Show me tough ECG and prominent finding

Reading File

Finding Sources

Reading File

Finding Sources

Reading File

Loading Image

Reading File

Loading Image

Reading File

Loading Image

Reading File

Loading Image

I now have a comprehensive collection of real ECG images and detailed textbook content. Let me compile the full answer.

Tough ECGs: High-Yield Patterns with Prominent Findings

Source: ROSEN's Emergency Medicine, Washington Manual of Medical Therapeutics

1. Anterior STEMI (LAD Occlusion)

Finding: ST elevation in V1-V4, obliquely straight or convex morphology.

Anterior STEMI - ST elevation V1-V4 with LAD occlusion

Key diagnostic criteria (4th Universal MI Definition):

Men >40 yrs: STE ≥2 mm in V2-V3, >1 mm elsewhere
Men <40 yrs: STE >2.5 mm in V2-V3
Women: STE >1.5 mm in V2-V3, >1 mm elsewhere

Pitfall: The very first ECG finding is the hyperacute T wave - tall, broad-based, asymmetric, appearing within minutes of occlusion. It precedes STE and is easy to miss.

2. Anterolateral STEMI (Proximal LAD / Left Main)

Finding: STE in V1-V6 + I + aVL, representing massive territory at risk.

Anterolateral STEMI with STE V2-V6, I, aVL - prior LAD stent in-stent thrombosis

3. aVR STE - Left Main / Proximal LAD Occlusion

Finding: ST elevation in aVR >1 mV with widespread ST depression across other leads.

aVR STE with diffuse ST depression - left main coronary artery disease

STE in aVR >0.5 mV is ~78% sensitive, 83% specific for left main disease. Greater aVR elevation than V1 elevation favors left main; greater V1 elevation favors proximal LAD.

4. Wellens Syndrome (Pre-Infarction LAD Pattern)

Finding: Deep symmetric T wave inversions (Type I) or biphasic T waves (Type II) in anterior precordial leads V2-V3, with isoelectric or minimally elevated (<1 mm) ST segments and no Q waves.

ST depression morphology patterns - (A) horizontal, (B) downsloping, (C) Wellens Type II biphasic, (D) deep symmetric inversions, (E) mixed

Why it's tough: The patient may be pain-free when the ECG is obtained, making it easy to dismiss. This pattern indicates a critical proximal LAD stenosis - the natural history is progression to anterior STEMI. Do NOT stress test these patients.

5. De Winter ECG Pattern (STEMI Equivalent)

Finding: J-point depression + upsloping ST depression in precordial leads + tall, prominent (hyperacute) T waves + ST elevation in aVR.

De Winter ECG - J-point depression with prominent T waves in V2-V4 and STE in aVR - proximal LAD obstruction

Why it's tough: This pattern doesn't show classic STE, so it often goes unrecognized. It is a STEMI equivalent - treat with emergent PCI. Associated with proximal LAD occlusion, same territory as anterior STEMI.

6. Pericarditis vs. STEMI

Finding: Diffuse concave-upward ("saddle-shaped") STE + PR depression in most leads + PR elevation in aVR + sinus tachycardia.

Pericarditis - diffuse concave STE, PR depression in II, PR elevation in aVR, sinus tachycardia

Distinguishing features from STEMI:

Feature	Pericarditis	STEMI
STE distribution	Diffuse (multiple territories)	Regional (contiguous leads)
ST morphology	Concave upward	Flat/convex/oblique
PR depression	Present (most leads)	Absent
Reciprocal STD	Absent (except aVR)	Present
Q waves	No	Develop over time

7. Benign Early Repolarization (BER) vs. STEMI

Finding: Concave-upward STE best seen in V4-V6, relatively large T waves in same leads, subtle J-point notching.

Benign early repolarization - concave STE V4-V6, large T waves, J-point irregularity (arrows)

The trap: BER can mimic anterior STEMI. Key differentiators: the STE is stable on serial ECGs, concave morphology, and absence of reciprocal changes.

8. Brugada Syndrome

Finding: Downward coved (Type 1) or saddleback (Type 2) ST elevation in V1-V3, sometimes simulating RBBB morphology. May be transient or unmasked only by sodium channel blockers (ajmaline, flecainide), fever, or vagotonic states.

Clinical context: Young male + unexplained syncope + Brugada pattern = admit for ICD evaluation. Inherited Na+ channelopathy causing ventricular fibrillation and sudden cardiac death without structural heart disease.

Differential for STE in V1-V3: Brugada, RBBB, anterior STEMI, RV strain, Hyperkalemia, Na+ channel drug toxicity.

9. Ventricular Tachycardia vs. SVT with Aberrancy

Finding: Wide-complex tachycardia. Brugada VT criteria (4-step algorithm):

VT - (A) RS >100ms in chest leads = VT, (B) morphologic criteria: notched S in V1, QR in V6, (C) QS in V6

Step 1: No RS complex in any chest lead? → VT Step 2: RS interval >100 ms in any chest lead? → VT Step 3: AV dissociation present? → VT Step 4: Morphologic criteria in V1 and V6 consistent with VT?

Bidirectional VT (alternating QRS axis beat-to-beat) = classic for digoxin toxicity or catecholaminergic polymorphic VT (CPVT):

10. Torsades de Pointes

Finding: Polymorphic VT with characteristic twisting of QRS complexes around the isoelectric baseline ("turning of the points"), preceded by prolonged QT.

Torsades de Pointes - classic spiraling of QRS complexes around the baseline

Treatment: IV magnesium sulfate 1-2 g rapidly (even without confirmed hypomagnesemia). Overdrive pacing at 100-120 bpm for acquired (pause-dependent) forms. Beta-blockers for congenital (adrenergic-dependent) forms.

Causes (Acquired): QT-prolonging drugs (class IA/IC antiarrhythmics, macrolides, haloperidol, TCAs, azoles), hypokalemia, hypomagnesemia, severe bradycardia.

Quick Reference: Anatomic STEMI Localization

ST Elevation Leads	Territory	Culprit Artery
V1-V2	Septum	Proximal LAD / septal branch
V2-V4	Anterior wall	LAD
V5-V6	Lateral wall	LCX
II, III, aVF	Inferior wall	RCA (90%) or LCX
I, aVL	High lateral	Diagonal or proximal LCX
V1-V6 + LBBB	Anterior + septal	Proximal LAD or left main
aVR + diffuse STD	Left main / proximal LAD	Left main / LAD

Sources: ROSEN's Emergency Medicine 9e (Ch. 64-65), Washington Manual of Medical Therapeutics

Am loving the info

This is a shared conversation. Sign in to Orris to start your own chat.