Need an explanation please...

[Quidam]

We do Nclex questions in preconference and this question came up.

I have gotten a few different answers of explanation...but nothing that makes sense to me. I thought I would try this forum and see if anyone here could help me out.

A client with chronic renal failure has lab results as follows:

BUN 186, NA 142, K 7.3

The nurse should give priority to which of the following interventions?

a. Initiate an IV of 0.9% NS

b. Give 40 mg furosemide IV

c. Infuse 100 mL D10W with 10 units Regular Insulin

d. Administer sodium polystyrene sulfonate (kayelexate) enema

The correct answer was said to be option c.

There was no rationale with this question and I feel that whatever it is that I am not understanding about administering the Insulin will be critical information for me to understand. Any help is greatly appreciated.

:wink2:

Quidam

[athena55, BSN, RN]

Hello Quidam:

Potassium is a major ion of the body and nearly 95% of potassium is intracellular (think Na+/K+ pump). The ratio of intracellular to extracellular potassium is important when you are talking about membrane potential. Even small changes in the extracellular potassium level can have profound effects on the function of the cardiovascular & neuromuscular systems.

Normal K+ level: 3.5-5.0 mEq/L

Our K+ levels are controlled by intracellular to extracellular exchange, again mostly by that Na+/K+ pump that is controlled by insulin and beta 2 receptors (beta 1 = heart, beta 2 = lungs, kidney....1 heart, 2 kidneys/lungs...a helpful hint to remember the difference between beta 1 and beta 2!)

So any K+ > 7.0 is severe and potentially life-threatening.

What can cause hyperkalemia? Acute or chronic renal failure, potassium sparing diuretics, urinary obstructions, sickle cell disease, Addison's disease, Lupus, over-use of potassium supplements, rhabdomyolysis, trauma, hemolysis, tumor lysis syndrome, burns, blood transfusions, acidosis, acute dig toxicity, beta blockers, DKA....

SO the primary cause of death is potassium's effect on cardiac muscle and function.

Changes you would see with hyperkalemia: peaked T waves, a shortened QT interval, ST-segment depression, wide QRS, increases in PR interval

Treatment: Insulin is administered with glucose to facilitate the uptake of glucose into the cell which helps to bring the K+ with it. Causes a temporary shift of the K+ back into the cells, so then you've got to find out the cause of the increased K+ levels

Going through those choices:

a) start an IV with 0.9% NS: Na 142 is normal and the IV fluid will not help the immediate problem of a life threatening electrolyte result

b) give 40 mg Lasix IV: again not an immediate solution as onset is 20-60 minutes and peaks in 1-2 hours

d) Adminsiter sodium polystyrene sulfonate: true it is "a potassium-removing resin that exchanges sodium ions for potassium ions in the intestine" (Nursing Drug Handbook; 2006, pg 1257) but the onset can take over 2 hours !

That is why answer "c" was the best choice.

I hope this helps.

athena 66H8A

[rotteluvr31, ADN, RN]

In my very simple way of viewing things, I imagine insulin as a big hammer that smacks K+ back into the cells, thereby lowering the K+ level.

Like I said, this is very simple. Athena55 provided a most excellent answer as to the pathophys behind the answer.