Hyperkalemia

Proceed to flow chart 15–3

Is the time period short and/or is the intake of K⁺ low?

Is there a reason to suspect a shift of K⁺ out of cells?

Yes

No

End

Pseudohyperkalemia

Repeated fist clenching, especially in a cachectic patient
Release of K⁺ from blood cells in the test tube (e.g., hemolysis, thrombocytosis, leukocytosis)
Leak of K⁺ from RBCs in vitro

Repeated fist clenching, especially in a cachectic patient
Release of K⁺ from blood cells in the test tube (e.g., hemolysis, thrombocytosis, leukocytosis)
Leak of K⁺ from RBCs in vitro

Tissue trauma or crush injury
Na-K-ATPase problem

hypoxia
lack of a stimulator (e.g., lack of insulin [e.g., DKA], use of β₂ blockers)
presence of an inhibitor (e.g., digoxin toxicity)

Hyperosmolality
-Adrenergic release
Metabolic acidosis due to non-monocarboxylic acids
K⁺ efflux from cells (e.g., administration of depolarizing agents [e.g., succinylcholine], fluoride intoxication)

Tissue trauma or crush injury
Na-K-ATPase problem

hypoxia
lack of a stimulator (e.g., lack of insulin [e.g., DKA], use of β₂ blockers)
presence of an inhibitor (e.g., digoxin toxicity)

Hyperosmolality
-Adrenergic release
Metabolic acidosis due to non-monocarboxylic acids
K⁺ efflux from cells (e.g., administration of depolarizing agents [e.g., succinylcholine], fluoride intoxication)

Tissue trauma or crush injury
Na-K-ATPase problem

hypoxia
lack of a stimulator (e.g., lack of insulin [e.g., DKA], use of β₂ blockers)
presence of an inhibitor (e.g., digoxin toxicity)

hypoxia
lack of a stimulator (e.g., lack of insulin [e.g., DKA], use of β₂ blockers)
presence of an inhibitor (e.g., digoxin toxicity)

Yes

No