[HSF] Inotropes,
ventricular fibrillation and myocardial protection
rwmfglycar at aol.com
rwmfglycar at aol.com
Fri Aug 3 03:19:50 EDT 2007
The suggestion that an episode of fibrillation during the recovery from
a period of aortic clamping with the addition of one of many methods
of trying to prevent myocardial damage from this otherwise fatal
maneuver may indicate myocardial damage has upset many HSF surgeons.
Can we agree that an episode of ventricular fibrillation in you or me,
walking down the street, is abnormal and indicates something wrong with
the heart? If an alert paramedic strolling by with his defibrillator
shocks our heart and it starts up, would we say " see, nothing happened
"? Could we say " since I have recovered there must have been nothing
wrong when it fibrillated"? It is obvious that the state of the heart
was not normal when it fibrillated. It is also quite possible that the
abnormal state was fleeting and because of our ability to reverse it
not permanent. But the mere fact that it can occur and not result in an
operative mortality or even permanent change in ventricular function
does not mean that it should be ignored.
If it occurs always with surgeon A's method of myocardial protection
and never with surgeon B's method , surgeon A must ask himself the
question am I routinely producing an abnormal state that makes my
patients fibrillate? Could this be harmful? Could this produce
permanent damage? If he is a scientist with a good mind and lots of
money he may even go so far as to ask "why?".
Both surgeons A and B must ask themselves, one year after surgery,
taking into account the many variables that affect ventricular
function, two questions:
If my patient's ventricular function was normal preop is it normal now?
If it was abnormal preop and I did something that should have improved
it, is it better now than it was?
I was blessed today to receive an Email here in the foothills of the
Beartooth Mountains in Montana. It was from a family to tell me that
their 86 year old mother on whom I had done triple bypass in 1975 at
the age of 54 had finally died. They thanked me for the 32 years of
excellent cardiac health and clear mind that she had enjoyed until the
end.
I have asked for a copy of her cath and operative reports. But there is
absolutely nothing that I could say, one way or the other, about any
methods I used that day, except that at least once the goal of "Primum
non nocere" was achieved.
-----Original Message-----
From: Ani Anyanwu <anianyanwu at hotmail.com>
To: openheart-l at lists.hsforum.com
Sent: Wed, 1 Aug 2007 9:42 am
Subject: RE: [HSF] Inotropes, ventricular fibrillation and myocardial
protection
Prasanna
What you do now is no less voodoo that what you graduated from; indeed
your
current cardioplegia recipe is very much a 'homemade cocktail'. We have
to be
careful in ascribing benefits to things we do without being able to
demonstrate
such benefits scientifically.Many never add drugs like adenosine and
esmolol, as
you might do, to cardioplegia and have good results. I recall recently,
one of
our senior members (maybe Dr Tom Martin?) said he still uses
crystalloid
cardioplegia and yet has fantastic results in very complex cases
several of
which he has shared on this forum. Indeed the more I quiz people about
this
'fibrillation is bad' theory the less I am convinced about it. A day or
two ago
I learnt from Hal that he sometimes defibrillates with the clamp on and
then
that later will count as the heart being in SR when you declamp? Tohru
induces
fibrillation in all patients and has good results. We also learnt that
many of
us actually don't even know what is in the cardioplegia or hot-shot we
use.
Cardioplegia is indeed still voodoo. There are basic principles which
have to be
adhered to depending on whether you are cold or warm, arrested or
beating; aside
from this, most of the rest is voodoo, including, I suspect, the
suggestion that
transient fibrillation indicates poor protection.
