Interpreting an ECG systematically, in the same order every time, reduces the risk of missing abnormalities. The eight steps below go through the rhythm and then the waveforms one by one, and conclude with comparison against previous ECGs and with the clinical context.
1. Rhythm
Check
- Is the ventricular rate regular at 50–100 beats/min?
- Is there a P wave in front of every ventricular complex?
Normal values and differential diagnoses
- In sinus rhythm the rate is 50–100/min; a P wave precedes every QRS complex; the PR interval is constant and the P wave is positive in lead II.
- Causes of bradyarrhythmia: sinus bradycardia, SA block, sinus arrest, sick sinus syndrome, second-degree or third-degree AV block. An escape rhythm may be present in any bradycardia. Bradycardia may be present despite a high atrial rate (for example atrial fibrillation) if the block in the AV node is high-grade.
- Causes of tachyarrhythmia with narrow QRS complexes (QRS duration < 0.12 s): sinus tachycardia, inappropriate sinus tachycardia, sinus node re-entry, atrial fibrillation, atrial flutter, atrial tachycardia, multifocal atrial tachycardia, AVNRT, AVRT (pre-excitation, WPW), junctional tachycardia. These tachyarrhythmias arise in the atria and are very rarely life-threatening.
- Causes of tachyarrhythmia with wide QRS complexes (QRS duration ≥ 0.12 s): the commonest cause is ventricular tachycardia, which is a potentially life-threatening condition. Note, however, that any arrhythmia arising in the atria may have wide QRS complexes if the ventricles cannot be depolarised normally (example: sinus tachycardia together with left bundle branch block).
2. P wave and PR interval
Check
- The P wave is always positive in II, III and aVF.
- P wave duration < 0.12 s.
- P wave amplitude ≤ 2.5 mm.
- PR interval 0.12–0.22 s.
Normal values and differential diagnoses
- The P wave must be positive in lead II, otherwise sinus rhythm cannot be present. The P wave is often biphasic in V1 (V2). It may be slightly bifid, particularly in lead II.
- P mitrale: increased P wave duration and increased bifid appearance in II, together with a more pronounced biphasic deflection in V1.
- P pulmonale: increased P wave amplitude in II and V1.
- If no P wave is apparent, look for a retrograde (negative) P wave (indicating that atrial activation is proceeding in the reverse direction). Look also for P waves within the ST–T segment.
- PR interval > 0.22 s: first-degree AV block.
- PR interval < 0.12 s: pre-excitation (WPW syndrome).
- Second-degree AV block, Mobitz I (Wenckebach): repeated episodes with progressive lengthening of the PR interval until an atrial beat is blocked (the QRS complex fails to appear).
- Second-degree AV block, Mobitz II: atrial beats are blocked (the QRS complex fails to appear) with a constant PR interval.
- Third-degree AV block: all atrial impulses are blocked in the AV conduction system and therefore cannot activate the ventricles. An escape rhythm arises (which may have narrow or wide QRS complexes). There is no relationship between P waves and QRS complexes. The atrial rate is usually higher than the ventricular rate (both are regular).
3. QRS complex
Check
- QRS duration < 0.12 s (normally 0.07–0.10 s).
- There must be a limb lead with an amplitude > 5 mm and an amplitude > 10 mm in some chest lead (otherwise low voltage is present). High voltage (excessive amplitudes) is present if the S wave in V1 or V2 + the R wave in V5 is > 35 mm.
- Q waves: pathological Q waves (≥ 0.03 s and/or an amplitude ≥ 25 % of the R wave amplitude in the same lead, in at least two contiguous leads).
- R wave progression is checked in V1–V6.
- The electrical axis should be −30° to 90°.
Normal values and differential diagnoses
- Prolonged QRS duration: left bundle branch block. Right bundle branch block. Non-specific intraventricular conduction delay. Hyperkalaemia. Class I antiarrhythmic drugs. Tricyclic antidepressants. Phenothiazines. Ventricular beats or rhythm. Pacemaker. Pre-excitation. Aberrant conduction.
- Short QRS duration: of no clinical relevance.
- High voltage: hypertrophy. Left bundle branch block. Right bundle branch block. Normal variant in younger, athletic or slim individuals.
- Low voltage: normal variant. Incorrectly connected leads. Cardiomyopathy. Chronic obstructive pulmonary disease. Perimyocarditis. Hypothyroidism (often with concomitant sinus bradycardia). Pneumothorax. Large myocardial infarction. Obesity. Pericardial effusion. Pleural effusion. Myxoma. Cardiac amyloidosis.
- Pathological Q waves: myocardial infarction. Left-sided pneumothorax. Perimyocarditis. Hyperkalaemia. Cardiomyopathy. Amyloidosis. Myxoma. Bundle branch block. Left anterior fascicular block. Pre-excitation. Ventricular hypertrophy. Acute right ventricular strain.
- A fragmented QRS may indicate previous infarction.
