Ischemia, injury, and necrosis on ECG
The development of myocardial infarction is accompanied by a complex of characteristic signs that depend on the depth of ventricular wall involvement. Three main stages of blood supply impairment are distinguished: ischemia, injury, and necrosis itself.
Changes in ischemia Ischemic changes primarily affect the shape of the T wave.
- Subendocardial ischemia: a tall, peaked T wave is registered on the ECG.
- Subepicardial ischemia: the T wave becomes inverted (negative).
- Transmural ischemia: encompasses the entire thickness of the myocardium, forming a deep inverted T wave.
Changes in injury The injury zone is characterized by displacement of the ST segment relative to the isoelectric line.
- Subendocardial injury: manifests as ST-segment depression.
- Subepicardial and transmural injury: lead to pronounced ST-segment elevation.
Changes in infarction (necrosis) Cardiomyocyte death is directly reflected in the ventricular complex. Non-transmural infarction leads to the appearance of a pathological Q wave and a noticeable decrease in R-wave amplitude. In transmural infarction, when the wall dies across its entire thickness, only the QS complex is registered. Typical signs of infarction also include the formation of a negative "coronary" T wave.
Stages of development and classification
The evolution of myocardial infarction is a dynamic process that is conventionally divided into several time intervals. Each phase reflects specific morphological alterations in the heart muscle.
- Hyperacute stage (injury stage): Develops within 15–60 minutes to several hours and can last up to 3 days. During this period, early signs of acute ischemia and injury are recorded, primarily ST-segment elevation.
- Acute stage: Begins on day 1 and lasts up to 2–3 weeks. During this time, active formation of necrosis takes place.
- Subacute stage: Lasts up to 6–8 weeks (up to 3 months).
- Scarring stage: The longest phase, lasting months, years, and persisting for the rest of life.
Infarctions are classified by the presence of ST-segment elevation (ST-elevation or non-ST-elevation) and by Q-wave formation:
- Non-Q-wave infarction: ST-segment changes (depression or elevation) and T-wave inversion are noted. The formation of a classical necrosis complex (QS or pathological Q) is absent.
- Q-wave infarction (transmural or large-focal): Follows a classical staging with obligatory formation of a necrosis zone, which is reflected on the ECG by the appearance of a pathological Q wave.
Topographic diagnosis by leads
Electrocardiography allows precise determination of the anatomical localization of the lesion. The appearance of pathological changes in specific leads serves as a reliable marker of necrosis topography.
- V1–V3: Anterior part of the interventricular septum (anteroseptal infarction).
- V3–V4: Apex of the left ventricle (anteroapical infarction).
- I, aVL, V5, and V6: Lateral wall (anterolateral infarction).
- I, aVL, V1–V6: Extensive involvement (extensive anterior infarction).
- II, III, aVF: Diaphragmatic surface (posterior diaphragmatic or inferior infarction).
- II, III, aVF, V5, V6: Combined involvement (posterolateral infarction).
ECG dynamics in extensive anterolateral infarction
To better understand the chronological evolution of ECG signs, let us consider a classic example of the development of an extensive transmural myocardial infarction.
One hour after pain onset (hyperacute stage), early signs of ischemia and deep tissue injury are recorded on the cardiogram, manifesting as ST-segment elevation.
One day later (acute/subacute stage), irreversible formation of necrosis occurs. Topographic diagnosis allows precise correlation of changes with anatomy:
- In lead V2, a pathological Q wave appears, indicating involvement of the interventricular septum.
- In lead V4, a pathological Q wave indicates damage to the apex.
- Changes in lead V6 confirm the spread of the process to the lateral wall.
Ten days later (scarring stage), the consolidation phase of changes begins. The electrocardiographic picture stabilizes, and the formed pathological Q wave remains as a reliable marker of the past event.
To memorize the infarction zones, imagine a target: right in the center (the "bullseye") is the necrosis zone, surrounded by a ring of the injury zone, and the outermost ring is the ischemia zone.
Class and exam questions
How does a transmural infarction differ from a non-transmural one on an ECG?
In transmural infarction (involvement of the entire wall thickness), only the QS complex is registered on the ECG. Non-transmural infarction is characterized by the appearance of a pathological Q wave and a decrease in R-wave amplitude.
What changes are characteristic of non-Q-wave myocardial infarction?
In non-Q-wave infarction, the necrosis complex (QS or pathological Q) is not formed. This form is characterized by ST-segment changes (depression or elevation) and T-wave inversion.
How to determine anterolateral myocardial infarction on an ECG?
Anterolateral myocardial infarction is diagnosed when typical ischemic and necrotic changes appear in leads I, aVL, V5, and V6.
What else to study on this topic
- Criteria for the pathological Q wave and QS complex.
- Mechanisms of ST-segment depression and elevation formation.
- Causes of the negative "coronary" T wave.
- Differences between acute myocardial infarction and post-infarction cardiosclerosis (scarring stage).
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