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![P waves
• Normal findings
• Upright in I, II, aVL
• Inverted in aVR
• amplitude < 2.5 mm [> 3mm abnormal]
• Duration < 9o msec [ > 120 msec abnormal]
• 1st half by RA Depolarisation & 2nd half by LA](https://image.slidesharecdn.com/habeebecgfinal-230302145729-6c5c85f1/85/Pediatric-ECG-final-pptx-8-320.jpg)
![• LAD
• Tall R in I, II, II, aVL,aVF, V5,
V6
• Deep S in V1/ V2
• R/S ratio in V1 < 1
• Deep Q wave [Q > 5 mm] +
tall symmetrical T wave in V5
& V6 (“LV diastolic load”)
• Strain pattern
• Inverted T wave in I, aVF
Criteria FOR LVH](https://image.slidesharecdn.com/habeebecgfinal-230302145729-6c5c85f1/85/Pediatric-ECG-final-pptx-31-320.jpg)
![• RVH + LVH in the absence of BBB /
preexcitation
• Large equiphasic QRS complexes in two or more
of the limb leads and in the mid- precordial
leads[V2-V5] KATZ-WACHTEL
PHENOMENON
Criteria FOR BVH](https://image.slidesharecdn.com/habeebecgfinal-230302145729-6c5c85f1/85/Pediatric-ECG-final-pptx-32-320.jpg)
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Pediatric ECG final.pptx
- 1. PEDIATRIC ECG- Abnormalities DrHABEEB REHMAN K M JUNIOR RESIDENT PEDIATRICS MES MEDICAL COLLEGE
- 2. OVERVIEW 1. READING OFAN ECG 2. INTERPRETATION OF ABNORMAL FINDINGS 3. NORMAL VARIATIONS IN PEDIATRICS 4. HEART BLOCKS 5. CHAMBER ENLARGEMENTS 6. CONGENITAL HEART DISEASE 7. ARRHYTHMIAS IN CHILDREN 8. DYSELECTROLYTEMIAS 9. SOME EXAMPLES OF ECG READING
- 4.
- 5. READING AN ECG SOLITUS RATE RHYTHM AXIS CHAMBER HYPERTROP HY PWAVE PR INTERVAL Q WAVE QRS COMPLEX QT INTERVAL ST SEGMENT T WAVE U WAVE
- 6.
- 8. P waves • Normalfindings • Upright in I, II, aVL • Inverted in aVR • amplitude < 2.5 mm [> 3mm abnormal] • Duration < 9o msec [ > 120 msec abnormal] • 1st half by RA Depolarisation & 2nd half by LA
- 9. ABNORMALITIES OF PWAVE • INVERTED IN I, aVL DEXTROCARDIA REVERSAL OF ARM LEADS LOW ATRIAL ECTOPICS • FLAT P WAVE HYPERKALEMIA • ABSENT P WAVE AF AV BLOCK PAROXYSMAL AT
- 10. • P- MITRALE-BROAD & NOTCHED P WAVES MS LARGE VSD • P- PULMONALE- TALL & PEAKED P WAVES TRICUSPID ATRESIA EBSTEIN ANOMALY TOF Severe PS HYPOPLASTIC RIGHT HEART SYNDROME COMPLEX CHD
- 11. PR Interval • Beginningof P wave to beginning of QRS complex • Normal: 120 – 200 msec • LOWER LIMIT OF NORMAL PR ▫ <3 YR : 80 msec ▫ 3-16YR : 100 msec ▫ ADULTS : 120 msec
- 12. • PROLONGED PR ▫HEART BLOCKS ▫ ENDOCARDIAL CUSHION DEFECT ▫ ACUTE RHEUM FEVER ▫ EBSTEIN’S ANOMALY ▫ HYPERKALEMIA ▫ DIGITALIS TOXICITY ▫ MYOCARDITIS ▫ ISCHEMIA/HYPOXIA ABNORMALITIES OF PR INTERVAL SHORT PR •WPW SYND •POMPE‘S DISEASE •FABRYS •MANNOSIDOSIS •LOWN-GANONG- LEVINE SYND VARIABLE PR •WENCKEBACH PHENOMENON •COMPLETE AV BLOCK
- 13. Q Wave • Bydepolarisation of ventricular septum • II, II, aVF • Normal- 0.02 sec • Never > 25% of R- wave DEEP & WIDE Q WAVE ALCAPA MI Q WAVE IN V1 Severe LVH C- TGA Single ventricle
- 14.
