1. Cardiac ArrhythmiasCardiac Arrhythmias

2. Cardiac ArrhythmiasCardiac Arrhythmias
Abnormal rate and or rhythm of the heart can beAbnormal rate and or rhythm of the heart can be
physiological or pathological, congenital or acquired,physiological or pathological, congenital or acquired,
transient or chronic, self-limited or life threatening. Fortransient or chronic, self-limited or life threatening. For
all of which ECG is essential to make a diagnosis.all of which ECG is essential to make a diagnosis.
((I) Tachyarrhythmia (increased H.R.):I) Tachyarrhythmia (increased H.R.):
1- Sinus tachycardia1- Sinus tachycardia: a physiological compensatory: a physiological compensatory
mechanism due to rapid discharge from S.A. node inmechanism due to rapid discharge from S.A. node in
response to:response to:
 A- Certain physiological events as crying, pain,A- Certain physiological events as crying, pain,
anxiety and exercise.anxiety and exercise.
 B- Certain pathological events as fever, shock,B- Certain pathological events as fever, shock,
hypoxia, H.F. , anemia orhypoxia, H.F. , anemia or
 C- Due to certain drugs as atropine, adrenaline orC- Due to certain drugs as atropine, adrenaline or
theophylline.theophylline.
ECG shows tachycardia with normal "P", normal 1:1 AVECG shows tachycardia with normal "P", normal 1:1 AV
conduction and normal QRS.conduction and normal QRS.

4. 2- Supra ventricular tachycardia2- Supra ventricular tachycardia "S.V.T."; the discharge is"S.V.T."; the discharge is
from an abnormal mechanism proximal to thefrom an abnormal mechanism proximal to the
bifurcation of "His" bundle. It is of 3 types:bifurcation of "His" bundle. It is of 3 types:
A- Paroxysmal S.V.T.: caused by "Re-entry"A- Paroxysmal S.V.T.: caused by "Re-entry"
phenomenon through the AV node or through otherphenomenon through the AV node or through other
conducting pathways. SVT affects all ages fromconducting pathways. SVT affects all ages from
fetal life onward.fetal life onward.
 The paroxysm occurs suddenly without an event cause orThe paroxysm occurs suddenly without an event cause or
follows an infection or a physical factor and usuallyfollows an infection or a physical factor and usually
occurs at rest. The H.R. is between 180 and 300 /min.occurs at rest. The H.R. is between 180 and 300 /min.
short attacks for minutes or hours may be tolerated butshort attacks for minutes or hours may be tolerated but
prolonged and severe forms may lead to C.C.F.prolonged and severe forms may lead to C.C.F.
 The attack may spontaneously terminate as suddenly asThe attack may spontaneously terminate as suddenly as
it began. Polyuria may occur due to release of atrialit began. Polyuria may occur due to release of atrial
nitriuretic peptide.nitriuretic peptide.
 Maneuvers that increase vagal tone (unilateral carotidManeuvers that increase vagal tone (unilateral carotid
sinus massage, valsalva maneuver, abdominal pressure,sinus massage, valsalva maneuver, abdominal pressure,
pressure on the eye ball [not in young infants] and icepressure on the eye ball [not in young infants] and ice
pack on the face) may successfully terminate the attackpack on the face) may successfully terminate the attack

