ECG Changes in Myocardial

Myocardial ischemia and infarction are critical conditions affecting millions worldwide. Rapid recognition and management are essential to reduce morbidity and mortality. Electrocardiography (ECG) is one of the most important diagnostic tools in detecting myocardial ischemia, injury, and infarction. Understanding ECG patterns allows clinicians to quickly identify affected myocardial regions, the severity of ischemia, and potential complications.

1. Introduction

The heart relies on a constant supply of oxygenated blood for optimal function. Any interruption in coronary blood flow can lead to ischemia (reversible injury) or infarction (irreversible myocardial necrosis). ECG serves as a window into the electrical activity of the heart, reflecting underlying ischemic or infarcted regions.

Key Points:

ECG changes can precede clinical symptoms, especially in silent ischemia.
Early recognition of changes facilitates timely interventions like thrombolysis or percutaneous coronary intervention (PCI).
Patterns vary depending on the location, extent, and timing of myocardial injury.

2. Basic Pathophysiology of ECG Changes

2.1 Myocardial Ischemia

Ischemia occurs when oxygen supply is insufficient to meet myocardial demand. This leads to:

Altered membrane potential
Slowed conduction
Altered repolarization

ECG Manifestation:

ST-segment depression
T-wave inversion
Sometimes transient arrhythmias

2.2 Myocardial Injury

Prolonged ischemia causes cellular injury without immediate necrosis.

Subendocardial injury: Inner layer affected, often causing ST depression.
Transmural injury: Full-thickness involvement, leading to ST elevation.

2.3 Myocardial Infarction (MI)

Irreversible necrosis due to prolonged ischemia. Pathophysiology includes:

Cell death releasing potassium and enzymes
Electrical conduction disturbances
Formation of scar tissue over time

ECG Manifestation:

ST elevation (acute phase)
Pathological Q waves (necrosis)
T-wave inversions (repolarization abnormalities)

3. Normal ECG Components

Before analyzing pathological changes, a review of normal ECG waves is important:

P wave: Atrial depolarization
PR interval: Conduction from atria to ventricles
QRS complex: Ventricular depolarization
ST segment: Plateau phase of ventricular action potential
T wave: Ventricular repolarization
QT interval: Total ventricular depolarization and repolarization

Normal Duration:

PR: 120–200 ms
QRS: <120 ms
QT: 350–450 ms
ST segment: isoelectric baseline

4. ECG Changes in Myocardial Ischemia

Ischemia primarily affects ventricular repolarization, leading to specific ECG patterns.

4.1 T-Wave Changes

Inverted T waves: Most common manifestation of ischemia; often symmetric inversion.
Peaked T waves: Can indicate hyperacute ischemia or early MI.
Flattened T waves: May indicate mild or chronic ischemia.

Clinical Significance:

T-wave inversion in V1–V4 may suggest anterior ischemia.
Lateral ischemia may show inversion in I, aVL, V5–V6.

4.2 ST-Segment Depression

Horizontal or downsloping ST depression indicates subendocardial ischemia.
Up-sloping depression is less specific.
Reciprocal changes may occur in leads opposite the ischemic region.

Example Patterns:

Anterior leads (V1–V4): ST depression in posterior MI.
Inferior leads (II, III, aVF): Lateral ischemia may produce reciprocal depression.

4.3 ST-Segment Elevation (Hyperacute Ischemia)

Early ischemic injury may initially cause tall, peaked T waves and slight ST elevation.
This phase often precedes full-blown infarction.

5. ECG Changes in Myocardial Infarction

Myocardial infarction evolves over time with dynamic ECG changes, reflecting injury, necrosis, and healing.

5.1 Hyperacute Phase

Duration: Minutes to a few hours
ECG Features:
- Tall, peaked T waves
- Slight ST elevation
- Minimal or no Q-wave development
Represents early transmural injury.

5.2 Acute Phase

Duration: Hours after onset
ECG Features:
- Significant ST-segment elevation (>1 mm in limb leads, >2 mm in chest leads)
- Hyperacute T waves may persist or normalize
Indicates transmural myocardial injury.

5.3 Evolving Phase

Duration: Hours to days
ECG Features:
- ST segments gradually return to baseline
- T-wave inversion develops
- Pathological Q waves begin to appear
Reflects cell death and necrosis.

5.4 Chronic or Old MI

Duration: Weeks to months
ECG Features:
- Deep, wide Q waves persist
- T waves may remain inverted or normalize
- ST segments are typically isoelectric
Represents scar formation.

6. Pathological Q Waves

6.1 Definition

Width > 0.04 seconds (1 small box)
Depth ≥ 25% of R wave in the same lead

6.2 Clinical Significance

Indicates transmural infarction.
Develops hours to days after MI onset.
Persistent Q waves reflect permanent myocardial damage.

