Pediatric

Cardiology

Second Edition
2015-2016

by

Dr Maged Zakaria IBRAHIM

Neonatologist and Pediatrician
MRCPCH, MSc. Pediatrics, IBCLC

Keynotes ®
Keynotes “Pediatric Cardiology ”

Copyright © 2015 by Maged Zakaria Mahmoud.

All rights reserved. No part of this publication may be reproduced
or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information
storage and retrieval system, without permission in writing from the
author. Queries on how to seek permission, and arrangements can be
sent to the author’s email: maged.zakaria@yahoo.com

Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional
practices, or medical treatment may become necessary. Practitioners and researchers must
always rely on their own experience and knowledge in evaluating and using any
information, methods, compounds, or experiments described herein. In using such
information or methods they should be mindful of their own safety and the safety of others,
including parties for whom they have a professional responsibility. With respect to any drug
or pharmaceutical products identified, readers are advised to check the most current
information provided (i) on procedures featured or (ii) by the manufacturer of each product
to be administered, to verify the recommended dose or formula, the method and duration of
administration, and contraindications. It is the responsibility of practitioners, relying on
their own experience and knowledge of their patients, to make diagnoses, to determine
dosages and the best treatment for each individual patient, and to take all appropriate safety
precautions. To the fullest extent of the law, the author does not assume any liability for any
injury and/or damage to persons or property as a matter of products liability, negligence or
otherwise, or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.

ISBN 978-977-94-1232-2
Printed in EGYPT

١٠٢٥ © ‫حلوق الطبع محفوظت‬

۲٠٢٥ - ٤۲٢٦٢ ‫زكم الايداع‬

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maged.zakaria@yahoo.com

https://www.facebook.com/keynotes.pediatrics
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Index
Chapter 1 - Congenital Heart disease 3
Fetal Circulation 4
Introduction to CHD 5
Acyanotic Congenital Heart Disease - The Left-to-Right Shunt Lesions 8
Atrial Septal Defect (ASDs) 8
Ventricular Septal Defect (VSD) 11
Atrioventricular Septal Defect (AVSD) 14
Patent Ductus Arteriosus (PDA) 16
Acyanotic Congenital Heart Disease - The Obstructive Lesions 19
Pulmonary Stenosis 19
Aortic Stenosis 22
Coarctation of the Aorta 23
Complete Interruption of the Aortic Arch 26
Congenital Cyanotic Heart Disease with  Pulmonary Blood Flow 27
Fallot Tetralogy 27
Tetralogy of Fallot with Pulmonary Atresia 31
Pulmonary Atresia with Intact Ventricular Septum 32
Double Outlet Right Ventricle (DORV) 33
Tricuspid Atresia 33
Ebstein Anomaly of the Tricuspid Valve 35
Congenital Cyanotic Heart Diseases with  Pulmonary Blood Flow 37
D-Transposition of the Great Arteries (d-TGA) 37
Total Anomalous Pulmonary Venous Return (TAPVR) 39
Truncus Arteriosus 41
Single Ventricle (Double-Inlet Ventricle, Univentricular Heart) 42
Hypoplastic Left Heart Syndrome 43
Abnormal Positions of Heart and the Heterotaxy Syndromes 45
Scimitar Syndrome 46
Anomalies of the Aortic Arch 47
Anomalies of Coronary Arteries 48
Extracardiac Complications of Cyanotic CHD and Eisenmenger Physiology 49
Chapter 2 - Cardiac Arrhythmias 50
Electrical System of the Heart 51
ECG: The Basics 52
Extrasystoles 56
Tachyarrhythmias 57
Ventricular Tachyarrhythmias 64
Long QT Syndromes (LQTS) 66
The Holter monitor (Ambulatory ECG monitoring) 67
Bradyarrhythmias 68
Principles of Antiarrhythmic Therapy 72
Chapter 3 - Acquired Heart Diseases 75
Acute Rheumatic Fever 76
Auscultatory Sites 85
Rheumatic Heart Disease 86
Mitral Insufficiency 86
Mitral Stenosis (MS) 88
Aortic Insufficiency 91
Aortic Stenosis 93
Tricuspid Valve Disease 95
Infective Endocarditis (IE) 97
Chapter 4 - Diseases of Myocardium and Pericardium 102
Diseases of the Pericardium 103
Diseases of the Myocardium 106