5.  SVT may be precipitated by nasal decongestantsSVT may be precipitated by nasal decongestants
(sympathomimetics).(sympathomimetics).
 ECG reveals a very fast rate, normal "P", normal 1:1 AVECG reveals a very fast rate, normal "P", normal 1:1 AV
conduction and normal QRS.conduction and normal QRS.
 Some patients with SVT have WPW syndrome and are atSome patients with SVT have WPW syndrome and are at
higher risk for sudden death from WPW syndrome.higher risk for sudden death from WPW syndrome.
 During the paroxysm the ECG misses WPW picture which isDuring the paroxysm the ECG misses WPW picture which is
in the form of short P-R and slow upstroke QRS (deltain the form of short P-R and slow upstroke QRS (delta
wave).wave).
 If the above measures fail I.V adenosine 0.05 mg/kg bolusIf the above measures fail I.V adenosine 0.05 mg/kg bolus
repeated every 2 min for several times.repeated every 2 min for several times.
 When available DC cardioversionWhen available DC cardioversion
 Other drugs used in SVT include; Phenylphrine,Other drugs used in SVT include; Phenylphrine,
Edrophonium, Amiodarone, Quinidine, Procainamide,Edrophonium, Amiodarone, Quinidine, Procainamide,
propranolol and Verapamil (not used in infants).propranolol and Verapamil (not used in infants).
 After cessation of the acute paroxysm maintenance drugsAfter cessation of the acute paroxysm maintenance drugs
as Digoxin (not in presence of WPW), Propranolol,as Digoxin (not in presence of WPW), Propranolol,
Amiodarone, Verapamil, etcAmiodarone, Verapamil, etc…….should be used for 1 year..should be used for 1 year.
 Recurrences are common in older children and may indicateRecurrences are common in older children and may indicate
for radiofrequency ablation therapy.for radiofrequency ablation therapy.

6. WPW syndromeWPW syndrome

9. B- Atrial flutter: a very uncommon form ofB- Atrial flutter: a very uncommon form of
tachyarrhythmia, caused by an abnormal atrial focustachyarrhythmia, caused by an abnormal atrial focus
discharging at a very high rate (300-500/min)discharging at a very high rate (300-500/min)
producing atrial "sawtooth" flutter waves on ECG.producing atrial "sawtooth" flutter waves on ECG.
 As the AV node can not transmit all these impulses a degreeAs the AV node can not transmit all these impulses a degree
of AV block occurs.of AV block occurs.
 ECG shows a regular sawtooth "P" waves and a regular QRSECG shows a regular sawtooth "P" waves and a regular QRS
complexes but there is one QRS for each 2 or 3 P waves.complexes but there is one QRS for each 2 or 3 P waves.
 This conduction is rare in normal heart.This conduction is rare in normal heart.
 Treatment includes vagal maneuvers, adenosine andTreatment includes vagal maneuvers, adenosine and
synchronized DC cardioversion.synchronized DC cardioversion.

10. C- Atrial fibrillation: mostly seen in older children withC- Atrial fibrillation: mostly seen in older children with
chronic rheumatic heart disease, usually mitralchronic rheumatic heart disease, usually mitral
stenosis. Thyrotoxicosis may be the cause. It isstenosis. Thyrotoxicosis may be the cause. It is
characterized by irregular discharges from atrialcharacterized by irregular discharges from atrial
foci resulting in an irregular disorganized atrial ratefoci resulting in an irregular disorganized atrial rate
of 350-600/min. patients are liable to haveof 350-600/min. patients are liable to have
thromboemboli and stroke.thromboemboli and stroke.
 The ventricular response is variable, resulting in a veryThe ventricular response is variable, resulting in a very
irregular beating.irregular beating.
 ECG shows:ECG shows:
 Absent "P" waves (irregular base lines)Absent "P" waves (irregular base lines)
 Irregular P-R intervals (irregular ventricularIrregular P-R intervals (irregular ventricular
contractions)contractions)
 Normal shapes QRS complex.Normal shapes QRS complex.
 Treatment is by digitalization which restores theTreatment is by digitalization which restores the
ventricular rate to normal although the atrial fibrillationventricular rate to normal although the atrial fibrillation
usually persists, followed by Amiodaroneusually persists, followed by Amiodarone±± Warfarin.Warfarin.

