Tag: sodium

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Edelman formula is fundamental to understanding sodium

Sodium is wildly misunderstood and mismanaged.

If you want to understand sodium you should spend the time to truly understand The Edelman Formula. I have seen no better explanation of this formula than this powerpoint by Graham Gipson (who incidentally also designed the 2023 NephMadness logo). It is 133 slides long, but he has printed each build of the slides separately, and I found it fairly self guided. He beautifully shows how the EdelsonFformula can be derived using first principles and algebra and ends with demonstrating how the formula (nearly) perfectly predicts the results of Edelman’s classic 1958 experiment.

QN_III-The-Edelman-Equation-full-lecture-from-2020-07-30Download
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Sodium is not like the other electrolytes

This thread by Screaming Pectoriloquy is perfect

And a screenshot for when Twitter disappears.

A ten percent reduction in sodium drops it from stone cold normal to rather significant hyponatremia. This is a great example of how precisely sodium is regulated. Sodium regulation is tighter than all other ions. Look at a CMP with calcium, phosphorus, and magnesium added in. (Data is from UCSF).

Range is calculated by taking the difference between high and low and dividing it by the low value. https://www.ucsfhealth.org/medical-tests/phosphorus-blood-test
https://www.ucsfhealth.org/medical-tests/magnesium-blood-test
https://www.ucsfhealth.org/medical-tests/comprehensive-metabolic-panel

Here is a graph of the spread.

Two things immediately should be obvious.

    1. BUN (233%) and creatinine (117%) are not regulated anywhere close to how electrolytes are regulated. Get those guys out of here.
    2. And, the sodium (7%) and chloride (10%) range are nearly identical. Outside of the anion gap, I almost always ignore chloride. 

So let’s simplify this and remove the outliers and shadow.

Look at how tightly sodium is regulated. Regulation of second place, calcium, is THREE times as relaxed.

Every electrolyte is important, but regulating sodium regulates the tonicity in all 42 liters of the internal ocean. Apparently, this is important and sodium is allowed to wander only slightly.

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An introduction to sodium and water

A number of years ago, I was invited to write a chapter introducing sodium and water for a new medical text book under the Scientific American brand. I remember being disappointed that I didn’t get hypo- or hypernatremia and being stymied for awhile before I figured out how I wanted to the topic. Ultimately, I had a great time writing the chapter and, at least at the time. I was quite proud of the work. The textbook was somehow abandoned somewhere between inviting the chapter authors and publication. The publisher pivoted to some online component that was supposed to rise out of the ashes of the text book and they asked me to do additional work. I never did that work and they never asked a second time, so I don’t know if that ever came to fruition.

Anyways, this chapter has been sitting in the bowels of my Google Drive for years.

I hadn’t thought about this until recording chapter seven of Channel Your Enthusiasm podcast where we are reading through Burton Rose’s classic Clinical Physiology of Acid Base and Electrolyte Disorders. In Chapter 7, Rose discussed using simple math to predict the changes in intracellular and extracellular fluid volume following various fluid and solute challenges. This is exactly what I did in my Scientific American chapter. I found the exercise to be a profound moment of understanding.

Here is a link to the Google Doc:

Google Doc

And a PDF of the same:

PDF

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More questions from the minds of the M2s at OUWB

The minds of OUWB continue to provide thoughtful questions.
My roommate and I have encountered a question regarding the content on Sodium/Water Balance and also its application to SIADH. We have been using some outside resources to supplement the learning in class, and I feel that they have been somewhat contradictory in these 2 scenarios. The following are the scenarios that I am trying to think through
1) Patient eats a high salt meal, increasing total body Na+, resulting in an increase in ADH release (via increased plasma osmolarity) and eventually reaching baseline Na+ concentration and osmolarity at a higher ECV. Now, the increase in ECV would result in a down regulation of Sympathetic NS and RAAS; however, what I am hearing is that this down regulation would just return the kidney to Na+ in = Na+ out and would not actually return the individual to the original ECV. So, my question is how does this person get back to original ECV? What I am reading is that the person will continue to operate at this higher ECV until sodium restriction takes place. However, I am wondering how decreased RAAS (decrease aldosterone – decrease Na+ reabsorption – increase sodium excretion) wouldn’t do this, and also if pressure natriuresis wouldn’t do this also? Basically, why don’t these mechanisms do the work automatically, and why do you have to sodium restrict?
You have it right. That is the currently accepted understanding of sodium metabolism. It is not quite complete, because, though some subjects increase their blood pressure with increased sodium intake, not all patients increase their blood pressure. As to why the renin-angiotensin aldosterone system does not down regulate itself sufficiently to fully correct the volume overload situation, it is not well understood. The sodium regulating systems in the body strive to match sodium absorption with sodium excretion. With an increase in sodium intake there will be a modest expansion of the extracellular compartment until the sodium excretion is upregulated to match sodium intake. We can see evidence of the increase total body sodium with an increase in body weight associated with increased sodium intake.
2) In SIADH – high levels of ADH cause increased water reabsorption but euvolemic hyponatremia. Fitting in with my previous questions in the earlier scenario, how does the patient maintain euvolemic status? If increased water reabsorption occurs and the ECV is increased, the same down regulation of Sympathetic NS and RAAS would occur. Now, the outside resources in this case state that a decreased RAAS would actually cause increased sodium excretion that would allow for increased water excretion that would maintain euvolemic status. This makes sense because then the hyponatremia that results is not only an effect of the dilution from increased water reabsorption, but also from the increased excretion of Na+. But, this goes directly against the whole logic of needing to sodium restrict in the earlier case (i.e. RAAS can’t do the work to return the individual in scenario 1 back to a normal ECV).
So again you are well versed in what is happening in SIADH. SIADH is largely euvolemic and largely is a situation where patients are in sodium balance, i.e. sodium = sodium out. However if you do meticulous metabolic balance studies you will find that patients do gain weight during SIADH. There is excess water and this does serve to expand the patient’s extracellular volume. This also will suppress the renin-angiotensin-aldosterone-system so that patients will get a modest increase in urine sodium excretion. But I don’t quite understand how you think this is any different than the first scenario. There is a modest increase in sodium excretion but in the presence of continued unremitting ADH activity the patient continues to deal with the modest increase in volume. So like the first scenario, the modulation of the RAAS is unable to fully restore euvolemia.
For more on SIADH and volume status see this post.