Ani
> Date: Wed, 1 Aug 2007 20:15:53 +0530> From: prasannasimha at gmail.com>
To:
OpenHeart-L at lists.hsforum.com> Subject: Re: [HSF] Inotropes,
ventricular
fibrillation and myocardial protection> CC: > > Ani,> Having graduated
from
voodoo homemade cocktails to blood and its > variants, you would easily
be able
to see that the bad cardioplegia's > did have a higher (more accurately
uniform)
incidence of fibrillation > which came down with better modifications
of
cardioplegia's. That does > make us wary and anyway fibrillation is not
something by any stretch > normal.Transient defibrillation may appear
innocuous
but then it has > been shown that such hearts have indeed been
improperly
preserved (from > works of Buckberg and Kirklin).Remember that
sometimes speed
etc etc may > compensate but this may become an issue in longer case.>
Prasanna>
Ani Anyanwu wrote:> > I still do not understand why we are alarmed
about
transient ventricular fibrillation on reperfusion and why using drugs
to
suppress it will have any impact on outcome.> > > > Ani> >> >> >> > >
>> Date:
Wed, 1 Aug 2007 11:51:47 +0530> From: prasannasimha at gmail.com> To:
OpenHeart-L at lists.hsforum.com> Subject: Re: [HSF] Inotropes,
ventricular
fibrillation and myocardial protection> CC: > > I am not saying that
the
procaine or lignocaine is still acting. What I> meant is that since the
fibrillation is occurring with the hotshot delivery> with high local
lignocaine
changing the drug class may be beneficial.> Prasanna> > On 8/1/07, Ben
Bidstrup
<benjamin.bidstrup at bigpond.com> wrote:> >> > I beg respectfully to
differ. The
lidocaine (a fast Na channel> > blocker) is all but gone after a short
while in
the cardioplegia> > scenario. Getting a suitable level back into the
circulation
and thus> > the heart at release of the clamp is what is needed.> >> >
Perhaps a
randomised study is in the offing.> >> >
http://circ.ahajournals.org/cgi/content/abstract/79/5/1106>
>> > This reference relates to defib energy levels but i think you
will> > see
where I am coming from.> >> > At James Cook, I was involved in the
development
of a non> > depolarising cardioplegia solution, which is slowly working
its way>
> up the development path. The main components are lidocaine and> >
adenosine.>
>> >> >> >> > >Ben,> > >I use Amiadorone in the pump for all emazes
(and postop)
and> > >Amiadorone in the pump for all aortic valves. Since the St
Thomas> >
>Cardioplegia (which we mix in blood) already has procaine adding> >
>Lignocaine
would be redundant.(Incidentally Amiadorone is very cheap> > >in India
!!)> >
>Prasanna> > >Ben Bidstrup wrote:> > >>Why the amiodarone. Surely with
some
perfusion, the electrolyte> > >>imbalances within the myocardium would
correct
and SR ensue. If> > >>anything use lidocaine. Less toxic and cheaper,
not a
negative> > >>inotrope. It is what Yacoub taught me many years ago, and
I have>
> >>used it to good effect (infrequently I might add).> > >>> >
>>>Tohru,> > >>>
I did an AVR on an 87 yo man as a 2nd case just a couple of> > >>>hours
ago.
Again, no LV vent, only a sump. While closing the> > >>>aortotomy, I
began the>
> >>>continuous warm retrograde blood. The heart began fibrillating> >
>>>after
a couple of> > >>>minutes. I gave amio and then cardioverted. The heart
had a> >
>>>slow junctional> > >>>rhythm until the clamp was released. A sinus
rhythm
developed shortly> > >>>afterwards. He came off with no inotropes. It's
much
easier on> > >>>the heart and> > >>>your nerves to cardiovert a
clamped, flaccid
heart rather than> > >>>trying to do it> > >>>after the clamp has been
released.> > >>> I look forward to your visit at the STS. As I said
before,
I'll> > try to> > >>>have a couple of interesting cases for you and
other
interested> > >>>members of HSF> > >>>to watch and criticize to your
heart's
content.> > >>>> > >>>Hal> > >>>> > >>>> > >>>> >
>>>**************************************
Get a sneak peek of the> > >>>all-new AOL at> >
>>>http://discover.aol.com/memed/aolcom30tour>
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> Daniel J Boorstin> >> > Ben Bidstrup FRACS FRCSEd FEBCTS> >
Consultant
Cardiothoracic Surgeon> >
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>> > > > -- > Prasanna Simha M>
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