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 hypo
ventilated 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.
Why were they giving calcium and 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 point me to places to read up on this?
Forgive my ignorance, doing the very best I can. Most grateful for any assistance.
bicarb and respiratory/metabolic alkalosis are intimately linked. when you see bicarb (hco3-) always think alkalosis and kidneys; when you see carbon dioxide (co2) always think acidosis and the lungs.
i'm just going to print out what is in my lab reference manual for you. . .(page 105-6, mosby's diagnostic and laboratory test reference
, 4th edition, by kathleen deska pagana and timothy james pagana, 1999)
"most of the co2 content in the blood is hco3-. the bicarbonate ion is a measure of the metabolic (renal/kidney)
component of the acid-base equilibrium. it is regulated by the kidney. the ion can be measured directly by the bicarbonate value or indirectly by the co2 content. as the hco3- level increases, the ph also increases; therefore, the relationship of bicarbonate to ph is directly proportional. hco3- is elevated in metabolic alkalosis and decreased in metabolic acidosis. the kidneys are also used to compensate for primary respiratory acid-base derangements. for example, in respiratory acidosis the kidneys attempt to compensate by resorbing increased amounts of hco3-. in respiratory alkalosis the kidneys excrete hco3- in increased amounts in an attempt to lower ph through compensation. in diabetic ketoacidosis hco3- ion does decrease because it is directly used to neutralize the plasma diabetic acids."
in the lung, hco3- converts to co2, it's useable form there. in the lung, co2 is referred to as the respiratory component
in the acid-base determination because it is controlled by the lung. as co2 levels increase, ph decreases. the lungs will be the organ that attempts to compensate for acidosis derangements. they would want to increase her kidney output because that is how you dump hco3- from the body. it is more efficient than working it off through the co2 of the lungs which is only a compensatory mechanism. kidneys are more direct. 30cc/hr of urine is minimal urine output.
the lactate in lactated ringer's iv solution is metabolized into bicarbonate (hco3-) once in the body. it is normally used to treat acidosis conditions. lactated ringers does not have enough potassium and calcium in it for homeostatic maintenance, so if she was not having a very good intake to begin with, she was not going to get adequate potassium and calcium replacement from the lactated ringers solution. Attachment 5949
my question is " how long did they have her on the lactated ringers?" if that is what happened, i'm thinking that maybe the docs just miscalculated and didn't give her enough electrolyte replacement. what i usually saw was the lactated ringers discontinued and changed to a sodium chloride solution to encourage diuresis and excretion of hco3- in order to correct the metabolic alkalosis. potassium replacement can be done through supplemental potassium added to the iv solutions.
the pathophysiology behind the hypocalcemia (low calcium) that occurs with metabolic alkalosis is that the high ph interferes with the ability of the calcium ions circulating in the blood to bind with serum proteins causing the calcium ions to have a greater affinity for protein. so the calcium ions in the blood end up binding to circulating serum proteins and reducing the amount of calcium ions in the blood. when a calcium level is drawn it will show that the calcium level is low. in actuality, the true total calcium concentration has most likely not changed, but the blood test can only detect the free ions. as the patient's body ph returns to a normalized range, the calcium level will more than likely correct itself as the circulating serum proteins release the calcium ions they hold in bondage.
a potassium of 3.2 is still within normal limits although at the low end of norm. she is most likely losing some potassium through the weeping fluid on her legs. hypokalemia is a symptom
of metabolic alkalosis. the pathophysiology of the hypokalemia symptomatology according to metheny occurs in two ways (page 165, fluid & electrolyte balance: nursing considerations
, 4th edition, by norma m. metheny) and i'm still trying to reason it out, but here it is:
metabolic alkalosis. . .can be produced by a gain of bicarbonate or a loss of hydrogen ion. . .hypokalemia produces alkalosis in two ways:
- in the presence of hypokalemia, the kidneys conserve potassium and thus increase hydrogen ion excretion (recall that these ions compete for renal excretion)
- cellular potassium shifts out into the ecf in an attempt to maintain near-normal serum levels (as potassium leaves the cell, hydrogen must enter to maintain electroneutrality).
calcium and potassium must be constantly replaced, most conveniently we do it through our diet.
this lady was on an ace inhibitor to lower her blood pressure which might be affecting her kidney function. some ace inhibitors are known to be nephrotoxic. bun can also rise when there is dehydration.
there is a list of acid-base tutorials and other weblinks on post #24 of this sticky thread:
Last edit by Daytonite on Apr 5, '08