Hyperkalemia: ECG Changes & Emergency Management (USMLE)

Why this matters

Hyperkalemia kills the indecisive. The difference between “hmm” and “give calcium now” is a cardiac arrest. This post gives you a rapid, exam‑proof playbook: what to look for, what to push, and what to stop.

Step 1 integration: Raising extracellular K⁺ depolarizes the resting membrane potential (less negative), inactivating fast Na⁺ channels → slowed conduction and arrhythmias. The Nernst equation & the Na⁺/K⁺‑ATPase pump live behind every ECG change you see.

The big picture (fast)

• When to panic: ECG changes (peaked T’s, PR prolongation, QRS widening → sine‑wave), severe K⁺, or symptoms.
• Immediate goal: stabilize myocardium with IV calcium.
• Shift K⁺ intracellularly: insulin + dextrose, high‑dose β‑agonist, bicarbonate (if acidemic).
• Remove K⁺ from body: loop diuretics, potassium binders, dialysis.
• Stop the cause: meds (ACEi/ARB, spironolactone, trimethoprim, NSAIDs), missed dialysis, tissue breakdown.
• Goal is to avoid cardiac arrest, ACS, and heart failure.

Step 1 integration: Insulin stimulates Na⁺/K⁺‑ATPase → K⁺ influx; β₂‑agonists increase cAMP with similar effect; acidemia shifts H⁺ into cells and K⁺ out via H⁺/K⁺ exchange—fixing pH helps fix K⁺.

Pathophysiology you actually use

• Renal excretion controls K⁺ long‑term. Aldosterone upregulates ENaC and Na⁺/K⁺‑ATPase in principal cells, favoring K⁺ secretion into the lumen. CKD, hypoaldosteronism, and drugs that block RAAS or ENaC/ROMK crank up serum K⁺.
  Step 1 integration: Aldosterone ↓serum K⁺ by ↑ENaC (apical) and ↑Na⁺/K⁺‑ATPase (basolateral). Removal of lumen‑negative potential (e.g., amiloride) reduces K⁺ secretion.
• Beware pseudo‑hyperkalemia: hemolyzed sample, prolonged tourniquet, leukocytosis/thrombocytosis. Always re‑draw if the ECG is pristine and the story smells off.

Clinical vignette #1 — DKA trap

A 22‑year‑old with DKA: fruity breath, K⁺ 6.8, bicarbonate 10, glucose 520. ECG shows tall, narrow, peaked T waves in V2–V4.
Moves:
1) Calcium gluconate 1–2 g IV (membrane stabilization).
2) Regular insulin 10 units IV + 25 g dextrose (add D10W if glucose <250 after bolus).
3) High‑dose nebulized albuterol (10–20 mg).
4) Fluids + insulin infusion to fix ketoacidosis (the real problem).
Pearl: Total body K⁺ is low in DKA from osmotic diuresis; serum is “fake high.” Once insulin flows, K⁺ plummets—replace K⁺ when serum K⁺ <5.0 and patient is urinating.
Step 1 integration: Insulin deficiency + acidosis shift K⁺ out of cells; therapy reverses both, driving K⁺ back in and unmasking total body depletion.

Clinical vignette #2 — Dialysis miss + drug stack

A 68‑year‑old with ESRD misses dialysis. Med list: lisinopril + spironolactone + TMP‑SMX. He’s weak; ECG shows PR prolongation, wide QRS. K⁺ 7.2.
Moves now:
1) Calcium chloride 1 g IV via central line (or gluconate peripherally) for immediate stabilization.
2) Insulin + dextrose and albuterol.
3) Call nephrology for urgent hemodialysis (definitive).
4) Hold offending meds.
Step 1 integration: ACEi/ARB ↓aldosterone; spironolactone antagonizes mineralocorticoid receptor; trimethoprim blocks ENaC (amiloride‑like). All three decrease distal K⁺ secretion.

ECG changes: what they actually look like

• Early: narrow, peaked T waves (especially precordial leads).
• Progression: short QT, PR prolongation, QRS widening, loss of P waves, finally sine‑wave and ventricular arrhythmias.
  Pro tip: ECG sensitivity is imperfect—treat the patient, not a pretty tracing.

Step 1 integration: Depolarized resting potential inactivates fast Na⁺ channels → slowed phase 0 upstroke → widened QRS; repolarization changes drive T‑wave morphology.

ED/ICU algorithm (simple and safe)

1) Confirm & strip errors: verify non‑hemolyzed sample; get ECG immediately.
2) If ECG changes or K⁺ ≥6.0 or symptomatic:

• Calcium gluconate 1–2 g IV (or calcium chloride 1 g IV, central). Repeat if QRS still wide.
  3) Shift K⁺ into cells (temporary):
• Regular insulin 10 units IV + 25 g dextrose (skip dextrose if glucose ≥250; re‑check glucose q30–60 min).
• Albuterol 10–20 mg nebulized (or 2–4 mg IV if available).
• Sodium bicarbonate 50–100 mEq IV if pH ≤7.1 or severe metabolic acidosis.
  4) Remove K⁺ (definitive):
• Loop diuretic + fluids if kidneys work.
• Potassium binders: sodium zirconium cyclosilicate or patiromer (onset hours; SPS is legacy and has GI risks).
• Hemodialysis for ESRD or refractory cases.
  5) Stop sources: RAAS blockers, K‑sparing diuretics, NSAIDs, trimethoprim, heparin (hypoaldo), supplements, salt substitutes.
  6) Re‑check K⁺ & ECG q1–2h until stable; watch for rebound.

Step 1 integration: Distal nephron K⁺ secretion needs a lumen‑negative potential (Na⁺ uptake via ENaC). Block ENaC (amiloride/trimethoprim) → less negativity → less K⁺ secretion.

Testing extras you might see

• TTKG (trans‑tubular K gradient): in true hyperkalemia, a low TTKG suggests impaired aldosterone effect or distal flow; not needed for emergent care but fair game for exams.
• Magnesium & calcium: correct concomitant abnormalities that worsen arrhythmias.
• Tumor lysis/rhabdo: aggressive fluids, treat underlying cause, consider rasburicase in TLS.

Step 1 integration: Cell lysis and acidosis raise serum K⁺; β₂ agonism and alkalosis lower it by intracellular shift.

Take‑home (tattoo this)

Stabilize with calcium, shift with insulin/β₂/bicarb, remove with diuretics/binders/dialysis, and stop the causes. If the QRS is fat, don’t philosophize—push calcium.

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