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Information

Editors

PekkaRaatikainen
HannuParikka

Interpretation of Adult ECG

Essentials

  • Electrocardiography (ECG) plays an essential role in the diagnostics and acute care of many heart diseases (e.g. acute coronary syndrome, arrhythmias).
  • The interpretation of an electrocardiogram should be performed systematically and taking all leads into account. The findings should always be set in proportion to the patient history.
  • Interpretations provided by the ECG device can be used in assistance but they should not be blindly relied upon.

Overview

  • The aim should be to obtain a quick overview of the patient's rhythm, AV conduction, the shape of the QRS complex and the possible presence of ST-T changes.
    • Essential pathology is often revealed but, for example, a long QT interval is easy to miss.
    • At the same time, it should be checked that all the leads have been recorded and are correctly marked.
    • The correct paper speed is 50 mm/s and the calibration 1 mV = 10 mm.
  • After the initial overview, it is recommended that the ECG is examined systematically to avoid unnecessary errors. However, the sequence of interpretation may vary according to the patient's symptoms.
    • If the patient presents with chest pain, attention must be paid to the ST segment and T wave changes as these reflect ischaemia.
    • If arrhythmias are the presenting symptom, the shape of the QRS wave and ventricular rate should be scrutinised.
    • The use of an ECG ruler and calliper should be considered to aid the interpretation.
    • Comparing the ECG with previous recordings will solve many problems.
  • Modern ECG devices automatically provide the majority of necessary measurements.
    • With a few exceptions, the measurements provided by the devices are very reliable. The most error prone areas in computerised ECG interpretation are P wave recognition and the measurement of the QT interval.
    • The examination of a computerised ECG report must take into account the fact that the programmes are sensitive by design, and this may often lead to overdiagnosis. On the other hand, if the device gives a report of a normal ECG it can usually be relied on.
    • Many devices allow the operator to enter the patient's age, sex and other relevant data into the programme memory. This will improve the accuracy of the reports.
    • The device will not take responsibility for erroneous reports; the final responsibility will always lie with the doctor!

Ventricular rate

  • The normal ventricular rate is 50-100 beats per minute, but individual variations are great.
    • Bradycardia < 50/min
    • Tachycardia > 100/min
  • If the heart rate is irregular, as for example in atrial fibrillation (AF), the rate should first be measured between several QRS complexes after which their average can be calculated. A computer will automatically calculate the average rate.

P wave

  • P wave reflects the activation of the atria and its normal duration is < 0.12 s. The first half of the P wave reflects the activation of the right atrium and the terminal half that of the left atrium.
  • The width, height and morphology of the P wave are determined first, and at the same time it should be checked whether each QRS complex is preceded by a P wave and whether the P waves are always followed by a QRS complex.
    • Because the sinus node lies high in the right atrium P waves are normally positive in the inferior leads and in the leads that look at the heart from the left (I, aVL, V5, V6).
    • In the benign coronary sinus rhythm, P waves are inverted in the inferior leads as the rhythm originates from the lower part of the right atrium.
    • In right atrial strain, the initial deflection of the P wave is abnormally high in inferior leads.
    • In left atrial strain, the duration of the negative terminal deflection of the P wave (s) x its depth (negativity; mm) in lead V1, i.e. the P-terminal force (PTF), is more negative than -0.03 mms. A positive PTF is a fairly specific but not a sensitive sign.
    • A prolonged (> 0.12 s) and notched (bifid) P wave (picture ) can also be a sign of slowed down conduction within or between the atria. It is often associated with predisposition to AF.
  • Computers often have difficulties recognising small P waves possibly leading to erroneous arrhythmia diagnosis (AF).
    • P wave is usually best seen in lead V1 or in the inferior leads (II, III, aVF).

PR interval (= PQ interval)

  • The PR interval reflects the conduction time between the atrium and ventricle (AV conduction) and is normally < 0.20 s.
  • In first degree AV block, the PR interval is prolonged (> 0.20 s), but each P wave is followed by a QRS complex.
    • A slightly prolonged PR interval (< 0.24 s) is a very common and usually harmless ECG abnormality; it does not prevent the use of beta blockers or digoxin. However, the patient's ECG should be checked a few days after medication has been started.
    • If other conduction defects coexist (e.g. LBBB, RBBB, LAHB, LPHB), a prolonged PR interval is a more serious finding and may carry a risk of progressing to complete AV block.
    • Functional prolongation of the PR interval due to enhanced vagal tone is seen at rest, for example in athletes. The PR interval normalises during exercise.
  • Mobitz type I (Wenckebach) second-degree AV block is characterised by a progressive prolongation of the PR interval until a QRS complex is missed after a P wave. The conduction defect is almost invariably located in the AV node, and the disturbance is usually benign and transient.
  • In Mobitz type II second-degree AV block, the PR interval does not increase gradually in length, but a QRS complex is occasionally missed (randomly or regularly) after a P wave. The conduction defect is usually located in the bundle of His or distal to it. This disturbance is usually serious and carries a risk of progressing to complete AV block.
  • In third degree AV block (complete AV block) no P waves are conducted to the ventricles, and there is complete dissociation between the atrial and ventricular activity. The QRS complexes may be either narrow or broad.
  • A PR interval shorter than normal (< 0.12 s) may be suggestive of WPW syndrome Supraventricular Tachycardia (SVT).
  • In problematic cases, an ECG calliper may be used to assist the determination of atrial rate and the identification of P waves hidden in the QRS complexes or T waves.