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Dilated Cardiomyopathy (DCM) 106
Hypertrophic Cardiomyopathy (HCM) 107
Restrictive Cardiomyopathy 108
Secondary Cardiomyopathy 109
Myocarditis 110
Endocardial Fibroelastosis (EFE) 111
Pediatric myocardial infarction 111
Tumors of the Heart 113
Chapter 5 - Cardiac Therapeutics 114
Congestive Heart Failure (CHF) 115
Cardiogenic Shock 120
Differential Diagnosis of Cardiomegaly without Heart Murmur 121
Systemic Hypertension 122
Hypertensive Crisis 132
Pulmonary Hypertension 134
Chapter 6 - Miscellaneous 138
Causes of Palpitation 139
Sudden Death 140
Innocent Cardiac Murmurs 141
Child with Chest Pain 142
Cyanosis 145
Syncope 147
Summary of Abnormal S2 153
Chest Radiography 154
Cardiac Manifestations of Systemic Diseases 158

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Chapter 1

Congenital
Heart Disease

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Introduction to CHD
- CHD occurs in ~ 0.8% of live births.
- Incidence is higher in stillborns (3-4%), spontaneous abortuses (10-25%) and premature
infants (2% excluding PDA).
- The most common CHD is VSD (35-50%).

Etiology

- The cause of most congenital heart defects is unknown.

- Most cases of CHD are multifactorial (combination of genetic predisposition and
environmental stimulus).

- Genetics Causes of Congenital Heart Disease:

 Structural Heart Defects
o DiGeorge syndrome
o Familial ASD ± heart block
o Alagille syndrome (Peculiar facies, bile duct hypoplasia, right-sided cardiac lesions)
o Holt-Oram syndrome (limb defects, ASD)
o Trisomy 21 (AV septal defect)
o Isolated familial AV septal defect (without trisomy 21)
o Cri du chat syndrome (5p deletion) (Cat-like cry in infancy, microcephaly, downward
slant of palpebral fissures)
o Familial (total anomalous pulmonary venous return; TAPVR)
o Noonan syndrome (PS, ASD, hypertrophic cardiomyopathy)
o Ellis–van Creveld syndrome (polydactyly, ASD)
o CHARGE association (Coloboma, heart defects, choanal atresia, growth or mental
retardation, genitourinary anomalies, ear anomalies, genital hypoplasia)
o Williams syndrome (supravalvular AS, branch PS, hypercalcemia)
o Marfan syndrome (connective tissue weakness, aortic root dilatation)
o Familial laterality abnormalities (situs inversus, complex CHD)

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 Cardiomyopathies
o Hypertrophic cardiomyopathy
o Hypertrophic cardiomyopathy with Wolff-Parkinson-White syndrome
o Dilated cardiomyopathy (X-linked or AR)

 Arrhythmias
o Complete heart block
o Long Q-T syndrome (AD, 6 types)
o Jervell and Lange-Nielsen syndrome (AR long QT syndrome, congenital deafness)
o Familial atrial fibrillation (autosomal dominant)
o Brugada syndrome (RBBB, ST segment elevation, unexpected sudden death)

- Environmental Factors:
 Maternal infection e.g. TORCH
 Maternal DM or SLE
 Teratogenic drugs:
o Amphetamines are associated with VSD, PDA, ASD and TGA.
o Phenytoin and Valproic acid are associated with pulmonary stenosis (PS), aortic stenosis
(AS), coarctation of the aorta (COA), and PDA.
o ACE inhibitors and angiotensin II receptor antagonists cause congenital malformations of
multiple systems, including cardiac defects (e.g., ASD, VSD, PDA, and PS).
o Lithium is associated with Ebstein’s anomaly.
o Retinoic acid may cause conotruncal anomalies.
o Progesterone and estrogen.
o Excessive alcohol intake is associated with VSD, PDA, ASD, and TOF (fetal alcohol
syndrome).

Genetic Counseling

- Incidence of CHD is ≈0.8% of live births.

- If one parent has CHD or for the 2nd pregnancy after a previous child with CHD, the incidence
increases to 2-6%
- When 2 1st degree relatives have CHD, the risk for a subsequent child may reach 20-30%.
- Fetal echocardiography improves rate of detection of CHD in high-risk patients.

