's assertion...but he's an A+E consultant and also a chest physician, so I have to assume he's got damn good reasons and experience on which to base his opinion.

    Interested to hear people's opinions, theories and experiences on this...


Comments

  • #2
    wheresthebeef
    Registered Users, Registered Users 2 Posts: 887 ✭✭✭wheresthebeef


    To be honest, I've always operated on the principal of prioritising ABC. So i would always use high flow oxygen 15lpm via NRB mask or BVM in the event of a cardiac arrest, pending the decision of the Doctor present. I've experienced actively titrating oxygen against O2 Sats and Co2 via Tosca monitoring in patients with COPD, but never during an arrest situation. I think its a call for the Doctor present to make. And until that call is made, or until the Doc arrives, I'd provide care as per the standard, which is high flow supplementary oxygen. If needs be, you can always supplement the rate by mechanical means. And a bit of respiratory acidosis can be corrected, dead brain or myocardium can not. Thats my two cents anyway.


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