ECG

The ECG in Chest Pain
An ECG should be performed on all patients presenting to the ED with chest pain à the baseline ECG is rarely normal but if it is, should be repeated every 15 minutes whilst the patient still has chest pain. NB: a normal ECG does not rule out the diagnosis of MI – this may be indicative of a ‘microinfarction’, a small MI causing myocardial necrosis[1].

The physician’s aim is to answer three questions[2], using the ECG:
1. Does the patient have acute ST segment elevation MI, non Q-wave MI, acute coronary syndrome, or unstable angina?
2. How much myocardium is at risk?
3. Which artery is the culprit?

ECG changes are usually confined to leads that ‘face’ the infarction. The ECG signs of AMI are as follows:
– T wave changes (ischaemia) à almost immediately after coronary artery occlusion, there are T wave changes (initially peaked T waves followed by T wave inversion) in the leads reflecting the involved surface
– ST segment displacement (injury) à the T waves changes are accompanied by a maximal elevation of the ST segment, which gradually evolves into inverted, symmetrical T waves as the pathologic condition progresses
– Abnormal Q waves (cellular death) à appear as early as two hours after the onset of chest pain and are usually fully developed within 12 to 24 hours
Successful reperfusion will dramatically alter this evolution of the ECG in patients with AMI. Early signs include rapid reduction in ST segment elevation and resolution of conduction abnormalities.

The ECG in a STEMI
Elevation of the ST segment is an indication of acute myocardial injury (as opposed to infarction), either due to:
– Recent infarction
– Pericarditis à not usually a localised affair, therefore causes ST elevation in most leads

The normal ST segment:
All layers of the myocardium are at the same electrical potential; this is the plateau of the action potential. Therefore there is no current flow between areas of the heart, resulting in an isoelectric ST segment. However, this is not the case when the myocardium is acutely injured.

The ST segment following acute injury:
New ST segment elevation of 1mm or more in the limb leads and 2mm or more in the precordial leads is a powerful diagnostic feature of AMI. This occurs due to severe ischaemia and lack of nutrients, which affects the tissue immediately surrounding the centre of the infarct:
o This is non-functional tissue
o But may receive blood supply from collateral circulation
o Collateral supply is sufficient to keep tissue alive
o But insufficient to maintain membrane integrity
o Therefore injured tissue has a less negative membrane potential from the healthy myocardium
This chain of events, and ultimately the less negative membrane potential, results in a current that flows from the healthy tissue to the injured tissue during the ST segment, causing ST segment elevation (or depression).

Typical ECG changes in myocardial infarction (STEMI) - THIS IS A PRETTY GOOD SUMMARY TABLE (kumar and clarke table 13.32) AND NOW LOOKS POXY BUT WILL BE ALL GOOD IN THE COMPILED VERSION
NB: these changes are usually confined to leads that ‘face’ the infarction

Infarct site
Leads showing ST elements
Anterior:

Small
V3-V4
Extensive
V2-V5
Anteroseptal
V1-V3
Anterolateral
V4-V6, I, AVL
Lateral
I, AVL
Inferior
II, III, AVF
Posterior
V1, V2 (reciprocal)
Subendocardial
Any lead
Right ventricle
VR4
Kumar and Clarke, 6th edition, Table 13.32, p. 813


Sources
Kumar and Clarke, 6th edition, pp. 812-13
The ECG made easy, 4th edition, pp.84-85
Conover MB. Understanding electrocardiography. 8th ed. Missouri: Mosby; 2003. pp. 332-39.


[1] Albert JS, Thyfesen K, Antman E, Bassand JP: Myocardial infaction redefined – a consensus document of the joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction, J Am Coll Cardiol 36:959-969, 2000.
[2] Wellens HJJ: Acute myocardial infarction and left bundle-branch block – can we lift the veil? N Engl J Med 334:528-529, 1996.