Hyperkalemia
Hyperkalemia questions and answers
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Q: 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?
A: 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.
Q: 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
A: 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.
Q: 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
A: Hi, the normal serum potassium level ranges from 3.5 - 5.2mEq/l. Potassium is mainly intracellular element & the cellular concentration is up to 20 folds the serum level.According to several factors e,g.pH, potassium ions may move across the cell membrane to the inside of the cell lowering the plasma level or to the outside increasing the plasma level. However you did not mention the cause of your hypokalemia, is it GIT problem? Some diuretic drugs also cause hypokalemia.Hyperkalemia above 5.5mEa should not take place as long as your kidneys function properly
My advise to you is to consult your doctor as soon as possible. I hope you find this helpful.
Q: What is the affect of hyperkalemia and hypokalemia on heart rate?
Also tell the mechanism of their affect on heart rate.
A: Either one can stop your heart and can go into cardiac arrest
Q: What is the affect of slight hyperkalemia and hypokalemia on heart rate?
Also tell the mechanism of their affect on heart rate.
A: Doc from India?..........................
Q: How does rhabdomyolysis cause hyperkalemia and metabolic acidosis?
Be specific.
Thanks. :]
A: 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.
Q: 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!
A: 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.
Q: why do your nerve and muscle cells get abnormally excited in hyperkalemia?
I was wondering if someone could explain this simply to me so I understand. a sudden increase in extracellular K+ makes nerve and muscle cells abnormally excitable. Why though? Also what is depolarization. Please help!
A: Hemolysis can cause an increase in potassium in the blood. Hemolytic anemia can be genetically passed on or acquired from drugs or toxins. It causes the breakdown of red blood cells and the hemoglobin is then released into the fluid surrounding these cells.
Repolarization is the return of membrane potential to negative (normal state) after an action potential changed it to a positive state.
Sodium-potassium pumps control the amount of sodium and potassium that enters a cell, which controls the membrane electrical potential by changing the ratio of these negative and positively charged ions. The myocytes (muscle cells) of the heart have these sodium-potassium pumps in their membranes in order to have a resting membrane potential of -90mV.
Now if our friend who has hyperkalemia has an abundance of potassium ions outside the cells, the concentration gradient across the membrane declines and causes a decrease in the resting membrane potential, which causes a decrease in the maximum action potential (the last point of depolarization). When the membrane potential becomes less and less negative and reaches -45mV, Calcium channels are stimulated so that calcium is released into the cells and potassium is released out. Then when the calcium channels close, the potassium channels continue to allow K+ to leave in order to restore the negative potential across the membrane.
The increase in extracellular K+ of people with hyperkalemia changes the effects of important antiarrhythmic agents (drugs that help keep the heart from pumping too fast) which work with the potassium pumps and the change allows the pumps to release even more K+ from the heart cells in a certain time. The higher concentration of potassium leaving makes the resting potential even more positive and even closer to the threshold potential (the membrane potential it must reach at depolarization for an action potential).
Edit: I didn't see you're 'simply' request. Basically the added extracellular K+ changes the membrane potential so that the action potential required for contraction is easier to reach.
Q: Pls help me on HyperKalemia and Insuline glucose treament?
I know hyperkalemia is k+ high in blood. We use insuline glucose to move k+ from the blood into the cell: how this works? And based on this treatment, the cell really won't care too much K+ in cellular level- will this cause cellular K+ toxicity?
Thank you so much.
A: It works because the pump is one of the sodium-potassium pumps, and the intracellular potassium level isn't increased markedly because almost all the total body potassium is intracellular, so you're basically spitting in the ocean.
Q: what is the effect of hypokelamia and hyperkalemia on cell excitability?
what is the effect of hypokelamia and hyperkalemia on cell excitability?
A: Hyperkalemia will do two things - it will depolarize the cell somewhat, but also, since the conductance of potassium channels is also dependent on extracellular potassium concentration, hyperkalemia increases potassium channel conductance.
So, in the hyperkalemic state, the delayed outward potassium current will be greater, decreasing repolarization time, so in a way, it increases excitability by allowing the cell to fire again sooner (which is why it leads to a susceptibility for arrhythmias in the heart). Because the cell is also slightly depolarized, at first, the excitability may also be increased because of this - however, being in a depolarized state also means that more sodium channels will be in the refractory state, which will eventually prevent excitability (which is why potassium is used to stop the heart).
