Although hyperkalemia has many etiologies (Table 74.1), there are three distinct pathways: (i) ineffective elimination of potassium during any interval in the perioperative period, almost always due to renal failure; (ii) acute potassium load from a medication error or massive transfusion of stored blood; (iii) movement of potassium ions from the intracellular space to the extracellular space. This last can occur with the use of succinylcholine, especially for burn patients or paralyzed patients. It can also be seen with changes in ventilation and/or acid-base status in patients on certain drug combinations (spironolactone/beta-blockers) or significant physiologic derangements such as diabetic ketoacidosis. At the cellular level, hyperkalemia interferes with neuromuscular transmission and thus produces skeletal and cardiac muscle abnormalities. Neuromuscular transmission depends on membrane excitability. Increased extracellular potassium depolarizes the cell membrane, making the cell more excitable, and requiring less of a stimulus to generate an action potential. The hyperexcitability eventually
inactivates sodium channels and leads to cardiac conduction abnormalities and muscle paralysis.

A valuable resource is the Cochrane Database of Systematic Reviews, which has published recommendations for emergency interventions for hyperkalemia. Current evidence suggests that intravenous (IV) insulin and glucose combined with nebulized beta-adrenergic receptor agonists were more effective than each treatment alone.