1. Potassium
Potassium changes are often described as pushing the T wave in one direction or the other — hyperkalemia "pulls it up," hypokalemia "pushes it down" — a genuinely useful way to remember the pattern, since the effects then cascade the same direction through the rest of the tracing.
| Stage | Hyperkalemia progression |
|---|---|
| Earliest | Tall, narrow-based ("tented") T waves, especially precordial — often the first sign, typically mild-moderate elevation |
| Moderate | P wave flattening, PR prolongation, atrial arrest / nodal rhythms |
| Severe | QRS widening, right axis deviation, tall terminal R in aVR (mimicking sodium-channel toxicity) |
| Pre-terminal | QRS and T merge into a "sine wave" pattern — a pre-arrest rhythm that can be mistaken for VT/idioventricular rhythm in the absence of visible P waves |
Counterintuitive finding: a retrospective study of 188 patients with severe hyperkalemia found that peaked T waves alone did not predict short-term adverse events — the ECG changes that did were more advanced (widened QRS, bradyarrhythmia, high-grade block). Don't let a reassuring-looking T wave alone talk you out of treating a severe lab value.
Hyperkalemia is the "great ECG imitator" — it can mimic an anterior STEMI closely enough (particularly in V1-V2) that patients have gone to the cath lab for hyperkalemia. If the pattern doesn't fully fit a coronary distribution, or the clinical picture doesn't fit ACS, check a potassium before assuming occlusion.
Hypokalemia runs the opposite direction: T-wave flattening/inversion, ST depression, and prominent U waves — sometimes fusing with the T wave into a T-U complex easy to mistake for QT prolongation. Hypokalemia also increases automaticity and reduces AV conduction in a manner that parallels digoxin toxicity — worth remembering when both are plausible in the same patient.
Critical interaction: IV calcium, the standard cardioprotective treatment for hyperkalemia, can precipitate fatal arrhythmia if the hyperkalemia is being driven by digoxin toxicity. Ask about digoxin use before pushing calcium in a hyperkalemic patient with any digoxin-effect features on the tracing.
2. Calcium
| Abnormality | ECG finding |
|---|---|
| Hypercalcemia | Shortened QT interval — often a symmetric, domed ST-T complex without a true ST segment. Can produce tall, peaked T waves in V2-V3, and can mimic a lateral occlusion MI pattern. |
| Hypocalcemia | Prolonged QT interval — the ST segment itself lengthens (distinct from a prolonged QT from repolarization/T-wave abnormalities), raising torsades risk if severe. |
QT shortening alone is nonspecific — catecholamine excess, acidosis, digoxin, and simply being critically ill can all shorten it. Hypercalcemia is one differential among several, not a diagnosis to make from the ECG in isolation.
3. Digoxin: Effect vs. Toxicity
This is one of the most consistently confused pairs in ECG interpretation, and the distinction changes what you do next: one is an expected finding in a patient taking the drug, the other is an emergency.
Digoxin effect (seen at therapeutic levels, does NOT imply toxicity): downsloping, "scooped" ST depression — variously called a reverse tick, hockey stick, or "Salvador Dali's moustache" — most prominent in leads with a tall R wave (V5-V6). Shortened QT interval. Flattened, biphasic, or inverted T waves. Increased U-wave amplitude. The scooped depression characteristically starts from the isoelectric line without J-point depression.
Digoxin toxicity can occur with or without the classic "effect" morphology present, and vice versa — the ECG "effect" pattern is not a reliable marker of toxicity either way. What actually signals toxicity: PVCs (the most common toxic dysrhythmia), any new bradycardia or AV block with increased automaticity elsewhere (atrial tachycardia with block, accelerated junctional rhythm, slow atrial fibrillation), and — near-pathognomonic when present — bidirectional ventricular tachycardia.
The clinical takeaway: don't diagnose toxicity from the scooped ST segment alone, and don't rule it out just because the classic scoop isn't there. Diagnose toxicity from the rhythm and the clinical picture (nausea, visual changes, hyperkalemia in acute overdose, renal function), with the level as supporting evidence, not the ST morphology.
4. Other Drug Effects
| Drug / class | ECG changes |
|---|---|
| Tricyclic antidepressants / Na-channel blockers | QRS widening, terminal R wave in aVR — the substrate for the sodium bicarbonate treatment covered in the Antidotes & Reversal Agents guide. |
| Amiodarone | QT prolongation, bradycardia — expected pharmacologic effect; distinguishing expected QT prolongation from a dangerous one is a clinical judgment call, not an ECG-alone one. |
| Beta-blockers / calcium channel blockers | Bradycardia, PR prolongation, AV block — overdose management for both lives in the Antidotes & Reversal Agents guide's poison-induced cardiogenic shock section. |
| Local anesthetic systemic toxicity | QRS widening, ventricular arrhythmias — management (lipid emulsion) also lives in that same guide. |
These four rows are intentionally thin — full mechanism and treatment detail for each already exists elsewhere in this reference set. This guide is the recognition layer; the antidotes guide is the action layer.
5. Quick Reference Card & Primary Sources
| Finding | Consider |
|---|---|
| Tall, tented T waves | Hyperkalemia (early) — but don't rely on this alone to gauge severity |
| Sine wave pattern | Severe/pre-terminal hyperkalemia — treat immediately |
| Flattened T, prominent U wave | Hypokalemia |
| Short QT, domed ST-T | Hypercalcemia (among other causes) |
| Long QT (ST-segment prolongation) | Hypocalcemia |
| Scooped ST depression, V5-V6 | Digoxin effect — not itself diagnostic of toxicity |
| Bidirectional VT | Near-pathognomonic for digoxin toxicity |
| Wide QRS, terminal R in aVR | Na-channel blocker toxicity (TCA, etc.) — see Antidotes guide |
Primary sources checked for this guide:
- Hyperkalaemia ECG changes. LITFL ECG Library, reviewed 2024.
- ECG Diagnosis: Hyperkalemia. The Permanente Journal.
- Hyperkalemia. ECG Stampede, including the 188-patient predictive-findings study.
- Long B, Warix JR, Koyfman A. Controversies in management of hyperkalemia. J Emerg Med. 2018;55(2):192-205.
- U-waves, QT interval, hypokalemia. EMCrit Project IBCC, reviewed 2025.
- Digoxin Effect. LITFL ECG Library Toxicology, reviewed 2024.
- Special Feature: Digoxin Effect on the Electrocardiogram. Clinician Reviews, 2001 (foundational description, still standard-referenced).
- Digoxin Toxicity. ECG Stampede and Atlas of Emergency Medicine, 5e.
- Surawicz B, et al. AHA/ACCF/HRS recommendations for standardization and interpretation of the electrocardiogram. Circulation. 2009.