oxygen..time to change the subject

  1. While researching information for my CV careplan I came across a few articles that recommended the lowest o2 flows possible for any patients on amiodarone P.O. or IV. This recommendation was based on the theory that acute pulmonary fibrosis (rare complication of amiodarone therapy as opposed to slower onset) is the result of free oxygen radical interaction with amiodarone metabolites.
    There have also been indications that NRP guidlines will soon change to recommend that newborns be rescusitated without extra oxygen as they are more likely to suffer acute oxygen toxicity.
    These things along with all the other information that seems to indicate oxygen therapy as a culprit in post-op morbidity has resulted in my placing most of my patients on the lowest o2 they can tolerate. I have worked with several CRNA's who would prefer I not do that (so when in rome..).

    What do you guys think? Is oxygen really a problem or just the latest target?
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  2. 6 Comments

  3. by   canoehead
    I think that the thought on newborns and oxygen is that premies are unable to deal with the free radicals on a long term basis, but full term babies are well equipped and we should provide lots of oxygen, especially during the initial resuscitation. In fact immediately after birth all infants get 100% oxygen, and are later weaned down to their tolerance.
  4. by   kids
    CNN story from 10/25/02 on a data being gathered on the relationship between ROP and O2.

    http://www.cnn.com/2002/HEALTH/paren....ap/index.html

    The majority of the premies I do home visits on that are getting home O2 are getting it at less than 50 cc per minute with target sats of 85-92%. The few (trach ed/vented) that are on my PDN case load have similar parameters (makes me wonder what they want us to do when they are sating at 100% on room air)
  5. by   kmchugh
    Well, O2.....

    I don't know that anyone has the real answers to your questions. I think part of the answer lies in how someone has always done it, and what they are comfortable with, and that's why some of the CRNA's you meet are resistant to lower O2 concentration. Here's my thoughts.

    We know pure O2, over prolonged periods of time, can cause pulmonary damage, probably though free radicals. By prolonged, that generally means (as I recall) more than 20 hours breathing pure O2. So, for the course of most surgeries, running a patient on pure O2 won't be harmful, because they are going to be there for less time than it would take for O2 to start causing damage.

    Generally, I adjust my gas flows based on a number of different factors. If the surgery is going to be very short, I don't generally mess with adjusting flows and leave the patient on 100% O2, for the reasons mentioned above. Also, if the patient has a cardiac history, I'll generally leave them on 100% O2, just to get the maximum O2 to the myocardium.

    For longer surgeries, and healthier patients, I will generally adjust my gas flows so I am delivering about 50% O2 to the patient. Other than that, I will adjust as the SaO2 directs. When I went to school, there was a real "anti-nitrous" sentiment, because there was some tenuous link between N2O and postoperative nausea. I almost never used N2O. Now, I have worked with N2O a bit more, and am more comfortable using it. Its great for use when you want something of a faster wake up (nothing like waiting for a patient asleep on forane to wake up after a 4 hour surgery). It's also great for increasing the depth of anesthesia in a rapidly reversible fashion. Again, I adjust to about 50% O2 flow. I have noticed no greater incidence of postoperative nausea in the patients I have used N2O in over other patients. I think the studies that suggested a link between N2O and nausea did not adequately account for other factors.

    Kevin McHugh, CRNA
  6. by   prmenrs
    in my nicu (FOR PREMIES) was to keep sats no higher than 92% on kids getting supplemental O2. We had a study in progress when I retired.

    NRP is by definition an emergency proceedure; I would be more worried about brain cells than pulmonary fibrosis.

    Premies on long term O2 are often given hefty doses of vit E to protect their eyes. (50IU 2x/d)

    The amiodarone/pulmonary fibrosis connection I am not at all familiar with.
  7. by   Qwiigley
    The reason the CRNA/MDA wants you to recover their patients with 100% O2 is because they know what they gave them for the procedure. They know if they gave 50-70% N2O, then the patient will have a nitrous effect of leaving the body faster than the Co2 and the patient's sats will drop. Yes, this effect is transient, but if the MDA/CRNA has asked the recovery team to keep the O2 at such a rate, you should ask them before deciding on your own to change it. Also, all cerebral/neurosurgery should have extra O2 24 hours after surgery preventatively. I would link the empirical data to prove this, but I really should be studying for a pharm exam.
    Lastly; O2 is a drug, as with any drug, there is different dosing for premies, newborn full terms and children. Different doses for normal adults and for COPDers. Really there are different reasons to go long and hard on O2 and reasons to go very minimal.
  8. by   smiling_ru
    This is one source re: amiodarone and O2:
    http://www.pharmacology2000.com/Card...arr/class3.htm
    excerpt:
    Anesthetic Implications: pulmonary
    Suggested restriction of inspired oxygen concentration in patients receiving amiodarone(Cordarone) and undergoing general anesthesia to as low a level as while retaining adequate systemic oxygenation -
    Postoperative pulmonary edema has been reported in patients treated with amiodaron(Cordarone) chronically--resembles acute onset form of amiodarone toxicity. -
    In patients with preexisting amiodarone-cause pulmonary damage are at increased risk for adult respiratory distress syndrome following surgery requiring cardiopulmonary bypass.

    PALS information:
    http://www.acutecare.com/palsnew.htm...concentrations

    Although 100% oxygen has been used traditionally for rapid reversal of hypoxia, there is biochemical evidence and preliminary clinical evidence to argue for resuscitation with lower oxygen concentrations. Current clinical data, however, is insufficient to justify adopting this practice


    Anyway these are some of the things I have been reading.

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