Potassium and Insulin Relationship

medicrn16 · Oct 9, 2008

Hey Standout...we JUST had a test on this two weeks ago, lol. Hardest dang test I ever took.

Basically, insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the famous sodium-potassium pump. However, this is only a temporary fix and monitoring for the hypokalemic/hypoglycemic effects would be necessary. You would have to give glucose with the insulin as part of the regimen. It depends on whether the person has an actual total body excess of K+ or the K+ has moved from ICF to ECF as to how well this will work and for how long.

Causes of movement from ICF to ECF would be tissue damage, acidosis, hyperuricemia, and uncontrolled DM.

Causes of excess total body K+ would be too much potassium foods, salt substitutes, transfusions of whole blood or PRBCs, and decreased K+ excretion from the kidneys due to K+ sparing diuretics, renal failure, or Addison's disease.

Hope this helps. For me to pass this test (fluids and electrolytes) I made a chart with similarities/differences. Thank God for this. I escaped the doom of much of the class with a B. Hoo-ray.

Daytonite, BSN, RN · Oct 9, 2008

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 liable 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.

medicrn16 · Oct 10, 2008

daytonite 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 liable 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.

I am printing this and putting in my notes for my final. Excellent! Thanks.

Daytonite, BSN, RN · Oct 10, 2008

Just found this:

http://www.kidneyatlas.org/book1/adk1_03.pdf - Disorders of Potassium Metabolism

spongebob6286, BSN, RN · Oct 12, 2008

Insulin moves glucose inside the cells and it brings along with it potassium and so that's why insulin is given to hyperkalemic pt.

HamsterRN, ADN, RN · Apr 9, 2009

Could someone explain to me why we give insulin and dextrose to treat hyperkalemia? I realize that insulin and glucose help drive potassium into the cells thereby reducing serum potassium levels, but given the choice wouldn't it be better to leave it in the serum rather than forcing it into the cells? The main risk of hyperkalemia is cardiac arrest caused by high potassium levels in cardiac muscle cells. Pushing more potassium into these cells seems idiotic. Since we can't directly measure intracellular potassium, we measure serum potassium which has a predictable correlation with intracellular potassium levels, while I agree that forcing potassium into the cells to 'hide' it makes your labs look better, it would seem like it could potentially kill your patient.

allnurses Guide · Apr 11, 2009

HamsterRN said:
The main risk of hyperkalemia is cardiac arrest caused by high potassium levels in cardiac muscle cells.

Hyperkalemia is not used as a surrogate measure of intracellular potassium levels. K+ is primarily an intracellular cation, and almost all of the body K+ stores are intracellular. High SERUM potassium directly causes cardiac arrhythmias. Otherwise, there's no reason that someone with hyperkalemia due to extracellular shifts, say from acidosis (ie. no increase in total body potassium stores), would get cardiac arrhythmias. They would not have an increase in INTRAcellular K+, just extracellular (serum).

The problems are caused generally by cell membrane instability due to an alteration in ICF/ECF ratio of K+, which leads to reduced resting membrane potential and delayed depolarization (ie. narrow peaked T waves, shortened QTi, loss of atrial activity).

Valharley · Feb 4, 2011

Actually there is a lab test for intracellular Potassium called an RBC Potassium test. I found this site looking for more information about my OWN issues as I have been on 120mEq potasisum for about 2 years now and just had to raise my insulin a little and now I am feeling the old low potassium symptoms again. It starts as muscle pain and fluid retention, so common in Diabetics I have to wonder how many on insulin need potassium and do not know it. My serum K was 4.2 when I started supplementing and now it is 4.0, but symptoms relief is amazing, I was ready to go into forced retirement 2 years ago now I am good to go for another 5-7 years. I also had 15 years chronic IBS that stopped like turning off a faucet when I started supplementing 40mEq potassium. Hip pain I thought was arthritis, gone, back pain, same. Urinary leakage I thought was due to early hysterectomy, gone. The lab that did my RBC potassium testing stated they had NEVER done this test before! Please become pioneers with Diabetics in running this test.

JROregon, ASN, BSN, RN · Feb 8, 2011

RBC = red blood cells. Red blood cell are part of the extracellular fluid so I don't understand your point Valharly. The serum and red blood cells are all part of blood and are extracellular not intracellular.

Valharley · Feb 9, 2011

RBC potassium tests what is inside the red blood cells which is where potassium is stored. SERUM tests extracellular potassium which is where the body used it from to take it inside the RBC when that falls low. Normal serum potassium does not preclude low potassium. Testing RBC levels will show up deficiencies not showing in serum.

JROregon, ASN, BSN, RN · Feb 9, 2011

RBCs are not true cells. They carry oxygen. They don't store potassium. Our real cells "store" potassium. Potassium and Sodium go back and forth between the plasma portion of blood/ interstitial fluid and the real cells. When you get a blood test to check potassium levels, the potassium is not in the red blood cells, it is in the plasma portion. Also, potassium isn't truly "stored" in the body. If we don't get enough dietary potassium, it will escape in the urine and leave the body depleted.