Electrocardiographic Examination

Patients with chest discomfort should be assessed by an appropriately qualified person and have an ECK recorded within 5 minutes of arrival at a healthcare facility to determine the presence and extent of myocardial ischaemia, the risk of adverse events, and to provide a baseline for subsequent changes. Most importantly, the ECK is essential to determine whether emergency reperfusion is required, and is recommended as the sole test for selecting patients for PCI or thrombolysis. Where ST segment monitoring is available, this should be continuous. Alternatively, if chest discomfort persists, ECGs should be repeated every 15 minutes. Even when chest pain resolves it is important to record a series of 12-lead ECGs over admission to determine changes over time.

Myocardial ischaemia, injury or infarction cause cellular alterations and affect depolarization and repolarisation. Myocardial ischaemia may be a transient finding on the ECG. Ischaemia results in T wave inversion or ST segment depression in the leads facing the ischaemic area. Ischaemic T waves are usually symmetrical, narrower and more pointed. St segment depression of 1 mm for 0.08 seconds is indicative of ischaemia, especially when forming a sharp angle with an upright T wave. These changes are reversible with reduction in demand (e.g. by rest, nitrates).

On acute presentation, myocardial injury (infaction) is most commonly associated with ST segment elevation on the ECG, although this is not universal. In addition, a typical pattern of ECG changes over time (evolution of the St segments, Q wave development and T wave inversion) are often seen (described below), but these changes too are not universal. The distinction between the various ‘acute coronary syndromes’, including both ‘ST elevation myocardial infarction’ (STEMI) and ‘non-ST elevation myocardial infaction’ (non-STEMI), is important for ensuring appropriate assessment and protocol-based treatment for the various presentations.

The location and extent of ischaemia or infarction may be evident on the ECG leads overlying the affected area, as follows :

- Anteroseptal wall of the left ventricle, V1-V4- Lateral wall of the left ventricle, I, aVL, V5 and V6- Inferior wall of left ventricle, II, III, and aVF

Additional leads are needed to view the right ventricle and posterior wall. Chest electrodes can be placed on the right chest wall using the same landmarks as the left chest to view the right ventricle. Further electrodes, V7-V9, may be placed over the posterior of the left chest to view the posterior wall.

Continuous ECG monitoring is essential to detect dysrhytmias, which often accompany AMI and are a common cause of death. The dysrhythmia may be due to poor perfusion of the conduction tissue. More often, dysrhythmias occur because ischaemic tissue has a lower fibrillatory

threshold and ischaemia is not being managed. Dysrhythmmias also often result from left ventricular failure.

Typical ECG Evolution Pattern

The initial ECG features of myocardial infarction are ST segment elevation with tall T waves recorded in leads overlying the area of damaged myocardium. These changes gradually change, or evolve, over time, with ST segments returning to baseline (within hours), while Q waves develop (hours to days) and T waves become inverted (days to weeks). The time course for the evolutionary changes is accelerated by reperfusion, e.g. PCI, thrombolysis or surgery. Thus an almost fully evolved pattern may be seen within hours if successful reperfusion has been undertaken.

Given the expected time course for evolution, it is possible to approximate how recently infarction has occurred, which is essential in determining management :

- Acute (or hyperacute)—there is ST elevation biut Q waves or T inversion have not yet developed.

- Recent—Q waves have developed. ST segment elevation may still be present. Evolution is underway. The infarction is more than 24 hours old.

- Old (fully evolved)—Q waves and T inversion are present. ST segments no longer elevated. Infarction occurred anything from a few days to years ago.

Bipchemical Markers

Intracellular cardiac enzymes enter the blood as ischaemic cells die, and elevated levels are used to confirm myocardial infarction and estimate the extent of cell death. The cardiac troponins T and I (cTnT and cTnI) have been found to be both sensitive and specific measures of cardiac muscle damage. Tropinin I is rapidly released into the bloodstream, so it is especially useful the diagnosis and subsequent risk stratification of patients presenting with chest pain in the early stages. Troponin I is also a more appropriate marker to use in postoperative and trauma patients than creatinin kinase-MB (CK-MB), as CK-MB levels woll be affected by muscle damage. However, CK-MB is less costly and more readily available, and so is still often used, particularly in the presence of a non-diagnostic ECG. C-reactive protein assays may prove to be useful, as baseline and discharge levels are predictive of subsequent cardiac events. However, the laboratory facilities are not readily available.