[HSF] Targeted Renal Therapy
Ani Anyanwu
anianyanwu at hotmail.com
Sun Apr 15 10:03:56 EDT 2007
Prasanna,
Somehow as you get to read comments on this forum you can get reasonable insight on members views, interests and practices. You had presented a case a while ago and mentioned something to do with coronary sinus lactate, so I was certain sampling coronary sinus blood had to be something you had interest in.
As this is diverting a bit from the thread I was wondering if you could start a new thread on coronary sinus sampling - the method, timing and how you use it to aid patient management. What do the numbers mean? I sampled one two weeks ago and found a sadly sick heart with ph 7.13 and lactate 9, O2 sat around 30 - needless to say, that patient is now on a VAD. Also could you tell us more about modulating coronary resistance? Do you add the nitrates to the cardioplegia solution? Finally, why do you need to clamp a sick heart to resuscitate it? What is the advantage over just leaving the heart perfusing via CPB to recover?
Thanks
Ani
----- Original Message -----
From: prasannasimha<mailto:prasannasimha at gmail.com>
To: OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com>
Sent: Sunday, April 15, 2007 1:42 AM
Subject: Re: [HSF] Targeted Renal Therapy
I missed this post of Ani and read it after I had sent my previous post.
Two things that I can iterate.
Coronary sinus sampling does show the oxygen consumption of the heart
and this is measurable (using flow + VA difference) and in fact if I
have a heart that doesn't come off cross clamp in NSR, I have reclamped
and reperfused and you can easily see that this heart has either a high
extraction or a high coronary vascular resistance or both which needs to
be dealt with. Once corrected you will see the heart defibrillates
spontaneously indicating that there was and is inadequate protection in
such hearts that actually needs attending to.
Continuous perfused hearts still have an AV difference indicating that
there is ongoing O2 consumption and the AV difference is around 5 % if
being adequately perfused.
I believe post clamp 2 minute AV difference is a more important value
indicating residual myocardial oxygen debt.This value should be above 45
% if the heart has been adequately perfused during arrest. If it is
below 45 % then things are wrong.
I used this system of analysis to change my myocardial protective regime
especially after had the spate of deaths/LCOS in patients with severe
AS with gradients > 100 mm Hg which I discussed some years back. The
increased risk was negated by adding Adenosine , Esmolol and checking
coronary vascular resistance and adding NTG and Adenosine boluses till
this comes down. At present I am evaluating whether cold continuous
preserves coronary resistance (which I think is a surrogate for coronary
endothelial integrity) has better effects than intermittent perfusion
with Esmolol /K cardioplegia.I have not really been able to do a true
continuous warm beating antegrade perfusion since I feel I will
interrupt it at times so I prefer to be cold at the times when I feel I
will interrupt perfusion. The rest of the time continuous perfusion with
the heart beating (like both Hal and I do) is very achievable
Incidentally, Ani, why did you suspect that I had interest in this ?
(Since I am actually doing some of this sampling at present).
Prasanna
Ani Anyanwu wrote:
> Thank you for your comments Murtaza. I too would be keen to know Dr Salerno's thoughts. My understanding though is that ischemia is a relative phenomenon and occurs when the demand (primarily of oxygen) exceeds the supply. If indeed the metabolic rate of the heart is such that most oxygen is not utilized even though blood is going through it, will this be defined as ischemia? Probably the cells have used whatever oxygen they need (which will not be much). When we give cold blood cardioplegia, we often see it going in bright red at one end and coming our dark at the other so surely some of the oxygen has been taken away? I suspect Prasanna may have some coronary sinus sampling data to support that the heart is indeed utilizing the oxygen. Of course one does not know what this all means - maybe the real benefit (if any) of continuous cold blood perfusion lies in maintaining tissue hypothermia rather than preventing ischemia.
>
> I am not sure though that we need mega amounts of K to keep a continually cold perfused heart arrested. I suspect that provided it is kept cold (by the continued cold perfusate) it is unlikely to beat (and if it does it defeats your argument that cardiac cell mechanisms stop working when they are below 16 degrees Celsius). Certainly I have never seen an explanted donor heart beat when taken out of the ice bucket, but as the heart warms (before the clamp is removed) one sometimes will see some fine fibrillation.
>
> The ideal I agree is no doubt warm or tepid perfusion but the question is whether, for those who like it cold, background continuous perfusion offers any advantage over intermittent cardioplegia.