QRS complex

  • The normal duration of a QRS complex is < 0.12 s. The duration of the complex may prolong, for example, in the presence of bundle branch block or delta wave.
    • LBBB is usually a pathological finding and may be associated, for example, with heart failure Bundle Branch Blocks in an ECG. RBBB may be encountered in a healthy heart Bundle Branch Blocks in an ECG.
    • Functional bundle branch block, i.e. aberration, is a benign phenomenon Bundle Branch Blocks in an ECG.
    • The morphology of a delta wave is dependent on the location of the accessory pathway, and it may also be negative. In WPW syndrome, delta waves are present in several contiguous leads, and the PR interval is abnormally short.
  • A QRS complex with abnormal morphology is usually caused by a myocardial infarct scar or ventricular hypertrophy.
  • A pathological Q wave appears in leads where it previously was absent. It is usually a sign of transmural myocardial infarction.
    • Any Q wave with length ≥ 20 ms in leads V2-V3 or QS complex in leads V2 and V3
    • A Q wave with length ≥ 30 ms and depth ≥ 1 mm or a QS complex in two contiguous leads: I and aVL; II and aVF; V4-V6
    • A transmural posterior wall infarction may cause a tall R wave (> 40 ms and R/S > 1) into leads V1-V2.
  • In ventricular hypertrophy, the amplitude of the complex increases. Criteria for left ventricular hypertrophy (LVH): see Assessment of Ventricular Hypertrophies from an ECG.
    • A deep (≥ 0.2 mV) but narrow Q wave may develop in hypertrophic cardiomyopathy.
  • Also decreased R wave may indicate damage caused by myocardial infarction.
  • The electrical axis of the QRS complex in the frontal plane can be roughly estimated by looking at limb leads I and aVF, which are perpendicular to each other.
  • The basic rule is that in atrial arrhythmias the QRS complexes are narrow and in ventricular arrhythmias broad.
  • In practice, a computer will interpret all broad complex extrasystoles as originating from the ventricles and is not able to recognise atrial premature beats with aberrant conduction.

T wave and U wave

  • T waves reflect the overall repolarisation of the various layers of the ventricular myocardium. Normally the T wave morphology does not change from beat to beat, they are uniphasic and have the same direction as the QRS complex.
    • Lead V1 forms an exception as T waves may be negative even in healthy adults.
    • A negative T wave may occur also in young individuals in association with acute sympathicotonia.
  • The causes of T wave abnormality include ischaemia, electrolyte disturbances (hypokalaemia), ventricular hypertrophy (strain pattern) and certain medications (e.g. digoxin).
    • Prominent and peaked T waves appear during the early phase of myocardial ischaemia, and T wave inversion occurs later on, i.e. the T waves become negative.
    • Beat to beat fluctuation in the morphology of the T wave is an abnormal finding and is often associated with arrhythmia susceptibility.
  • A negative T wave is a non-specific sign and, in addition to ischaemia, may be associated with
    • numerous factors that may cause damage or strain to the heart
    • ventricular hypertrophy
    • poisoning
    • recovery from a prolonged episode of tachycardia
    • subarachnoid haemorrhage or elevated intracranial pressure.
  • A U wave occasionally follows the T wave; it is a separate ECG deflection that is smaller than the T wave but has the same direction. It should not be confused with the T wave, and it is not included in the QT interval.
    • A fairly rare finding, which may be caused by, for example, hypokalaemia, ischaemia, hypertrophy and electrolyte disturbances
    • The U wave may be associated with the risk of developing arrhythmias but in a young person it may occur without accompanying heart disease.

