[HSF] Coronary Sinus Sampling

[prasannasimha]

I use coronary sinus lactate or retroperfusion aortic effluent lactate 
in two situations - in hypertrophied hearts or sick hearts especially 
who have been preoperatively unstable (eg crashes on induction or 
severely unstable patients). I also use it when I have had cases where I 
have had problems and use it using the near hit miss concept (ie any 
case type that required more than 3-5 mics dopamine + 3-5 mics 
dobutamine and Adlib SNP while weaning off CPB. It helps at least in 
settling myocardial protection issues and forces you to reanalyze the 
case. (Bojan will attest to the fact that I dramatically have been able 
to decrease inotropic requirements especially when my cardioplegic 
protocol is adhered to).

The coronary sinus sat should always be above 45 % in a beating heart 
off CPB (Subject to normal arterial concentration). This represents the  
value acceptable and is lower than the rest of the body as the O2 
extraction is higher for the myocardium normally. The coronary Sinus 
lactate  should ideally be below 2 mmol (aerobic threshold) and 
definitely be below 4 mmol (anerobic threshold).
Trends are also more important than just absolute numbers.
Coronary resistance - should be normally 40 - 60 mm Hg at a flow of 350 
ml/min of cardioplegic solution at the aortic root. To be more precise 
it (Coronary flow) should be 1ml/gm myocardium/min if you have the LV 
mass ascertained preoperatively on Echo.If it is higher you have a 
delivery problem. Usually Adenosine acts as a good coronary vasodilator. 
If this does not then boluses of NTG need to be given typically 50 mic 
shots or "flush " preparations till you can deliver this.  Unfortunately 
many a time we do not have that and 350 ml seems to be the minimum flow 
since this represents the normal flow in an adult heart (albeit 
pulsatile) and LV mass estimations are also inaccurate to some extent by 
Echo but you get a rough Idea.

I do not routinely add NTG to the cardioplegia since I already give 
Adenosine but add it when I seem to have a delivery problem.Esmolol also 
relaxes the myocardium and also decreases subendocardial wall stress and 
I believe it enhances subendocardial perfusion (Something that I have 
seen bitterly in a cut heart). I have toyed with the idea but have 
desisted as it makes the cardioplegia more and more complex. Giving 
boluses  as per a protocol to the perfusionists seems to be something 
they understand and can easily do.

As far as clamping a sick heart to resuscitate it, it is something that 
I have done repeatedly with success.
I bet all of you have seen an unclamped heart that has mildly bluish 
blotches. This represents a no reflow phenomenon and represents non 
perfusion despite coronaries being perfused. This represents a case of 
failure of adequate myocardial protection and over a prolonged period of 
time the heart becomes pink. This is not the state at which a heart 
needs to be unclamped. Being on CPB with a heart beating may also do two 
things - unload the heart and thus reduce myocardial oxygen demand or 
paradoxically decrease supply due to a decreased pressure head. All of 
us have seen ST's at times increasing when you go on CPB emergently. I 
believe that a beating perfused heart with low coronary resistance and 
no  "no flow" or "no reflow" is OK. If there is anything to the contrary 
you need to manage it differently. In these cases the heart needs to be 
arrested, coronary vascular resistance modified, myocardial oxygen 
delivery optimized and tissues be given a chance to manage their oxygen 
debt and I feel this is best done with an aerobic arrested heart - 
rested thus using less energy for beating and more for repairing with 
plegic arrest and beta blockade , vascular resistance being lowered 
pharamcologically with adenosine and NTG and appropriate substrate 
enhancement - oxygenated nonacidotic blood till the coronary sinus 
/retroperfusion aortic effluent  crosses a minimum of 90 % and better 
still 95 %  with normalization of lactate to the aerobic threshold 
(2mmol/dl) thus biochemically telling us that we have at least repayed 
the oxygen debt (Better still fi you can give Kreb cycle intermediates 
which I do not have but Adensoine is supposed to break down and give 
some intermediatesk. Further reperfusion pressure can then be slowly 
raised over a period of time to allow low pressure head perfusion to 
allow the myocardium to progressively adapt to the pressure without 
causing myocardial edema and then the clamp can be removed. At times 
this needs patience and can even take upto an hour. All this cannot be 
done with a beating blue heart.
I believe that there are two phases were CS lactates need to be measured 
- one after delivery of plegia either at the time of initial arrest or 
reperfusion phase or secondary cardioplegic phase - this is to check the 
adequacy of delivery and supply demand mismatch monitoring and two - 3 
minutes off CPB to test wether your  strategy has worked in the loaded 
heart. In fact in some cases I have left a long neck line and pushed it 
into the CS and feel that probably that would be a better monitor of 
myocardial function than systemic sampling - tells us the state of the 
oxygen status of the heart- the primary organ in relation to LCOS
If weaning still cannot be achieved - the myocardium has been 
dead/killed or there is a mechanical problem in your correction needing 
to be readdressed.
Does this seem to be a convincing argument ?

Prasanna

Ani Anyanwu wrote:
> 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
>
>