[Courtney1202]

Hey you might want to clarify with your instructor. Was this a cardiac patient or is it a diabetic ketoacidosis crisis patient question? Maybe the insulin was already running on a pump, and they went into arrest because they didn't replace the K+ quickly enough.

[rgroyer1RNBSN]

You might want to add in there to we also use Kaexylate for hyperkalemia

[neneRN]

Only reason I can think of is to treat a high K as cause of arrest, but even then Calcium works faster.

[ICUadmirer]

Possibly treating H's and T's (refer to your ACLS manual)

[msjangir]

I am working in a critical care setup but i have never heard insulin during the code. She may want to convey dextrose + insulin which is used to revert hyperkalemia.

[RN Randy]

Never seen insulin in a code either...? We do have a "K-Lowering Cocktail" that we drip for hyperkalemia... I believe it includes insulin/D50, Calcium Gluconate and HC03 in a 250 bag.

rb

[SEOBowhntr]

Therapy: Insulin plus glucose .. Dose: (use 1 U insulin/5 g glucose) Regular insulin 10 U IV plus 50 g glucose ... Mechanism: Shifts ... Onset: 30 min .. Duration: 4-6 h

The key here is that it lasts longer. Certainly in acute management, Calcium is optimal, but how long will it last, and at what point does TOO much Calcium become problematic. I was involved in a code when the Dr. decided on 3 amps of Calcium, guess what....Way too much. Overshot the problem, the first amp stabilized the patient, and he was actually doing ok, but when the doc heard that the serum K+ was 8.8, he decide that we should give 2 more amps. Nearing the end of the second amp, the patient went into VT and we never got him back.

You also have to look at the overall condition of the patient. If it's a post abd. surgery patient with an ileus, certainly Kayexalate isn't such a good choice. Renal failure patients seem to respond well to the Insulin therapy, while Lasix in complete renal failure would be a waste of your efforts.

Certainly it's not the first choice in all cases, and it's not overly common, but...it does have it's place. I've given it during code or "peri-arrest" situations at least half a dozen times when we had a known hyperkalemia.

[platon20]

There's a lot of misinformation on this thread.

1) Insulin does not treat cardiac arrest specifically, its used for hyperkalemia which can lead to cardiac arrest. Insulin has no role in a non-hyperkalemic cardiac arrest patient.

2) The problem with necrosis of myocytes is NOT that they dont have enough glucose and therefore need insulin. The cells die because of lack of oxygen, not lack of glucose. Giving insulin to these cells wont do a thing to help them.

3) Calcium does not correct hyperkalemia, its used ONLY for stabilizing the cardiac membrane potential to prevent cardiac arrest. High K levels shift the resting membrane potential upwards and shut off ingoing Na channels, which causes wide QRS and eventually arrest if not corrected due to the inability to depolarize because of hte closed Na channels. Supplying calcium opens up the Na/Ca exchanger, which allows depolarization and lowers the resting membrane potential back to its previous level of -85 to -95 mV.

4) Kayexalate is the best way to treat the actual hyperkalemia, but as somebody else said you need properly functioning bowels to make it work. If somebody has a compromised GI tract or otherwise cant take PO, then you need to use an alternate method. It works thru a binding resin sodium/potassium exchange system. Basically it binds potassium int the gut and its expelled in the feces.

5) Insulin is a commonly used alternate method. The insulin protein partially activates the H/K ATPase pump on cell membranes, which releases H+ while allowing K+ in. Beta agonists and bicarbonate work the same way. Diuretics can increase K+ excretion from kidneys and are also used occassionally.

[sirI]

There's a lot of misinformation on this thread.

Yes, there is.

1) Insulin does not treat cardiac arrest specifically, its used for hyperkalemia which can lead to cardiac arrest. Insulin has no role in a non-hyperkalemic cardiac arrest patient.

True. Insulin has no role in non-hyperkalemic cardiac arrest.

3) Calcium does not correct hyperkalemia, its used ONLY for stabilizing the cardiac membrane potential to prevent cardiac arrest. High K levels shift the resting membrane potential upwards and shut off ingoing Na channels, which causes wide QRS and eventually arrest if not corrected due to the inability to depolarize because of hte closed Na channels. Supplying calcium opens up the Na/Ca exchanger, which allows depolarization and lowers the resting membrane potential back to its previous level of -85 to -95 mV.

Yes, it does. Calcium does correct hyperkalemia. Calcium choloride/gluconate does stabilize the myocardial cell membrane to shift potassium back into the cell, where it belongs, and thereby allow potassium elimination. And, the former (choloride) is indicated for severe hyperkalemia (over 7) during cardiac arrest.

4) Kayexalate is the best way to treat the actual hyperkalemia, but as somebody else said you need properly functioning bowels to make it work. If somebody has a compromised GI tract or otherwise cant take PO, then you need to use an alternate method. It works thru a binding resin sodium/potassium exchange system. Basically it binds potassium int the gut and its expelled in the feces.

Since we are discussing cardiac arrest, kayexalate would definitely not be indicated.

5) Insulin is a commonly used alternate method. The insulin protein partially activates the H/K ATPase pump on cell membranes, which releases H+ while allowing K+ in. Beta agonists and bicarbonate work the same way. Diuretics can increase K+ excretion from kidneys and are also used occassionally.

True. Insulin, along with glucose, is indicated in hyperkalemic cardiac arrest. But, it is short term and should be followed with methods to remove total body potassium.

[platon20]

Yes, it does. Calcium does correct hyperkalemia. Calcium choloride/gluconate does stabilize the myocardial cell membrane to shift potassium back into the cell, where it belongs, and thereby allow potassium elimination. And, the former (choloride) is indicated for severe hyperkalemia (over 7) during cardiac arrest.

Thats wrong. Calcium DOES NOT CAUSE K+ TO MOVE INTRACELLULARLY. Only insulin, bicarb, and beta agonists do that. Stabilizing the myocardial membrane has NOTHING to do with K+ transcellular shifts. In a low threshold environment (created by excess K+ shifting the resting membrane potential upwards by the Nernt equation: Em = KT/N ln (Kout/Kin). As the membrane potential shifts up, sodium channels become less responsive. Calcium influx induces the sodium channels to open again. Calcium has NOTHING to do with opening K channels.

There are 2 ways to eliminate excess K+

1) Fecal losses
2) Renal losses

Shifting K+ into cells is a temporary fix ONLY. Once the K+ shifts intracellularly, it is not "eliminated" it just hangs out and is then shifted back outside the cell once the acidotic/alkalotic pH shifts, insulin decreases, beta agonist decreases, etc