Table of Contents
Page created on May 23, 2019. Last updated on May 4, 2020 at 14:58
Acute myocardial infarction (AMI) is characterised by ischaemia and infarction of the myocardium. These pathological processes cause characteristic signs of the ECG that we can use to diagnose it (in addition to cardiac enzymes and symptoms). Most of these signs appear only in the leads that correspond to the where the myocardial infarction occurs.
According to the location of the infarct, the following leads often show signs:
|Localization of infarct
|V1 + V2
|V1 + V2 + V3 + V4
|V2 + V3 + V4
|I + aVL + V1 + V2 + V3 + V4 + V5 + V6
|I + aVL + V6
|V5 + V6
|II + III + aVF
|Mirror signs in V1 + V2 + V3
|V1 + V2 + (V4R + V5R)
The progression of AMI follows three phases, the hyperacute, acute and chronic phases.
Pathomechanism of ST abnormalities:
When myocardiocytes are ischaemic, their ATP levels decrease. The Na+/K+ ATPase will therefore be impaired, causing intracellular K+ concentration to decrease. As a result, the cells will be hypopolarized, i.e. their outer surface will be more electronegative than the outer surface of intact myocardiocytes.
This creates a potential difference between the injured and intact myocardiocytes, called the current of injury. This current of injury causes the baseline of the ECG to be shifted upwards or downwards.
The current of injury is not present when the ventricles are depolarized, which is during the ST segment. As a result, the ST segment will appear elevated or depressed compared to the rest of the ECG, depending on whether the baseline was shifted downwards or upwards, respectively.
ST elevation is often present in the leads that represent the injured part of the myocardium. In the opposite leads “mirror image” ST depression often develops.
Phases of acute myocardial infarction
The hyperacute phase begins 30 minutes after the occlusion of the coronary and lasts until 6 – 8 hours after the occlusion. During this phase, the following ECG abnormalities are present:
- High, pointed positive T-waves – a sign of subendocardial ischaemia
- ST elevation – in the leads corresponding to the area of the infarct
- Often convex ST elevation
- Sometimes “T-en-dome”
- ST depression – in the leads opposite to the area of the infarct
The acute phase begins 8 hours after occlusion and lasts until 48 – 72 hours after occlusion. The following ECG abnormalities are present:
- Pathological Q – a sign of myocardial necrosis – in the leads corresponding to the area of the infarct
- Q-wave which is > 40 ms wide or its amplitude is > 25% of the corresponding R-wave
- Lack of R-propagation – in the leads corresponding to the area of the infarct
24 hours after occlusion, still in the acute phase, two more abnormalities can be seen:
- QS complex – a sign of transmural necrosis
- Coronary T
- Negative, pointed T-wave
The chronic phase begins 48 – 72 hours after the occlusion and lasts for months. It’s characterised by reconstruction of the necrotic myocardium, often involving fibrosis.
The following ECG abnormalities are present:
- Pathological Q
The ST segment is usually normalized. If the ST elevation never normalizes, a ventricular aneurysm is most likely. If the ST elevation initially normalizes but eventually returns, it is a re-infarction.
Posterior myocardial infarction
The posterior side of the heart is not “looked at” during a routine ECG with just 12 leads. Dorsal ECG leads can be used to check for posterior myocardial infarctions, but we can see signs of it with a 12-lead ECG as well.
In a posterior myocardial infarction “mirror signs” are often seen in lead V1 – V3. These signs are:
- ST depression – the mirror of ST elevation
- High R-wave – the mirror of pathological Q
- Positive, peaked T – the mirror of coronary T
Posterior infarcts are often seen together with inferior infarcts.
Other forms of acute myocardial infarction
When studying pathophysiology, it feels like all myocardial infarctions present with ST elevation. In the clinical practice so-called non-ST elevation myocardial infarctions (NSTEMIs) are more common than ST elevation myocardial infarctions (STEMIs). The former is associated with non-transmural ischaemia while the latter is associated with transmural ischaemia.