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