- 15. QRS DURATION AGE TIME(mSec) PREMATURE 40 TERM INFANT 50 1- 3 YEAR 60 ADULTS 80 WIDE QRS •RBBB •LBBB •WPW •Arrythmias of ventricular origin
- 16. QRS amplitude • Highvoltage ▫ Ventricular hypertrophy ▫ Ventricular conduction disturbances • Low voltage ▫ Myocarditis ▫ Pericardial effusion
- 17. QRS axis • AtbirthRAD normal • Causes Of LAD at birth ▫ Tricuspid atresia ▫ AV septal defects ▫ Very premature < 28 weeks
- 18. QT INTERVAL • Onsetof Q wave to End of T wave • BAZETT’S FORMULA ▫ Corrected QT QTc= QT/RR ▫ Normal QTc= 0.42- 0.43 sec ▫ QTc Upto 0.49 sec is normal in 1st 6 months of life PROLONGED QT SHORT QT ▫ Hypocalcemia - Hypercalcemia ▫ Rheumatic carditis -Digitalis effect ▫ Long QT syndromes ▫ Cardiomyopathies ▫ Head injury ▫ Severe malnutriotion ▫ Drugs
- 19. QTc INTERVAL &LQTS
- 20. ST Segment • STelevation upto 1 mm is normal • ST Elevation ▫ Hyperkalemia ▫ IC Bleed ▫ Pneumothorax ▫ ALCAPA ▫ KD related Coronary artery disease ▫ Brugada syndrome( ST + RBBB) • ST Depression ▫ Pressure overload strain
- 21. T Waves • Lookin V1 • At birth- upright • After 7 days- inverts • Inverted T-wave upto 7 yr
- 22. • UPRIGHT TWAVE IN V1 B/W 7 DAY- 7 YR ▫ RVH • T INVERSION ▫ ALCAPA ▫ KD+ CORONARY ARTERITIS ▫ PRESSURE OVERLOAD STRAIN • TALL TENTED T WAVE ▫ HYPERKALEMIA ▫ LVH • FLAT T WAVE ▫ HYPOKALEMIA ▫ NEONATAL HYPOTHYROIDISM ▫ PERICARDITIS ▫ MYOCARDITIS ▫ MI
- 24.
- 25. P WAVE INATRIAL HYPERTROPHY RA ENLARGEMENT: •Tall & peaked P •P pulmonale •Amplitude high > 3 mm •Duration normal LA ENLARGEMENT •P mitrale •Increased terminal negative deflection-Diphasic P wave •Prolonged p wave duration
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- 29. VENTRICULAR HYPERTROPHY GENERAL CHANGES: •QRS Axis directed towards hypertrophied ventricle • QRS Amplitude increases in the direction of ventricle hypertrophied • change in R/S ratio: increased R/S in right precordial leads suggest RVH and in left precordial leads suggest LVH • Changes in T-axis: strain pattern- wide QRS-T angle with the T-axis outside the normal range
- 30. • RAD • TallR in V1 • Deep S in V6 • High R/S ratio in V1 • R/S ratio in V6 < 1 • Upright T in V1 b/w 7 days – 7 years • Q wave in V1( qR or qRs pattern • RVH+ wide QRS-T angle with T axis outside normal range • Persistent pattern of RV dominance Criteria FOR RVH
- 31. • LAD • TallR in I, II, II, aVL,aVF, V5, V6 • Deep S in V1/ V2 • R/S ratio in V1 < 1 • Deep Q wave [Q > 5 mm] + tall symmetrical T wave in V5 & V6 (“LV diastolic load”) • Strain pattern • Inverted T wave in I, aVF Criteria FOR LVH
- 32. • RVH +LVH in the absence of BBB / preexcitation • Large equiphasic QRS complexes in two or more of the limb leads and in the mid- precordial leads[V2-V5] KATZ-WACHTEL PHENOMENON Criteria FOR BVH
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- 52. BRADYARRYTHMIAS SA BLOCK 1° 2° 3° AV BLOCK 1°2° MOBITZ TYPE 1 MOBITZ TYPE 2 3° BUNDLE BRANCH BLOCK RBBB LBBB
- 53. CONDUCTION ABNORMALITIES • Bundlebranch blocks are diagnosed as they would be in adults; RBBB occurs most commonly after repair of congenital heard defects and LBBB is very rare • First degree AV block and Mobitz type 1 (Wenckebach) can be a normal variant in 10% of kids • Complete AV block is usually congenital or secondary to surgery
- 54. Sinus Bradycardia • Deviationfrom NSR - Rate < 60 bpm ▫ Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval). ▫ Hypothermia, sleep, raised ICT, hypoxia, vagal stimulation, hypothyroidism
- 55. Sinus Tachycardia Deviation fromNSR - Rate > 100 bpm • Anxiety • Fever • Exercise • Shock • Anemia • CCF • Thyrotoxicosis
- 56. 1st Degree AVBlock • Etiology: Prolonged conduction delay in the AV node or Bundle of His. • PR interval > 5 small divisions, 200 msec • Causes: myocarditis, acute rheumatic fever, drugs