Hypokalemia will decrease potassium channel conductance and lengthen repolarization time and the refractory period (when the cell can't fire again), decreasing excitability in that sense.
Q: How does hyperventilation treat hyperkalemia?
On a patient who is on a vent, how does hyperventilation help lower K+ level?
A: Hydrogen and potassium have a specific relationship within the body. If hydrogen (H) moves out of the cell, potassium (K) moves into the cell, and vice versa (this happens to maintain electrical neutrality, they are both positively charged ions). When a person is hyperventilating, they are blowing their carbon dioxide (CO2) out at a higher than normal rate (that's why they give them a bag to breathe in, so they can inhale the carbon dioxide back in). There is an important chemical equation that will help you understand this better: CO2 + H2O => H2CO3 => H + HCO3 (this happens in the extracellular fluid). H2CO3 dissosiates into HCO3 (bicarbonate, which is a very important buffer in the body) and H (hydrogen, concentrations of which determine if pH of the medium is acidic, high amount of H meaning low pH; or basic, low amount of H meaning high pH). So, by following the formula we can see that if CO2 is going to decrease (because it is being exhaled from the body at a higher than normal rate), then the equilibrium of the equation will shift to the left, meaning that there will be less H2CO3 produced, and that means that there will be less H (hydrogen) and HCO3 (bicarbonate) produced as well. Because there is now a concentration gradient between the inside and the outside of the cell, there is more H inside the cell than outside, H will now move out of the cell into the extracellural fluid so that equilibrium can be established. As I mentioned from the start, when H moves out of the cell, K (potassium) moves into the cell. This movement of K into the cell decreases the amount of K in the extracellular fluid thus lowering the hyperkalemia. Hyperventilation, however, will produce respiratory alkalosis (an increase in blood pH due to lower blood H levels, although there will also be a slight decrease in HCO3, Hydrogen will decrease more).
I haven't heard of this being used as a treatment for hyperkalemia though, because of the fact that respiratory alkalosis will develop. I'd rather give a diuretic (most of them promote K excretion, except K sparing diuretics). Or give a cation exchanger medication, that will bind K and together will be excreted via the gastrointestinal tract. Or give IV glucose and insulin, which will promote movement of K back into the cells.
In a normal person (who doesn't have ion disturbances), hyperventilation will lead to hypokalemia, and hypoventilation, will lead to hyperkalemia.
Hope this answer helped :)
All the best
Q: How does acidosis cause hyperkalemia?
What is the mechanism behind this?
A: Well, in general terms it is like this:
"Acidic blood plasma, or acidosis, is an occasional cause of hyperkalemia. Acidosis, which occurs in a number of diseases, is defined as an increase in the concentration of hydrogen ions in the bloodstream. In the body's attempt to correct the situation, hydrogen is taken up by muscle cells out of the blood in an exchange mechanism involving the transfer of potassium ions into the bloodstream. This can abnormally elevate the plasma's concentration of potassium ions. When acidosis is the cause of hyperkalemia, treating the patient for acidosis has two benefits: a reversal of both the acidosis and the hyperkalemia."
That's pretty general, but it covers the basics. Are you looking into a specific condition?
Q: 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?
A: 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
Q: How does glucose help hyperkalemia?
does it move K+ into the cells? If so, how?
A: 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.
Q: how can a diuretic cause hyperkalemia?
I know it causes the body to store potassium but I need a little more detail...thanks!
A: To understand how different diuretics work, it's critical to understand the physiology of the nephron. If an agent work such that potassium is not properly eliminated from the bloodstream, the consequences can be bad to fatal. To get into the complexities of why certain diuretics are particularly bad actors (especially in patients who already have underlying renal insufficiency) is beyond the scope of a simple explanation. It would require a discussion of the underlying physiology of the kidney and the pharmacology of the different types of diuretics. Not all diuretics have the capacity to produce hyperkalemia (but some do and we have to be very vigilant in ensuring that the serum K level is below toxic levels, otherwise people can die).