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Congenital Cyanotic Heart Disease

with  Pulmonary Blood Flow
 Fallot Tetralogy

- Infundibular pulmonary stenosis

- VSD (usually nonrestrictive and large)
- Dextro-position of aorta so that it overrides the ventricular septum
- RV hypertrophy

tetralogy of Fallot can be associated with DiGeorge syndrome

Pathophysiology

- Blood from RV is shunted across VSD into aorta (with marked PS) resulting in desaturation
and cyanosis (variable according to severity of pulmonary obstruction).
- Pulmonary blood flow may be compensated by a PDA.
The degree of RV outflow obstruction determines timing of onset of symptoms, severity of cyanosis and
degree of RV hypertrophy.

- With mild to moderate PS, patient may not be visibly cyanotic (acyanotic or “pink” tetralogy
of Fallot). With severe PS, cyanosis will be present from birth and worsen with ductal closure.

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Clinical Picture

- Often, cyanosis is not present at birth; but with increasing RV hypertrophy over time,
cyanosis occurs later in the 1st yr of life (expect in neonates with severe PS; in whom
pulmonary flow is PDA dependent). A heart murmur is audible at birth.

- Dusky blue skin with marked clubbing of fingers and toes (extracardiac manifestations of
long-standing cyanotic CHD)

- Infants with mild PS may present with CHF (e.g. dyspnea on exertion and easy fatigability)
caused by ventricular left-to-right shunt.

- FTT and delayed puberty.

- Squatting (for relief of dyspnea caused by physical effort):

 Kinking of femoral arteries causes  intra-aortic pressure and thus  systemic pressure to
overcome pulmonary pressure so blood is pushed through the stenosed RV outflow.

- Paroxysmal Hypercyanotic Attacks (hypoxic or “blue” Spells):

Mechanism of hypoxic spell

 PaO2 stimulates respiratory center causing
hyperventilation. The hyperpnea  systemic
venous return (SVR). In the presence of a fixed
right ventricular outflow tract (RVOT), the 
SVR results in  right-to-left (R-L) shunt,
worsening cyanosis (vicious circle)

 Episodes of hyperpneic, restless,  cyanosis, gasping and syncope; frequently in morning on

awakening or after vigorous crying and last from a few minutes to hours
 Caused by infundibular spasm with reduction of an already compromised pulmonary blood
flow, which may result in severe hypoxia and metabolic acidosis

- Inspection and Palpation:

 Left anterior hemithorax bulge because of long-standing RV hypertrophy
 Systolic thrill along left sternal border in the 3rd and 4th parasternal spaces

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- Auscultation:
 S2 is single ( pulmonary component)
 Ejection systolic murmur over left parasternal area ( in intensity with more severe PS)

Investigations

- Chest X-ray: pulmonary oligemia, RV hypertrophy with uplifted apex, large aorta (Cœur en
sabot, French for "clog-shaped heart").
- ECG: RV hypertrophy, right axis deviation with tall peaked P wave suggesting RA enlargement.
- Echocardiology establishes diagnosis, degree of RV outflow tract obstruction and PDA flow.
- Cardiac Catheterization with angiography (5-10% have coronary artery abnormalities).

Tetralogy of Fallot (Cœur en sabot)

Complications

- Cerebral thrombosis (due to polycythemia, dehydration, associated iron-deficiency anemia).

- Brain abscess with seizures, localized neurologic signs and  ICT.
With a right-to-left shunt bypassing pulmonary circulation, bacteria in bloodstream are not filtered
through pulmonary macrophages. G+ve organisms are more common than G-ve

- Bacterial endocarditis.
- CHF is unusual except in young infants with “pink” or acyanotic tetralogy of Fallot

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Treatment

- In neonates with critical PS, prostaglandin E1 (0.05-0.2 μg/kg/min IVI).