ST segment

  • The ST segment normally lies flat on the isoelectric line.
    • ST segment changes should be assessed visually from all leads, and the measurement should be done to half a millimetre.
    • ST elevation is measured from the J point in order to avoid false positive interpretation due to early repolarisation.
  • ST elevation is associated with acute ischaemia and is the most important sign of imminent myocardial injury.
    • The area of the injury can be determined by noting the leads which show changes since, in imminent infarction, ST elevation is only observed in the leads looking at the area supplied by the occluded coronary artery.
    • Reciprocal ST segment depression is typically seen in the leads looking at the opposite side of the injury.
    • After successful reperfusion (acute PTCA, thrombolysis), ST elevation quickly normalises. Persistent ST elevation is a sign of poor prognosis.
    • Slight ST elevation may also be a normal finding in anterior chest leads (early repolarisation), particularly in an "athlete's heart". An upward sloping ST segment is suggestive of benign ST elevation as is a T wave with a peak which is clearly higher than the initial part of the ST segment.
  • As well as ischaemia, possible causes of ST elevation include early repolarisation, myocarditis, pulmonary emboli, hyperkalaemia, hypertrophic cardiomyopathy and Brugada syndrome.
    • In myopericarditis, ST elevation does not follow the anatomy of the coronary arteries, and changes are seen in almost all the leads whilst reciprocal ST depression is lacking. Moreover, PR segment depression is often present in myopericarditis.
  • ST depression is caused particularly by ischaemic heart disease but also by certain medicines (e.g. digoxin), left ventricular hypertrophy and cardiomyopathy.
    • The classic ST depression induced by digoxin is ”scooped” (or ”bowl shaped”) in appearance, most obvious at the end of the segment.
    • In LVH, a typical strain pattern is evident in the ST segment Assessment of Ventricular Hypertrophies from an ECG.
    • Sympathicotonia, particularly in women, may cause ST-T changes, which mimic ischaemic changes. A beta blocker test may be used in differential diagnosis since sympathicotonic ECG changes will resolve when the heart rate slows down to 50-60/min.
  • Computers have been programmed for safety reasons to be particularly sensitive to interpret ST changes as being caused by ischaemia. This causes some overdiagnosis. If the computer reports ”non-specific ST elevation”, the final interpretation is the responsibility of the clinician.

QT interval

  • An ECG ruler should always be used to measure the QT interval, which reflects the repolarisation phase of the heart, rather than rely on the values produced by the ECG machine. The measurement is made from the beginning of the QRS complex to the end of the T wave.
    • Where the identification of the termination of the T wave is difficult, the interval is measured to the intersection of the isoelectric line and the tangent of the down slope of the T wave.
    • A separate U wave is excluded from the measurement, but if the T wave and U wave form a continuous wave, the QT interval is measured to the end of the complex.
  • The QT interval shortens as heart rate increases and becomes prolonged as heart rate slows down. A measured QT interval is corrected to heart rate by dividing it by the square root of the previous R-R, measured in seconds (QTc = QT/(R-R)1/2 ).
    • A correction for heart rate will always add unreliability to the measurement, and the most reliable measurement is therefore obtained from an ECG where the heart rate is close to the baseline level (60/min).
    • In practice, a QTc > 470 ms in women and > 450 ms in men is to be considered abnormal and warrants specialist consultation, unless an explanatory condition or co-morbidity coexists.
    • An ECG ruler will provide the upper limit for a QT interval corrected to the heart rate. A variation of over 10% is abnormal, and the cause of it should be sought for.
    • Exceptionally short QT time (QTc < 340 ms) may be associated with predisposition to ventricular arrhythmias (short QT syndrome).
  • The cause of prolonged QT interval is usually either a congenital ion channel abnormality or a drug effect. Drugs that may prolong the QT interval include some antiarrhythmic drugs, antimicrobial drugs, antihistamines and antipsychotics Long QT Syndrome (LQTS).
  • A long QT interval increases the risk of torsade de pointes ventricular tachycardia. The risk is increased, among others, in hypokalaemia, hypomagnesaemia and hypocalcaemia and by drug interactions.
    • Transient loss of consciousness may be a warning sign of an episode of torsade de pointes.

Arrhythmias

Essential clues to be noted on a resting ECG or an ECG taken during arrhythmia when considering an arrhythmia diagnosis.

ECG findingProbable diagnosis
Abnormal P wave morphologyEctopic atrial rhythm
Broad, notched (bifid) P waveAtrial fibrillation
Pathological Q waveMonomorphic VT associated with old myocardial infarction
ST elevationPolymorphic VT associated with acute ischaemia
Delta waveWPW syndrome (atrioventricular reciprocating tachycardia AVRT)
Long QT intervalAcquired or congenital long QT syndrome (torsade de pointes VT)
Partial RBBB and ST elevation in leads V1-V3Brugada syndrome (VT/VF)
Negative T wave and epsilon wave in right sided chest leadsArrhythmogenic right ventricular cardiomyopathy (VT/VF)
Symptomatic bradycardia or sinus arrestSinus node dysfunction
Long PR timeFirst degree AV block
Each P wave is not followed by QRS complexSecond or third degree AV block
Bundle branch blockTransient complete AV block, VT
Bifascicular block (LBBB or RBBB + LAHB/LPHB)Transient complete AV block
Irregular ventricular rate, no recognisable P wavesAtrial fibrillation
Negative F waves with a sawtooth pattern in inferior leadsTypical atrial flutter
Narrow complex, regular tachycardia, with no recognisable P waves or abnormal P wavesSupraventricular tachycardia (SVT)
Broad complex monomorphic tachycardiaVT, SVT with aberrant conduction, antidromic tachycardia
Broad complex polymorphic tachycardiaPolymorphic VT, torsade de pointes, AF with aberrant conduction or pre-excitation