Myocardial infarction

Note that the initial ECG may be normal in about half of patients with AMI.

The earliest change is ST elevation, which may occur within 30 minutes of onset of pain, and is the basis upon which a decision regarding thrombolysis or angioplasty is made.

ST elevation

• ST elevation ≥ 1 mm in LI and aVL suggests a lateral AMI (Figure 12.1), usually due to occlusion of the circumflex artery.

• ST elevation ≥ 1 mm in LII, III and aVF suggests inferior AMI, usually due to occlusion of the right coronary artery; in some cases, the left coronary system may be the site of occlusion, if the left coronary artery (LCA) is ‘dominant’.

• ST elevation ≥ 2 mm in chest leads suggests anterior or anteroseptal (if only in V_1–3) AMI, which occurs with occlusion of the left main coronary or its branches.

Figure 12.1 Inferior AMI, earliest changes: minimal ST elevation in II, III, aVF

If a coronary thrombus is treated early with thrombolysis or angioplasty, the ST elevation can regress, and further myocardial damage may be prevented. It is therefore vital that the cardiology unit is notified at the first moment a diagnosis of suspected AMI is made, usually on the basis of a history of chest pain and the early ST-T wave changes described above.

Normal ‘high ST-take-off’ in anterior chest leads can confuse the diagnosis when the chest pain is atypical, but it is better to err in suspecting an acute cardiac event than to clear the patient, when in doubt. Consult with an emergency physician, cardiologist or registrar.

Q waves

Q waves > 2 mm, > 40 ms follow in those leads showing ST elevation, if the infarct evolves (Table 12.1). They may appear within the first hour or, more commonly, within 2–6 hours (Figure 12.2). Differentiate from nonpathological septal Q waves in LI, LII, aVF or V₅,V₆, which are small (< 2 mm) and narrow.

Table 12.1 Infarct localisation—the ECG pattern distribution (early ST elevation, later Q waves)—will help to localise the site of infarction, and the usual coronary artery occluded

ECG pattern distribution	Site	Infarct-related artery
I, aVL	Lateral	Circumflex
II, III, aVF	Inferior	Right coronary, circumflex
V2–4	Anterior	Left anterior descending (LAD)
V1,2 (large R, ↓ST)	Posterior	Right coronary

Figure 12.2 Anterior AMI, later changes: Q waves, prominent coved ST elevation V_2–5

A nonpathological Q wave can occur in LIII; it is narrow, < 2 mm and < one-third the height of the QRS complex, and may disappear during deep inspiration. A small Q wave in LIII is significant if associated with one in LII.

Sometimes Q waves do not develop, but AMI can still be suspected if there are small R waves with ‘lack of progression of R waves’ across the anterior leads (normally the R wave increases in amplitude from V₂ to V₄). These infarcts are often associated with inverted T waves.

Non-Q AMI refers to subendocardial infarcts. Up to 40% of infarcts are not transmural, but they predispose to reinfarction. Blood should be sent for cardiac enzymes on arrival of the patient with chest pain so that, where there is no ECG evidence of AMI, the diagnosis is not missed.

Unstable angina, acute coronary syndrome, acute ischaemia

The ECG may be normal, but acute ischaemia is confirmed by 2 mm or more ST depression in anterior or standard leads. This may be induced by exercise. If angina is prolonged greater than 20 minutes, then this can be regarded as pre-infarctional.

Left ventricular hypertrophy

Pericarditis

Myocarditis

Aortic dissection

The ECG is nonspecific, with associated hypertensive changes in the majority.

If the dissection involves the coronary ostia, resultant myocardial ischaemia or infarction may be seen. The cardiac surgeon should be notified urgently.

Pulmonary embolus (PE)

Over 40% show no significant change; therefore, a normal ECG does NOT rule out a pulmonary embolus. ECG findings include:

Figure 12.3 Acute pulmonary embolism: partial RBBB, inverted T waves V_1–4

Anticoagulation is indicated (see Chapter 10, ‘Pulmonary emboli and venous thromboses’). Consult urgently for compromised patients following massive PE as they may need urgent thrombolysis or embolectomy.

AMI, acute ischaemia, unstable angina or acute coronary syndrome

These can cause syncope or coma as a result of vasovagal reaction, cardiogenic shock, tamponade or any of the following arrhythmias.

Ventricular asystole

Absence of any electrical activity with a ‘flat’ ECG is asystole requiring cardiac massage, full cardiopulmonary resuscitation (CPR) and the use of adrenaline as in advanced life support (ALS) guidelines.

Ensure that leads are attached and recording amplitude is correct, as low voltage VF may be misinterpreted as asystole. Direct current reversion should be tried, if there is any doubt.

Ventricular fibrillation (VF)

This grossly irregular and variable amplitude arrhythmia is easy to recognise (Figure 12.4), unless it is low in amplitude, when it can be mistaken for asystole (if in doubt, treat as VF).

Figure 12.4 Ventricular fibrillation

It requires immediate defibrillation beginning with 200 J biphasic or 360 J monophasic according to full CPR and ALS protocols, with adrenaline 1 mg IV, repeated every 3 minutes as required, and lignocaine 1–1.5 mg/kg or 100 mg bolus IV or amiodarone 5 mg/kg or 300 mg bolus IV as the mainstays of drug therapy. Magnesium 5 mmol should also be considered.

Lack of response to treatment will lead to deterioration, agonal rhythm with a sine-wave pattern, asystole and death.

Rarely, continued ALS may still rescue a patient with a preterminal rhythm.

Ventricular tachycardia (VT)