- For Hypercyanotic Attacks (Hypoxic Spells):
 Knee-chest position (traps systemic venous blood in the legs, thereby
temporarily  SVR and helping to calm the baby. The knee–chest position
may also  SVR by  arterial blood flow to the lower extremities).
 Administration of O2
 SQ morphine (max 0.2 mg/kg) (suppresses the respiratory center and
abolishes hyperpnea)
 Correction of metabolic acidosis with IV NaHCO3 (in severe spells) ?!
 Intubation and sedation (for resistant spells)
 IV phenylephrine (to  systemic vascular resistance)
 β-Adrenergic blockade (IV propranolol; 0.1 mg/kg)
- Brain Abscess:
 IV antibiotics with surgical drainage
- Cerebral Thromboses:
 Adequate hydration, phlebotomy (for severe polycythemia)
- Surgical Correction:
 Palliative Surgery (to bypass PS):
o Blalock-Taussig shunt (anastomosis between subclavian and pulmonary artery).
o Waterston shunt (anastomosis between ascending aorta and pulmonary artery).
o Potts shunt (anastomosis between descending aorta and pulmonary artery).
 Total surgical correction

Blalock-Taussig Shunt Waterston Shunt Potts Shunt

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Chapter 2

Cardiac
Arrhythmias

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Chapter 3

Acquired
Heart Diseases

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Auscultatory Sites

Mitral area is at the apex beat, as LV is closest to the thoracic cage.

The apical impulse is normally at the 5th intercostal space in the midclavicular line after age 7 years.
Before this age, the apical impulse is in the 4th intercostal space just to the left of the midclavicular line.

Tricuspid area is at the inferior left sternal margin.

Pulmonary area is at the left 2nd intercostal space close to sternum.

Aortic area is at the right 2nd intercostal space close to sternum.

Erb's Area (mid-sternal area or the 2nd aortic area) corresponds to the inner end of the 3rd left
interspace. Soft early diastolic murmur of aortic insufficiency is best heard here.

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Mitral Insufficiency Mitral Stenosis Aortic Insufficiency Aortic Stenosis

Chambers Enlarged

Symptoms PVC and Low COP
General Examination Signs of Low COP and SVC
Cardiac Examination – Inspection, Palpation and Percussion
Localized
Apex Hyperdynamic
Downward, Outward Shift
Left Parasternal Area (±) Heave
Aortic Area - -
(±) Palpable S2
Pulmonary Area
(±) Dull on percussion
Cardiac Examination – Auscultation
 S1
Holosystolic; to axilla
Apex
PVC, hemoptysis and Low COP Palpitations, Dyspnea, angina Low COP, Syncope
de Musset's - Corrigan’s
Water Hammer Pulse
Malar flush
Quincke's pulse Low COP
Signs of Low COP and SVC
Wide Pulse pressure
Durozier - Traube's - Hill’s
Diffuse Localized Localized
Slapping Hyperdynamic Heaving
Outward Shift Downward, Outward Shift Downward, Outward Shift
Heave - -
- Systolic thrill
(±) Palpable S2
- -
(±) Dull on percussion
 S1
Diastolic; localized
Austin Flint Murmur -

(±)  P2
Pulmonary Area (±)  P2 - -
(±) Garaham Steell Murmur
 S1
Ejection Systolic; to neck
Aortic Area

Diastolic; to apex
2nd Aortic Area

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Chapter 4

Diseases of
Myocardium and
Pericardium

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Chapter 5

Cardiac
Therapeutics

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Chapter 6

Miscellaneous

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Syncope
Syncope is a transient loss of consciousness and muscle tone that result from inadequate cerebral perfusion

1. Autonomic (non-cardiac) Disorders:

- Vasovagal syncope (simple syncope, neurocardiogenic syncope, or neutrally mediated syncope)
- Orthostatic (postural) hypotension (dysautonomia)
- Exercise-related syncope
- Situational syncope:
 Breath holding
 Cough, micturition, defecation, and so on
 Carotid sinus hypersensitivity
- Excess vagal tone.

2. Cardiac Disorders:
- Arrhythmia:
 Tachycardia: SVT, atrial flutter or fibrillation, VT (seen with long QT syndrome, arrhythmogenic
RV dysplasia, Brugada syndrome)
 Bradycardia: sinus bradycardia, asystole, complete heart block, pacemaker malfunction
- Obstructive lesions:
 Outflow obstruction: AS, PS, hypertrophic cardiomyopathy, pulmonary hypertension
 Inflow obstruction: MS, tamponade, constrictive pericarditis, atrial myxoma
- Myocardial diseases:
 Coronary artery anomalies
 Hypertrophic cardiomyopathy, dilated cardiomyopathy, MVP, arrhythmogenic RV dysplasia.

3. Neuropsychiatric Disorders:
- Anxiety disorders: panic disorders, agoraphobia (fear of open space)
- Hyperventilation
- Seizure disorders
- Migraine
- Brain tumors
- Hysterical (conversion reaction)

4. Metabolic Disorders:
- Dehydration (or inadequate hydration)
- Hypoglycemia and Electrolyte disorders
- Drugs and toxins: anti-seizure drugs, sedatives and tranquilizers, antihypertensive drugs.
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Proposed pathophysiology of neurocardiogenic (vasovagal) syncope.

Presumed points of action of various pharmacologic agents are also shown by open arrows.

Evaluation of a Child with Syncope

- Most children who present with presyncope (without loss of consciousness) or even syncope
have vasovagal phenomena or other benign causes of syncope.
- The goal of the evaluation is to identify high-risk patients with underlying heart disease.
- Evaluation may extend to other family members when a genetic condition is suspected.

History
- Because physical examinations are almost always normal long after the event, accurate history
taking is most important. Sometimes a complete history cannot be obtained owing to amnesia
about the event, but witness accounts are useful.

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- Aspects of history taking:
 About the syncopal event:
o The time of the day:
Syncope after rising in the morning or after morning shower suggests vasovagal syncope.
Hypoglycemia (a very rare cause), occurring in a fasting state in the morning
o Patient’s position (supine, standing, or sitting):
Syncope while sitting or recumbent suggests arrhythmias or seizures.
Syncope after standing for some time suggests vasovagal syncope.
o Relationship to exercise:
Syncope occurring during exercise suggests arrhythmias.
Syncope occurring immediately after cessation of physical activities suggests venous
pooling in the leg (with reduced venous return and cardiac output).
o Associated symptoms:
Palpitation or a racing heart rate suggests tachycardia or arrhythmias
Chest pain suggests possible myocardial ischemia
Shortness of breath or tingling or numbness of the extremities suggests hyperventilation
Nausea, epigastric discomfort, and diaphoresis suggest vasovagal syncope
Headache or visual changes suggest vasovagal syncope
o Duration of syncope:
Syncope < 1 min suggests vasovagal syncope, postural hypotension, or hyperventilation.
A longer duration of syncope suggests convulsive disorders, migraine, or arrhythmias.
o Patient’s appearance during and immediately after the episode:
Pallor indicates hypotension
Abnormal movement or posturing, confusion, focal neurologic signs, amnesia, or muscle
soreness suggests the possibility of seizure
 History of a cardiac, endocrine, neurologic, or psychological disorders
 Medication history
 Family history:
o Coronary heart disease risk factors e.g. history of MI in family members < 30 years of age
o Cardiac arrhythmia, CHD, cardiomyopathies, long QT syndrome, seizures, metabolic and
psychological disorders
o A positive family history of fainting is common with vasovagal syncope.

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 Social history is important in assessing whether there is a possibility of substance
abuse, pregnancy, or a conversion reaction.

Physical Examination
- The results of the physical examination are usually normal:
 If orthostatic intolerance group is suspected, the heart rate and BP should be measured
repeatedly while the patient is supine and after standing without moving for up to 10
minutes. In a well-hydrated state, positive test results for vasovagal syncope or postural
hypotension in the office setting are uncommon.
 Careful auscultation to detect a heart murmur or an abnormally loud 2nd heart sound.
 Neurologic examination should include a funduscopic examination, test for Romberg’s sign,
gait evaluation, test of deep tendon reflexes, and test of cerebellar function.

Differential Diagnosis
- Epilepsy:
 Patients may have incontinence, marked confusion in the postictal state, and abnormal EEG.
 Patients are rigid rather than limp and may have sustained injuries.
 Patients do not experience the prodromal symptoms of syncope (e.g., dizziness, pallor,
palpitation, and diaphoresis).
 Duration of unconsciousness is longer than that typically seen with syncope (<1 minute).

- Hypoglycemia:
 Characteristics include pallor, perspiration, abdominal discomfort, lightheadedness,
confusion, unconsciousness, and possible subsequent occurrence of seizures.
 Hypoglycemic attacks differ from syncope in that the onset and recovery occur more
gradually, they do not occur during or shortly after meals, and the presyncopal symptoms
do not improve in the supine position.

- Hyperventilation:
 Hyperventilation is believed to produce hypocapnia, resulting in intense cerebral
vasoconstriction, and causes syncope (may also have a psychological component).

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 Patient often experiences air hunger, shortness of breath, chest tightness, abdominal
discomfort, palpitations, dizziness, numbness or tingling of face and extremities, and rarely
loss of consciousness. It often is associated with emotional disturbances.

- Conversion reaction:
 Not associated with injury and occurs only in the presence of an audience.
 Episodes are rare before 10 years of age.
 Spells are not related to postural changes and are not improved by the supine position.

Diagnostic Studies
- A complete cardiac evaluation is indicated if there is a heart murmur, a family history of
sudden death or cardiomyopathy, or an abnormal ECG finding.
- Serum glucose and electrolytes is of limited value (patients seen after the episode).

- With suspected arrhythmia as the cause of syncope, the following may be indicated:
 ECG for all patients presenting with syncope.
 Ambulatory ECG monitoring e.g. Holter monitor.
 Exercise stress test (if syncope is associated with exercise).
 Echocardiographic studies.
 Cardiac catheterization and electrophysiologic testing (rarely indicated).

 Head-up tilt table test: If patients with syncope have

autonomic symptoms (e.g., pallor, diaphoresis, or
hyperventilation), tilt table testing is useful to provoke
symptoms exactly during orthostatic stress while being
closely monitored for cardiac rhythm and rate and BP
responses associated with symptoms.
Several distinct abnormal patterns have been
identified after head-up tilt table tests:
 Vasovagal: An abrupt  BP usually with bradycardia
 Dysautonomia (or postural hypotension): A gradual  BP leading to syncope.
 Postural orthostatic tachycardia syndrome (POTS): excessive  HR to maintain an
adequate BP to prevent syncope.

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- Neurologic consultation and EEG are indicated with:
 Prolonged loss of consciousness
 Seizure activity
 Postictal phase with lethargy or confusion

Treatment of Cardiac Causes

- Beginning empiric treatment without performing a head-up tilt table test may be reasonable.
- Most patients show spontaneous resolution of syncope in 6-12 months; therefore, long-term
medical prophylaxis is usually not necessary.

- Orthostatic Intolerance Syndromes (including vasovagal syndrome):

 Adequate intravascular volume is the most important preventive element:
o Patient is recommended to drink 2-3 L of water a day.
o Physical activities, especially in a hot environment, require more fluid intake, preferably
electrolyte-containing fluids (e.g. sport drinks with additional sodium).
o Liberal use of salt with meals and non-fatty salted snacks.
o Caffeinated beverages should be avoided (because of their renal diuretic effect).
o Wearing elastic support hose (waist-high) may be useful in postural hypotension.

 Medications:
o Fludrocortisone (Astonin-H®)  intravascular volume and also produces both venous
and arterial vasoconstriction. It can be given in a low dosage (0.1 mg by mouth once or
twice a day) with  salt intake or a salt tablet (1 g daily).
o α-Agonist (e.g. pseudoephedrine) stimulates heart rate and  peripheral vascular tone,
preventing reflex bradycardia and vasodilation.
 Cardiac Pacemaker is generally not indicated in pediatric patients.

- Cardiac Arrhythmias:
 Antiarrhythmic medications as indicated.
 Patients with long QT syndrome are treated with beta-blockers, pacemakers, or implantable
cardioverter defibrillators.
 Propranolol may be indicated with symptomatic MVP syndrome.
 Catheter ablation may be indicated in patients with WPW syndrome causing frequent SVT.

Keynotes Pediatric Cardiology

 1. Pediatric Cardiology 2. Pediatric Gastroenterology 3. Pediatric Hepatology

5. Genetic Disorders of
4. Pediatric Genetics 6. Immunology and Allergy
Metabolism (IEM)

7. Pediatric Endocrinology 8. Pediatric Nephrology 9. Pediatric Nutrition

11. Pediatric Psychiatry, 12. Pediatric Rheumatology,

10. Pediatric Neurology
Growth & Development Bone Disorders

15. Neonatologists’ Pocket

13. Neonatology (Volume I) 14. Neonatology (Volume II)
Drug Reference

18. Pediatric Infections

16. Pediatric Hematology 17. Pediatric Oncology
(coming soon)

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Pediatric Postgraduate Series

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