Memory palace technique for Hypokalemia & hyperkalemia

You’re going to see potassium disorders constantly on Step—and they’re one of the easiest places to pick up points fast if you have a tight, visual framework. Here’s a shareable “memory palace” you can run through in seconds to nail hypokalemia vs hyperkalemia: causes, ECG changes, acid–base tie-ins, and what to do next.

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The Potassium Palace: One Hallway, Two Doors

Picture a palace hallway labeled “K+ Corridor” with two doors:

• Left door = “LOW-K Lounge” (Hypokalemia)
• Right door = “HIGH-K Hall” (Hyperkalemia)

You’ll “walk” into each room and grab the same items every time:

1. What causes it? (Intake/shift/loss)
2. What does the ECG look like?
3. What symptoms show up?
4. How do I treat it—fast?

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Door #1: LOW-K Lounge (Hypokalemia)

The visual

In the lounge, you see:

• A “DIUretic” dripping water into a drain (renal K+ wasting)
• A vomit bucket + diarrhea toilet (GI losses)
• A bottle of insulin and a β-agonist inhaler pushing K+ into cells
• A “Licorice” rope tied to a mineralocorticoid crown (pseudo-hyperaldosteronism)

One-liner

Hypokalemia = K+ lost (GI/renal) or shifted into cells (insulin/β-agonists/alkalosis).

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High-yield causes (Step-ready buckets)

1) Renal K+ loss (think: “kidneys dumping K+”)

• Diuretics: loop, thiazide (↑ distal Na+ delivery → ↑ K+ secretion)
• Hyperaldosteronism (or increased mineralocorticoid effect)
• Renal tubular disorders
  • Type 1 RTA (distal): hypokalemia + urine pH > 5.5 (can’t acidify urine)
  • Type 2 RTA (proximal): hypokalemia (bicarb wasting)
• Hypomagnesemia (big testable trap)
  • Low Mg → disinhibits ROMK channels → renal K+ wasting
  • If K won’t correct, check/replete Mg

2) GI K+ loss

• Diarrhea (K+ lost in stool)
• Vomiting/NG suction can indirectly cause hypokalemia via metabolic alkalosis and renal K+ wasting (volume depletion → aldosterone)

3) Shift into cells

• Insulin
• β2-agonists (albuterol)
• Alkalosis (H+ leaves cells, K+ enters)

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ECG + symptoms (test-favorite)

ECG in hypokalemia

• Flattened T waves
• U waves
• ST depression
• Prolonged QU → torsades risk

Symptoms

• Weakness, cramps
• Constipation/ileus
• Arrhythmias (especially if on digoxin)

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What to do (fast, safe, board-style)

Treatment approach

• Mild/asymptomatic: oral KCl (preferred if gut works)
• Severe (<2.5), symptomatic, or ECG changes: IV KCl
• Always consider magnesium: replete Mg if low

Step pearls

• Never give dextrose-containing fluids when trying to correct K+ quickly → insulin release can worsen hypokalemia.
• KCl is often preferred because many cases are “chloride-responsive” (e.g., vomiting/diuretics with metabolic alkalosis).

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Door #2: HIGH-K Hall (Hyperkalemia)

The visual

In the hall, you see:

• A crushed “K cell” spilling bananas (cell lysis → K+ release)
• A kidney with a clogged filter (renal failure)
• A “K-sparing” shield labeled ACEi/ARB, spironolactone/eplerenone, amiloride/triamterene, TMP-SMX
• A sign that says “Acidosis opens the exit doors” (K+ shifts out of cells)

One-liner

Hyperkalemia = impaired excretion (kidney/aldosterone) or K+ shifted out of cells (acidosis/cell lysis).

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High-yield causes (the classic Step list)

1) Decreased excretion (most common clinically)

• CKD/AKI (can’t excrete K+)
• Hypoaldosteronism / Aldosterone resistance
  • Type 4 RTA: hyperkalemia + normal anion gap metabolic acidosis
  • Diabetic nephropathy → low renin → low aldosterone
• Drugs:
  • ACE inhibitors / ARBs (↓ aldosterone)
  • Spironolactone/eplerenone
  • Amiloride/triamterene
  • Heparin (↓ aldosterone synthesis—high-yield, often forgotten)
  • TMP-SMX (acts like amiloride at ENaC)
  • NSAIDs (↓ renin → ↓ aldosterone)

2) Shift out of cells

• Acidosis (especially mineral acidosis; boards love “metabolic acidosis → hyperkalemia”)
• Insulin deficiency (DKA)
• β-blockers (less cellular uptake)
• Hyperosmolarity (water out of cells → K+ follows)

3) Increased release (cell breakdown)

• Rhabdomyolysis
• Tumor lysis syndrome
• Hemolysis
• Severe burns
• Succinylcholine (esp. burn/neuromuscular injury patients)

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ECG + symptoms (don’t miss)

ECG progression in hyperkalemia (the “tall-to-wide-to-sine” story)

1. Peaked T waves
2. Prolonged PR, flattened/absent P waves
3. Widened QRS
4. Sine wave → VF/asystole

Symptoms

• Weakness, paresthesias
• Arrhythmias (can be sudden)

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What to do (the board algorithm)

When you see ECG changes or K+ is very high, think in 3 steps:

1) Stabilize the cardiac membrane

• IV calcium gluconate (or calcium chloride via central line)
  • Works fast; does not lower K+, just buys time

2) Shift K+ into cells (temporary fix)

• Insulin + glucose (unless already hyperglycemic)
• β2-agonist (albuterol)
• Sodium bicarbonate if metabolic acidosis (variable effect, but testable)

3) Remove K+ from the body (definitive)

• Loop diuretics (if making urine)
• Potassium binders (e.g., patiromer, sodium zirconium cyclosilicate; SPS is older/less favored)
• Hemodialysis (best for severe/refractory, especially in renal failure)

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Acid–Base tie-in (quick, high-yield)

Use this mental link:

• Acidosis → K+ out of cells → hyperkalemia
• Alkalosis → K+ into cells → hypokalemia

And remember: Type 4 RTA is the hyperkalemic RTA (low aldosterone effect).

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Rapid comparison table (shareable)

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Mini-mnemonics you can recall under time pressure

Hypokalemia: “DIU + GI + IN”

• DIUretics (renal loss)
• GI loss (diarrhea)
• INsulin/β2 (shift INto cells)

Hyperkalemia: “K can’t get OUT”

• Kidney failure / low aldosterone = can’t excrete OUT
• Acidosis/cell lysis = K moves OUT of cells

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Common USMLE traps (don’t fall for these)

• Refractory hypokalemia? Think hypomagnesemia.
• DKA: total body K is depleted, but serum K may be normal/high initially (lack of insulin + acidosis shift K out).
• Type 4 RTA: hyperkalemia + normal anion gap metabolic acidosis—often tied to diabetes and ACEi/ARB use.
• Hyperkalemia with ECG changes: calcium first—don’t “wait for insulin to work.”