- 57. 2nd Degree AVBlock, Type I • Deviation from NSR ▫ PR interval progressively lengthens, then the impulse is completely blocked (P wave not followed by QRS). ▫ Wenckebach phenomenon
- 58. 2nd Degree AVBlock, Type II • Deviation from NSR ▫ Occasional P waves are completely blocked (P wave not followed by QRS). ▫ Etiology: Conduction is all or nothing (no prolongation of PR interval); typically block occurs in the Bundle of His. • MOBITZ TYPE 2
- 59. • There’s fullAV dissociation • P waves and QRS have no definite association in it 3rd Degree AV Block
- 60. RIGHT BUNDLE BRANCHBLOCK 1. Wide QRS > 120 msec ( >3 small divisions) 2. R > r in rSR 3. VAT is > 80 msec 4. ST depression 5. T inversion • M morphology in V1 V1 “Rabbit Ears”
- 61. LEFT BUNDLE BRANCHBLOCK 1. Wide QRS > 120 msec ( > 3 small divisions) 2. VAT 80 msec 3. M morphology in V 6 (monophasic tall R ) 4. Q wave absent in V5-V6 5. ST depression 6. T inversion • morphology in V 6 and W in V1
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- 64. Interpretation? 2nd DegreeAV Block, Type I
- 65. Interpretation? 2nd DegreeAV Block, Type II
- 66. Interpretation? 3rd DegreeAV Block
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- 70. • Due topremature conduction of atrial impulses to ventricle via accessory pathway • CAUSES OF WPW 1. Ebstein’s anomaly 2. c-TGA 3. HCM 4. Rhabdomyoma WPW SYNDROME
- 71. •WPW- 3 features 1.Short PR interval 2. Delta wave on upstroke of QRS 3. Slightly wide QRS> 110 msec( fusion complex)
- 72.
- 74. VSD • Normal ECG NORMALPUL RESISTANCE • LAD, LVH, PR / N MODERATE PUL RESISTANCE + MODE SHUNT • BVH • KATZ-WACHTEL PHENOMENON LARGE VSD
- 75. ASD • LAD • rSR’in V4R/ V1 • Notched S wave • Prolonged PR OSTIUM PRIMUM • RAD • RVH • Incomplete RBBB • Prolonged PR • Tall peaked P wavesRAH OSTIUM SECONDUM
- 76. PDA • NORMAL SMALL SHUNT •LVH • LAH MODERATE SHUNT • BVH LARGE SHUNT • RVH • PEAKED P WAVES EISENMENGER’S SYNDROME
- 77. ENDOCARDIAL CUSHION DEFECT SUPERIORAXIS DEVIATION BVH DEEP SPLINTERED S WAVES PR PROLONGATION
- 78. PULMONARY STENOSIS MILD PS •NORMAL • MILD RVH MODERATE PS • RVH • PEAKED P WAVE SEVERE PS • RVH • PEAKED P WAVE • TALL V1R • DEEP V6S • RV STRAIN PATTERN • T INVERSION • RAD
- 79. Sinus, RAD, RVForces: SEVERE PULMONIC STENOSIS
- 80. AORTIC STENOSIS • NORMAL •LVH MILD TO MODERATE • LVH • ST DEPRESSION • ASYMMETRIC T INVERSION SEVERE
- 81. EBSTEIN’S ANOMALY • Tall& peaked P waves • PR prolongation • RBBB • Bizarre 2nd QRS attached to preceding normal complex- SPLINTERED QRS • WPW features • SVT • AF, A Fl • Q waves in V1 & V4
- 82. Sinus, Tall P ,splintered QRS: Ebstein’s anomaly
- 83. COARCTATION OF AORTA A.INFANTS RAD RVH RAE B. CHILDREN Normal LVH ± LAE
- 84. TOF • RVH • RAD •Abrupt change of Tall R in V1 to rS pattern in V2
- 85. Sinus, RAD, RVforces, Early transition: TOF
- 86. TGA • RAH • RAD •AV Blocks • Atrial arrythmias • QR in V4R & RS in V5, V6 • Upright T waves in all chest leads • V1 has tall T wave than V6
- 87. TRICUSPID ATRESIA • LEFTANTERIOR HEMIBLOCK • LAD • LVH • RAE • LAE
- 88. Sinus tachycardia, LAD,LV forces: TRICUSPID ATRESIA
- 90. HYPERKALEMIA ECG CHANGES TallTented T wave QRS prolongation PR prolongation Disappearance of P wave Wide , bizzare diphasic QRS complex (sine wave)
- 93. HYPOKALEMIA 1.Depressed ST segment 2.DiphasicT wave 3.Prominent U Wave
- 95. QT prolongation inhypocalcemia
- 96. BIBILIOGRAPHY: 1. PARK pediatriccardiology for practitioners 2. Fundametals of pediatric cardiology David J Driscol 3. Kulkarni pediatric cardiology 4. CHD- Management issues- pediatric cardiology division TRIVANDRUM 5. Sushma Bhai Clinical Evaluation Of Newborns & Children
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