- Abnormal R wave progression: previous infarction. Right ventricular hypertrophy (reversed R wave progression). Left ventricular hypertrophy (accentuated R wave progression). Cardiomyopathy. Chronic right ventricular strain. Left bundle branch block. Pre-excitation.
- An unusually tall R wave in V1/V2: misplaced chest electrodes. Normal variant. Situs inversus. Rightward displacement of the heart. True posterolateral infarction (if there is chest pain). Right ventricular hypertrophy. Hypertrophic cardiomyopathy. Right bundle branch block. Pre-excitation.
- Right axis deviation: right ventricular hypertrophy. Acute right ventricular strain. Chronic right ventricular strain (obstructive pulmonary disease, pulmonary hypertension, pulmonary stenosis). Left posterior fascicular block. Reversed arm electrodes (negative P and QRS–T in lead I). Situs inversus. Lateral myocardial infarction. Pre-excitation. Normal in the newborn.
- Left axis deviation: left bundle branch block. Pre-excitation. Left ventricular hypertrophy. Left anterior fascicular block.
- Extreme axis deviation: rare, and probably due to misplaced electrodes. In tachycardia it argues for ventricular tachycardia.
4. ST segment
Check
- It is isoelectric, slightly upsloping, and merges smoothly into the T wave.
- ST elevation and ST depression are measured at the J point.
Normal values and differential diagnoses
- Differential diagnoses of ST elevation: ST elevation myocardial infarction. Prinzmetal angina. Male/female pattern. Early repolarisation. Acute perimyocarditis. Left bundle branch block or other intraventricular conduction delay. Left ventricular hypertrophy. Brugada syndrome. Takotsubo syndrome. Hyperkalaemia. After electrical cardioversion. Pulmonary embolism. Pre-excitation. Aortic dissection occluding the coronary ostia. Ventricular aneurysm.
- Differential diagnoses of ST depression: physiological normal response to exertion. Acute myocardial ischaemia. Hypokalaemia. Increased sympathetic tone. Digoxin. Left bundle branch block. Right bundle branch block. Left ventricular hypertrophy. Right ventricular hypertrophy. Pre-excitation. Prolonged tachycardia. Heart failure.
5. T wave
Check
- It is concordant with the QRS complex.
- Positive in all or most leads.
- In the limb leads the amplitude is greatest in II; in the chest leads in V2–V3.
Normal values and differential diagnoses
- Normal variants: isolated T wave inversion is accepted in V1 and III. In unusual cases the T wave inversions of childhood may persist into adult life in V1–V3 (V4) (juvenile T wave pattern). Rarer still is global idiopathic T wave inversion (V1–V6).
- T wave inversion without ST deviation: does not indicate acute ischaemia, but may be post-ischaemic. If most of the chest leads are involved and the patient has angina, suspect Wellens syndrome. Cerebrovascular catastrophe. Pulmonary embolism. Perimyocarditis in the healing phase. Cardiomyopathy.
- T wave inversion with ST deviation: acute myocardial ischaemia.
- Tall positive T waves: normal variant. Early repolarisation. Hyperkalaemia. Left ventricular hypertrophy. Left bundle branch block. Occasionally perimyocarditis. Acute myocardial infarction may present with hyperacute T waves.
6. QTc interval and U wave
Check
- QTc interval ≤ 0.45 s in men, ≤ 0.46 s in women. A prolonged QTc interval can cause malignant arrhythmias. A shortened QTc interval is exceedingly rare but can also cause malignant arrhythmias.
- A U wave is sometimes seen, more often in young athletic individuals; it should be positive, is best seen in V3–V4, and should be considerably smaller than the T wave.
Normal values and differential diagnoses
- Acquired QTc prolongation: class Ia antiarrhythmic drugs (procainamide, disopyramide) and class III drugs (amiodarone, sotalol). Psychotropic drugs (tricyclic antidepressants, phenothiazines, haloperidol, lithium, SSRIs). Antimicrobials (macrolides, quinolones, pentamidine, atovaquone, chloroquine, amantadine, foscarnet, atazanavir). Hypokalaemia. Hypocalcaemia. Hypomagnesaemia. Cerebrovascular event (haemorrhage, stroke). Acute myocardial ischaemia. Cardiomyopathy. Bradycardia. Hypothyroidism. Hypothermia.
- Congenital QTc prolongation (LQTS): likely if no other cause can be found.
- Shortened QTc (≤ 0.32 s): hypercalcaemia and digitalis treatment, which may likewise lead to malignant ventricular arrhythmias.
- A negative U wave: high specificity for cardiac disease.
7. Compare with previous ECGs
It is fundamental always to compare the current ECG with previous recordings. Any change is of interest and may indicate pathology.
8. Clinical context
The ECG changes must be interpreted in their context.
Source
The method and the normal values have been compiled from established ECG literature and from clinical consensus on systematic ECG interpretation.
