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An overview of paediatric ECG

This document provides a comprehensive guide on interpreting pediatric electrocardiograms (ECGs), detailing the anatomy of the cardiac conduction system, waveform characteristics (P, QRS, T waves), and intervals (PR, QT). It discusses normal and abnormal rhythms like sinus bradycardia, tachycardia, and various types of ectopic beats, emphasizing the significance of clinical context, patient age, and ECG standards in accurate diagnosis. Key analysis points include measurement of heart rate, examination of waveforms, and intervals to identify potential cardiac issues.

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An Overview of Paediatric Electrocardiogram Sid Kaithakkoden MBBS,DCH,DipNB,MD.MRCPCH,FCPS sidkaithakkoden@nhs.net
2 The Electrocardiogram: Basics
3 The Cardiac Conduction System Sino-atrial node Purkinje fibresRight & left bundle branches Atrioventricular bundle (bundle of His) Atrioventricular node 3.3 RA LA RV LV
4
5 Conventional Placement for 3-lead Monitoring
6 Rough Direction of Depolarisation
7 It’s all about being able to relate…… This…. To this!
8 ECG Waveform… P R Q S T
9
10 Sequence of Electrical Activity in the Heart Forming the P-Q-R-S-T Waves • P wave: – Atrial depolarization – Axis: 0-90 – P wave is upright in I & AVF
11 The P Wave: Spread of Electrical Activity through the Atria P
12 The P Wave • Represents atrial depolarisation and activation – Either from the SA node (sinus rhythm) – Or from somewhere else in atria (ectopic) • In sinus rhythm P wave rate is regular • The only normal exception where P wave rate varies is sinus arrhythmia – usually only seen in people under 40
13 The P Wave: Characteristics • P waves should be present! • If absent, atrial activity may be: – Truly absent (No coordinated atrial activity) – Present but not visible on ECG • No more than 0.12 secs duration • No more than 2.5 mm high in lead II • Upright in lead II (usually upright in all leads except aVR)
14 Analysis of P waves: • Are the P waves regular? • Is there one P wave for every QRS? • Is the P wave normal and upright in Lead II? • Are there more P waves than QRS complexes? • Do all of the P waves look alike?
15 • PR interval: – Slow AV node conduction – No electrical activity recorded by ECG – PR interval is flat
16 The PR Interval • Measures the time from the beginning of atrial depolarisation to the beginning of ventricular depolarisation – i.e. from beginning of P wave to beginning of QRS complex • A major portion of the PR interval is the slow conduction through the AV node • AV nodal conduction under autonomic control
17 PR interval analysis: • Normal PR interval (PRI) is 0.12 - 0.2 secs in adults (age dependant in children) • Is the PRI measurement within the normal range? • Are all of the PRI’s the same? • If the PRI varies, is there a pattern to the changing measurements?
18 • Q wave: – Depolarization of the ventricular septum – Axis: 180-270 – Negative deflection in I & AVF
19 • R Wave: – Depolarization of the ventricles – Axis: 0-90 – Upright in I & AVF
20 • S Wave: – Depolarization of the heart base – Axis: 180-270 – Negative deflection in I & AVF
21 The QRS Complex • Represents ventricular depolarisation and activation • Usually much bigger than P and T wave as much larger muscle mass • NB. The QRS complex may comprise of a Q, R and S wave – but often not all three in same complex!
22 The QRS Complex • Q waves usually absent from most leads of the 12-lead ECG • The duration of the QRS complex is termed the “QRS Interval” (Normal range for is 0.07 – 0.11 secs) • QRS amplitude (on 12-lead ECG) varies considerably – up to 3.0 mV (30mm) may be normal
23 QRS Waveform Nomenclature R r qR qRs Qrs QS Qr Rs rS qs rSr’ rSR’ 7.1
24 Analysis of QRS Complex • What is the duration of the QRS complex? • Are all of the QRS complexes of equal duration? • Do all of the QRS look alike? • Are the unusual QRS complexes associated with ectopic beats? • Is the QRS complex preceded by a P wave?
25 The ST Segment • The ST segment lies between the end of the S wave and the start of the T wave • It represents the time between end of depolarisation and beginning of repolarisation
26 Analysis of the ST Segment • The ST segment is normally isoelectric • Can be abnormal in two ways: –Are the ST segments elevated? • May indicate myocardial infarction –Are the ST segments depressed? • May indicate myocardial ischaemia
27 ECG complex with isoelectric ST segment
28 12-lead ECG showing ST Segment Depression
29 12-lead ECG showing ST Segment Elevation
30 • T Wave: – Repolarization of the Ventricles – upright deflection in I & AVF
31 The T Wave • Represents repolarisation (“recharging”) of the ventricular muscle to its resting electrical state • Analysis of the T wave would examine: – Its direction – Its shape – Its height
32 Repolarisation of Ventricle The T wave: Repolarisation of the ventricle T 3.6
33 The QT Interval • The QT interval measures the total time taken for depolarisation and repolarisation of the ventricles – Beginning of the QRS complex to the end of the T wave • Usually measured rather than the duration of the T wave alone • Varies with heart rate, age and sex
34 The U Wave • The U wave is normally either absent or present as a small rounded wave following the T wave • Normally oriented in the same direction as T wave • Origin of U wave is uncertain • More prominent in hypokalaemia, hypercalcaemia or hyperthyroidism
35 Age HR bpm QRS Axis degrees PR interval seconds QRS interval seconds R in V1 mm S in V1 mm R in V6 mm S in V6 mm 1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10 1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10 1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10 3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10 6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7 1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7 3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5 5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4 8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4 12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4 > 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4 Normal Values
36 QT interval: • the duration from the beginning of the QRS complex to the end of the T wave • count the number of small squares, then multiply by 0.04 seconds, that the QT in seconds • Corrected QT interval – Normal QT is determined by the HR – QTc = QT / square root of RR interval
37
38 Reading and Interpreting Electrocardiograms • Age: unless the patient’s age is known, the paediatric ECG cannot be interpreted • Is the ECG "full standard"? • Is the ECG "standard speed"? • The standard speed of paper is 25 mm/sec • Occasionally it is made to run at a double speed (50 mm/sec) in cases of tachyarrhythmia to enable the visualization of an otherwise hidden p waves • Additional clinical information : • Indication • Clinical diagnosis: cardiac and other • Medications: cardiovascular drugs, others eg. cisapride, tricyclics • Electrolytes
39 Systematic reading of ECG: 1. Heart rate 2. P wave axis 3. Rhythm 4. QRS axis 5. Intervals PR, QRS, QT/QTc 6. P wave amplitude and duration 7. QRS amplitude, R/S ratio, Q waves 8. ST segments and T wave
40 Heart Rate
41 Heart Rate - Basics • The standard UK and USA speed for ECG recording is 25mm / second • Before you measure the heart rate always check that this speed has been used! • At this speed, a one-minute ECG tracing covers 300 large squares
42 ECG Paper: Dimensions 5 mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = Rate Voltage ~ Mass
43 Method 1 • Count the number of large squares between two consecutive R waves and divide into 300. – Quick – Not very accurate with fast rates – Used ONLY with regular rhythms
44 Method 2 • Count the number of small squares between two consecutive R waves and divide into 1500. – The most accurate method – Time-consuming – Used only with regular rhythms
45 Rhythms Arising From the Sinoatrial Node
46 Rhythms Arising From the Sinoatrial Node • (Normal) sinus rhythm • Sinus tachycardia • Sinus bradycardia • Sinus arrhythmia • Sick sinus syndrome
47 Normal Sinus Rhythm • Sinus rhythm is the normal cardiac rhythm • The sinoatrial node is acting as the natural pacemaker • Heart rate is between 60-100 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex
48 Normal Sinus Rhythm
49 Sinus Bradycardia • Sinus bradycardia is sinus rhythm with a heart rate of less than 60 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex • It is unusual for sinus bradycardia to be slower than 40 / min – Consider alternative e.g. Heart block
50 Sinus Bradycardia
51 Sinus Bradycardia & Escape Beats • If sinus bradycardia is severe, escape beats or rhythms may occur • While these beats and rhythms may look abnormal, they are protective mechanisms
52 Sinus Tachycardia • Sinus tachycardia is sinus rhythm with a heart rate of more than 100 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex • Unusual for sinus tachycardia to be faster than 180 beats / min, except in fit athletes – Consider alternative eg. Nodal tachycardia
53 Sinus Tachycardia
54 Sinus Arrhythmia • Sinus arrythmia is the variation of heart rate seen with inspiration & expiration • Each P wave followed by QRS complex • Uncommon in age over 40 years • Harmless • Cause: heart rate increases during inspiration as reflex response to more blood returning to heart
55 Sinus Arrhythmia
56 Sick Sinus Syndrome • This refers to a collection of impulse generation and conduction problems related to the sinus node • Any or all of the following may be seen: – Sinus bradycardia – Sinus arrest – Sinoatrial block • May be associated with paroxysmal tachycardias (“tachy–brady syndrome”)
57 Sick Sinus Syndrome Sinus arrest • This is when the sinus node fails to discharge on time, • P wave fails to appear as expected, causing a variable-length gap Sinoatrial block • Sinus node depolarises normally, but impulse doesn’t reach the atria • P wave fails to appear, but next one appears in exactly the right place
58 Sinus Arrest
Ectopics & Escape Beats:
60 Ectopics • The word “ectopic” implies “outside” – (eg. ectopic pregnancy outside the uterus) • Ectopic beats therefore could be defined as beats arising from outside the normal cardiac conduction pathway ie. not starting at the sinoatrial node • Ectopic beats are also called: – Extrasystoles – Premature beats (or complexes)
61 Ectopics • Ectopic beats appear earlier than the next expected beat • They can arise from any region of the heart, but are normally classified into: – Atrial – AV junctional – Ventricular
62 Ectopics • Ectopic beats may occur as: – Isolated single beats – Multiple beats – The dominant rhythm (usually defined as three or more successive ectopic beats) having “taken over” from the SA node
63 Cardiac Conduction System: Inherent Rates Sino-Atrial (SA) Node: • 60-100 / min Atrioventricular (AV) Node: • 40-60 / min. Ventricles: • 20-40 / min. Escape rhythms generated by the AV node and ventricles will therefore be at the above respective rates
64 Beats & Rhythms Arising From the Atria • Atrial ectopics • Atrial tachycardia • Atrial flutter • Atrial fibrillation
65 Atrial Ectopics • Atrial ectopics are identified by a P wave which appears earlier than expected and has an abnormal shape • They will usually be conducted through to the ventricles giving a QRS complex – A normal QRS complex meaning normal ventricular conduction – Wide (>0.12 sec or 3 small squares) QRS complex indicating aberrant ventricular conduction
66 Atrial Ectopics • Atrial ectopics are also known as: – Premature atrial complexes (PAC’s) – Atrial extrasystoles • They may occur as: – Isolated single beats – Two beats together (a pair or couplet) – As a run of ectopics (ie. more than 3) becoming a tachycardia – One ectopic for every sinus beat (bigeminy)
67 Atrial Ectopics • Atrial ectopics may all arise from the same focus in the atria (unifocal) – All the abnormal P waves would look the same • Atrial ectopics may arise from different foci in the atria (multifocal) – Abnormal P waves would vary in shape
68 Atrial Ectopic – Single
69 Atrial Bigeminy
70 Atrial Tachycardia • Atrial tachycardia is a tachycardia originating from impulses generated in the atrial myocardium – From an ectopic focus – Via a “re-entry” mechanism • Characteristics: – Heart rate greater than 100 / min – Abnormally shaped P waves
71 Atrial Tachycardia • Atrial (P wave) rate is usually 120-250 / min • Above atrial rates of 200 / min, the AV node struggles to keep up with conduction so AV block may occur
72 Atrial Tachycardia
73 Atrial Flutter • Differs from atrial tachycardia in that the atrial (P wave) rate is higher • Results from: – Either an ectopic focus – Or depolarization circling the atrium (“Circus Movement”) • Atrial rate is usually 250-350 / min, but often almost exactly 300 / min • The rapid rate gives it a classic “sawtooth” appearance
74 Atrial Flutter • AV node cannot keep up with that rate, so AV block occurs • Most common is 2:1 block, giving ventricular rate of around 150 / min • 3:1 = ventricular rate of 100 / min • 4:1 = ventricular rate of  75 / min • AV block may also be variable
75 Atrial Flutter
76 Atrial Flutter – Variable Block
77 Atrial Fibrillation • Much more common than atrial flutter • Affects 5-10% of elderly people • Can be permanent • May be transient or paroxysmal – particularly in younger people • Caused by rapid, chaotic depolarisation of the atria (350 - 650 impulses / min)
78 Atrial Fibrillation • Characteristics: – No P waves seen – Baseline consists of high frequency, low amplitude oscillations (fibrillation or “f” waves) – Conduction through AV node is erratic, therefore ventricular (QRS) rate is irregular (often described as “irregularly irregular”) – Ventricular rate usually  120 – 180 / min • Unless patient medicated eg. digoxin
79 Atrial Fibrillation
80 Atrial Fibrillation
81 • The term “supraventricular tachycardia” (SVT) is frequently misused • Literally, it refers to any heart rhythm over over 100 / min that originates above the ventricles, including: – Sinus tachycardia – Atrial fibrillation – Atrial tachycardia – AV re-entry tachycardia Supraventricular Tachycardia (SVT)
82 Rhythms Arising From The Ventricles
83 Beats & Rhythms Arising From the Ventricles • Ventricular ectopics • Ventricular escape beats & rhythms • Accelerated idioventricular rhythm • Ventricular tachycardia including Torsade de Pointes • Ventricular fibrillation
84 Ventricular Ectopics • Ventricular ectopics are also known as: – Premature ventricular complexes (PVC’s) – Ventricular extrasystoles • They may occur as: – Isolated single beats – Two beats together (a pair or couplet) – As a run of ectopics (ie. more than 3) becoming a tachycardia – One ectopic for every sinus beat (bigeminy)
85 Ventricular Ectopics • They activate the ventricles early, giving rise to an early and wide QRS complex – Wide QRS because the ventricular conduction does not follow the specialised pathways for fast conduction (bundle branches) • They may retrogradely conduct to & activate the atria
86 Ventricular Ectopics • Characteristics: – Early & wide QRS complex – Compensatory pause – No P wave (or inverted P wave) • Ventricular ectopics may: – All look the same if there is just one ectopic focus (unifocal) – Vary in morphology if there is more than one ectopic focus (multifocal)
87 Ventricular Ectopics - Unifocal
88 Ventricular Ectopics - Multifocal
89 Ventricular Bigeminy
90 Ventricular Ectopics: The “R-on-T” Phenomenon
91 Ventricular Tachycardia • Ventricular tachycardia (VT) is a broad- complex tachycardia defined as three or more successive ventricular ectopic beats at a heart rate above 120 / min • Normally occurs at a rate of 150 – 250 / min • Symptoms of VT can range from mild palpitations only, through to cardiac arrest
92 Ventricular Tachycardia Ventricular tachycardia may be described as: • Monomorphic – Where all the ventricular complexes look the same • Polymorphic – Where the ventricular complexes vary in morphology (eg. Torsade de Pointes)
93 Ventricular Tachycardia: Torsade de Pointes • Torsade de Pointes is a polymorphic variant of VT associated with a long QT interval • Can cause significant haemodynamic disturbance, and can also precipitate ventricular fibrillation • Establishing the cause of the long QT interval is very important in its treatment
94 Ventricular Tachycardia: Monomorphic
95 Ventricular Tachycardia: Torsade de Pointes
96 “Broad Complex Tachycardias” (Not everything that looks like VT is VT!)
97 “Broad Complex Tachycardias” • Broad complex tachycardias are often ventricular tachycardia • However, sometimes supraventricular (ie arising from above the ventricles) rhythms can produce broad complexes if there is abberant conduction (e.g. bundle branch block or an accessory pathway)
98 “Broad Complex Tachycardias” • Distinguishing between VT and SVT with abberant conduction is not always easy (even if you are a cardiologist!) • It is important, however, to tell the difference for correct management • Luckily, in an emergency – both can be treated with DC shock!
99 “Broad Complex Tachycardias” Atrial Fibrillation with Abberant Conduction (Accessory Pathway) Ventricular Tachycardia
100 Ventricular Fibrillation • Ventricular fibrillation (VF) can be defined as rapid and totally disorganised ventricular activity without discernible QRS complexes or T waves in the ECG • Untreated VF is a rapidly fatal arrhythmia – Requires immediate DC shock • Sometimes described as “coarse” or “fine” VF depending on amplitude & frequency – Fine VF can sometimes look like asystole – check monitor gain
101 Ventricular Fibrillation
102 Asystole • Asystole implies the absence of ventricular activity • P waves may still be seen (P wave asystole or “ventricular standstill”) • Characterised by a flat(tish) line – Don’t forget a completely straight line is often a loose lead – Clue – check the patient!!
103 Asystole
104 “Heart Block” (Or to be more correct Atrioventricular Block!)
105 Atrioventricular (AV) Block • Atrioventricular (AV) block refers to an abnormality in electrical conduction between the atria and the ventricles • Caused by conduction abnormality in one or more of the below: – The AV node – Bundle of His – Both the right and left bundle branch
106 Atrioventricular (AV) Block The term degree is used to describe the severity of AV block: • First degree (minor): – All impulses conducted with delay • Second degree (moderate): – Some impulses are not conducted • Third degree (complete): – No impulses conducted
107 First-Degree AV Block • First-degree AV block is defined as a prolongation of AV conduction to longer than 0.2 secs (5 small squares) – ie. PR interval is greater than 0.2 secs • Can be: – A normal variant – Pathological due to cardiac problem or drug interaction (eg beta blockers)
108 First-Degree AV Block
109 Second-Degree AV Block • Second degree AV block is when one or more, but not all, atrial impulses reach the ventricles • It may be intermittent or continuous • Commonly described as two types: – Mobitz Type 1 AV block (or Wenkebach phenomenon) – Mobitz Type 2 block
110 Mobitz Type 1 AV block (Wenkebach phenomenon) Characteristics of this type of second degree AV block are: • Progressive lengthening of the PR interval until one P wave fails to be conducted and fails to produce a QRS complex • The PR interval then “resets” to normal and the cycle repeats
111 Mobitz Type 1 AV block (Wenkebach phenomenon)
112 Mobitz Type II AV block Characteristics of this type of second degree block are: • Most P waves are followed by a QRS complex • The PR interval is normal and constant • Occasionally a P wave is not followed by a QRS complex
113 Mobitz Type II AV block • Mobitz Type II AV block is thought to result from abnormal conduction below the AV node • It is considered more serious than Mobitz Type I as it can progress without warning to third degree (complete) AV block
114 Mobitz Type II AV block
115 Third-Degree AV Block (Complete Heart Block) • There is complete interruption of conduction between the atria and the ventricles • The atria and the ventricles therefore are working independently • Any atrial rhythm may co-exist with 3rd degree block • The QRS complexes are usually the result of a ventricular escape rhythm
116 Third-Degree AV Block (Complete Heart Block) Main characteristics are therefore: • P wave (atrial) activity may be normal, abnormal or absent • QRS complexes are slower & usually broad • No relationship between P waves and QRS complexes
117 3rd Degree AV block (Complete Heart Block)
Axis Determination
119 • Axis is perpendicular to a lead where QRS complex is isoelectric ( equal parts positive & negative)
120 • Mean QRS axis calculated in the frontal plane • Looking at lead I (0 degree) and lead aVF(90 degree) • if net QRS deflection is positive in leads I & aVF - axis is normal • if net QRS deflection is positive in leads I but negative in aVF - LAD • if net QRS deflection is negative in leads I but positive in aVF – RAD • if net QRS deflection is negative in leads I & aVF – axis is indeterminate How to determine QRS axis?
121 Net QRS deflection Lead I Lead aVF Normal axis positive positive LAD positive negative RAD negative positive Indeterminate negative negative Axis Determination
Atrial Enlargement
123 Right Atrial Enlargement (RAE) • The P wave is taller than two small squares in infants and small children and more than three small squares in older children and adults
124 Left Atrial Enlargement (LAE) • The P waves are wide, more than two small squares (> 0.08 sec) in infants and small children and more than three small squares (> 0.12 sec) in older children and adults
Chamber Hypertrophy
126 LVH • R in V6 taller than 95% of normal and S in V1 deeper than 95%
127 Age HR bpm QRS Axis degrees PR interval seconds QRS interval seconds R in V1 mm S in V1 mm R in V6 mm S in V6 mm 1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10 1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10 1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10 3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10 6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7 1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7 3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5 5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4 8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4 12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4 > 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4 Normal Values
128 Right Ventricular Hypertrophy (RVH) • R in V1 taller than 95% of normal PLUS S in V6 deeper than 95%
129 • rsR’ in V1 & V2 without widening of QRS complex as in bundle branch block.
130 • qR in V1 & V2
131 • Pure R wave in V1 & V2 , with or without ST & T changes indicative of strain
Age related ECG progression
133 • Full Term Newborn infant – Right axis deviation (up to +180) – RV dominance in praecordial leads: – tall R in V1 ( >10mm suggests RVH) – deep S in V6 – R/S ratio >1 in right chest leads, relatively small in left – QRS voltages in limb leads relatively small T waves – low voltage – T wave in V1 maybe upright for < 48 hours (>48 hours suggests RVH)
134 • 1 week - 1 month – Right axis retained – R waves remain dominant across to V6, although dominant S maybe normal – T wave negative V1 – T wave voltage higher in limb leads
135 • 1 – 6 months – QRS axis rotates to leftward (less than +120) R wave remains dominant in V1 R/S ratio in V2 close to I but maybe >1 in V1 RSR’ pattern in V1 not abnormal – Large voltages in praecordial leads suggestive of BVH – T waves negative across right chest leads
136 • 6 months – 3 years – QRS axis usually < +90 – R wave dominant in V6 – R/S ratio in V1 close to or less than 1 Large voltages in praecordial leads persist
137 • 3 - 8 years – Adult QRS progression in praecordial leads: • dominant S in V1 • dominant R in V6 • Large praecordial voltages persist q waves in left chest leads may be large (< 5mm) • T waves remain negative in right praecordial leads
Normal Variants
139 Normal variants • T wave inversion: – Infants older than 48 hours of age should have inverted T waves in the right praecordial leads – T inversion persist throughout childhood with inversion to V4 being accepted as normal – There is a progressive change to an upright T wave across the praecordial leads from left to right as the child grows older – Until 8 years of age an upright T wave in V1 is considered a sign of right ventricular hypertrophy – Many children will show persistence of an inverted T wave in V1 until their late teens
140 References • Houghton A.R., Gray D. Making Sense of the ECG. A Hands-on Guide. Arnold. London. 1999. (If you only buy one book on ECGs make it this one! Simple to read but still comprehensive, pocket-size, not too expensive) • Hampton J.R. 1992. The ECG Made Easy. 4th Ed. Churchill Livingstone. Edinburgh. • Hampton J.R. 1992. The ECG in Practice. 2nd Ed. Churchill Livingstone. Edinburgh • Wagner G.S. Marriott’s Practical Electrocardiography. 10th Ed. Lippincott. Philadelphia. 2001. (Very good book for those wanting to study ECGs in more depth) • Hatchett R., Thompson D. Cardiac Nursing. A Comprehensive Guide. Churchill Livingstone. Edinburgh • “ECG Learning Centre”: http://medlib.med.utah.edu/kw/ecg/ (Excellent website - loads of example ECGs)
An overview of paediatric ECG

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An overview of paediatric ECG

  • 1.
    An Overview of Paediatric Electrocardiogram SidKaithakkoden MBBS,DCH,DipNB,MD.MRCPCH,FCPS sidkaithakkoden@nhs.net
  • 2.
  • 3.
    3 The Cardiac ConductionSystem Sino-atrial node Purkinje fibresRight & left bundle branches Atrioventricular bundle (bundle of His) Atrioventricular node 3.3 RA LA RV LV
  • 4.
  • 5.
  • 6.
  • 7.
    7 It’s all aboutbeing able to relate…… This…. To this!
  • 8.
  • 9.
  • 10.
    10 Sequence of ElectricalActivity in the Heart Forming the P-Q-R-S-T Waves • P wave: – Atrial depolarization – Axis: 0-90 – P wave is upright in I & AVF
  • 11.
    11 The P Wave: Spreadof Electrical Activity through the Atria P
  • 12.
    12 The P Wave •Represents atrial depolarisation and activation – Either from the SA node (sinus rhythm) – Or from somewhere else in atria (ectopic) • In sinus rhythm P wave rate is regular • The only normal exception where P wave rate varies is sinus arrhythmia – usually only seen in people under 40
  • 13.
    13 The P Wave:Characteristics • P waves should be present! • If absent, atrial activity may be: – Truly absent (No coordinated atrial activity) – Present but not visible on ECG • No more than 0.12 secs duration • No more than 2.5 mm high in lead II • Upright in lead II (usually upright in all leads except aVR)
  • 14.
    14 Analysis of Pwaves: • Are the P waves regular? • Is there one P wave for every QRS? • Is the P wave normal and upright in Lead II? • Are there more P waves than QRS complexes? • Do all of the P waves look alike?
  • 15.
    15 • PR interval: –Slow AV node conduction – No electrical activity recorded by ECG – PR interval is flat
  • 16.
    16 The PR Interval •Measures the time from the beginning of atrial depolarisation to the beginning of ventricular depolarisation – i.e. from beginning of P wave to beginning of QRS complex • A major portion of the PR interval is the slow conduction through the AV node • AV nodal conduction under autonomic control
  • 17.
    17 PR interval analysis: •Normal PR interval (PRI) is 0.12 - 0.2 secs in adults (age dependant in children) • Is the PRI measurement within the normal range? • Are all of the PRI’s the same? • If the PRI varies, is there a pattern to the changing measurements?
  • 18.
    18 • Q wave: –Depolarization of the ventricular septum – Axis: 180-270 – Negative deflection in I & AVF
  • 19.
    19 • R Wave: –Depolarization of the ventricles – Axis: 0-90 – Upright in I & AVF
  • 20.
    20 • S Wave: –Depolarization of the heart base – Axis: 180-270 – Negative deflection in I & AVF
  • 21.
    21 The QRS Complex •Represents ventricular depolarisation and activation • Usually much bigger than P and T wave as much larger muscle mass • NB. The QRS complex may comprise of a Q, R and S wave – but often not all three in same complex!
  • 22.
    22 The QRS Complex •Q waves usually absent from most leads of the 12-lead ECG • The duration of the QRS complex is termed the “QRS Interval” (Normal range for is 0.07 – 0.11 secs) • QRS amplitude (on 12-lead ECG) varies considerably – up to 3.0 mV (30mm) may be normal
  • 23.
    23 QRS Waveform Nomenclature Rr qR qRs Qrs QS Qr Rs rS qs rSr’ rSR’ 7.1
  • 24.
    24 Analysis of QRSComplex • What is the duration of the QRS complex? • Are all of the QRS complexes of equal duration? • Do all of the QRS look alike? • Are the unusual QRS complexes associated with ectopic beats? • Is the QRS complex preceded by a P wave?
  • 25.
    25 The ST Segment •The ST segment lies between the end of the S wave and the start of the T wave • It represents the time between end of depolarisation and beginning of repolarisation
  • 26.
    26 Analysis of theST Segment • The ST segment is normally isoelectric • Can be abnormal in two ways: –Are the ST segments elevated? • May indicate myocardial infarction –Are the ST segments depressed? • May indicate myocardial ischaemia
  • 27.
    27 ECG complex withisoelectric ST segment
  • 28.
    28 12-lead ECG showingST Segment Depression
  • 29.
    29 12-lead ECG showingST Segment Elevation
  • 30.
    30 • T Wave: –Repolarization of the Ventricles – upright deflection in I & AVF
  • 31.
    31 The T Wave •Represents repolarisation (“recharging”) of the ventricular muscle to its resting electrical state • Analysis of the T wave would examine: – Its direction – Its shape – Its height
  • 32.
    32 Repolarisation of Ventricle TheT wave: Repolarisation of the ventricle T 3.6
  • 33.
    33 The QT Interval •The QT interval measures the total time taken for depolarisation and repolarisation of the ventricles – Beginning of the QRS complex to the end of the T wave • Usually measured rather than the duration of the T wave alone • Varies with heart rate, age and sex
  • 34.
    34 The U Wave •The U wave is normally either absent or present as a small rounded wave following the T wave • Normally oriented in the same direction as T wave • Origin of U wave is uncertain • More prominent in hypokalaemia, hypercalcaemia or hyperthyroidism
  • 35.
    35 Age HR bpm QRS Axis degrees PR interval seconds QRS interval seconds R in V1 mm S inV1 mm R in V6 mm S in V6 mm 1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10 1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10 1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10 3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10 6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7 1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7 3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5 5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4 8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4 12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4 > 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4 Normal Values
  • 36.
    36 QT interval: • theduration from the beginning of the QRS complex to the end of the T wave • count the number of small squares, then multiply by 0.04 seconds, that the QT in seconds • Corrected QT interval – Normal QT is determined by the HR – QTc = QT / square root of RR interval
  • 37.
  • 38.
    38 Reading and Interpreting Electrocardiograms •Age: unless the patient’s age is known, the paediatric ECG cannot be interpreted • Is the ECG "full standard"? • Is the ECG "standard speed"? • The standard speed of paper is 25 mm/sec • Occasionally it is made to run at a double speed (50 mm/sec) in cases of tachyarrhythmia to enable the visualization of an otherwise hidden p waves • Additional clinical information : • Indication • Clinical diagnosis: cardiac and other • Medications: cardiovascular drugs, others eg. cisapride, tricyclics • Electrolytes
  • 39.
    39 Systematic reading ofECG: 1. Heart rate 2. P wave axis 3. Rhythm 4. QRS axis 5. Intervals PR, QRS, QT/QTc 6. P wave amplitude and duration 7. QRS amplitude, R/S ratio, Q waves 8. ST segments and T wave
  • 40.
  • 41.
    41 Heart Rate -Basics • The standard UK and USA speed for ECG recording is 25mm / second • Before you measure the heart rate always check that this speed has been used! • At this speed, a one-minute ECG tracing covers 300 large squares
  • 42.
    42 ECG Paper: Dimensions 5mm 1 mm 0.1 mV 0.04 sec 0.2 sec Speed = Rate Voltage ~ Mass
  • 43.
    43 Method 1 • Countthe number of large squares between two consecutive R waves and divide into 300. – Quick – Not very accurate with fast rates – Used ONLY with regular rhythms
  • 44.
    44 Method 2 • Countthe number of small squares between two consecutive R waves and divide into 1500. – The most accurate method – Time-consuming – Used only with regular rhythms
  • 45.
  • 46.
    46 Rhythms Arising From theSinoatrial Node • (Normal) sinus rhythm • Sinus tachycardia • Sinus bradycardia • Sinus arrhythmia • Sick sinus syndrome
  • 47.
    47 Normal Sinus Rhythm •Sinus rhythm is the normal cardiac rhythm • The sinoatrial node is acting as the natural pacemaker • Heart rate is between 60-100 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex
  • 48.
  • 49.
    49 Sinus Bradycardia • Sinusbradycardia is sinus rhythm with a heart rate of less than 60 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex • It is unusual for sinus bradycardia to be slower than 40 / min – Consider alternative e.g. Heart block
  • 50.
  • 51.
    51 Sinus Bradycardia &Escape Beats • If sinus bradycardia is severe, escape beats or rhythms may occur • While these beats and rhythms may look abnormal, they are protective mechanisms
  • 52.
    52 Sinus Tachycardia • Sinustachycardia is sinus rhythm with a heart rate of more than 100 / min • P wave upright in lead II • PR interval 0.12 – 0.2 secs • Each P wave followed by QRS complex • Unusual for sinus tachycardia to be faster than 180 beats / min, except in fit athletes – Consider alternative eg. Nodal tachycardia
  • 53.
  • 54.
    54 Sinus Arrhythmia • Sinusarrythmia is the variation of heart rate seen with inspiration & expiration • Each P wave followed by QRS complex • Uncommon in age over 40 years • Harmless • Cause: heart rate increases during inspiration as reflex response to more blood returning to heart
  • 55.
  • 56.
    56 Sick Sinus Syndrome •This refers to a collection of impulse generation and conduction problems related to the sinus node • Any or all of the following may be seen: – Sinus bradycardia – Sinus arrest – Sinoatrial block • May be associated with paroxysmal tachycardias (“tachy–brady syndrome”)
  • 57.
    57 Sick Sinus Syndrome Sinusarrest • This is when the sinus node fails to discharge on time, • P wave fails to appear as expected, causing a variable-length gap Sinoatrial block • Sinus node depolarises normally, but impulse doesn’t reach the atria • P wave fails to appear, but next one appears in exactly the right place
  • 58.
  • 59.
  • 60.
    60 Ectopics • The word“ectopic” implies “outside” – (eg. ectopic pregnancy outside the uterus) • Ectopic beats therefore could be defined as beats arising from outside the normal cardiac conduction pathway ie. not starting at the sinoatrial node • Ectopic beats are also called: – Extrasystoles – Premature beats (or complexes)
  • 61.
    61 Ectopics • Ectopic beatsappear earlier than the next expected beat • They can arise from any region of the heart, but are normally classified into: – Atrial – AV junctional – Ventricular
  • 62.
    62 Ectopics • Ectopic beatsmay occur as: – Isolated single beats – Multiple beats – The dominant rhythm (usually defined as three or more successive ectopic beats) having “taken over” from the SA node
  • 63.
    63 Cardiac Conduction System: InherentRates Sino-Atrial (SA) Node: • 60-100 / min Atrioventricular (AV) Node: • 40-60 / min. Ventricles: • 20-40 / min. Escape rhythms generated by the AV node and ventricles will therefore be at the above respective rates
  • 64.
    64 Beats & RhythmsArising From the Atria • Atrial ectopics • Atrial tachycardia • Atrial flutter • Atrial fibrillation
  • 65.
    65 Atrial Ectopics • Atrialectopics are identified by a P wave which appears earlier than expected and has an abnormal shape • They will usually be conducted through to the ventricles giving a QRS complex – A normal QRS complex meaning normal ventricular conduction – Wide (>0.12 sec or 3 small squares) QRS complex indicating aberrant ventricular conduction
  • 66.
    66 Atrial Ectopics • Atrialectopics are also known as: – Premature atrial complexes (PAC’s) – Atrial extrasystoles • They may occur as: – Isolated single beats – Two beats together (a pair or couplet) – As a run of ectopics (ie. more than 3) becoming a tachycardia – One ectopic for every sinus beat (bigeminy)
  • 67.
    67 Atrial Ectopics • Atrialectopics may all arise from the same focus in the atria (unifocal) – All the abnormal P waves would look the same • Atrial ectopics may arise from different foci in the atria (multifocal) – Abnormal P waves would vary in shape
  • 68.
  • 69.
  • 70.
    70 Atrial Tachycardia • Atrialtachycardia is a tachycardia originating from impulses generated in the atrial myocardium – From an ectopic focus – Via a “re-entry” mechanism • Characteristics: – Heart rate greater than 100 / min – Abnormally shaped P waves
  • 71.
    71 Atrial Tachycardia • Atrial(P wave) rate is usually 120-250 / min • Above atrial rates of 200 / min, the AV node struggles to keep up with conduction so AV block may occur
  • 72.
  • 73.
    73 Atrial Flutter • Differsfrom atrial tachycardia in that the atrial (P wave) rate is higher • Results from: – Either an ectopic focus – Or depolarization circling the atrium (“Circus Movement”) • Atrial rate is usually 250-350 / min, but often almost exactly 300 / min • The rapid rate gives it a classic “sawtooth” appearance
  • 74.
    74 Atrial Flutter • AVnode cannot keep up with that rate, so AV block occurs • Most common is 2:1 block, giving ventricular rate of around 150 / min • 3:1 = ventricular rate of 100 / min • 4:1 = ventricular rate of  75 / min • AV block may also be variable
  • 75.
  • 76.
    76 Atrial Flutter –Variable Block
  • 77.
    77 Atrial Fibrillation • Muchmore common than atrial flutter • Affects 5-10% of elderly people • Can be permanent • May be transient or paroxysmal – particularly in younger people • Caused by rapid, chaotic depolarisation of the atria (350 - 650 impulses / min)
  • 78.
    78 Atrial Fibrillation • Characteristics: –No P waves seen – Baseline consists of high frequency, low amplitude oscillations (fibrillation or “f” waves) – Conduction through AV node is erratic, therefore ventricular (QRS) rate is irregular (often described as “irregularly irregular”) – Ventricular rate usually  120 – 180 / min • Unless patient medicated eg. digoxin
  • 79.
