[Indaemed_Freelist.Org] Re: [indaemed] Re: Syncope evaluation [wasRe: Re: NMS]
- From: SS Mishra <ssmhialt@xxxxxxxx>
- To: indaemed@xxxxxxxxxxxxx
- Date: Sun, 21 Mar 2004 13:39:22 +0530
First of all, VVS is not essentially a baroreceptor induced
phenomenon!!!!!!! Today, more and more evidence is gathering for it to be a
centrally mediated process. Secondly, typical absence seizures should give
some
indication on provocation EEGs. In any case typical absence seizures DO NOT
have a loss of postural tone. They do not occur so sporadically but are
typically recurrent, and are more generally noticed from childhood, become
more frequent during adolescence and are unlikely to occur the first time at
20-21 yrs of age.
In this case, if it is a GABA Vs Glutamate imbalance absence seizure,
lasting more than 15 seconds and with loss of postural tone, it is more
likely to be astatic atypical absence seizure (eg. Lennox-Gestaut type).
Just not possible, as this type has a typical EEG (2-5 /sec slow spike and
wave discharge), typical age of occurence is 2-10 years, and attacks are
very recurrent. Treatment is generally ineffective in controlling absence
and faint spells.
The current case has the features of a susceptibility to vasovagal syncope,
if provoking factors like lack of sleep, fatigue, anxiety, hypoxia,
hypoglycemia etc. etc. etc. are present. Contemptuously discarding this by
saying that he is not likely to get oxygen system failure in the air, he is
not likely to get decompression in the trainer ac etc. etc. is not
pertinent. What is pertinent that the stress that we noticed was hypoxia in
this case. Couldn't it have led to hyperventilation which ultimately
provoked the episode. Cannot hyperventilation occur due to reasons other
than hypoxia? How about provocation like thermal stress, anxiety, abdominal
discomfort, lack of sleep occuring again. True, that we do not do these
things to rule out VVS susceptibility, or there would be no end, but this
was the best possible guess, and a decision well taken by IAM. Even if it
was more on administrative considerations, still it was justified. Now,
even if it were TA, will he be allowed to fly????
Sudhanshu
----- Original Message -----
From: "USM Bish" <bish@xxxxxxxxxxx>
To: <indaemed@xxxxxxxxxxxxx>
Sent: Sunday, March 21, 2004 10:58 AM
Subject: [Indaemed_Freelist.Org] Re: [indaemed] Re: Syncope evaluation [was
Re: Re: NMS]
> On Sat, Mar 20, 2004 at 10:44:04PM +0530, Lt Col KK Tripathi wrote:
> >
> > This observation was made during his second exposure to hypoxia
> > at the 'OTHER CENTRE' referred to by Wg Cdr Sharma .
> >
> > I was in attendance. Pulse oximetry was available throughout
> > (except when he fell and probe got detached).
>
> Hmmm ... this was during the Hypoxia run, and assumingly after
> disconnection of oxygen at 30,000 ft.
>
> >
> > Details are available in my posting dt 19 Mar 2004.
> > Additionally, he had cold clammy extremities (nose included).
>
> Yeah, now I get it. This is from your post of 18 Mar :
>
> > --------------------<snip old mail>----------------------------
> > Even in the hypobaric chamber, the candidate did suffer from a
> > vaso-vagal syncope. It is reported (in almost all the text
> > books of Aviation Medicine) that about 20% of the cases of
> > syncope in hypoxia are of vaso-vagal in nature (and not due to
> > the effects of de-saturation of haemoglobin, per se). There was
> > a precipitous fall in pulse rate which was remained as low as
> > 37 per minute for about 15-20 sec even after restoration of
> > 100% oxygen. The event occurred without any premonition at a
> > haemoglobin saturation of about 65%. There was no apparent
> > hyperventilation.
> > --------------------</snip old mail>---------------------------
>
> This still may not indicate VVS. The initial response evoked by
> hypoxia stress (during the compensatory and distrurbance
> phases) are tachycardia, tachypnoea etc etc. But once critical
> phase is crossed, it would be exactly as described, with fall
> in pulse, BP, respn, sweating, cold skin etc. This is a common
> end point for virtually all syncopes. Acute Hypoxia induced LOC
> by itself present like this when going into syncope.
>
> The same would be true for absence seizures with any stimulus
> causing acute GABA depletion leading to symptoms.
>
> VVS is a baro-receptor mediated/ failure response, and usually
> caused by things like phychological factors (sight of blood or
> some repulsive thing), sudden changes in posture (specially
> after periods of recumbancy) etc. Normally baro-receptor based
> phenomena are demonstrateable/ repeatable/ reproduceable under
> HUT (albeit, may not be 100% of the times).
>
> Remember, desaturation of Hb% is necessary for Hypoxia induced
> LOC but not GABA depletion faints. Secondly, persistance of
> bradycardia after restoration of Oxygen is the expected thing,
> and NOT an exception. It may even have dropped further ! Please
> have a look at "oxygen paradox" under the heading "Recovery
> from Hypoxia" in the golden book authored by Gilles (which seem
> to be fallen out of favour these days) ! Too old ?
>
> You need to find explanation for observations that have been
> made. More credence is to be given to spontaneous episodes,
> rather than stress induced ones.
>
> >
> > There was no confusion, lethargy or fatigue.
> > I did not notice any myoclonia.
> >
>
> These are not likely to persist in Hypoxia induced GABA
> depletion which would be restored after resumption of Oxygen.
> The spontaneous faints of absence seizures is because of
> absolute GABA depletion (usually preceded by high psychological
> burn out), unlike transient oxidative failures produced by
> Hypoxia, where the quanta of available mediators are not
> effectively reduced, only made transiently ineffective.
>
> The facts stated above, indicate a condition which has caused
> syncope under hypoxia state, even with 65% or above Hb
> saturation. To me, absence seizure seems to be the most likely
> cause. This does NOT look like any baro-receptor mediated
> phenomenon to me ... YMMV.
>
> Just my POV
>
> Bish
>
>
>
>
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