Potassium Disorders

A Tactical Framework for the Wards

When you get a consult for “potassium 2.8” or “potassium 6.1,” don’t think of it as a number to fix — think of it as a signal. Potassium disorders involve total body stores and distribution: where potassium is sitting and why. Only after considering the distribution of potassium should you begin worry about how much potassium the body actually has.

Your job is to determine three things:

1. Is it a shift problem or a total body problem?

2. Is the kidney excreting potassium appropriately?

3. How quickly and safely do I need to act?

Step 1: Verify and Classify

Confirm the value

Repeat the potassium level if the sample was hemolyzed or if the clinical picture doesn’t fit.

Classify

Hypokalemia = K⁺ < 3.5 mmol/L

Hyperkalemia = K⁺ > 5.0 mmol/L

Assess severity and symptoms.

Mild: 3.0–3.5 (often asymptomatic)

Moderate: 2.5–3.0 (weakness, cramps, ileus)

Severe: <2.5 (paralysis, arrhythmia)

Hyperkalemia >6.0 or with ECG changes is an emergency.

Step 2: Think in Compartments

Roughly 98% of potassium is intracellular. Anything that drives K⁺ into or out of cells changes serum potassium without altering total body stores.

Causes of transcellular shift:

Hypokalemia: Insulin, beta-agonists, alkalosis, periodic paralysis, rapid cell production after chemotherapy.

Hyperkalemia: Acidosis, tissue breakdown (rhabdo, tumor lysis, hemolysis), insulin deficiency, beta-blockade.

When potassium changes quickly, think redistribution. When it changes slowly, think total body balance (intake, excretion, or both).

Step 3: Check the Kidney’s Response

Once you rule out a shift, the next question is whether the kidney is doing its job.

Obtain a spot urine potassium, urine creatinine, and ideally urine chloride if the patient is hypokalemic.

Hypokalemia

Use the urine potassium/creatinine ratio as a quick screen:

Ratio < 13 → appropriate renal conservation.

Ratio > 13 → inappropriate renal loss.

If renal wasting, think through these categories:

1. Diuretics (especially loop and thiazide; check medication list).

2. Hyperaldosteronism or excess mineralocorticoid effect.

3. Magnesium deficiency (impairs ROMK channel closure).

4. Distal renal tubular acidosis (urine pH > 5.5, non-anion gap metabolic acidosis).

Hyperkalemia

If the patient has hyperkalemia with no evidence of a transcellular shift, the patient has impaired renal potassium excretion. End of story.

Step 4: Identify Medications and Triggers

For either direction, review every medication.

Hypokalemia: Loop diuretics, thiazides, insulin, diarrhea, beta-agonists, amphotericin, zosyn.

Hyperkalemia: ACE inhibitors, ARBs, potassium-sparing diuretics (especially spironolactone), finerenone, NSAIDs, trimethoprim, heparin, tacrolimus, succinylcholine, and potassium supplements. Look for dietary changes or supplements (salt substitutes, protein shakes, licorice).

Step 5: Evaluate Acid–Base Status

Acid–base disorders shift potassium.

Metabolic alkalosis drives K⁺ into cells → hypokalemia.

Metabolic acidosis (especially mineral acid types) drives K⁺ out of cells → hyperkalemia.

Diabetic ketoacidosis often causes combined acidosis and total body K⁺ deficit despite normal or high serum potassium.

Step 6: Management Principles

Hypokalemia

1. Address the cause. Stop diuretics or laxatives, treat vomiting or diarrhea, replete magnesium if low.

2. Replace potassium.

   1. Oral preferred if possible. Each 10 mEq KCl raises serum potassium by roughly 0.1 mmol/L in a 70-kg adult (less if losses ongoing). When the potassium level is <3.0, it takes 20mEq KCl to raise the potassium by 0.1mmol/L.

   2. IV replacement if K⁺ < 2.8, symptomatic, or cannot take PO. Typical rate: 10 mEq/hr via peripheral line, 20 mEq/hr via central line with cardiac monitoring.

   3. Replace to a potassium level of 4.0. If the patient has CKD, AKI, or is at risk for hyperkalemia with overreplacement, calculate the

3. Avoid glucose-containing fluids (insulin drives K⁺ into cells).

4. Monitor frequently. Recheck every 2–4 hours during IV repletion.

5. If alkalotic, consider KCl; if acidotic, K bicarbonate.

Hyperkalemia

1. If ECG changes or K⁺ ≥ 6.5, act immediately.

2. Stabilize membrane: Calcium gluconate 1 g IV over 5–10 min.

   1. Shift K⁺ into cells:

   2. Regular insulin 10 units IV + D50 (25–50 g glucose).

   3. Nebulized albuterol 10–20 mg.

   4. If acidotic (i.e. a pH <7.1, start a sodium bicarbonate drip.

3. Remove K⁺ from body:

   1. Loop diuretics if making urine.

   2. Sodium zirconium cyclosilicate or patiromer for stable patients.

   3. Dialysis for severe or refractory cases.

4. Review and stop offending medications.

5. Monitor potassium and ECG closely.

Step 7: Integrate Physiology with Context

When evaluating potassium disorders, always ask:

1. Is the kidney handling potassium appropriately?

2. Is the acid–base status contributing?

3. Is there magnesium deficiency?

4. Are there drugs altering aldosterone, distal sodium delivery, or Na⁺/K⁺ ATPase activity?

5. Are there shifts related to insulin, beta-agonists, or pH?

Step 8: Special Considerations

1. Hypokalemia with metabolic alkalosis: Usually due to vomiting, diuretics, or hyperaldosteronism. Check urine chloride:

   1. Urine chloride < 20 → vomiting, prior diuretic use.

   2. Urine chloride > 20 → ongoing diuretic use or mineralocorticoid excess.

2. Hyperkalemia with metabolic acidosis: Think of type 4 RTA (hyporeninemic hypoaldosteronism), often in diabetics with mild CKD. 

3. Hyperkalemia out of proportion to the level of kidney function: think urinary obstruction, Bactrim use, spironolactone use.

Step 9: Monitoring and Consultation

1. For severe abnormalities or ongoing instability, recheck potassium every 2–4 hours until stable.

2. Continuous cardiac monitoring for K⁺ < 3.0 or > 6.0.

3. Consult nephrology for refractory hyperkalemia, unclear renal handling, or dialysis requirement.

Core Mental Framework

1. Confirm and classify.

2. Ask if it’s a shift or total body problem.

3. Determine if the kidney is responding appropriately.

4. Review acid–base and medications.

5. Replace or remove potassium deliberately

6. Understand that potassium movement mirrors the electrochemical life of the cell — insulin, beta-adrenergic tone, and aldosterone are its primary conductors.