Chapter 12 Clinical electrocardiography and arrhythmia management
This chapter examines the clinical use of the ECG, one of the most important diagnostic tools in an emergency department. It must be stressed, however, that the ECG may appear normal, even in the presence of severe cardiac disease.
The reader should have knowledge of basic cardiac electrophysiology and anatomy, which will help in diagnosing and localising lesions from the ECG.
INDICATIONS
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:
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).
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
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.
ST depression
ST depression > 2 mm in V1 may indicate a posterior infarct, and this may be confirmed in ECG leads V7,8,9. V1,2 will also have a prominent R wave and tall T waves. Posterior infarcts are usually caused by occlusion of the right coronary artery (RCA).
The RCA also supplies the sinoatrial (SA) and atrioventricular (AV) nodes and the bundle of His. Occlusion of the RCA is associated with potentially serious bradyarrhythmias.
Minor ST or Q wave changes in V1 with signs of right ventricular failure, e.g. elevated jugular venous pressure (JVP), may point to a right ventricular infarct: right ventricular leads RV3,4,5 may show characteristically slight ST elevation.
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 |
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.
Left bundle branch block (LBBB)
New LBBB, with chest pain, indicates AMI. The location may be diagnosed by inspecting the affected leads to see whether there is concordance of ST segments with QRS complexes (in non-AMI LBBB, the ST segments are discordant with the QRS, i.e. they point in opposite directions).
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.
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:
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.
2 Collapse, palpitations, syncope, dizziness, altered consciousness
The ECG can help to determine a cardiac cause.
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).
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.
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