INDICATIONS

ECGs are indicated:

• early, to assist in diagnosis and treatment of potentially life-threatening disorders

• routinely, as part of cardiac assessment.

They should be performed in all cases of chest pain, upper abdominal pain, dyspnoea, collapse, arrest, palpitations, syncope, dizziness, non-traumatic loss of consciousness and shock; also, in any patient with a history of hypertension, fluid or electrolyte imbalance, drug overdose or other conditions that may affect the heart.

ECG INTERPRETATION

This is most usefully done in the context of the presenting symptoms and signs, which fall into three main groups:

1. chest and upper abdominal pain, dyspnoea, shock

2. collapse, palpitations, syncope, dizziness, altered consciousness

3. electrolyte disturbances, drug overdose, environmental emergencies.

The ECG should be examined for rate, rhythm, P wave, PR interval, QRS morphology and axis, ST-T segment, T wave and QT interval.

With chest pain, particular attention is paid to the ST-T segment and Q waves. The underlying lesions may be determined by ECG pattern recognition. It is useful to have a previous ECG for comparison, since any changes will have more significance.

1 Chest and upper abdominal pain, dyspnoea, shock

History and examination are the mainstays of assessment, with the ECG playing a complementary role. The main conditions requiring early diagnosis are acute myocardial infarction (AMI), unstable angina, aortic dissection and pulmonary embolism (PE).

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
V_2–4	Anterior	Left anterior descending (LAD)
V_1,2 (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.

R wave

A prominent R wave in V₁, and often V₂, suggests a posterior infarct, as well as incomplete right bundle branch block (RBBB), right ventricular hypertrophy (RVH) or left accessory pathway.

T waves

Hyperacute peaked T waves in V leads may be the only sign of AMI; they may occur in hyperkalaemia or without a known cause.

Right bundle branch block (RBBB)

RBBB does not mask AMI, as ST elevation does not occur in non-AMI RBBB.

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

• Left axis deviation (LAD)

• S inV₂ + R inV₅ > 35 mm

• ST depression anterior chest leads (LV strain)

Pericarditis

• Extensive ST elevation, concave upwards

• P-R depression

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:

• sinus tachycardia

• RBBB, usually partial

• R axis deviation

• S₁Q₃T₃ (acute cor pulmonale)

• ST elevation in aVR

• anterior T wave inversion V_1–4 (Figure 12.3); differentiate from the normal T-wave inversion found in some youths, athletes and Black people in V_1–3.

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.