>
> Ani
> ----- Original Message -----
> From: murtaza chishti<mailto:cmurtaza at hotmail.com<mailto:cmurtaza at hotmail.com>>
> To: OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com>>
> Sent: Saturday, April 14, 2007 1:37 PM
> Subject: Re: [HSF] Targeted Renal Therapy
>
>
> dr Anyanwu
>
> congrtulaions on successful surgery of this very sick patient. certainly,
> continuos perfusion is better than intermittent perfusion. There are two
> things that must be taken cognizance of, though.
>
> 1) temperature in the cardiac capillaries needs to be 16-20 degrees cel
> before any significant amount of oxygen gets released. So contineous
> perfusion must mean warm perfusion( or tepid) , or else the very purpose of
> preventing ischemia and subsequent reperfusion injury is defeated. i wonder
> if you moniter myocardial temp. Blood delivered at 4 deg probaly ends up
> being at 12 degrees in the capillaries.
>
> 2)keeping a contineously perfused heart arrested means large amounts of K+
> and perhaps other additives like glucose, with attendent problems of their
> own, and ,therefore, comes at a price which could be significant. the point
> is if you are perfusing cotineously , is arrest
> ' really necessary in someone with normal coronaries.A case could be made
> for (tepid)arrest in some one with coronary artery disease if you argued
> that retrograde plegia is about 25% nutritive.
>
> i look forward to dr. salerno' post on this
>
>
> murtaza chishti
> EHIRC DELHI.
>
>
>
>
>
>
> >From: "Ani Anyanwu" <anianyanwu at hotmail.com<mailto:anianyanwu at hotmail.com<mailto:anianyanwu at hotmail.com<mailto:anianyanwu at hotmail.com>>>
> >Reply-To: OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com>>
> >To: <OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com<mailto:OpenHeart-L at lists.hsforum.com>>>
> >Subject: Re: [HSF] Targeted Renal Therapy
> >Date: Sat, 14 Apr 2007 07:55:27 -0400
> >
> >
> >I used targeted renal therapy for first time earlier this week. Patient was
> >50 year old with dilated cardiomyopathy EF ranging between 8 and 12%,
> >severe pulmonary hypertension who underwent triple valve surgery (was not
> >transplant candidate). His preoperative creatinine ranged from 1.9 to 2.6.
> >His renal arteries were off-set by 5cm so was not possible to cannulate
> >them both with single catheter so left a unilateral catheter in left renal
> >artery and infused 0.4 mcg.kg/min of fenoldapam for 24 hours. He was never
> >oliguric post-operatively and his creatinine did not 'bump' as they usually
> >do. Maybe has nothing to do with catheter - will try on some more patients
> >before forming opinion, but I know Hal seems to be convinced it may be
> >beneficial.
> >
> >Another thing I did differently is to apply Salerno's logic and perfuse
> >this very sick heart continuously during clamping via cannulae sutured into
> >the coronary ostia so that the heart was never ischemic during the case
> >(other than for very brief period when placing cannulae) . That way without
> >ischemia there could be no ischemic injury and also no reperfusion injury
> >and must say for a heart which barely moved before I was impressed by
> >function coming off. No IABP even. I think this makes sense and I will do
> >it more on sick ventricles. I have not gone all the way yet though and was
> >not bold enough to leave the heart warm and beating - I arrested the heart
> >and ran cold (4 degrees) blood through the case - also packed heart with
> >slush (yes - some archaic surgeons like me still use topical cooling!).
> >
> >Ani
> >
> >
> >Hgrmd at aol.com Hgrmd at aol.com
> ><mailto:openheart-l at lists.hsforum.com?Subject=[HSF<mailto:openheart-l at lists.hsforum.com?Subject=[HSF<mailto:openheart-l at lists.hsforum.com?Subject=[HSF<mailto:openheart-l at lists.hsforum.com?Subject=[HSF>>] Targeted Renal
> >Therapy&In-Reply-To=>
> >Mon Jan 22 07:26:45 EST 2007
> >
> >
> >--------------------------------------------------------------------------------
> >
> >Dear Ahmed,
> > To be honest, I found out about TRT from the rep coming by my office
> >last
> >Wednesday. I've read some of the brochures he left. From what I've seen,
> >there's really nothing concrete about its efficacy, only a few case
> >reports.
> >Apparently, intraop testing has shown that the GFR is increased by 25%
> >with
> >the infusion. All I know is it's fairly straight forward to insert, and
> >seems
> >to have little downside. Look at their website _www.flowmedica.com_
> >(http://www.flowmedica.com<http://www.flowmedica.com/<http://www.flowmedica.com<http://www.flowmedica.com/<http://www.flowmedica.com<http://www.flowmedica.com/<http://www.flowmedica.com<http://www.flowmedica.com/>>>)
> >Hal
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