Electrolytes and Drug Effects on the EKG
Key EKG patterns for potassium, calcium, digoxin, and QT-prolonging drugs.
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Questions Covered in This Set
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Earliest EKG sign of hyperkalemia?
Peaked T waves (~5.5–6.5 mEq/L): tall, narrow, symmetric, tent-shaped with a narrow base, best seen in V2–V4.
Sequence of hyperkalemia changes as potassium rises
Peaked T waves → P-wave flattening and PR prolongation → bizarre QRS widening → sine wave (>9 mEq/L, peri-arrest).
Treatment for the sine-wave pattern of severe hyperkalemia
IV calcium immediately — it stabilizes the myocardial membrane within minutes but does not lower the potassium level.
Hypokalemia EKG findings
Flattened T waves, prominent U waves (sometimes larger than the T), ST depression, and an apparently long QT (really QU) with torsades risk.
Hypercalcemia vs. hypocalcemia on EKG
Hypercalcemia = short QT (ST segment nearly disappears); hypocalcemia = long QT from a long, flat ST segment with a normal-width T wave.
How to distinguish hypocalcemic long QT from drug-induced long QT?
Hypocalcemia stretches the flat ST segment before the T; drugs widen or notch the T wave itself.
What is 'digoxin effect'?
Expected at therapeutic levels: downsloping, scooped/sagging ST depression (Salvador Dalí mustache) in leads with tall R waves, with short QT — not toxicity or ischemia.
Hallmark rhythms of digoxin toxicity
Increased ectopy plus block: atrial tachycardia with 2:1 block, bidirectional VT, frequent PVCs, junctional rhythms, and regularized atrial fibrillation.
Wide-complex bradycardia with no P waves in a dialysis patient — think what?
Hyperkalemia until proven otherwise; treat empirically rather than waiting for the lab.
Common QT-prolonging drug classes
Antiarrhythmics (sotalol, amiodarone, procainamide), antipsychotics (haloperidol, quetiapine), antidepressants (citalopram, TCAs), and antibiotics (macrolides, fluoroquinolones) — all block the hERG potassium channel.
