FAQ - hyperkalemia
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Hyperkalemia?


What is the rationale for giving calcium gluconate to treat hyperkalemia?? How does it treat it, and do you put your patient at risk for hypercalcemia?
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Calcium gluconate acts as a diuretic when a patient is not on diuretics. It aids in treating hyperkalemia without causing hypercalcemia if given at the right dose. This is why when it is given CBC blood test are done 4hrs after giving the medication so adjustments can be made to ensure not to much or to little is being given.  (+ info)

How do I reply to an answer to my Hyperkalemia question?


I just posted a question about my husband needing a low potassium diet due to hyperkalemia. Someone was kind enough to answer me but I don't know how to post and answer to a question he/she asked in return. I'm new to this. Please guide me through the process.

Thanks, YoungAtHeart
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You cannot answer your own question. But you can add additional information. If you have another e-mail address with yahoo. then you can answer the question under that name.  (+ info)

Is it normal to have hypokalemia for it to change into hyperkalemia?


From low potassium levels.. getting treated for it. And then a few months later having hyperkalemia. Is it normal? thanks
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There can be exogenous causes such as potassium replacement leading to hypokalemia. This tends to happen if the situation isn't monitored.  (+ info)

Please explain why someone with Hyperkalemia would be prescribed?


High doses of Potassium 3x daily and why would a person who has low bloodpressure 90/50 and CHF be prescribed drugs like Coreg, and Imdur, both of which cause reduction in blood pressure?
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Wow, this is not good. Hyperkalemia as you know is high potassium, so I don't know why a doctor would prescribe potassium 3 times per day when they already have a high potassium level. And you are right about Coreg. Coreg is used for people who have high blood pressure. Imdur is used for people who have angina, but one of the precautions with Imdur is not to take it if you have low blood pressure.

I am unsure if you are talking about yourself or someone you know, but the physician needs to be questioned regarding this and personally I would find another physician.

I know that does not answer your question as to why, but I have no answer as to why this would be done. It does not make any sense as to why these would be prescribed with the information you have given.

Best wishes.  (+ info)

How does rhabdomyolysis cause hyperkalemia and metabolic acidosis?


Be specific.
Thanks. :]
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This sounds suspiciously like a Homework question but I'll give you the benefit of a doubt.

First, you must understand what rhabdomyolysis is and how it affects the body. Hyperkalemia is RARELY caused by rhabdo but rhabdo can be caused by hyperkalemia. When hyperkalemia is caused by rhabdo, it often goes unnoticed becaue of the counteracting effect of rhabdo on serum potassium.

Rhabdo is a disease of the skeletal muscle that involves the breakdown & destruction (lysis) of muscle tissue and thus muscle cells. As a result of cell lysis, electrolytes such as potassium and phosphate and myoglobin & creatine kinase (CK) are leaked from ruptured muscle tissue cells into the plasma of circulating blood. If tissue destruction is significant enough, the amount of K+ will reach hyperkalemic levels. Because K+ is leaking from an intracellular area of high concentration to a plasma area normally of low concentration, hyperkalemia is develop quickly. That's the key -- it's because plasma is normally an area of low K+ concentration. The normal range of serum K+ is quite narrow, 3.5-5.5 mEq/dL. You can easily see that it doesn't take much to go outside the range either direction.

Rhabdo is a rare cause of met acidosis. Myocyte is another word for muscle cell and you should be as familiar with this as you are with your own name. Recall that rhabdo is a lysis of muscle tissue and that tissue is made up of cells. The lysis action injures myocytes so that other substances besides myoglobin, CK, K+ and P+ are leaked. Lactic acid and other organic acids are also leaked from ruptured myocytes, promoting lactic acidosis which is one type of metabolic acidosis.  (+ info)

Why do ACE inhibitors sometimes cause hyperkalemia?


I've been looking on the internet, but there aren't really any explanations at the cellular level. I just need to wrap my brain around it a little more to help my memory. Any help would be greatly appreciated!
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This mechanism is somewhat complex, but let a good ol' pharmacist give you some insight into the potassium-sparing property of the ACE inhibitors:

These agents work by competitively inhibiting the Angiotensin Converting Enzyme (ACE), which normally hydrolyzes angiotensin I to angiotensin II via peptide cleavage. This step is important for homeostatic maintenance of the RAAS System (Renin-Angiotensin-Aldosterone System). When an ACE inhibitor is on board, Angiotensin I accumulates, thereby causing feedback inhibition of renin release from the juxtaglomerular apparatus near the glomerulus and proximal convoluted tubule of the nephron. Now, the RAAS System in full swing in a hypertensive patient normally generates supraphysiologic amounts of Angiotensin II, which stimulates Aldosterone release from the adrenal cortex (Angiotensin II receptors exist there). Aldosterone, in the distal tubules/collecting duct of kidney nephrons, normally binds to mineralocorticoid receptors, which results in the net reabsorption of sodium in exchange for the tubular secretion/loss (into urinary filtrate) of potassium. As stated before, when an ACE Inhibitor or Angiotensin Receptor Blocker (ARB) inhibits that pivotal point (angiotensin I => angiotensin II conversion) in the RAAS system, a lower level of aldosterone is released from the adrenal cortex, making it less available to the mineralocorticoid receptors in the distal nephrons. This understimulation of mineralocorticoid receptors results in the net retention of potassium at this site in the nephron. Of course it is noteworthy to mention that Angiotensin II itself has sodium and potassium altering effects in the kidney, so this mechanism may be a little more complicated. However, the above mechanism is the most common and widely accepted.

Most patients adapt to this effect via compensatory ion exhange upstream (proximal) mechanisms throughout the nephron. Some patients are at a particularly higher risk due to other drugs that alter potassium exhange favoring retention (amiloride, triamterene) and spironolactone/eplerenone (antagonize the aforementioned mineralocorticoid receptor). Remember that Tekturna (aliskiren), the new direct renin inhibitor inhibits the RAAS system at the first step, conversion of angiotensinogen to angiotensin I; this drug can cause hyperkalemia.

By the way, contact me anytime via email for questions. I check it daily.  (+ info)

Hyperkalemia causing muscle weakness in nursing?


I understand why hypokalemia a decrease in muscle activity, but why does hyperkalemia cause muscle weakness?

In hyperkalemia, wouldn't there be more K+, causing increase in muscle activity? Would there be muscle weakness in hyperkalemia because the muscles are being used too much?
I understand why hypokalemia would cause a decrease in muscle activity, but why does hyperkalemia cause muscle weakness?

In hyperkalemia, wouldn't there be more K+, causing increase in muscle activity? Would there be muscle weakness in hyperkalemia because the muscles are being used too much?
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How does hyperventilation treat hyperkalemia?


In a patient with high potassium level, how does hyperventilation help lower K+?
yes, it most certainly does. Just because it doesn't list it there does not mean it isn't an actual treatment for hyperkalemia.

Attention: Anesthesiologists / anesthetists / internist !
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Treatment of hyperkalemia may include any of the following measures, either singly or in combination:

* A diet low in potassium (for mild cases).

* Discontinue medications that increase blood potassium levels.

* Intravenous administration of glucose and insulin, which promotes movement of potassium from the extracellular space back into the cells.

* Intravenous calcium to temporarily protect the heart and muscles from the effects of hyperkalemia.

* Sodium bicarbonate administration to counteract acidosis and to promote movement of potassium from the extracellular space back into the cells.

* Diuretic administration to decrease the total potassium stores through increasing potassium excretion in the urine. It is important to note that most diuretics increase kidney excretion of potassium. Only the potassium-sparing diuretics mentioned above decrease kidney excretion of potassium.

* Medications that stimulate beta-2 adrenergic receptors, such as albuterol and epinephrine, have also been used to drive potassium back into cells.

* Medications known as cation-exchange resins, which bind potassium and lead to its excretion via the gastrointestinal tract.

* Dialysis, particularly if other measures have failed or if renal failure is present.

Treatment of hyperkalemia naturally also includes treatment of any underlying causes (for example, kidney disease, adrenal disease, tissue destruction) of hyperkalemia.

Last Editorial Review: 3/7/2008

In short....it doesn't.  (+ info)

multivitamins, lots of fruit/veg; is it poss that i could get hyperkalemia,hypercalcemia?


I take one centrum, and one 600mg calcium supplement each day along with a balanced diet that includes alot of friuts/veg. I was wondering if it was possible for me to get hyperkalemia or hypercalcemia, or will my kidneys just excrete the excess vitamin/electrolytes?
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Good question. Well your liver and kidneys can put up with a lot, but some things they just cant process. Like for instance too much carrots can turn you yellow, and thiamine acid can turn you reddish, but it would take a lot to do so. Also each person is different so consult your doctor. Bit from my point of view eating healthy is OK, just REALLY mo niter those supplements because accidents happen, and it could really hurt you. Your best bet is just to go talk to a doctor or nutritionist  (+ info)

How does glucose help hyperkalemia?


does it move K+ into the cells? If so, how?
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Glucose doesn't, but insulin does. In severe cases of hyperkalimia it can be treated by starting the patient on IV dextrose (a sugar) and giving them insulin. The insulin causes k+ to move back into the cells and the IV keeps the blood sugar from going too low. If a person had a lot of glucose in their blood the body could release insulin which would help with high potassium, but again, it's not the glucose, it's the insulin.  (+ info)

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