6.3 Localization

Inferior MI: Q waves in II, III, aVF
Anterior MI: Q waves in V1–V4
Lateral MI: Q waves in I, aVL, V5–V6
Posterior MI: Reciprocal Q waves in V1–V2

7. ST-Segment Elevation Patterns

7.1 Criteria

ST elevation ≥1 mm in limb leads
ST elevation ≥2 mm in chest leads

7.2 Morphology

Convex (“tombstone”) ST elevation: Classic acute MI
Concave ST elevation: Often pericarditis or early repolarization
Reciprocal changes: ST depression in opposite leads strengthens MI diagnosis

8. Lead Localization of MI

MI Location	Leads Showing Changes	Reciprocal Changes	Coronary Artery Involved
Anterior	V1–V4	II, III, aVF	LAD
Lateral	I, aVL, V5–V6	II, III, aVF	LCX
Inferior	II, III, aVF	I, aVL	RCA or LCX
Posterior	V1–V2 (tall R, ST depression)	V7–V9	RCA or LCX
Septal	V1–V2	Rare	LAD

9. Reciprocal Changes

Occur in leads opposite the infarcted region.
Examples:
- Inferior MI: ST depression in I, aVL
- Anterior MI: ST depression in inferior leads
Reciprocal changes support diagnosis of acute MI and help differentiate true ST elevation from pericarditis.

10. Special ECG Patterns

10.1 Wellens’ Syndrome

Characterized by biphasic or deeply inverted T waves in V2–V3
Indicates critical proximal LAD stenosis
Patients are at high risk for anterior MI

10.2 De Winter’s T Waves

Up-sloping ST depression at J-point in V1–V6 with tall, peaked T waves
Suggests proximal LAD occlusion
Considered an anterior STEMI equivalent

10.3 Posterior MI

Often missed because ST elevation occurs on posterior leads (V7–V9)
ECG clues:
- ST depression in V1–V3
- Tall R waves in V1–V2

10.4 Right Ventricular MI

ST elevation in right-sided leads (V3R–V6R)
Often accompanies inferior MI
Can cause hypotension and bradycardia

11. ECG Changes in Subendocardial vs Transmural MI

Feature	Subendocardial MI	Transmural MI
ST Segment	Depression	Elevation
T Wave	Inversion	Hyperacute then inversion
Q Wave	Usually absent	Develops after hours/days
Extent of Damage	Partial-thickness	Full-thickness
Clinical Presentation	Often NSTEMI	STEMI

12. Dynamic Nature of ECG Changes

ECG changes in MI are time-dependent.
Serial ECGs increase diagnostic accuracy.
Important phases:
1. Hyperacute: Minutes to hours
2. Acute: Hours
3. Evolving: Days
4. Chronic: Weeks to months

Key Clinical Tip: A single ECG may be normal early; repeated ECGs are crucial.

13. Complications Detected by ECG

13.1 Arrhythmias

Ventricular tachycardia/fibrillation
Atrial fibrillation/flutter
Heart blocks (AV block, bundle branch block)

13.2 Mechanical Complications

Ventricular aneurysm: Persistent ST elevation
Ventricular septal rupture: New murmurs may correlate with ECG changes
Papillary muscle rupture: Associated with inferior MI

14. ECG in Prognosis and Risk Stratification

Extent of ST elevation: Correlates with infarct size
Q-wave development: Indicates permanent damage
Reciprocal changes: Suggest larger infarcts
Persistent ST elevation: Risk for ventricular aneurysm
Arrhythmias: Predict early mortality

15. ECG in Modern Clinical Practice

Integration with biomarkers: Troponins confirm myocardial injury.
High-risk features: ST elevation, Wellens’ sign, or De Winter pattern trigger emergent PCI.
Non-ST elevation MI: Requires risk scoring (e.g., TIMI or GRACE scores) alongside ECG changes.
Continuous ECG monitoring: Essential in acute coronary syndrome (ACS) units for early detection of arrhythmias.

16. Limitations of ECG

May be normal in early MI or posterior infarction.
Baseline abnormalities (LVH, LBBB, pacemaker) can obscure ischemic changes.
Serial ECGs and additional imaging (echocardiography, cardiac MRI) improve diagnostic accuracy.

17. Summary Table: ECG Changes in Ischemia and Infarction

Phase	ECG Changes	Leads Affected	Clinical Significance
Ischemia	ST depression, T-wave inversion	Region-specific	Reversible, indicates oxygen deficit
Hyperacute Injury	Tall, peaked T waves	Localized	Early MI, precedes ST elevation
Acute MI	ST elevation	Infarct territory	Transmural injury
Evolving MI	ST returns to baseline, T inversion, Q waves	Infarct territory	Necrosis confirmed
Chronic/Old MI	Persistent Q waves, T changes may normalize	Infarcted area	Scar formation, previous MI

18. Clinical Case Example

Case: 55-year-old male presents with acute chest pain. Initial ECG shows:

ST elevation in II, III, aVF
Reciprocal ST depression in I, aVL
Hyperacute T waves in II, III

Interpretation:

Inferior STEMI likely due to RCA occlusion
Emergent PCI indicated
Serial ECG monitoring recommended for arrhythmias

19. Key Takeaways

ECG is rapid, non-invasive, and essential in diagnosing myocardial ischemia and infarction.
T-wave changes are earliest signs of ischemia; ST elevation indicates transmural injury.
Pathological Q waves develop hours to days, signifying necrosis.
Reciprocal changes and lead localization assist in identifying the infarct territory.
Special patterns (Wellens, De Winter, posterior MI) indicate high-risk lesions.
Serial ECGs are critical; early MI may be missed on a single ECG.
ECG changes guide urgent interventions, risk stratification, and prognosis.