[alaskalala]

I'm a nursing student, doing clinical rotations in the MICU.

I am digging into acid/base a little deeper than I have before. My patient had metabolic alkalosis with a little respiratory compensation, and her K+ was low (3.2), and Calcium was little low too.

The docs were rounding and one of them was saying, "We're trying to get her kidney's to dump that bicarb..."

I'm trying to figure out what they were doing to facilitate that. She's 40-ish, HTN, DM, morbidly obese (nearly 700 lbs). She was on LR at 100mL/hr, abx, on PC vent, an ACE inhibitor, and a minibag of calcium gluconate.

It had to be either the vent settings or the calcium, right? If they hypoventilated her that could lower her pH, but wouldn't that take the pressure off her kidney's, rather than pushing them to do their job?

On the subject of her kidneys, she was putting out more than 30mL/hr, her BUN was a slightly elevated, but her creatinine was fine. She might have been a little dry because she wasn't enthusiastic about PO fluids, and she was loosing a lot from weepy skin. (I don't know what her GFR was because they use an eGFR that has different values than what I learned in school).

Anyway, why were they giving calcium, but not potassium?

I can't find anything in my nursing texts about the relationship between K+ and metabolic alkalosis. I'm kind of lousy at Googling, always end up 250,000 hits, the first 20 of which are completely over my head, at which point I usually give up, and go back to studying what I'll actually be tested on, instead of these clinical rotation mysteries.

Anyway, on the internet, I come across something that says depleted potassium can contribute to reabsorption of bicarb in the proximal tubule.

Then I come across something else that says that in metabolic alkalosis K+ shifts into the intracellular space. In that case, low K+ isn't really depletion, it's just a low serum level because it's disappeared into the cells.

So, that might explain why the docs wouldn't correct the hypokalemia with potassium, because it's not a question of too little, it's a question of where it is. But I'm severely muddled on this.

My question is: does hypokalemia contribute to alkalosis, or is it a result of alkalosis?

And, what can be done to help the kidneys reverse the alkalosis?

And what does calcium gluconate have to do with it all (if anything)?

O.K., that's three questions.

Can anyone shed some light on my dim head, or point me to places to read up on this?

Forgive my ignorance, doing the very best I can. Most grateful for any assistance.

[Sister S]

This is before looking it all up again, but isn't it something to do with excess extracellular H+ means that potassium comes out of the cells to compensate? and therefore you get hyperkalaemia? And if there's a deficency in H+ in the extracellular fluid then K+ goes into the cells causing hypokalaemia. I could be compelety wrong - but something rings a bell!

[RN1980]

your kidneys act as part of your acid/base buffer system, they will retain some hco3 but the excessive hc03 will be dumped into the urine. i also think they will try to hold onto any chloride due to its neg charge (now chem was a few semesters ago) so it will attempt to help correct the base. and you will typically have a decrease k+ with alkalosis.

[dayshiftnurse]

hi, i'm also an icu nurse but i just finished my nephrology courses and so i hope i can help you understand a little better....these are difficult concepts especially when factoring in a vented patient.

first though, primary metabolic alkalosis generally has to do with GI losses of KCL; can also be from getting lots of bicarb drip.

whenever there is metatbolic alkalosis, ususally hypokalemia follows; and the converse is true.

potassium participates in acid base balance in the serum by correcting for a high or low H+ concentration. so for example, if H+ is low, potassium will shift into the cell and kick H+ out to help restore proper acid base. this results in a lower H+ serum concentration . (the opposite occurs in metabolic acidosis) my notes explained that the mechanism for how this occurs really is not that well understood.

in addition, the kidney dont conserve potassium even if a deficit occurs. so for example in metabolic alkalosis--for every 3 potassium ions that move into the cell (to help correct acid-base) 2 H+ and 1 sodium ion move into the cell. but it becomes a vicious cycle because k+ and H+ compete for exchange in the distal tubule, but since there isnt any K+, the H+ ends up getting lost instead, causing metabolic alkalosis..

i always try to remember that in acidosis, hyperkalemia and hypercalcemia go togther and in alkalosis hypokalemia and hypocalcemia go together...therefore much easier to remember. but also understanding how potassium works to help control acid-base balance helps me understand the labs.

they could be giving calcium supplement to help protect the heart--in this type of imbalance where potassium is affected, it is irritating to the heart so calcium helps protect heart function.

always keep an eye on blood pressure with electrolyte replacement...especially magnesium iv replacement can cause hypotension. in hypotensive patient i tend to run it slower and spaced away from my anti-hypertensive iv drugs if possible.

[GoldenFire5]

My notes say that alkalosis increases Calcium binding to albumin with a decrease in serum Calcium. So there would be less free, available Calcium with alkalosis.

The opposite is true with acidosis: it decreases calcium bound to albumin and increases serum Calcium.

[dayshiftnurse]

i tried to edit my post to include this but itwouldn't let me so ...

in addition in the proximal tubules of kidney, sodium is resorbed with either chloride or bicarb...so if there is a deficit of chloride, the bicarb is conserved causing a metabolic alkalosis
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i have a little note in my book with a very simplified notes of what to see with met acid/alk resp acid/alk for quick reference...then eventually it sticks in your mind and makes sense so you don't have to memorize. i hope this helps a bit

[Zookeeper3]

There is potassium and calcium in the LR. Plus there is more potassium in the cells which needs to be shifted out and a longer acting calcium gluconate helps some. The ACE will help conserve the potassium so this is a good choice.

Now on a vent, it's so much easier to correct... adjust the RR, the tidal volume and up the sedation so the patient does not breathe over the vent and undo what your trying to fix. Sometimes you have to paralyze if the alkalosis is life threatening. Use the vent! Don't let the vent complicate it.. it's there to help fix it.

most importantly.... what is causing this... fix the source if it's the gut. The vent can fix the numbers, but you have to fix the source.

[alaskalala]

Thank you to all who replied. What a great resource you are, tremendously helpful. I went back to my A&P text, reread Acid/Base, F&E, and Renal chapters – surprisingly: not much there. Searched this forum for other related threads, many more details to sink my teeth into, then to the library for more books.

I’m so glad this patient didn’t have something very…for lack of better words, “dramatic” or “complex” going on that would have dazzled me (a ventriculostomy, multiple organ dysfunction syndrome).

Otherwise, I would have missed the opportunity delve into this essential business. Can’t believe how in the dark I was about it. Alarming. You study like a fiend and get good grades and think you know what you’re supposed to. I’m only being introduced to the bare minimum the state requires, good thing to keep in mind.

As to the source of her problem, what’s causing the alkalosis: she’s not on diuretics, not vomiting, no NG suction, no steroids. She’s not losing acid, soooo…

Even though the numbers looked like metabolic alkalosis with respiratory comp, I think the trouble was really (initially, anyway) respiratory.

Here’s what I think is going on: her obesity (almost 700 lbs) has been mechanically suppressing her respirations for a long time, so she’s been chronically retaining CO2, and her kidneys have been compensating. Now that she’s on a vent and blowing off more than she’s used to, she’s alkalotic because her kidneys have been holding onto bicarb and haven’t adjusted yet to the lower CO2. The potassium/hydrogen exchange is what’s lowering her serum K+ values. The hypokalemia is a result of rather than a cause of her alkalosis.

Maybe. What do you all think of my latest interpretation?