Del Nido: It’s ALL about the Calcium Baby!

“What it boiled down to is that Del Nido, when deployed for long complex cases becomes a clinical dance.  You go from a Mechanic to an Artist if you stay true to basic principals, have the patient’s welfare as your primary concern, and you have a strong negotiating relationship with your surgeon.  Anything less is a compromise.”

Editor’s Note:

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Had an interesting case coming up, that was going to involve a valve replacement as well as multiple grafts and so forth.  A lot of tension surrounding the case, as the patient was pretty sick, had poor LV function, and a few other co-morbidities that we as perfusionists recognize and deal with more often than not.  We were planning on using Del Nido cardioplegia to arrest the heart, and reap the benefits of 90 minute dosing intervals during the procedure.  What presented a challenging proposition was the surgeons’ proclivity to perfuse the SVG after each distal, establish graft patency and Q rates, do the valve replacement after completing the distals, and then go on to do the proximals with a partial X-Clamp.

The considerations are as follows:  The loading dose is roughly 1000 ml of 4:1 Del Nido (4 parts crystalloid to 1 part blood).   Typically, we would allow 90 minutes or so before considering the need to re-dose (subsequent 500 ml alliquots per 90 min)- depending on what point we are at in the procedure.  With intermittent dosing of cardioplegia- to enable SVG distension, measuring Q rates, and myocardial perfusion, the total Del Nido dose becomes cumulatively larger, and then begs the following questions:

  • How much Del Nido is too much?
  • At what point, with these partial cardioplegia doses down the vein grafts do you consider it a true REPLENISHING dose of cardioplegia- therefore RESETTING your ischemic countdown timetable (theoretically 90 min with a full dose)?
  • Do multiple 200 ml alliquats  of SVG perfusion constitute an acceptable and viable cardioplegia dose delivery- thus moving your time table further down the road in terms of myocardial preservation?

These were all legitimate concerns I had prior to the operation, but the next questions to be dealt with were the following:  In order to mitigate the sheer volume, hemodilution, and impact to the myocardium in what basically translates to delivering continuous Del Nido cardioplegia in order to sustain this SVG perfusion, do you consider either:

  • Changing the perfusate concentration from 4:1 to 1:4 (as in regular crystalloid delivery configurations?
    • This was an option I thought about and wanted to try until I read some literature (see below) and it was exactly counter to the principals that Del Nido works on:  One of the more over looked factors is that blood contains calcium. Using a 4:1 blood to crystalloid cardioplegia means a higher level of calcium as compared to a mostly crystalloid solution. The dilution and control of calcium is a key factor in DelNido.

 

  • Switch intermittently to cold blood- and augment with KCL- to limit and control the Del Nido volume?
    • I tried this as a resort- after having washed out the perfusate in the coronaries with straight cold blood- and the surgeon let me know the “heart was starting to beat- “

 

  • Continue the status Quo and end up with a cumulative dose of 2500 ml or more?
    • I couldn’t get myself to go there.

What it boiled down to is that Del Nido, when deployed for long complex cases becomes a clinical dance.  You go from a Mechanic to an Artist if you stay true to basic principals, have the patient’s welfare as your primary concern, and you have a strong negotiating relationship with your surgeon.  Anything less is a compromise.

Here is a collage of Del Nido Graphics I looked at in order to simplify this discussion.  You tell me if looking at any of these images will or does improve your overall comprehension of the physiology implied with Del Nido- and how it affects your daily practice?  If anyone reading this has a comprehensive diagram of how the CA+ inhibition impacts the RMP for an action potential- well that would be appreciated and very helpful 🙂

 

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Good luck- and God Bless 🙂

Frank

Del Nido: It’s ALL about the Calcium Baby!

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Lidocaine is classified as a sodium channel blocker and is a frequently used in practice as an antiarrhythmic.
The sodium channel blockade helps counteract the negative effects of a hyperkalemic depolarized arrest by polarizing the cell membrane to some degree and preventing sodium and calcium accumulation within the cell. A depolarized arrest can result in calcium and sodium accumulation within the cell so blocking the sodium channel prevents this.
This concept indicates that Del Nido is truly a depolarizing agent due to the addition of lidocaine and magnesium.
With all of the aforesaid information given it should be clear that Del Nido is truly advanced in its composition. The key is a low calcium concentration solution which results in decreased oxygen consumption due to the reduced excitability of the cells. Individual myocyte excitability is not reflective on the EKG. Why is it a crystalloid solution?
Why not use a 4:1 blood to crystalloid composition including the key ingredients like lidocaine and magnesium?
One of the more over looked factors is that blood contains calcium. Using a 4:1 blood to crystalloid cardioplegia means a higher level of calcium as compared to a mostly crystalloid solution. The dilution and control of calcium is a key factor in DelNido.

 

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