Help, K+ and metabolic alkalosisRegister Today!
This is a discussion on Help, K+ and metabolic alkalosis in Nursing Student Assistance, part of Nursing Student ... I am digging into acid/base a little deeper than I have before. My patient had metabolic alkalosis...by alaskalala Apr 5, '08I 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.
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.Last edit by brian on Apr 5, '08 : Reason: Changed Hyperventilated to Hypoventilated per user request
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- Apr 5, '08 by AnnaN5I can answer some of your questions for you. Metabolic alkalosis or Respiratory alkalosis results in hypocalcemia and hypokalemia. Acidosis results in hyperkalemia and hypercalcemia. The body is actually not depleted of the potassium, it is a relative hypokalemia. Potassium enters cells from the ECF in exchange for H+ leaving the cell.
The IV calcium gluconate was to correct the calcium imbalance. Hypocalcemia can be treated with IV calcium gluconate, calcium chloride or oral replacement.
Hyperventilation causes respiratory alkalosis because you are blowing off more carbon dioxide. Hypoventilation results in respiratory acidosis because the lungs retain more carbon dioxide.
- Apr 5, '08 by alaskalalaThanks, Anna,
For confirming the intracellular shift thing.
But if both calcium and potassium are shifting to the intracellular space because of the alkalosis, why replace one and not the other?
I meant to say "if they HYPOventilate her" it would drop her pH, too late to be posting...brain dead.
Maybe it will all be clear to me in the morning.
- Apr 5, '08 by brianI edited your first post to read hypo instead of hyper
- Apr 5, '08 by Daytonitebicarb 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:calcium and potassium must be constantly replaced, most conveniently we do it through our diet.
- 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).
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
- http://allnurses.com/forums/f205/pat...es-145201.html - pathophysiology/ a & p/ microbiology/ fluid & electrolyte resources
- Apr 6, '08 by alaskalalaI went back to my A&P textbook and reread the Acid/Base, F&E chapter, then the renal chapter. I’m still awash. This is one complex balancing act.
Then you, Daytonite, come up with the excerpt from Methany, and blow my tentative grip on things apart. Item number two, with alkalosis shifting K+ from ICF to ECF, is what got me. Everything else I read had it the other way around: high pH shifting K+ from ECF to ICF.
Methany stands alone regarding the direction of shift, but it…actually makes sense. I think it’s the missing piece!
I believe it may depend on which imbalance is getting a priority correction: the pH or the K+. If hypokalemia is the priority, you get alkalosis. If alkalosis is the priority, you get hypokalemia.
Here’s how I’m seeing it, please correct me if I got it wrong.
If potassium is the priority:
Kidneys hold on to K+
Kidneys dump H+
Higher K+ (greater good)
Higher pH (necessary evil)
cells give up K+
cells take in H+
Higher K+ (greater good)
Higher pH (necessary evil)
If pH is the priority:
Kidneys hold more H+
Kidneys dump more K+
Lower pH (greater good)
Lower K+ (necessary evil)
Cells give up H+
Cells take in K+
Lower pH (greater good)
Lower K+ (necessary evil)
So hypokalemia can either be a cause, or a result, of alkalosis, and vice versa.
Daytonite, you are likely right about the contributing factors in terms of the hypokalemia: insufficient intake of potassium, LR running for too long, loss through sweating and weeping. I still can’t figure out if the alkalosis is caused by, or merely exacerbating, her hypokalemia. And if it’s not the hypokalemia, what the heck is causing the alkalosis? She’s not on diuretics, not vomiting, no NG suction, no steroids.
But here are a few curve balls:
1) She was receiving calcium gluconate to correct the low Ca2+, doesn’t calcium gluconate lower potassium levels (bad)?
2) She was on an ACE inhibitor, that blocks aldosterone, this should increase her potassium (good)?
3) I was thinking her urinary output was O.K. because it was more than 30mL/hr, but I forgot this is just a rough number based on an average 175 lb individual. She’s nearly 700 lb. Urinary output should be (more precisely) .5mL/kg/hr, or in her case, about 160 mL/hr.
HOLY COW! No wonder her urine was so dark. This can’t be right! Does the .5mL/kg/hr still hold up for the morbidly obese? She’s in the ICU of a major academic institution, there are docs of every stripe rounding constantly, would none of the nephrologists have mentioned to me that her urine output needs to be way, way higher, and would they not do something about it (diuretics)? Are her kidneys only working good enough for a 175 lb person, and essentially, failing, given her size? If so, why was her creatinine just fine?
And why is nobody ordering supplemental potassium? If not for the hypokalemia, then for the alkalosis?
Could it be that they were thinking the alkalosis had caused a big intracellular shift of K+, and that if they corrected the alkalosis, the ICF K+ would come rushing out, sending her into hyperkalemia?
And once again, what, exactly were they doing to correct the alkalosis? Diamox is the only drug I could find that causes the kidneys to excrete bicarb. She wasn’t on it.
Enlightened by your post (as always), still flummoxed (a perpetual state).
Care to shed more light?
And thanks also for the calcium piece, binding to serum proteins, you made my night, I love to get the details on this stuff so I can understand why and how things are happening instead of just memorizing “pH up, calcium down.”
Ever in your debt, you patron saint of nursing students.