In emergent management of hyperkalemia

Q: All of the following can be used in emergent management of hyperkalemia EXCEPT? - Select one

A) Intravenous Epinephrine 

B) Nebulized Albuterol

C) Intravenous Albuterol

D) Subcutaneous Terbutaline

E) Insulin with glucose 

Answer: A

Beta-2-adrenergic agonists (B2AA) are used as adjuvant treatment in emergent hyperkalemia. Although 'Epi' (choice A) is a B2AA, it can induce angina. A large proportion of patients who developed hyperkalemia usually have renal failure/insufficiency and are prone to have underlying subclinical coronary disease.

Mechanism of Action (MoA): The B2AA drives potassium into the cells by increasing the activity of the Na-K-ATPase pump in skeletal muscle. Beta-2-adrenergic receptors in skeletal muscle also activate the inwardly directed Na-K-2Cl cotransporter, which may account for as much as one-third of the uptake response to catecholamines. B2AA in the acute treatment of hyperkalemia lowers the serum potassium concentration by 0.5 to 1.5 mEq/L. The reason B2AA is used only as an adjuvant treatment is that it takes approximately 30 minutes to achieve peak effect with intravenous infusion and 90 minutes with nebulization.

Albuterol (choices B and C) is relatively selective for the beta-2-adrenergic receptors. The dose for emergent hyperkalemia administered via nebulizer is 4 to 8 times the dose for bronchodilation, i.e., 10 to 20 mg in 4 mL of saline, administered over 10 minutes by nebulization. Less well known is the fact that Albuterol can be given IV in a dose of 0.5 mg. Similarly, SQ terbutaline (choice D) is a suitable option when an IV line or nebulizer is unavailable or the patient can't tolerate them.

Insulin (choice E) is not a B2AA, but it drives potassium inside the cell and decreases the extracellular potassium transiently. Glucoce is added to insulin to avoid hypoglycemia.

Emergent dialysis is an effective way of lowering K, but arrangements may take time.

#electrolytes

References:

1. Clausen T, Everts ME. Regulation of the Na,K-pump in skeletal muscle. Kidney Int 1989; 35:1.

2. Gosmanov AR, Wong JA, Thomason DB. Duality of G protein-coupled mechanisms for beta-adrenergic activation of NKCC activity in skeletal muscle. Am J Physiol Cell Physiol 2002; 283:C1025.

3. Sowinski KM, Cronin D, Mueller BA, Kraus MA. Subcutaneous terbutaline use in CKD to reduce potassium concentrations. Am J Kidney Dis 2005; 45:1040.

4. Palmer BF, Carrero JJ, Clegg DJ, Colbert GB, Emmett M, Fishbane S, Hain DJ, Lerma E, Onuigbo M, Rastogi A, Roger SD, Spinowitz BS, Weir MR. Clinical Management of Hyperkalemia. Mayo Clin Proc. 2021 Mar;96(3):744-762. doi: 10.1016/j.mayocp.2020.06.014. Epub 2020 Nov 5. PMID: 33160639.