Evaluation of Potassium Disorders

Last updated: April 6, 2026, 6:50 PM Pacific Time (PDT)

Shared bedside framework for hypokalemia and hyperkalemia. Choose whether the active potassium problem is low or high, then use the adaptive assistant to sort redistribution, renal handling, medication effects, acid-base context, and urgent ECG-risk situations.

Interactive diagnostic assistant

Activate the assistant to adapt the page to either hypokalemia or hyperkalemia and re-rank likely mechanisms from entered data.

Potassium pattern Hypokalemia present Hyperkalemia present

Potassium (mEq/L)

History and bedside clues

ECG changes or major arrhythmia concern Acute onset or rapidly changing potassium AKI, CKD, or impaired renal excretion concern

Other labs

Core labs

Bicarbonate / CO2 (mEq/L, ref about 22-28)
Creatinine (mg/dL, ref about 0.6-1.3)
Magnesium (mg/dL, ref about 1.7-2.2)
Urine potassium (free text)

Optional labs

Glucose (mg/dL, ref about 70-180)
Phosphate (mg/dL, ref about 2.5-4.5)
CK / tumor-lysis markers (CK often abnormal if >1000 U/L)
Renin / aldosterone (free text)

Free-text entries are interpreted automatically when they look high, normal, low, suppressed, elevated, or clearly abnormal.

Likely mechanisms

Likely diagnoses from entered data

This is a simplified teaching assistant for bedside potassium reasoning. Severe potassium abnormalities, ECG changes, or arrhythmia concern still need immediate clinical judgment and urgent treatment planning.

Flowchart

Step 1

Define direction and urgency first

Before chasing mechanism, decide whether the active problem is low potassium or high potassium and whether ECG changes, weakness, or arrhythmia risk make the pace urgent.

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Step 2

Use shared anchors

Medication review, kidney function, acid-base context, magnesium, and whether the kidney is appropriately excreting potassium prevent premature anchoring.

Hypokalemia branch

Loss

GI loss or renal potassium wasting

Vomiting, diarrhea, diuretics, hyperaldosterone states, and magnesium deficiency live here.

Shift

Intracellular shift or refeeding pattern

Insulin, beta-agonists, alkalosis, and refeeding can lower serum potassium without the same degree of total-body deficit.

Hyperkalemia branch

Excretion

Reduced renal excretion or medication-associated hyperkalemia

AKI, CKD, RAAS blockade, mineralocorticoid deficiency, and type 4 physiology are common anchors.

Release / shift

Cellular release, acidosis, or pseudohyperkalemia

Tumor lysis, rhabdomyolysis, hemolysis, acidosis, and sample artifact need to stay on the list.

Teaching pearl: potassium disorders are often a kidney-handling problem, a medication problem, or a shift problem. Asking which of those three is active usually gets you close fast.