13. 3- Ventricular tachyarrhythmia3- Ventricular tachyarrhythmia: the rapid heart rate: the rapid heart rate
originates from abnormal ventricular mechanisms.originates from abnormal ventricular mechanisms.
Two main forms are known:Two main forms are known:
A-A- Ventricular tachycardiaVentricular tachycardia; a serious condition which may; a serious condition which may
change to fatal ventricular fibrillation, predisposed bychange to fatal ventricular fibrillation, predisposed by
myocarditis, cardiomyopathy, digoxin toxicity, hypoxiamyocarditis, cardiomyopathy, digoxin toxicity, hypoxia
or severe electrolyte imbalance.or severe electrolyte imbalance.
Clinically there is tachycardiaClinically there is tachycardia ±± syncope and suddensyncope and sudden
death may occur. ECG shows rapid wide QRS notdeath may occur. ECG shows rapid wide QRS not
preceded by P waves.preceded by P waves.
I.v. lidocaine is essential to prevent fibrillation and death.I.v. lidocaine is essential to prevent fibrillation and death.
B-B- Ventricular fibrillationVentricular fibrillation: a potentially fatal dysrhythmia: a potentially fatal dysrhythmia
which cause death within few minutes unlesswhich cause death within few minutes unless
immediate resuscitative measures ere provided.immediate resuscitative measures ere provided.
Clinically the patient suddenly loses consciousness withClinically the patient suddenly loses consciousness with
no detectable heart beat and the ECG shows totalno detectable heart beat and the ECG shows total
disorganization with absent QRS.disorganization with absent QRS.
Immediate cardiac massage, i.v. amiodarone orImmediate cardiac massage, i.v. amiodarone or
lidocaine,intracardiac adrenaline and artificial ventilationlidocaine,intracardiac adrenaline and artificial ventilation
+ cardioversion when available.+ cardioversion when available.

14. (II) Bradyarrhythmia:(II) Bradyarrhythmia:
Bradycardia is considered to be present when the heartBradycardia is considered to be present when the heart
rate is less than the lower normal limit for age .rate is less than the lower normal limit for age .
The lower limit of heart rate in awake state is:The lower limit of heart rate in awake state is:
Newborn 90/min.Some what less during sleepNewborn 90/min.Some what less during sleep
Infant 100/min.Infant 100/min.
Young children 80/min.Young children 80/min.
Older children 60/min.Older children 60/min.
Bradyarrhythmias include:Bradyarrhythmias include:
1- Sinus bradycardia (S.B.);1- Sinus bradycardia (S.B.); characterized by abnormallycharacterized by abnormally
slow heart rate caused by discharge from S.A. node.slow heart rate caused by discharge from S.A. node.
Sinus bradycardia may be physiological (during sleepSinus bradycardia may be physiological (during sleep
and in athletes), pathological (syncope or raised intra-and in athletes), pathological (syncope or raised intra-
cranial pressure) or caused by drugs (Digoxin orcranial pressure) or caused by drugs (Digoxin or
propranolol)propranolol)
Clinically there is bradycardia which increases withClinically there is bradycardia which increases with
exertion (crying), a point which differentiates sinusexertion (crying), a point which differentiates sinus
bradycardia from AV block.bradycardia from AV block.
ECG shows a slow rate but normal P-QRS-T complexes.ECG shows a slow rate but normal P-QRS-T complexes.

15. 2- Atrioventricular block;2- Atrioventricular block; it is of three types:it is of three types:
A- First degree AV block: prolonged P-R interval but allA- First degree AV block: prolonged P-R interval but all
the atrial impulses are conducted to the ventricle.the atrial impulses are conducted to the ventricle.
B- Second degree; failure of conduction of some of theB- Second degree; failure of conduction of some of the
atrial impulses to the ventricle.atrial impulses to the ventricle.
It is subdivided in to two forms:It is subdivided in to two forms:
Mobitz type I (wenckebach);Mobitz type I (wenckebach); in which the P-P intervalin which the P-P interval
remains constant, but there is progressive increase of theremains constant, but there is progressive increase of the
P-R interval until a "P" wave is not conducted. After thisP-R interval until a "P" wave is not conducted. After this
dropped beat the cycle starts again with a short P-Rdropped beat the cycle starts again with a short P-R
interval.interval.
Mobitz type IIMobitz type II; P-R interval remains constant, but an; P-R interval remains constant, but an
occasional atrial beat does not conduct to the ventricle.occasional atrial beat does not conduct to the ventricle.
Syncope may occur and the conduction may change toSyncope may occur and the conduction may change to
complete AV block.complete AV block.

