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Sun Oct 7 13:47:47 BST 2007

Hi Mike
well, l guess that lactic acidosis due to hypoxia cannot be fully reversed
by CPR because there's only so much the O2 that can be delivered during CPR
to those tissues, but certainly can reduce level of acidosis. normal liver
can manage all the piruvate that is produced during hypoxia.
a for apoptosis issue l think that mitochondria play central part due to
their caspase-induced increased permeability with all its consequences(ATP
depletion, NAD/NADH depletion, increas in Ca...)
and for extending CPR before defib,if you witness arrest defib
instantly,prior to bls' but if you didn't witness the arrest then you should
due 5 cycles prior to defib. this wouldn't be more riskier because this way
you get them a bit more O2 and increase chances of successful defib
ante

2007/10/5, Mike Smertka <medic0947969 at yahoo.com>:
>
>
> Hello everyone,
>
>   I posed a question about the topic of delayed resuscitation and
> oxygenation on the EMS-L list and hoped maybe somebody here could answer my
> questions.
>
>   1. Does effective CPR adequetly perfuse the body enough to stop/reverse
> anaerobic metabolism in the Brain/kidnetys/heart/liver?
>
>   2. What causes an apoptotic rxn when o2 is reindroduced? My only guess
> is a capsase chain in the mitochondria. Possibly from the others in the cell
> as well. By I lean towards mitochondria.
>
>   3. Would continued/exteded CPR prior to defib then be more harmful?
>
>   I accept that immediate cpr, would perfuse enough heart and brain to
> stop acidosis there, but what about the liver especially?
>
>   I ask because of a study that was recently announced about possibly
> delaying defib longer for more cpr. I am very skeptical about that. I know
> that refractory v-fib is likely from the AHA study if during prolonged
> downtime the heart is defibed without reoxgenation. But how does all this
> play out?
>
>
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