[indaemed] Re: Re NMS
- From: anujc@xxxxxxxx
- To: indaemed@xxxxxxxxxxxxx
- Date: Mon, 15 Mar 2004 18:40:51 +0500
With ref to Bish sir's mail,
I agree 110% that the diagnosis of VVS MUST NOT be done based on LOC in a
altitude chamber. Let me clarify that this was not the case. If I remember
correctly, the diagnosis of VVS was made independent of the LOC episode. I may
be corrected on this since I was not privy to the initial work up of this
cadet. My aim of posting the VVS and HUT part was since somebody mentioned that
HUT was not done for this subject during the last review and suggested that it
should have been done. Since I was the one who turned down the HUT request in
this case, I thought I must share my POV. I may also add that in a large
percentage of cases labelled as VVS, none of the ANS studies show any
abnormality. If one goes thrrough available literature on the subject, the
etiopathology of VVS may vary from ANS dysfunction to cerebral blood flow
autoregulation problems to peculiar neural activity in the brain. There are
even reports to suggest that VVS may be a manifestation of abnormal electrical
act
ivity in the brain, on the lines of temporal lobe epilepsy!
It would be worth remembering that if this cadet did have a VVS as an
independent occurence, he could be prone for other reflex neural phenomenon as
well. (this is documented in literature. I think even Gillies mentions this
somewhere.) In such a setting his LOC under hypoxia is not surprising at all!
The second factor that should be kept in mind is his high degree of aerobic
conditioning. He had a resting HR of about 50 beats per min. I have seen
syncope cases in NDA cadets while at AFMC where simply going easy on aerobic
conditioning cuts down the recurrence of syncope. The point however in this
case is that the cadet had a solitary episode of syncope and not recurrent
ones. Whether this was in any way subsequently related to his LOC in the
chamber can be argued.
cheers
Anuj
----- Original Message -----
From: USM Bish <bish@xxxxxxxxxxx>
Date: Sunday, March 14, 2004 8:33 pm
Subject: [indaemed] Re: Re NMS
> On Sun, Mar 14, 2004 at 06:19:58PM +0500, anujc@xxxxxxxx wrote:
> >
> > I have been reading with interest the discussion on the
> > evaluation of a case of NMS and the correct disposal. This is
> > not the first time that such a discussion has taken place. For
> > my part as a physiologist I would like to share my
> > understanding of the head up tilt test and its relevance in
> > such cases. This is important because an opinion was voiced
> > suggesting that the test should have been repeated for the
> > cadet in question and so on. The following points of view are
> > offered. The head up tilt test is not the gold standard for
> > diagnosis of vaso vagal syncope In a large number of cases the
> > test may actually be normal and vice versa. The diagnostic
> > yield of this test is about 65- 70% ...
> >
> [rest snipped]
> >
>
> The point that you make is very valid. However, the point here
> is a bit different. It must be clearly understood that Acute
> Hypoxia induced LOC is NOT VVS. It is a normal response of the
> body on exposure to Critical levels of Hypoxia. It is a
> physiological response of the body to stresses well beyond
> compensatory mechanisms.
>
> The time for total loss of consciousness would vary from person
> to person and the gap between TUC (Time of Useful
> Consciousness) to LOC is not well defined/ measured. TUC is the
> parameter which has been recorded in various studies, and
> normally under Hypoxia training flights this is the stage when
> re-oxygenation is commenced. If my memory serves me right, the
> 50%ile value for TUC at 30,000 ft is about 125 sec or so with a
> SD of about 40 or so. In which case, in about 5% of NORMAL
> individuals TUC would be expected to be less than 10 sec. In
> such susceptible individuals, it is my guess that the gap to
> LOC is less, and therefore, LOC may be expected within 10 - 15
> sec. The duration at 30,000 ft was missing in the Original Post
> (OP), so things are left to conjecture.
>
> The diagnosis of VVS would normally be based on:
>
> a) CVS evidences like severe bradycardia, SSS, ECG abnoramali-
> ties, arrythmias, episodes of asystolic spells or anything
> affecting cardiac output (even transiently/ momentarily).
>
> b) Neurological abnormalities like asynchronous epileptogenic
> discharges need exclusion. I am assuming here that things
> like Hysterical Reactions are ruled out by circumstantial
> evidence.
>
> c) ANS studies (of which HUT is one) or even things like cold-
> pressor, vagal stimulation etc would give some indication.
> A positive test would definitely indicate ANS insufficiency.
> Even if a negative test is inconclusive.
>
> d) Concurrent minor ailments like viral episodes, or major pre-
> disposing factors like anaemia at the time of the LOC must
> also be excluded. What was his ventilation state like just
> before the LOC ?
>
> If all these have been done (maybe even repeated), and has been
> seen to be normal, the diagnosis of VVS is NOT tenable.
>
> Shortented TUC or shortened LOC latency under acute hypoxia
> episoded is NOT sufficient to label a case as VVS. Low Hypoxia
> tolerance, yes. However, that would also need all physiological
> parameter records within compensatory phase of hypoxia to just-
> ify such a label, not at critical+ levels of 30,000 !.
>
> The diagnosis of VVS should be established INDEPENDENT of these
> hypoxic LOC episodes ... Shortened TUC or LOC on acute hypoxic
> exposures beyond critical phase is NOT a ground for rejection
> from flying duties.
>
> The details furnished, based on which we are progressing with
> our discussions perhaps lacks full details. It would be nice if
> full details can be furnished by anybody in knowledge of the
> case.
>
> Frank as ever ...
>
> Bish
>
>
>
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