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Ischaemic heart disease

Created: 18/8/2006
Updated: 10/8/2006
 
The ECG is commonly used in the investigation of suspected ischaemic heart disease (IHD). The ECG provides information about the myocardium and the specialised conducting tissues that have undergone ischaemia. It should also be remembered that a percentage of patients with unequivocal angina pectoris may have normal resting 12-lead ECGs when first seen.

The ECG in acute myocardial infarction (MI)

Acute MI may cause changes in the QRS complex, ST segment or the T wave. However, the only definitive diagnostic changes of myocardial infarction are changes in the QRS complex.

The QRS complex in infarction


Two types of QRS abnormalities may indicate infarction:
1) Inappropriately low R wave voltage in a local area and
2) Abnormal Q waves

The above two abnormalities are actually part of the same process - i.e. the development of a negative Q wave and the reduction in size of the positive wave.

The loss of positivity is the result of myocardial necrosis beneath the exploring electrode. The size of the positive wave in each precordial lead is related to the thickness of viable myocardium underneath that electrode.

Abnormal Q waves and QS complexes

In a transmural infarction (endocardium to epicardium), there will be total loss of R waves in leads overlying the infracted zone. This gives rise to entirely negative waves - i.e. QS complexes. These negative waves are the result of depolarisation of the posterior wall of the ventricle travelling from endocardium to epicardium (i.e. away from the anterior leads).

The reduction in R wave voltage can only be confirmed if either a previous ECG shows a significantly greater R wave height in the appropriate leads before the infarction occurred, or the leads involved are two or more of the leads V2 to V5.

Therefore, the four possible QRS changes indicative of infarction are:
1) Reduced R wave voltage (confirmed by previous ECGs)
2) Abnormal Q waves without any conclusive evidence of R wave reduction
3) Reduced R wave voltage in association with abnormal Q waves and
4) QS complexes.

These four changes represent increasing thickness of infarction as part of a common process. A combination of these findings is seen in an infarction of non-uniform thickness.

Abnormal Q waves

Q waves may be recognised to be abnormal because of:
1) Abnormal width (duration) - i.e. Q wave = 0.04 s or
2) Abnormal depth (relative to the following R wave) - i.e. depth of Q wave >25% of the height of the following R wave is abnormal.

ST segment changes in myocardial infarction

Dramatic ST segment changes occur in the early stages of myocardial infarction. Such changes indicate myocardial injury rather than infarction.

The injury state is unstable, and acute ST segment elevation always resolves to some extent and usually resolves completely. The resolution of the acute ST elevation is usually accompanied by development of the QRS changes of frank infarction, although occasionally, it may resolve without the development of diagnostic changes of infarction.

The ST segment shift is produced by myocardial injury, which causes a disturbance in the current flow across the cell membrane.

The essential change of myocardial injury is ST segment elevation above the isoelectric line.

The normal ST segment does not deviate by more than 1 mm above or below the isoelectric line.

Abnormal ST segment elevation occurs in leads facing the infarction, both in transmural and subepicardial infarction. Reciprocal ST segment depression may be seen at the same time as the above primary changes in leads recording from positions opposite to the infarct.

Primary ST segment depression is seen in leads facing the infarct when a
subendocardial infarction occurs.

T wave changes of infarction

The spectrum of changes in the T waves during infarction includes flattening of the T waves, bi-phasic T waves, inverted T waves and abnormally tall T waves.

The most typical T wave change in acute MI is deep, symmetrical T wave inversion. 


Sequence of changes in acute MI



Acute myocardial infarction


A) Shows the normal QRS complex in a lead.

B & C) Within hours of the clinical onset of an MI, there is ST segment elevation. At this stage no QRS or T wave changes have occurred. This indicates myocardial damage only, not definitive evidence of infarction.

D) Within days, the R wave voltage falls and abnormal Q waves appear. This is sufficient evidence of an infarction. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before.

E) Within one or more weeks, the ST segment changes revert completely to normal. The R wave voltage remains low and the abnormal Q waves persist. Deep, symmetrical T wave inversion may develop at this stage.

F) Months after the MI, the T waves may gradually return to normal. The abnormal Q waves and reduced R wave voltage persist.

Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.

Location of changes in MI

Because primary ECG changes occur in leads overlying the infarct, the location of an infarct can be derived by looking at the primary changes occurring in such leads. This is depicted in the following table:


Location of infarction Leads showing primary changes
Typical changes
Anterior infarction
Antero-septal V1, V2, V3
Anterior Some of V1-V3 plus some of V4-V6
Anterior extensive V1, V2, V3, V4, V5, V6,I, aVL
Antero-lateral V4, V5, V6, I, aVL, possibly II
High lateral aVL and/or I
Inferior infarction
Inferior II, III, aVF
Infero-lateral (= apical) II, III, aVF, V5, V6 & sometimes also I, aVL
Infero-septal II, III, aVF, V1, V2, V3
Other changes
Posterior infarction V1, V2 (inverse of usual changes elsewhere)
Subendocardial infarction Any lead (usually multiple leads)


 Examples of ECGs depicting MI


Click here for a larger image

Antero-septal MI: Fully evolved

The QS complexes, resolving ST segment elevation and T wave inversions in V1-2 are evidence for a fully evolved antero-septal MI. The inverted T waves in V3-5, I, aVL are also probably related to the MI.

