Shifting potassium from the extracellular to the intra- cellular compartment remains a mainstay of acute treat- ment. Insulin and beta-2 adrenergic agonists (e.g., salbu- tamol/albuterol) decrease serum potassium by stimulat- ing the Na/K-ATPase pump, shifting potassium from the extracellular to the intracellular compartment in exchange for sodium. Beta-2 adrenergic stimulants combined with insulin have been shown to have potassium-lowering effect greater than when used alone, and also have been shown to reduce the incidence of insulin induced hypo- glycemia. The efficacy of beta-2 adrenergic agonists is variable, and these agents should not be used as mono- therapy. There is growing evidence for the role of al- buterol in treating severe hyperkalemia [15]. Catechola- mines activate Na-K ATPase pumps through B2 receptor stimulation that may add to the effects on insulin [16]. In addition to insulin, sodium bicarbonate buffers hydrogen ions extracellularly while shifting potassium intracellu- larly to maintain electrical neutrality. Sodium bicarbon- ate should be reserved for cases with metabolic acidosis because effects may be delayed or unreliable especially in patients with renal dysfunction.