Heart attack ecg

Reading File

Finding Sources

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Finding Sources

Here is a thorough breakdown of heart attack ECG findings, drawn from Harrison's, Ganong's, and Rosen's Emergency Medicine.

ECG Changes in Myocardial Infarction (Heart Attack)

Physiology Behind the Changes

When coronary artery occlusion cuts off blood supply to the myocardium, three electrical abnormalities develop in the infarcted cells:

Defect	Current Flow	ECG Change
Rapid repolarization (K+ channels open)	Out of infarct	ST elevation
Decreased resting membrane potential (K+ loss)	Into infarct	TQ depression (recorded as ST elevation)
Delayed depolarization	Out of infarct	ST elevation

All three changes produce the hallmark finding: ST segment elevation in leads overlying the infarct, with reciprocal ST depression in leads on the opposite side.

Temporal Evolution of ECG Changes

The ECG evolves through a characteristic sequence after coronary occlusion:

1. Hyperacute T-Waves (Minutes)

Tall, peaked, broad T-waves appear within minutes of occlusion
Represents the earliest sign of ischemia - often missed as it is transient

2. ST Elevation (Hours)

The classic finding of STEMI
Convex ("tombstone") or flat ST segment elevation
Criteria: ≥1 mm in limb leads, ≥2 mm in precordial leads (≥2.5 mm in men <40 years, ≥1.5 mm in women in V2-V3)
Reciprocal ST depression appears in mirror-image leads

The diagram below illustrates how subendocardial vs. transmural ischemia produce opposite ST vector directions:

Subendocardial (ST depression) vs. transmural/epicardial ischemia (ST elevation) - current of injury diagrams

3. Q-Wave Development (Hours to Days)

Pathological Q waves appear as necrotic tissue becomes electrically silent
Criteria: width ≥40 ms (≥0.04 s) or depth >25% of R-wave amplitude
Reflect loss of depolarization forces in the infarcted zone
Note: transmural infarcts may occur without Q waves ("non-Q wave MI"); subendocardial infarcts can sometimes produce Q waves

4. T-Wave Inversion (Days)

Develops in same leads as ST elevation, typically within 24-48 hours
May persist for weeks to months

5. ST Normalization (Days to Weeks)

ST segments return toward baseline
Persistent ST elevation (weeks or more) after Q-wave infarction suggests ventricular aneurysm or severe wall motion disorder

The precordial leads below show deep T-wave inversions in V1-V6 - the Wellens T-wave sign, indicating critical LAD stenosis:

Severe anterior wall ischemia with prominent T-wave inversions in precordial leads V1-V6 (Wellens pattern)

Lead Localization - Where Is the Infarct?

Territory	Leads with ST Elevation	Likely Artery
Anterior	V1-V4	LAD (left anterior descending)
Anterolateral	V1-V6, I, aVL	LAD or LCx (left circumflex)
Lateral	I, aVL, V5-V6	LCx or diagonal branch
Inferior	II, III, aVF	RCA (right coronary artery)
Posterior	Reciprocal ST depression V1-V3; tall R in V1	RCA or LCx
Right ventricular	V4R (right-sided leads)	Proximal RCA

For posterior MI, there are no directly overlying leads in a standard 12-lead - it is recognized by reciprocal ST depression in V1-V3 and a tall R-wave in V1. Right-sided leads (especially V4R) are needed to detect right ventricular infarction, which occurs with proximal RCA occlusion.

The ECG below shows a real STEMI with concordant ST elevation in I and aVL (lateral wall MI):

12-lead ECG showing ST segment elevation myocardial infarction with concordant ST elevation in leads I and aVL consistent with lateral wall AMI

STEMI vs. NSTEMI

	STEMI	NSTEMI
ECG	ST elevation ≥1-2 mm in ≥2 contiguous leads	ST depression, T-wave inversion, or normal ECG
Biomarkers	Elevated troponin	Elevated troponin (required for diagnosis)
Mechanism	Complete occlusion	Partial occlusion or demand ischemia
Reperfusion	Emergency PCI within 90 min	Risk-stratified approach

Important Mimics and Pitfalls

Left Bundle Branch Block (LBBB): masks ischemic changes; new LBBB in chest pain treated as STEMI equivalent (Sgarbossa criteria used)
Benign Early Repolarization: ST elevation in young patients, concave morphology, "fishhook" J-point notching
Pericarditis: diffuse saddle-shaped ST elevation in most leads, PR depression
Hyperkalemia: peaked T-waves can mimic hyperacute T-waves
Takotsubo (stress) cardiomyopathy: can produce STEMI pattern without coronary occlusion
WPW preexcitation: can mask or simulate ischemic changes

A normal ECG does not rule out MI - it occurs in a minority of true infarctions. Serial ECGs every 20-30 minutes and ST-trend monitoring significantly improve sensitivity for STEMI detection.

Sources: Harrison's Principles of Internal Medicine 22E (2025); Ganong's Review of Medical Physiology 26E; Rosen's Emergency Medicine 9E; Tintinalli's Emergency Medicine

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