Acute anterior MI



Click here for a larger image

Extensive anterior/antero-lateral MI

Significant pathological Q waves (V2-6, I, aVL) plus marked ST segment elevation are evidence for this large anterior/antero-lateral MI. The exact age of the infarction cannot be determined without clinical correlation and previous ECGs, but this is likely to be a recent MI.


Click here for a larger image

High lateral wall MI

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Inferior MI: Fully evolved


Click here for a larger image

Significant pathological Q waves are seen in leads II, III and aVF along with resolving ST segment elevation and symetrical T wave inversion. This is a classic inferior MI.

Inferior & antero-septal MI + RBBB

Pathological Q waves are seen in leads II, III, aVF (inferior MI) and in leads V1-3 (antero-septal MI). RBBB is recognised by the wide QRS (>0.12 s) and the anterior/rightwards orientation of terminal QRS forces. When an antero-septal MI complicates RBBB (or vice versa), the rSR' complex in V1 (typical of RBBB) becomes a qR complex.


Click here for a larger image

Postero-lateral MI: Fully evolved


Click here for a larger image

The "true" posterior MI is recognised by pathological R waves in leads V1-2. These are the posterior equivalent of pathological Q waves (seen from the perspective of the anterior leads). Tall T waves in these same leads are the posterior equivalent of inverted T waves in this fully evolved MI. The loss of forces in V6, I, aVL suggest a lateral wall extension of this MI.

Infero-posterior MI with RBBB

This is an unusual RBBB because the initial R wave is taller than the R' wave in lead V1. This is the clue for true posterior MI. The tall initial R wave in V1 is a "pathological R" wave analagous to the "pathological Q" wave of an anterior MI.


Click here for a larger image

Diagnostic criteria for MI

A definitive diagnosis of MI from the ECG can only be made on the basis of abnormalities in the QRS complex. The following changes are seen:

1) q waves which are either 0.04 s or longer in duration (excluding aVR and lead III) or have a depth which is more than 25% of the height of the following R wave (excluding aVR and lead III).
2) qs or QS complexes (excluding aVR and lead III).
3) Local area of inappropriately low R wave voltage.

Additional changes frequently associated with MI are:

a) ST segment elevation (convex upwards) in leads facing the infarcted zone.
b) ST segment depression occurs as a reciprocal change in leads mutually opposite to the primary leads showing evidence of infarction.
c) Horizontal ST segment depression may occur as a primary change in subendocardial infarction.

Reciprocal changes

In addition to the primary changes that occur in the ECG leads facing the infarcted myocardium, "reciprocal changes" may occur in leads opposite to the site of infarction. The changes are just the inverse of the primary changes.

Thus, "ST segment elevation and T wave inversion" will appear as "ST segment depression and tall pointed T waves", respectively.

The inferior limb leads on the one hand and the precordial leads, together with leads I and aVL, on the other hand are "mutually opposite". Thus, primary changes in one of the above groups will usually be accompanied by reciprocal changes in the other group.

It will be safe to assume that if on the ECG there is ST segment elevation in one group (as above) and ST segment depression in the other group, the elevation is the primary change and the ST segment depression is the secondary change.


True posterior MI

Infarction evident in the inferior leads (II, III and aVF) was previously called posterior infarction (now called inferior infarction).

However, true posterior infarction is quite rare and is not easily recognised, as none of the ECG leads are actually situated posteriorly.

Hence, it is only recognisable by looking for "reciprocal" changes in the anterior leads. Primary changes are not seen, as there are no actual posterior leads.

The changes in the ECG of a true posterior infarction are:

1) Abnormally tall and broad "R" waves in V1 (reciprocal to abnormally deep and wide q waves in a posterior lead, if there were any) and
2) ST segment depression in V1 in recent infarcts; in infarcts of intermediate age, tall T waves may be present in V1, V2 and V3.


True posterior myocardial infarction

Right-sided chest leads, V1R - V6R, are shown. The true posterior MI is evidenced by the marked ST segment elevation in V1R (actual V2) and V2R (actual V1). The RV MI is evidenced by the ST elevation in V3R to V6R.

Subendocardial infarction

Infarcts are most commonly intramural infarcts (transmural or subepicardial). Subendocardial infarcts are relatively rare and may encircle the interior of the left ventricle.
 
The ECG shows primary ST segment depression or deep symmetrical T wave inversion without any changes in the QRS complexes. Since these changes can also be produced by myocardial ischaemia without infarction, the diagnosis of a subendocardial infarction cannot be made with a single ECG (unless correlated with clinical or enzyme evidence of infarction).

When ST depression is the primary change, it will be seen in all or most leads except the cavity leads (aVR - always a cavity lead, aVL - a cavity lead in a vertical heart and aVF - a cavity lead in a horizontal heart). By definition, cavity leads inevitably show QS complexes.


Changes in myocardial ischaemia

Hypoxia of the myocardium may occur in the absence of infarction and necrosis. The changes may occur following stress (physical or emotional) or even spontaneously.
Significant degrees of ischaemia may exist with no evidence of ECG abnormalities. The changes, when present, are confined to the ST segment and T waves. There will be no change in the QRS complexes.

The following ECG changes may accompany myocardial ischaemia:
1) Flattening of T waves
2) Inverted T waves
3) Abnormally tall T waves
4) "Normalisation" of primarily abnormal T waves
5) Sloping ST segment depression
6) Horizontal ST segment depression
7) ST segment elevation
8) Any combination of the above changes


ArticleDate:20060818
SiteSection: Article
 
   
    
                                            
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