ECG Patterns: Electrolytes, Drugs, Bundle Branch Blocks & STEMI Mimics
Spot the tracings that call for calcium, bicarbonate, or the cath lab
Electrolytes and temperature
Hyperkalemia. Changes appear in a predictable order, but the potassium level at which each appears varies widely.
- Peaked T wavesTall, narrow-based, and symmetric; the earliest sign.
- Atrial slowingPR prolongation, then flattening and loss of P waves.
- QRS wideningBizarre wide complexes, bradycardia, and new blocks.
- Sine waveThe QRS merges with the T wave; VF or asystole follows.
Any hyperkalemic ECG change calls for IV calcium gluconate first; it stabilizes the membrane within minutes but does not lower potassium.
Hypokalemia. T waves flatten, the ST segment sags, and U waves appear after the T wave, best seen in V2–V3; a fused T and U can mimic a long QT that is really a long QU interval. Ectopy, torsades, and digoxin toxicity become more likely. Hypokalemia that will not correct usually reflects hypomagnesemia, which causes renal potassium wasting, so magnesium is replaced too.
Calcium. Calcium sets the length of the ST segment. Hypercalcemia shortens it, giving a short QT with the T wave rising straight off the QRS. Hypocalcemia lengthens it, giving a long QT with a normal-width T wave and a risk of torsades, classically after thyroidectomy or parathyroidectomy with perioral tingling and carpopedal spasm. Hypomagnesemia also prolongs the QT.
Hypothermia. Below about 32 °C, Osborn (J) waves appear: a positive hump at the QRS–ST junction, largest in the inferior and lateral leads and growing as temperature falls. Sinus bradycardia, prolonged PR, QRS, and QT intervals, shivering artifact, and atrial fibrillation are typical. Below about 28 °C ventricular fibrillation threatens, so handle the patient gently, rewarm, and continue resuscitation until the patient is warm.
Drug effects: digoxin and tricyclics
Digoxin effect vs toxicity. Therapeutic digoxin produces scooped ("reverse tick") ST depression, flattened T waves, and a short QT, best seen laterally; this is expected and not a sign of toxicity. Toxicity combines excess automaticity with AV block: PVCs and bigeminy, atrial tachycardia with block, accelerated junctional rhythm, and bidirectional VT, which is nearly pathognomonic.
Tricyclic overdose. TCAs block fast sodium channels and are also anticholinergic and α-blocking. The ECG shows sinus tachycardia, QRS prolongation, a terminal R wave >3 mm in aVR, and QT prolongation.
Bicarbonate is the antidote. IV sodium bicarbonate alkalinizes the serum (target pH about 7.45–7.55) and loads sodium, overcoming the channel blockade and narrowing the QRS. Hypotension is treated with fluids and norepinephrine.
In TCA toxicity avoid class IA and IC antiarrhythmics such as procainamide and flecainide, which deepen sodium-channel blockade, and avoid physostigmine and flumazenil, which can provoke asystole or seizures.
Bundle branch and fascicular blocks
| Feature | RBBB | LBBB |
|---|---|---|
| QRS duration | ≥120 ms | ≥120 ms |
| V1–V2 | rSR′ ("rabbit ears," M shape) | Deep, broad QS or rS |
| I, aVL, V5–V6 | Wide, slurred S wave | Broad, notched, monophasic R; no septal q waves |
| ST-T | Discordant T inversion in V1–V3 | Discordant ST-T changes in most leads |
| Meaning | May be a normal variant; also PE, ASD, RV strain | Almost always structural disease: HTN, CAD, cardiomyopathy, aortic stenosis |
LBBB and ischemia. The discordant ST-T changes of LBBB mask ischemia, and new or presumed-new LBBB alone is no longer treated as a STEMI equivalent. The Sgarbossa criteria are highly specific but insensitive:
- Concordant ST elevation ≥1 mm in leads with a positive QRS: 5 points.
- ST depression ≥1 mm in V1, V2, or V3: 3 points.
- Excessively discordant ST elevation ≥5 mm in leads with a negative QRS: 2 points.
