Hyperkalemia and glucose / insulin...

[ohmg]

So, I'm a student. I graduate in a few weeks. I've heard that they give glucose for hyperkalemia. While researching this, I see that it is insulin and glucose that is given to push the potassium into the cells. http://www.aafp.org/afp/2006/0115/p283.html

So, I'm wondering what the mechanism is for this.

Please don't respond based on assumption, I'd like to know the actual mechanism and not the assumed one.

I'm thinking that glucose must be electronegative and thereby creates a complex with potassium and pulls it into the cells with it.

I've only taken chemistry to organic II, but not biochemistry yet.

Thanks for your informed responses!

[Rob72, ASN, RN]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1413606/

[Esme12, ASN, BSN, RN]

Yup what he said.......Potassium levels are decreased by insulin. Hypokalemia suppresses insulin release leading to glucose intolerance. this was the best explanation of why it happens that I could find and seems to be tied to ATP activity:

Insulin is the first-line defense against hyperkalemia. A rise in plasma K+ stimulates insulin release by the pancreatic beta cell. Insulin, in turn, enhances cellular potassium uptake, returning plasma K+ towards normal. The enhanced cellular uptake of K+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium ATPase located in cell plasma membranes.

The insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. Insulin deficiency allows a mild rise in plasma K+ chronically and makes the subject liabel to severe hyperkalemia if a potassium load is given. Conversely, potassium deficiency may cause decreased insulin release. Thus plasma potassium and insulin participate in a feedback control mechanism.

http://www.kidneyatlas.org/book1/adk1_03.pdf

http://www.aafp.org/afp/2006/0115/p283.html

[ImThatGuy, BSN, RN]

In a nut shell, it's not the glucose. It's the insulin that does the job, but even though you're using it to reduce the extracellular potassium content, but facilitating its (K+) diffusion back into the cells, the insulin still going to have the same effect on blood sugar levels. That's why you've got to administer some sugar with it so you don't drop the sugar content.

[xtxrn, ASN, RN]

And it's a whole lot more pleasant than kayexolate

[zcoq72mehs]

In a nut shell, it's not the glucose. It's the insulin that does the job, but even though you're using it to reduce the extracellular potassium content, but facilitating its (K+) diffusion back into the cells, the insulin still going to have the same effect on blood sugar levels. That's why you've got to administer some sugar with it so you don't drop the sugar content.

that is correct, it is the insulin

elevated serum k is cardiotoxic.

insulin does not lower total body potassium, nor do we want this to be the case in the majority of hyperkalemic presentations. In the case of diabetic ketoacidosis, for instance, it is the hydrogen ions from anaerobic metabolism intracellulary that has displaced the potassium out of the cell (you must have a balance of anions and cations), producing the increased extracellular potassium, and hyperkalemic presentation

we dont want to use kayexalate (resin binding) in these kinds of presentations, generally.

instead, we correct the underlaying cause of the acidosis. in the case of dka, the osmolarity/osmolality of the serum was greatly increased (due to the sugar), producing diuresis and dehydration.

we therefore must begin fluid volume administration

our goal is not to lower the glucose more than 100mg/dl to avoid cerebral edema from the rapid fluid shift and possible pontine demyelination.

once we get to 250-300mg/dl, we begin dextrose infusions, and depending on sodium and fluid balance, possibly 1/2 to normal saline.

more importantly, we must closely monitor serum potassium, because as we correct the acidosis, the beforementioned hyperkalemia becomes hypokalemic in the majority of cases, as the kidneys exchanged potassium for sodium to try to maintain fluid hemostasis--thus our hyperkalemia is actually a total body hypokalemia.

we can only replace K at a slow rate, depending on access and the literature, about 20meq/hr and it may take 150meq to restore 1 point rise in serum potassium

some literature (the icu book) suggests 60-80meq, but i would be cautious as we use it in cardiac surgery for a reason

so, the tx is usually something like this:

5-10units IV insulin followed by 1-2amps D50% and 5units/hr of insulin drip (0.9mg/kg)

normal saline 200-400ml/hr depending on serum osmolality and cardiac status

monitoring serum glucose q15min--not because we are trying to fix hyperglycemia, but because it is an indirect measurement of acid balance

once the potassium gets to 5, strongly consider k replacement, ie 40meq per liter and up

if the K is very high and we have ecg changes (widened complex, tented t waves, flattened p waves etc, dysrhthmias) we can use cacl 1gm iv for cardioprotective measures

furthermore, we can use sodium bicarbonate, not because we are trying to correct the acidosis, but because it begins the association disassociation process of carbonic acid, tying up hydrogen for exhalation (thus the patient hyperventilates or we do so for them)--now that this transient event is occuring rapidly back and forth, association disassocition, potassium is opposed, moving intracellularly, where again hydrogen is now pushed out cause potassium is back in (hydrogen's affinity to bicarbonate is extreme)

we werent trying to correct the cellular acidosis by giving the bicarb, it just happens this way synergistically (because really we need to correct the cellular hypoxia, whether it be from anaerobic metabolism, cyanide, carbon monoxide, tricyclic OD or what have you)

in the case of tricyclic od, nahco3 has the added benefit of causing ionization once in the bladder, thwarting re-absorption across the lipid-membrane of the bladder wall, thus inactivating the slightly acidic medication

hope that is clear as mud.

my point is that u dont just give bicarb for acidosis as without proper measures it simply goes back and forth with the carbonic acid system--understanding the process allows you to intervene accordingly

that is all i can think of off hand

it is as the two other ppl said--it aint the glucose that treats hyperkalemia, it is indeed the insulin and the cell wall channels

but the brain is very sensitive to blood sugar changes, much more so than absolute serum levels

[nurseprnRN, BSN, RN]

one other quick tip: people always get spazzed about remembering whether intracellular or extracellular na+ and k+ are higher or lower.

hint: when you get your serum lab work back, is the k+ a big number or a little one? is the na+ a big number or a little one? there ya go.