Yes, you are correct in noting that lactic acid is a product of the anaerobic metabolism that occurs when tissues are not perfused...as in cardiac/respiratory arrest. However, the quantities of lactic acid produced are not the primary contributor to the acidosis. It is the accumulation of CO2, in the form of carbonic acid, that is THE primary contributor to serum acidosis.
By the time that lactic acid would accumulate in pathological levels, the organism/patient has reached end stage organ death.
It's fun and wonderful to see that people are thinking and exploring the basic science behind what we do. Keep in mind what we do is PRE-hospital medicine. Critical lactic acidosis requires dialysis. My service, although progressive, is cheap and won't give me the latest greatest portable dialysis unit.
Where to begin...
Ok, since it would take no less than a book to explain all of this, and I have no intention of writing one, let me try to point out a few key problems here.
Bicarb is the major buffer system of the serum. RBCs in the serum are subject to acidosis in the form of protein denaturing and enzymatic alteration of normal function.
Irrespective of the effects of end organ lactic acidosis, losing the ability to carry and donate oxygen molecules ends in organ damage.
Because the RBCs do not use TCA as a substrate producing path, they are particularly vulnerable because they are already using lactic acid metabolism.
Brain cells requiring oxygen in high concentration to get substrate primarily from the TCA cycle are dependant on this o2 transport and delivery. For a bit, there is alterantive sources for brain, but it is rather a short time.
Then you have the issue of renal papilae being rather vulnerable to oxygen deprivation. Once they start to denature, slough, and die, there can be a sequele of renal dysfunction (I'd love to explain it, but like I said I am not writing a book)
When the area surrounding the hepatic venous system loses it's meager oxygen supply, it also contributes to hepatic dysfunction in a short time. The conventional wisdom was that since hepatocytes can regenerate this was not a major issue. However, I am hoping to win my Nobel in medicine demonstrating that temporary liver dysfunction impacts the rest of the ability of the total organism to compensate in the periarrest state, when liver products are absent or altered. After all, what good is a heart full of oxygen without fatty acid metabolism? Of course what good is any organ if you have oxygen but no substrate?
Once bicarb and phosphate buffers are overloaded or in effective, it takes the body days to adjust. (providing the kidneys are functioning) In the meantime you have RBC permiability if not lysis. (for a variety of reasons like shape and structural integrity) Once the membrane is permiable, you start to lose adenosine. (which if you need atp, is going to be a really big problem)
Moreover, once you have mitochondrial membrane leakage in any mito. containing cell, irresgardless of the PH level, the caspase cascade is going to finish off the cell. (think of it at a grand level like in megaMoles or gross organs)
and i will not bother to type ot the systemic inflammatory sequele except to mention it also plays a part.
This is why the whole cardiac arrest algorythm will never get survivial beyond its epidemilogical value. It is why all the studies showing the benefit or lack of specific drugs are inherintly flawed. Because you are hoping your subjects pathology falls into your treatment, rather than targeted treatments to specific pathology.
Have you ever seen a study that shows the effects of bicarb on patients in cardiac arrest secondary to DKA? I haven't.
Or epi in hypertensive crisis secondary to pheocrhomocytoma?
Or amiodarone in arrest secondary to hyperkalemia?
But instead they pick things identifiers like V-fib. Which may or may not correlate sometimes. I wonder about the quality of the professionals that pick extraordinarily vague parameters like this for studies.
It is why all of us old gys have anectdotes about seeing bloodletting and cautery save lives or some studies show minor benefit and some show harm. If you read these studies regularly, you will notice the pathology report is never included. (if even performed)
In the publish or perish environment of evidence based medicine, most studies are not worth the paper they are printed on. It is why clinical judgement and proficency along with sound demonstrated basic scientific knowledge is what will be required to save lives.
Anything less is just a trial and error, with saves being accidents rather than definitive care.
While I agree that the ICU in a hospital is more suited to saving lives than the back of a truck on the street, it is important to remember that in coaglative necrosis, the time period is about 4 days. So what happens in the truck on the street that is not apparent or easily demonstratable, directly affects the sequele once the pt. gets to the ICU. The reason survival to discharge is so low, is becase by the time the pt. makes it to the ICU, the irreversible cascades have started and the deal was done 8-20 minutes into the prehospital phase.
I once had the idea we could be more effective by moving this intensive medicine into the earlier stages of care like the field or ED. But there was so much resistance to it from field providers, I gave up.
h34r:
