Presentation on basic principles of pediatric ecg with important examples: BY Dr. Nivedita Mishra (PGY2 PEDIATRICS, TRIBHUVAN UNIVERSITY TEACHING HOSPITAL,KATHMANDU,NEPAL)
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
Ecg in children
1. READING ECG IN CHILDREN
• Presenter- Dr. Nivedita Mishra
• Duration : 1hr 30 mins
2. Objectives
• To discuss conducting system of heart and techniques of obtaining pediatric ECG
• To enumerate indication of ECG in children
• To enumerate the age related changes in the pediatric ECG
• To enumerate the steps involved in interpreting the ECG
• To discuss the common ECG abnormalities associated with commonly
encountered conditions in children.
3. Introduction ECG
Electrocardiogram
• Recording of the electrical activity of the heart.
Electrocardiograph
• Sophisticated galvanometer – detects changes in electromagnetic potential.
Lead Axis
• Theoretical straight line joining the paired electrodes (Vector measurement)
4. Conducting system of the heart
No mechanical activity of the heart takes place in the absence of a preceeding electrical activity.
5. About current vectors of the Heart:
• Heart = moving dipole
• Generates current (action potential) between excited (Depol.= in +ve, out -ve)
and non excited (pol./repol/resting = in –ve , out +ve) state.
• Direction of electric current (by convention): direction in which the +ve charge
would move , i.e towards –ve terminal.
• Current flows from endocardial surface to epicardial surface to reach the
recording electrode placed on the skin.
• ECG like a Galvanometer records electric potentials between 2 points on the body
surface.
• Surface last to Depolarise is the first to Repolarise.
• Depolarisation current is +ve current (towards electrode)
• Repolarisation current is –ve current (away from electrode)
6.
7. ECG – Leads
The hexaxial reference system
• Leads I, II, and III (sup,inf/ rt,lt) - bipolar limb leads
(Frontal projection)
• Leads aVR, aVL, and aVF (sup,inf/ rt,lt) - unipolar limb
leads (Frontal projection)
• Leads V1–V6 (ant,post/ Rt to Lt) - unipolar precordial leads
(Horizontal projection)
8. Chest Leads – Electrode Placement
Leads Positive Electrode Placement View of
Heart
•V1 4th Intercostal space to right of
sternum
Septum
•V2 4th Intercostal space to
left of sternum
Septum
•V3 Directly between V2 and V4 Anterior
•V4 5th Intercostal space at
left midclavicular line
Anterior
•V5 Level with V4 at left anterior
axillary line
Lateral
•V6 Level with V5 at left midaxillary
line
Lateral
9.
10. By combining scalar (only magnitude, no direction) leads that represent the
frontal projections and horizontal projections of vector( magnitude as well
as direction) we can derive the direction of force from scalar ECG.
I / AVF
II / AVL
III/ AVR
11. Indications for a Pediatric ECG
• Tachyarrhythmia
• Bradyarrhythmia
• Electrolyte disturbance
• Syncope/seizure
• Congenital heart diseases
• Cyanotic episodes
• Heart Failure
• Kawasaki disease
• Pericarditis
• Drug ingestions
• Post cardiac surgery
• Rheumatic fever
• Myocarditis
ABC of clinical electrocardiography
Paediatric electrocardiography
Clinical review
BMJ , 2002
12. Pediatric ECG is different than adult
• The pediatric ECG characteristics:
• The heart rate is faster than in the adult.
• All the durations and intervals (PR interval, QRS duration, and QT interval) are
shorter than in the adult.
• Inferior and lateral Q waves
• RSR’ pattern in V1
• Marked sinus arrhythmia
• The RV dominance of the neonate and infant
• 15 leads instead of 12 leads in adults( V7, V3R, V4R) to better evaluate RV
13. Developmental Changes
• Neonates: RV larger than LV(right ventricular dominance)
• Right axis deviation(mean QRS frontal plane axis +60 to +180 degrees)
• Large precordial R waves(forces) (tall R waves in aVR and the right precordial leads [ V1,
and V2]
• Upright T waves in the right precordial leads (V1).
• Deep S waves in lead I and the left precordial leads ( V5 and V6).
• Upright T waves that persist in leads V1 beyond 1 week of life – indicate RVH or strain, even
in the absence of QRS voltage criteria.
• By age 6 years, pediatric ECGs resemble those of the adult
16. Steps of ECG interpretation
• Standardization,
• Age of the child
• Rate
• Rhythm
• QRS axis
• Intervals
• P wave morphology
• QRS Complex abnormalities
• ST and T wave abnormalities
• U waves if present
17. MOST IMPORTANT!!!!
• NEVER diagnose only on ECG
• Should be interpreted keeping in mind the clinical context
18. ECG Conventions & Intervals
• Depolarisation towards electrode : +ve deflection
• Depolarisation away from electrode : - ve deflection
• Sensitivity : 10mm = 1 mv
• Paper speed : 25mm/sec
• Each large square (5mm) = 0.2 sec
• Each small square (1mm) = 0.04 sec
• Heart rate = 300/ no. of large squares between each R-R interval
19. The ECG Paper- Standardisation
Amplitude
Full standard 10mm/mV
Time
21. Electrical Components
Deflection Description
P wave
Ht= <2.5 mm (2.5
sm sq)
Width= <2.5 mm
(0.10sec)
First wave, rounded, upright in all leads
except aVR
Atrial depolarization
PR interval
0.12-0.20 sec
3- 5 sm.sq
From beginning of P wave to beginning of
QRS
Depolarization reaches from atria to the
ventricles
QRS Complex
Axis = -30* to
+110*
0.10 sec
Three deflections following P wave
Ventricular depolarization
Q Wave: First negative deflection
R Wave: First positive deflection
S Wave: First negative deflection after R wave
22. Electrical components
Deflection Description
ST
segment
From end of S wave to beginning of T wave
Time between ventricular depolarization
and beginning of repolarization
T wave Rounded upright wave following QRS
Represents ventricular repolarization
QT interval
0.40 sec
QTc=0.44
From beginning of QRS to end of T wave
Total ventricular activity
U wave Small rounded, upright wave following T wave
Repolarization of Purkinje fibers.
23. Rate
• Both atrial and ventricular rates should be measured
• Fast HR:
• 1500/No. of small boxes
• Slow HR:
• 300/No. of large boxes
• For irregular Heart rate:
• No. of R waves in a 6 sec strip(30 large boxes) X 10
• Countdown method: Find a QRS on thick line, countdown 300, 150, 100, 75, 60, 50 for
each thick line till next QRS
26. Rhythm
Sinus rhythm
• Depolarization originating from SA node.
• Two characteristics
• P wave preceding each QRS complex ,
with a constant PR interval.
• The P axis between 0 and +90 degrees(P
wave upright in leads I and aVF.)
Normal rate of SAN= 60 to 100 / min
Non-sinus rhythm
• Some have p waves in front of every QRS but
with an abnormal P axis (inverted in lead II).
27. Rhythm disturbances
• Altered automaticity (heart rate)
• Altered conductivity
• To recognise arrythmias,look at:
1.Presence and Rate of P waves
2.QRS COMPLEX (0.12 sec) – wide (ventricular)
narrow (supraventricular)
3. Relationship between P & QRS
ORIGIN : SAN/ Atria/ AV Junction/ Ventricles
29. Sinus Rhythms
Sinus Bradycardia - <60/min
Sinus Tachycardia – 100 -150/ min in
exercise,fear,pain,haemorrhage,thyrotoxicosis
Sinus Arrythmia- H.R goes up and down with phases of
inspiration (vagal inhibition) and expiration respectively.
Beat to beat variability seen.
Common in 3-12 yrs olds.
Reduces with exercise.
30.
31.
32.
33.
34. Atrial Rhythms
• Atrial ectopics : normal QRS complex following an abnormal P wave
(morphologically different from the other sinus P waves present in
the same lead)
• Atrial tachycardia (150-250/min) : >3 atrial ectopics occuring in a row.
• Atrial Flutter : “Saw toothed appearance” of P waves with no
isoelectric segments in between them. Associated with AV BLOCK at
rates > 180-200.
• Atrial fibrillation (>350/min): irregularly irregular RR interval.P waves
of variable shapes and sizes throughout ECG.
35.
36.
37.
38. JUNCTIONAL RHYTHM
• AVN controlling atrial and ventricular depolarisation.
• AVN discharges when SAN dead (intrinsic junctional rhythm @ 50/min)
or
AVN is abnormally excitable e.g hypoxia.(1.Accelerated junctional rhythm @
50- 100/min, 2. Junctional tachycardia @>100/min)
• ABSENT P
• Seen in: Digoxin toxicity (the classic cause of AJR)
Beta-agonists, e.g. isoprenaline, adrenaline
Myocardial ischaemia, Myocarditis
40. Ventricular Rhythms
• Ventricular tachycardia:
Rate= >100/min
TYPES: 1. Monomorphic VT – all ventricular complexes look the same
2. Polymorphic VT – variant : TORSADES DE POINTES
risk of V- Fib.
• Ventricular Fibrillation: no definite QRS. Immediately requires
Asynchronised D.C shock
• Ventricular Flutter: only QRS complexes seen.
Rate= 200- 250/min
41.
42.
43.
44.
45. QRS axis
• Represents the mean vector of ventricular depolarization process in the vertical
plane.
• Successive approximation method using hexaaxial reference system
• Measured from zero reference point (Lead I)
• Direction of QRS complex in leads I and aVF determines the axis quadrant in
relation to the heart
• Step 1. Locate a quadrant using leads I and aVF
• Step 2. Find a lead with equiphasic QRS complex (in which the height of the R wave and
the depth of the S wave are equal).The QRS axis is perpendicular to the lead with
equiphasic QRS complex.
• Inspect the QRS complexes in leads adjacent to the equiphasic lead.If lead to its left side
is +ve then axis is 90*to the equiphasic lead towards the left
• QRS axis is normally positive in aVF
49. QRS Axis
• Normal QRS Axis in neonates
: +30 to +180 degrees
In adults : -30 to +110
• LAD
• LVH, LBBB, and left anterior
hemiblock
• Superior QRS axis (S>r in Avf)
• Characteristically seen with
endocardial cushion defect [ECD] and
tricuspid atresia)
• RAD
• RVH and RBBB.
50. P wave- Amplitude and duration
Absent in junctional rhythms, A- FIB
• Normal P wave amplitude - less than 3
mm.
The duration of the P waves –
children <0.09 seconds
infants < 0.07 seconds
• Atrial hypertrophy:
• Tall Peaked P waves – RAH = P
PULMONALE
• Wide P wave ( height is normal ) – LAH =
P-mitrale
• Biphasic P wave is normal in V1
• Bifid P wave normal in lead II IF ECG
machine is very sensitive
51.
52. Progression of R wave
• R-wave progression: Generally a
normal increase in R-wave size
and decrease in S-wave size from
leads V1 to V6
• Represents dominance of left
ventricular forces
• Reversed in RVH
53.
54.
55.
56. Criteria for RVH
a. RAD for the patient’s age
b. Increased rightward and anterior QRS voltages in
the presence of normal QRS duration
(1) R in V1, V2, or aVR greater than the upper
limits of normal
(2) S in I and V6 greater than the upper limits of
normal
c. Abnormal R/S ratio
(1) R/S ratio in V1 and V2 “greater”than upper
limit for age
(2) R/S ratio in V6 < 1, after 1 month of age.
d. Upright T wave in V1 in patients more than 7 days of
age, provided that the T is upright in the LPLs (V5, V6).
e. A Q wave in V1 (qR or qRs pattern) - severe RVH
57. LVH
Criteria for LVH
a. LAD for the patient’s age
b. QRS voltages in favor of the LV in the presence
of normal QRS Duration
(1) R in I, II, III, aVL, aVF, V5, or V6 greater than
the upper limits of normal
(2) S in V1 or V2 greater than the upper limits of
normal
c. Abnormal R/S ratio: An R/S ratio in V1 and V2
“less” than the lower limits of normal for the
patient’s age
d. Q in V5 and V6, 5 mm or more, coupled with
tall symmetric T waves in the same leads
e. Inverted T waves in lead I or aVF.
63. PR Interval
• PR interval-measured from the onset of the P wave to the beginning of the QRS complex.
• Prolonged PR interval (first-degree AV block)
• Myocarditis (viral, rheumatic, or diphtheric)
• Digitalis or quinidine toxicity
• CHDs (ECD, ASD, Ebstein anomaly)
• Hyperkalemia
• Otherwise normal hearts.
• A short PR interval is present in
• Wolff-Parkinson-White (WPW) preexcitation
• Duchenne muscular dystrophy
• Glycogen storage disease
• Otherwise normal children.
• Variable PR intervals are seen in
• Wenckebach (Mobitz type I) second-degree AV block
65. QT interval
• Normally varies primarily with heart rate.
• The heart rate–corrected QT interval (QTc)
Bazett formula: QTc = QT/√RR interval
• Normal QTc interval (mean± SD) is 0.40 (± 0.04) seconds with the upper limit of normal 0.44 seconds in
children 6 month and older
• Short QT interval(QTc is ≤300 milliseconds) - hypercalcemia , digitalis effect.
• Prolong QT interval-
• Hypocalcaemia
• Myocarditis
• Long QT syndromes
• Head injury
• Drugs
66. ST segment
• Elevation or depression of up to 1 mm in the limb
leads and up to 2 mm in the precordial leads is within normal limits.
• Non-pathologic ST segment shift
• J depression and
• Early repolarization
68. T wave
• The precordial T-wave configuration changes over time
• Tall, peaked T waves are seen in
• Hyperkalemia
• LVH (volume overload)
• Benign early repolarization
69. Abnormalities of T wave
• Flat T waves are seen in:
• Normal newborns
• Hypothyroidism
• Hypokalaemia
• Digitalis
• Pericarditis
• Myocarditis
• Myocardial ischaemia
• Large, deeply inverted T waves are seen with:
• Raised intracranial pressure (e.g. intracranial haemorrhage, traumatic brain injury)
72. DIGOXIN: Effects on ECG
• m/c side effect : AV Block
(all types except Mobitz
type 2)
• Most characteristic side
effect : Bidirectional V- Tach
(i.e changing axis in
alternate cycle)
• Most toxic effect:
ventricular ectopics
(bigemini)
• Inverted tick sign,QT
shortening
73. Summary
• Pediatric ECG should be interpreted based on clinical context.
• Be aware of age related differences, the normal ranges for electrocardiographic variables,
and the typical abnormalities in infants and children.
• Normal ECG is the most important one to learn.
• The ECG should always be evaluated systematically to avoid the possibility of
overlooking a minor, but important, abnormality.
• No substitute to repeated practice of actually interpreting from REAL LIFE ECGs.Mere
understanding of principles will not help!
74. References
• Paediatric Electrocardiography by Steve Goodacre and Karen
McLeod, from the BMJ’s “ABC of Clinical Electrocardiography”
series
• ECG Made Easy: John R.Hampton 6TH Edn.
• Guyton’s textbook of Medical Physiology
• The Harriet Lane handbook
• A primer of ECG: Simple deductive approach by K.P Misra
• Nelsons Textbook of Pediatrics, 21st edition
An ECG is a recording of a series of waves and deflections from the body surface of the electrical changes that occur within a heart from a certain “view” during the cardiac cycle.
Direction of atrial depol.= rt to lt
Direction of atrial to ventricular depol. = sup to inf
Normally, inside of the cells in resting state is more –ve than outside. Cells lose their internal negativity by depolarisation and restore their resting polarity by repolarisation,this is accomplished by membrane pumps which reverse the flow of ions.
Galvanometer only measures the magnitude of potential difference, not the direction.
More negative the current, more is the potential difference, more is the amplitude recorded by the galvanometer.
Direction is told by lead placement:
towards +ve electrode=+ ve deflection,
away from +ve electrode = _ve deflection,
perpendicular to electrodes = biphasic
Lead = combination of 2 wires with their electrodes to make a complete circuit with the ECG machine.
Bipolar lead = 2 electrodes on different sides of the heart.
+ve electrode on Lt side & LOWER LT. FOOT
Largest P wave in lead II as it is exactly along the current of atrial depolarisation.
Leads I, II, and III are bipolar leads, which consist of two electrodes of opposite polarity (positive and negative).The third (ground) electrode minimizes electrical activity from other sources.
Leads aVR, aVL, and aVF unipolar limb leads -positive electrode and indifference electrode with very high resistance d/t which it remains at zero potential thus making a reference point at the center of the heart’s electrical field.
The augmented unipolar leads are of low elrctrical potential and are thus instrumentally augmented.
Chest leads are near the heart (on the chest wall) so no augmentation needed.
Augmented leads are perpendicular to limb leads.
One lead looking at heart @ every 30* interval. Low amplitude complexes are recorded d/t more body fat.
V1 + V2 = septum + Post. Wall(-ve deflections)
V3 + V4 = Ant. Wall
V5 + V6 = Lat. Wall
I, II, AVL = left lateral
III, AVF = Inferior
AVR = Rt atrium
Slightly peaked P waves (< 3mm in height is normal if ≤ 6 months)
Slightly long QTc (≤ 490ms in infants ≤ 6 months)
Q waves in the inferior and left precordial leads.
At birth, the right ventricle is larger and thicker than the left ventricle, reflecting the greater physiological stresses placed upon it in utero (i.e. pumping blood through the relatively high-resistance pulmonary circulation).
This produces an ECG picture reminiscent of right ventricular hypertrophy in the adult: marked rightward axis, dominant R wave in V1 and T-wave inversions in V1-3.
Conduction intervals (PR interval, QRS duration) are shorter than adults due to the smaller cardiac size.
Signal with amplitude of 1mV moves the recording stylus vertically by 1cm. 0.1 mV=1mm=1 small square.
ECG paper moves @ 25 mm/sec. 1 min is represented on ECG Paper by 25* 60= 1500 mm
1 large square= 0.2 sec 5 large squares/sec & 300 large squares/min.
Each RR Interval represents 1 cardiac cycle.
All intervals in ECG contain some waves, whereas segments do not!
In supraventricular rhythms, the wave of depolarisation spreads to ventricles via normal way i.e BOH so narrow QRS.
In ventricular rhythms, the wave of depolarisation spreads through the ventricles by abnormal slower pathway through purkinje fibres so broad QRS.
Accelerated junctional rhythm (AJR) occurs when the rate of an AV junctional pacemaker exceeds that of the sinus node.
This situation arises when there is increased automaticity in the AV node coupled with decreased automaticity in the sinus node.
Digoxin toxicity (= the classic cause of AJR)
Beta-agonists, e.g. isoprenaline, adrenaline
Myocardial ischaemia
Myocarditis
Cardiac surgeryJunctional rhythms are arbitrarily classified by their rate:
Junctional Escape Rhythm: 40-60 bpm
Accelerated Junctional Rhythm: 60-100 bpm
Junctional Tachycardia: > 100 bpm
They may also be classified by aetiology:
Automatic Junctional Rhythms (e.g. AJR) = Due to enhanced automaticity in AV nodal cells
Re-entrant Junctional Rhythms (e.g. AVNRT) = Due to re-entrant loop involving AV node
Narrow complex rhythm; QRS duration < 120ms (unless pre-existing bundle branch block or rate-related aberrant conduction).
Ventricular rate usually 60 – 100 bpm.
Retrograde P waves may be present and can appear before, during or after the QRS complex.
Retrograde P waves are usually inverted in the inferior leads (II, III, aVF), upright in aVR + V1.
AV dissociation may be present with the ventricular rate usually greater than the atrial rate.
There may be associated ECG features of digoxin effect or digoxin toxicity.
Rapid AJR may be difficult to distinguish from re-entrant junctional tachycardias such as AVNRT or AVRT.
Irregularity of rhythm and heart-rate variability are suggestive of automatic junctional tachycardia.
Automatic junctional tachycardia is typically non-responsive to vagal manoeuvres — there may be some transient slowing of the ventricular rate but reversion to sinus rhythm will not occur.
AJR with aberrant conduction may be difficult to distinguish from accelerated idioventricular rhythm.
The presence of fusion or capture beats indicates a ventricular rather than junctional focus.
This occurs when the site below the SA
node usurps control from the SA node by
accelerating its own automaticity, or because the
SA node abdicates its role by decreasing its
automaticity. The conduction to the SA node is
retrograde while to the AV node it is in an antegrade
fashion.
QR FIRST INCREASES THEN DECREASES.
1*=One p wave per qrs complex.PR interval prolonged.
2*=Progressive PR Prolongation ultimately following with faliure of conduction of atrial beat.recovery with a conducted beat with shorter PR interval in a cyclical pattern.
3*=PR interval is constant in each beat, but some beats don’t get through.
4*=No relationship between p and qrs.atria and ventricles beat at their own rate independently.
S1Q3T3= Deep S in lead 1,presence of q wave in LEAD 3, T wave inversion in lead 3
A superior QRS axis is present when the S wave is greater than the R wave in aVF. It includes the left anterior hemiblock (in
the range of −30 degrees to −90 degrees) and extreme RAD(LAD-with the QRS axis less than the lower limits of normal)
(RAD-with the QRS axis greater than the upper limits of normal)
The P wave in V1 is often biphasic.
Morris index= depth*width >0.04mm-sec indicates left atrial enlargement.
RSr in V1= RBBB,
M PATTERN in V5/V6=LBBB
(with dominant S waves in right precordial leads and dominant R waves in left precordial leads),
R-wave progression: Generally a normal increase in R-wave size and
decrease in S-wave size from leads V1 to V6 (with dominant S waves
in right precordial leads and dominant R waves in left precordial
leads), representing dominance of left ventricular forces.
R Wave prominence >7mm in V1 is a significant change for Rt. Ventricle.
R Wave in V5/V6 >25 mm
S wave depth (in V1) + R wave height (in V5/V6) >35 mm
Short pr interval <0.12sec d/t bypassing AVN by fast conducting accessory pathway
presence of delta wave(slurring on the upstroke of r wave)
Broad qrs= wpw (BUNDLE OF KENT joining atria to ventricles) depolarisation of venticles is not simultaneous.so slurring of upstroke of r and broadening of qrs seen.
Normal qrs = lown ganong levine syndrome ( JAMES PATHWAY joining atria to bundle of his)
PR SHORTENING=DIASTOLIC DYSFUNCTION=PULMONARY CONGESTION IMMEDIATELY AFTER SVT.
The lower limits of normal PR interval are as follows:
(a) <3 years, 0.08 seconds
(b) 3–16 years, 0.1 seconds
(c) >16 years, 0.12 seconds
PR interval
Infants and younger children : approx 100 milliseconds
Childhood to normal adults : approx 150 milliseconds
QRS duration
Infants and young children : 50 to 80 milliseconds
Childhood to normal adults : 80 to 100 milliseconds
QTc
Infants younger than 6 months : upto 490 milliseconds
More than 6 months : 440 milliseconds
(average 3 measurements taken from same lead)a familial cause of sudden death by ventricular tachycardia
The duration of the Q-T interval varies with the cardiac rate; a corrected
Q-T interval (Q-Tc) can be calculated by dividing the measured
Q-T interval by the square root of the preceding R-R interval.
J depression is a shift of the junction between the QRS complex and the ST segment (J point) without sustained ST segment
Depression.J POINT IS ELEVATED IN HYPOTHERMIA,HYPOTHYROIDISM.
In early repolarization, all leads with upright T waves have elevated ST segments, and leads with inverted T waves have depressed ST segments. This condition, seen in healthy adolescents and young adults, resembles the ST segment shift seen in acute pericarditis; in the former, the ST segment is stable, and in the latter, the ST segment returns to the isoelectric line.
Pathologic ST segment shift. Abnormal shifts of the ST segment often
are accompanied by T wave inversion. A pathologic ST segment shift
assumes one of the following forms.
• Downward slant followed by a diphasic or inverted T wave (see Fig.
2-20, B).
• Horizontal elevation or depression sustained for >0.08 seconds (see
Fig. 2-20, C).
Examples of pathologic ST segment shifts and T wave changes include
LVH or RVH with strain; digitalis effects; pericarditis; myocarditis; and
myocardial infarction
(more than 5mm in limb leads and >15 mm in chest lead)
In severe ventricular hypertrophy with relative
ischemia of the hypertrophied myocardium, the T axis changes. In the
presence of criteria of ventricular hypertrophy, a wide QRS-T angle (90
degrees or greater) with the T axis outside the normal range indicates
a strain pattern. When the T axis remains in the normal quadrant (0 to
+90 degrees), a wide QRS-T angle indicates a possible strain pattern
Hypokalemia = Prolongation of the PR interval
T wave flattening and inversion
ST depression
Prominent U waves (best seen in the precordial leads)