A score ≥3, or LBBB with chest pain plus shock or acute heart failure, warrants emergent catheterization. The Smith modification replaces the 5-mm rule with discordant ST elevation ≥25% of the preceding S-wave depth and is more sensitive; the same criteria apply to ventricular paced rhythms.
Fascicular and bifascicular block. Left anterior fascicular block causes left axis deviation (−45° or beyond) with qR in aVL and rS in II, III, and aVF; left posterior fascicular block causes right axis deviation. Bifascicular block is RBBB plus either hemiblock, usually the anterior one. Asymptomatic patients need no pacemaker. Syncope suggests intermittent infranodal high-grade AV block and calls for monitoring or an electrophysiology study, with pacing if block is documented. Alternating RBBB and LBBB warrants a permanent pacemaker.
Voltage, effusion, and the right heart
Left ventricular hypertrophy. Sokolow-Lyon: S in V1 plus R in V5 or V6 ≥35 mm. Cornell: R in aVL plus S in V3 >28 mm in men or >20 mm in women. The strain pattern is downsloping ST depression with asymmetric T-wave inversion in I, aVL, and V5–V6; causes include hypertension, aortic stenosis, and hypertrophic cardiomyopathy. The ECG is specific but insensitive, and thin young athletes often meet voltage criteria, so echocardiography is the test of choice.
Low voltage and electrical alternans. QRS amplitude <5 mm in every limb lead (or <10 mm in every precordial lead) suggests effusion, obesity, emphysema, hypothyroidism, or infiltrative disease; low voltage despite thick walls on echocardiography is the classic clue to cardiac amyloidosis. Electrical alternans, a beat-to-beat change in QRS height, reflects a heart swinging in a large effusion. With sinus tachycardia, hypotension, and JVD, obtain a bedside echocardiogram and proceed to pericardiocentesis for tamponade.
Pulmonary embolism. Sinus tachycardia with nonspecific ST-T changes is the most common finding, and the tracing may be normal. S1Q3T3 (deep S in I, Q wave and inverted T in III) is classic but present in only a minority. Right ventricular strain signs (new RBBB, right axis deviation, T-wave inversion in V1–V4, P pulmonale, atrial fibrillation) imply a larger clot and worse prognosis. The ECG can neither confirm nor exclude PE.
STEMI equivalents and STEMI mimics
Posterior MI. No standard lead faces the posterior wall, so posterior STEMI appears as its mirror image in V1–V3: horizontal ST depression, tall broad R waves (R/S ratio >1 in V2), and upright T waves. It results from LCx or RCA occlusion and often accompanies inferior MI. ST elevation ≥0.5 mm in posterior leads V7–V9 confirms it, and it is treated as a STEMI with emergent reperfusion.
Wellens pattern. Biphasic (type A) or deep, symmetric inverted (type B) T waves in V2–V3 in a patient who is pain-free after angina, with normal or mildly elevated troponin and no Q waves. It marks critical proximal LAD stenosis with a high short-term risk of extensive anterior MI. Management is coronary angiography; stress testing is contraindicated because it can precipitate infarction.
de Winter pattern. Ongoing chest pain with upsloping ST depression at the J point in V1–V6 and tall, symmetric T waves indicates acute proximal LAD occlusion, a STEMI equivalent that needs emergent catheterization.
| Feature | Pericarditis | Early repolarization | LV aneurysm |
|---|---|---|---|
| Setting | Pleuritic, positional pain; friction rub; often post-viral | Young, healthy, asymptomatic | Weeks after a large anterior MI |
| ST elevation | Diffuse, concave, nonterritorial | Modest, mainly precordial, with J-point notching | Persistent, in the infarct territory |
| Other clues | PR depression (PR elevation in aVR); reciprocal depression only in aVR and V1 | No PR depression; unchanged on serial ECGs | Deep Q waves; dyskinetic wall on echo |
Telling mimics from infarction. STEMI is territorial, shows reciprocal ST depression, and evolves Q waves. In pericarditis the T waves invert only after the ST segments return to baseline, and an ST-elevation to T-wave amplitude ratio >0.25 in V6 favors pericarditis over early repolarization. LBBB, paced rhythms, LVH, and hyperkalemia can also elevate ST segments without coronary occlusion.