  • 80.
  • 81.
    81 • The term“supraventricular tachycardia” (SVT) is frequently misused • Literally, it refers to any heart rhythm over over 100 / min that originates above the ventricles, including: – Sinus tachycardia – Atrial fibrillation – Atrial tachycardia – AV re-entry tachycardia Supraventricular Tachycardia (SVT)
  • 82.
  • 83.
    83 Beats & RhythmsArising From the Ventricles • Ventricular ectopics • Ventricular escape beats & rhythms • Accelerated idioventricular rhythm • Ventricular tachycardia including Torsade de Pointes • Ventricular fibrillation
  • 84.
    84 Ventricular Ectopics • Ventricularectopics are also known as: – Premature ventricular complexes (PVC’s) – Ventricular extrasystoles • They may occur as: – Isolated single beats – Two beats together (a pair or couplet) – As a run of ectopics (ie. more than 3) becoming a tachycardia – One ectopic for every sinus beat (bigeminy)
  • 85.
    85 Ventricular Ectopics • Theyactivate the ventricles early, giving rise to an early and wide QRS complex – Wide QRS because the ventricular conduction does not follow the specialised pathways for fast conduction (bundle branches) • They may retrogradely conduct to & activate the atria
  • 86.
    86 Ventricular Ectopics • Characteristics: –Early & wide QRS complex – Compensatory pause – No P wave (or inverted P wave) • Ventricular ectopics may: – All look the same if there is just one ectopic focus (unifocal) – Vary in morphology if there is more than one ectopic focus (multifocal)
  • 87.
  • 88.
  • 89.
  • 90.
  • 91.
    91 Ventricular Tachycardia • Ventriculartachycardia (VT) is a broad- complex tachycardia defined as three or more successive ventricular ectopic beats at a heart rate above 120 / min • Normally occurs at a rate of 150 – 250 / min • Symptoms of VT can range from mild palpitations only, through to cardiac arrest
  • 92.
    92 Ventricular Tachycardia Ventricular tachycardiamay be described as: • Monomorphic – Where all the ventricular complexes look the same • Polymorphic – Where the ventricular complexes vary in morphology (eg. Torsade de Pointes)
  • 93.
    93 Ventricular Tachycardia: Torsade dePointes • Torsade de Pointes is a polymorphic variant of VT associated with a long QT interval • Can cause significant haemodynamic disturbance, and can also precipitate ventricular fibrillation • Establishing the cause of the long QT interval is very important in its treatment
  • 94.
  • 95.
  • 96.
    96 “Broad Complex Tachycardias” (Noteverything that looks like VT is VT!)
  • 97.
    97 “Broad Complex Tachycardias” • Broadcomplex tachycardias are often ventricular tachycardia • However, sometimes supraventricular (ie arising from above the ventricles) rhythms can produce broad complexes if there is abberant conduction (e.g. bundle branch block or an accessory pathway)
  • 98.
    98 “Broad Complex Tachycardias” • Distinguishingbetween VT and SVT with abberant conduction is not always easy (even if you are a cardiologist!) • It is important, however, to tell the difference for correct management • Luckily, in an emergency – both can be treated with DC shock!
  • 99.
    99 “Broad Complex Tachycardias” Atrial Fibrillationwith Abberant Conduction (Accessory Pathway) Ventricular Tachycardia
  • 100.
    100 Ventricular Fibrillation • Ventricularfibrillation (VF) can be defined as rapid and totally disorganised ventricular activity without discernible QRS complexes or T waves in the ECG • Untreated VF is a rapidly fatal arrhythmia – Requires immediate DC shock • Sometimes described as “coarse” or “fine” VF depending on amplitude & frequency – Fine VF can sometimes look like asystole – check monitor gain
  • 101.
  • 102.
    102 Asystole • Asystole impliesthe absence of ventricular activity • P waves may still be seen (P wave asystole or “ventricular standstill”) • Characterised by a flat(tish) line – Don’t forget a completely straight line is often a loose lead – Clue – check the patient!!
  • 103.
  • 104.
    104 “Heart Block” (Or tobe more correct Atrioventricular Block!)
  • 105.
    105 Atrioventricular (AV) Block •Atrioventricular (AV) block refers to an abnormality in electrical conduction between the atria and the ventricles • Caused by conduction abnormality in one or more of the below: – The AV node – Bundle of His – Both the right and left bundle branch
  • 106.
    106 Atrioventricular (AV) Block Theterm degree is used to describe the severity of AV block: • First degree (minor): – All impulses conducted with delay • Second degree (moderate): – Some impulses are not conducted • Third degree (complete): – No impulses conducted
  • 107.
    107 First-Degree AV Block •First-degree AV block is defined as a prolongation of AV conduction to longer than 0.2 secs (5 small squares) – ie. PR interval is greater than 0.2 secs • Can be: – A normal variant – Pathological due to cardiac problem or drug interaction (eg beta blockers)
  • 108.
  • 109.
    109 Second-Degree AV Block •Second degree AV block is when one or more, but not all, atrial impulses reach the ventricles • It may be intermittent or continuous • Commonly described as two types: – Mobitz Type 1 AV block (or Wenkebach phenomenon) – Mobitz Type 2 block
  • 110.
    110 Mobitz Type 1AV block (Wenkebach phenomenon) Characteristics of this type of second degree AV block are: • Progressive lengthening of the PR interval until one P wave fails to be conducted and fails to produce a QRS complex • The PR interval then “resets” to normal and the cycle repeats
  • 111.
    111 Mobitz Type 1AV block (Wenkebach phenomenon)
  • 112.
    112 Mobitz Type IIAV block Characteristics of this type of second degree block are: • Most P waves are followed by a QRS complex • The PR interval is normal and constant • Occasionally a P wave is not followed by a QRS complex
  • 113.
    113 Mobitz Type IIAV block • Mobitz Type II AV block is thought to result from abnormal conduction below the AV node • It is considered more serious than Mobitz Type I as it can progress without warning to third degree (complete) AV block
  • 114.
  • 115.
    115 Third-Degree AV Block (CompleteHeart Block) • There is complete interruption of conduction between the atria and the ventricles • The atria and the ventricles therefore are working independently • Any atrial rhythm may co-exist with 3rd degree block • The QRS complexes are usually the result of a ventricular escape rhythm
  • 116.
