Electrocardiographic Changes in Ischemia

Electrocardiography (ECG) is one of the most valuable tools in diagnosing and monitoring ischemic heart disease (IHD). Since ischemia, injury, and infarction alter the electrical activity of the myocardium, these changes are reflected in the ECG waveform. A systematic approach to interpreting ischemic changes on the ECG helps in early diagnosis, localization, and risk stratification of patients with suspected ischemic events.

This article explores ECG changes in acute and chronic ischemia, ST-segment deviations, T wave abnormalities, pathological Q waves, and localization of ischemia using ECG leads.

1. Acute vs. Chronic Ischemia on ECG

1.1 Acute Ischemia

Acute ischemia refers to sudden reduction of coronary blood flow, often due to plaque rupture and thrombosis. It is commonly associated with acute coronary syndromes (ACS) such as unstable angina, NSTEMI, and STEMI.

Key ECG findings in acute ischemia:

ST-segment elevation (STEMI): Marker of acute transmural injury.
ST-segment depression (NSTEMI/unstable angina): Marker of subendocardial ischemia.
Hyperacute T waves: Early phase of acute infarction.
Dynamic changes: ECG evolves over minutes to hours.

1.2 Chronic Ischemia

Chronic ischemia results from fixed atherosclerotic narrowing of coronary arteries, often presenting as stable angina.

Key ECG findings in chronic ischemia:

ST-segment depression during exertion (stress ECG).
ECG may be normal at rest, with changes only induced by increased oxygen demand.
Chronic Q waves: Evidence of old infarction and myocardial scarring.

Summary:

Acute ischemia: Dynamic and often dramatic ECG changes.
Chronic ischemia: Stable patterns, typically exercise-induced or fixed from past infarcts.

2. ST-Segment Changes: Elevation and Depression

The ST segment represents the period between ventricular depolarization and repolarization. It is normally isoelectric. Deviations from baseline are hallmark features of ischemia.

2.1 ST-Segment Elevation (STE)

Indicates transmural injury (involving full thickness of myocardium).
Seen in acute STEMI or sometimes in coronary vasospasm (Prinzmetal angina).
Criteria for STEMI:
- New ST elevation at the J-point in ≥2 contiguous leads:
  - ≥2.0 mm in men ≥40 years.
  - ≥1.5 mm in women.
  - ≥1.0 mm in other leads.
Evolution:
1. Hyperacute T waves → ST elevation → Q wave development → T wave inversion.
Mechanism: Injured myocardial cells remain depolarized, shifting the electrical baseline and causing ST elevation.

Mimics of ST elevation:

Pericarditis (diffuse STE).
Early repolarization.
Left ventricular aneurysm.
Hyperkalemia.

2.2 ST-Segment Depression (STD)

Indicates subendocardial ischemia.
More often seen in NSTEMI or stable angina.
Patterns:
- Horizontal or downsloping depression: Strongly suggestive of ischemia.
- Upsloping depression: Less specific, can be exercise-related.
Seen during exercise stress tests as an indicator of inducible ischemia.

Mechanism:
Subendocardial ischemia alters repolarization, shifting the ST segment downward.

3. T Wave Inversions and Q Waves

3.1 T Wave Inversions

T wave reflects ventricular repolarization.
Ischemia distorts repolarization, producing inverted T waves.

Types:

Symmetrical, deep inversions: Strongly associated with ischemia.
Dynamic changes: Seen in evolving ACS.
Persistent inversions: Indicate prior infarction or ongoing ischemia.

Clinical examples:

Wellen’s syndrome: Deep, symmetrical T wave inversions in anterior leads (LAD stenosis).
NSTEMI: T wave inversions without ST elevation.

3.2 Pathological Q Waves

Q waves represent absence of electrical activity due to myocardial necrosis.
Appear when infarction is transmural and irreversible.

Criteria for pathological Q waves:

Width ≥0.04 seconds (1 small box).
Depth ≥25% of R wave in the same lead.
Present in ≥2 contiguous leads.

Significance:

Indicates old myocardial infarction.
May persist indefinitely, serving as a “scar marker.”
Helps distinguish acute ischemia (no Q yet) vs. prior infarction (established Q).

4. Localizing Ischemia by ECG

The ECG is not only diagnostic but also helps localize ischemia/infarction to specific myocardial regions based on the involved leads. This corresponds to coronary artery territories.

4.1 Anterior Wall Ischemia/Infarction

Leads involved: V1–V4.
Culprit artery: Left anterior descending (LAD).
Findings: ST elevation or Q waves in V1–V4.

4.2 Lateral Wall Ischemia/Infarction

Leads involved: I, aVL, V5, V6.
Culprit artery: Left circumflex (LCx) or diagonal branch of LAD.
Findings: ST elevation or Q waves in lateral leads.

4.3 Inferior Wall Ischemia/Infarction

Leads involved: II, III, aVF.
Culprit artery: Right coronary artery (RCA) in most, sometimes LCx.
Findings: ST elevation or Q waves inferiorly.
Reciprocal changes: ST depression in I, aVL.

4.4 Posterior Wall Ischemia/Infarction

Leads involved: V7–V9 (posterior leads).
Clues on standard ECG: ST depression and tall R waves in V1–V3.
Culprit artery: RCA or LCx.

4.5 Right Ventricular Ischemia/Infarction

Leads involved: V3R, V4R (right-sided precordial leads).
Culprit artery: Proximal RCA.
Findings: ST elevation in right-sided leads.

5. Evolution of Ischemic ECG Changes

Understanding the temporal sequence of ECG changes helps distinguish acute evolving infarction from chronic ischemia.

Minutes: Hyperacute peaked T waves.
Minutes–hours: ST elevation (injury pattern).
Hours–days: Development of Q waves and T wave inversion.
Days–weeks: Resolution of ST elevation, persistent T wave inversion.
Weeks–months: Pathological Q waves may persist; T waves normalize or remain inverted.

6. Clinical Applications of ECG in Ischemia

Diagnosis: Distinguishes STEMI from NSTEMI/unstable angina.
Localization: Identifies infarcted region and culprit artery.
Risk Stratification: Large ST deviations, multiple lead involvement = higher risk.
Monitoring: Detects reinfarction, recurrent ischemia, or post-PCI changes.
Guiding therapy: Immediate reperfusion strategies for STEMI.

7. Limitations of ECG in Ischemia

May be normal in early ischemia or silent ischemia.
Baseline abnormalities (bundle branch block, LVH, paced rhythm) obscure changes.
Non-ischemic ST-T changes (electrolyte imbalance, pericarditis) mimic ischemia.
Requires correlation with clinical context and biomarkers (troponins).

8. Summary Table of Ischemic ECG Changes

Finding	Mechanism	Condition	Localization
ST elevation	Transmural injury	STEMI, vasospasm	Depends on leads
ST depression	Subendocardial ischemia	NSTEMI, angina	Reciprocal in STEMI
Hyperacute T waves	Early repolarization change	Very early infarct	Localized to artery
T wave inversion	Abnormal repolarization	Ischemia, evolving infarct	Region-specific
Pathological Q waves	Transmural necrosis	Old infarct	Contiguous leads