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Ischaemic heart disease continues to rank as one of the leading reasons for mortality in Singapore. Clipping is a handy way to collect and organize the most important slides from a presentation.
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.
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.
A definitive diagnosis of MI from the ECG can only be made on the basis of abnormalities in the QRS complex. 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.
Infarction evident in the inferior leads (II, III and aVF) was previously called posterior infarction (now called inferior infarction). It is only second to cancer, claiming 18 percent of all deaths. What lies behind this silent killer and how much does society really know about this dreaded disease?
The ECG provides information about the myocardium and the specialised conducting tissues that have undergone ischaemia. However, the only definitive diagnostic changes of myocardial infarction are changes in the QRS complex. However, true posterior infarction is quite rare and is not easily recognised, as none of the ECG leads are actually situated posteriorly. It should also be remembered that a percentage of patients with unequivocal angina pectoris may have normal resting 12-lead ECGs when first seen. Thus, "ST segment elevation and T wave inversion" will appear as "ST segment depression and tall pointed T waves", respectively. 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).
The exact age of the infarction cannot be determined without clinical correlation and previous ECGs, but this is likely to be a recent MI.
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".

The loss of positivity is the result of myocardial necrosis beneath the exploring electrode. Additional changes frequently associated with MI are: a) ST segment elevation (convex upwards) in leads facing the infarcted zone.
Thus, primary changes in one of the above groups will usually be accompanied by reciprocal changes in the other group. The size of the positive wave in each precordial lead is related to the thickness of viable myocardium underneath that electrode. 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. 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. In addition, T wave inversion will also have appeared but the ST segment elevation may be less obvious than before. 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). The true posterior MI is evidenced by the marked ST segment elevation in V1R (actual V2) and V2R (actual V1). When an antero-septal MI complicates RBBB (or vice versa), the rSR' complex in V1 (typical of RBBB) becomes a qR complex.
These negative waves are the result of depolarisation of the posterior wall of the ventricle travelling from endocardium to epicardium (i.e. Postero-lateral MI: Fully evolvedThe "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). 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. Tall T waves in these same leads are the posterior equivalent of inverted T waves in this fully evolved MI. 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.
Occasionally, all evidence of infarction may be lost with the passing of time; this is due to shrinkage of scar tissue.

These four changes represent increasing thickness of infarction as part of a common process.
Infero-posterior MI with RBBB This is an unusual RBBB because the initial R wave is taller than the R' wave in lead V1. The tall initial R wave in V1 is a "pathological R" wave analagous to the "pathological Q" wave of an anterior MI.
ST segment changes in myocardial infarction Dramatic ST segment changes occur in the early stages of myocardial 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.

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