    116 Third-Degree AV Block (CompleteHeart Block) Main characteristics are therefore: • P wave (atrial) activity may be normal, abnormal or absent • QRS complexes are slower & usually broad • No relationship between P waves and QRS complexes
  • 117.
    117 3rd Degree AVblock (Complete Heart Block)
  • 118.
  • 119.
    119 • Axis isperpendicular to a lead where QRS complex is isoelectric ( equal parts positive & negative)
  • 120.
    120 • Mean QRSaxis calculated in the frontal plane • Looking at lead I (0 degree) and lead aVF(90 degree) • if net QRS deflection is positive in leads I & aVF - axis is normal • if net QRS deflection is positive in leads I but negative in aVF - LAD • if net QRS deflection is negative in leads I but positive in aVF – RAD • if net QRS deflection is negative in leads I & aVF – axis is indeterminate How to determine QRS axis?
  • 121.
    121 Net QRS deflection LeadI Lead aVF Normal axis positive positive LAD positive negative RAD negative positive Indeterminate negative negative Axis Determination
  • 122.
  • 123.
    123 Right Atrial Enlargement(RAE) • The P wave is taller than two small squares in infants and small children and more than three small squares in older children and adults
  • 124.
    124 Left Atrial Enlargement(LAE) • The P waves are wide, more than two small squares (> 0.08 sec) in infants and small children and more than three small squares (> 0.12 sec) in older children and adults
  • 125.
  • 126.
    126 LVH • R inV6 taller than 95% of normal and S in V1 deeper than 95%
  • 127.
    127 Age HR bpm QRS Axis degrees PR interval seconds QRS interval seconds R in V1 mm S inV1 mm R in V6 mm S in V6 mm 1st week 90-160 60-180 0.08-0.15 0.03-0.08 5-26 0-23 0-12 0-10 1-3wks 100-180 45-160 0.08-0.15 0.03-0.08 3-21 0-16 2-16 0-10 1-2 mo 120-180 30-135 0.08-0.15 0.03-0.08 3-18 0-15 5-21 0-10 3-5 mo 105-185 0-135 0.08-0.15 0.03-0.08 3-20 0-15 6-22 0-10 6-11 mo 110-170 0-135 0.07-0.16 0.03-0.08 2-20 0.5-20 6-23 0-7 1-2 yr 90-165 0-110 0.08-0.16 0.03-0.08 2-18 0.5-21 6-23 0-7 3-4 yr 70-140 0-110 0.09-0.17 0.04-0.08 1-18 0.5-21 4-24 0-5 5-7 yr 65-140 0-110 0.09-0.17 0.04-0.08 0.5-14 0.5-24 4-26 0-4 8-11 yr 60-130 -15-110 0.09-0.17 0.04-0.09 0-14 0.5-25 4-25 0-4 12-15 yr 65-130 -15-110 0.09-0.18 0.04-0.09 0-14 0.5-21 4-25 0-4 > 16 yr 50-120 -15-110 0.12-0.20 0.05-0.10 0-14 0.5-23 4-21 0-4 Normal Values
  • 128.
    128 Right Ventricular Hypertrophy(RVH) • R in V1 taller than 95% of normal PLUS S in V6 deeper than 95%
  • 129.
    129 • rsR’ inV1 & V2 without widening of QRS complex as in bundle branch block.
  • 130.
  • 131.
    131 • Pure Rwave in V1 & V2 , with or without ST & T changes indicative of strain
  • 132.
    Age related ECGprogression
  • 133.
    133 • Full TermNewborn infant – Right axis deviation (up to +180) – RV dominance in praecordial leads: – tall R in V1 ( >10mm suggests RVH) – deep S in V6 – R/S ratio >1 in right chest leads, relatively small in left – QRS voltages in limb leads relatively small T waves – low voltage – T wave in V1 maybe upright for < 48 hours (>48 hours suggests RVH)
  • 134.
    134 • 1 week- 1 month – Right axis retained – R waves remain dominant across to V6, although dominant S maybe normal – T wave negative V1 – T wave voltage higher in limb leads
  • 135.
    135 • 1 –6 months – QRS axis rotates to leftward (less than +120) R wave remains dominant in V1 R/S ratio in V2 close to I but maybe >1 in V1 RSR’ pattern in V1 not abnormal – Large voltages in praecordial leads suggestive of BVH – T waves negative across right chest leads
  • 136.
    136 • 6 months– 3 years – QRS axis usually < +90 – R wave dominant in V6 – R/S ratio in V1 close to or less than 1 Large voltages in praecordial leads persist
  • 137.
    137 • 3 -8 years – Adult QRS progression in praecordial leads: • dominant S in V1 • dominant R in V6 • Large praecordial voltages persist q waves in left chest leads may be large (< 5mm) • T waves remain negative in right praecordial leads
  • 138.
  • 139.
    139 Normal variants • Twave inversion: – Infants older than 48 hours of age should have inverted T waves in the right praecordial leads – T inversion persist throughout childhood with inversion to V4 being accepted as normal – There is a progressive change to an upright T wave across the praecordial leads from left to right as the child grows older – Until 8 years of age an upright T wave in V1 is considered a sign of right ventricular hypertrophy – Many children will show persistence of an inverted T wave in V1 until their late teens
  • 140.
    140 References • Houghton A.R.,Gray D. Making Sense of the ECG. A Hands-on Guide. Arnold. London. 1999. (If you only buy one book on ECGs make it this one! Simple to read but still comprehensive, pocket-size, not too expensive) • Hampton J.R. 1992. The ECG Made Easy. 4th Ed. Churchill Livingstone. Edinburgh. • Hampton J.R. 1992. The ECG in Practice. 2nd Ed. Churchill Livingstone. Edinburgh • Wagner G.S. Marriott’s Practical Electrocardiography. 10th Ed. Lippincott. Philadelphia. 2001. (Very good book for those wanting to study ECGs in more depth) • Hatchett R., Thompson D. Cardiac Nursing. A Comprehensive Guide. Churchill Livingstone. Edinburgh • “ECG Learning Centre”: http://medlib.med.utah.edu/kw/ecg/ (Excellent website - loads of example ECGs)