17. C- Third degree (complete heart block): no atrialC- Third degree (complete heart block): no atrial
impulse reaches the ventricles.impulse reaches the ventricles.
The cause may be;The cause may be;
Congenital, usually associated with maternal SLE.Congenital, usually associated with maternal SLE.
Acquired; digixin, post cardiac surgery, or bacterialAcquired; digixin, post cardiac surgery, or bacterial
endocarditis.endocarditis.
Clinically; most are asymptomatic, heart rate is aroundClinically; most are asymptomatic, heart rate is around
50/min, may increase by 10-20 on exercise or atropine.50/min, may increase by 10-20 on exercise or atropine.
Symptoms include fatigue, exercise intolerance, syncopeSymptoms include fatigue, exercise intolerance, syncope
(stokes-Adams attacks) and rarely sudden death may(stokes-Adams attacks) and rarely sudden death may
occur.occur.
Systolic murmurs are commonly heared. CardiomegalySystolic murmurs are commonly heared. Cardiomegaly
and elevated blood pressure may be detected.and elevated blood pressure may be detected.
ECG: QRS duration may be prolonged.ECG: QRS duration may be prolonged.
Prognosis of the congenital complete heart block is good.Prognosis of the congenital complete heart block is good.
Some who have exercise intolerance, progressiveSome who have exercise intolerance, progressive
cardiomegaly or Stokes-Adams attacks need implantationcardiomegaly or Stokes-Adams attacks need implantation
of the permanent cardiac pace maker.of the permanent cardiac pace maker.

19. 3- Sick Sinus Syndrome "SSS"3- Sick Sinus Syndrome "SSS"
This form of Bradyarrhythmia usually follows cardiac surgery,This form of Bradyarrhythmia usually follows cardiac surgery,
myocarditis, myocardial ischemia or cardiomyopathy. SSS ismyocarditis, myocardial ischemia or cardiomyopathy. SSS is
characterized by profound unresponsive sinus bradycardia withcharacterized by profound unresponsive sinus bradycardia with
or without periods of tachycardia (bradycardia- tachycardiaor without periods of tachycardia (bradycardia- tachycardia
syndrome) manifests as dizziness and syncope. In symptomaticsyndrome) manifests as dizziness and syncope. In symptomatic
cases drugs as digoxin or ventricular pacemaker are necessary.cases drugs as digoxin or ventricular pacemaker are necessary.
4- Asystole;4- Asystole; complete cessation of cardiac contraction, (flat ECG)complete cessation of cardiac contraction, (flat ECG)
may follow bradycardias or results from sever hypoxia,may follow bradycardias or results from sever hypoxia,
acidosis, shock, hypothermia, electrolyte disturbances oracidosis, shock, hypothermia, electrolyte disturbances or
hypovolemia. Stressful procedures as lumber puncture,hypovolemia. Stressful procedures as lumber puncture,
intubation or intra venous canulation may cause cardiacintubation or intra venous canulation may cause cardiac
arrest.arrest.
Extrasystoles (premature beat): these are mostly benign andExtrasystoles (premature beat): these are mostly benign and
occur in normal children. They may also accompany variousoccur in normal children. They may also accompany various
organic (inflammation, ischemia, fibrosis) heart disease or beorganic (inflammation, ischemia, fibrosis) heart disease or be
drug induce (digoxin)drug induce (digoxin)
They result from isolated discharge from an ectopic atrial orThey result from isolated discharge from an ectopic atrial or
ventricular focus.ventricular focus.
The atrial extrasystoles are shown on ECG as;The atrial extrasystoles are shown on ECG as;
Abnormally shaped "P" waveAbnormally shaped "P" wave
Normal QRSNormal QRS
No compensatory pauseNo compensatory pause

20. The ventricular extrasystoles are shown on ECG by:The ventricular extrasystoles are shown on ECG by:
Wide bizarre QRS, inverted "T" and a compensatory pause.Wide bizarre QRS, inverted "T" and a compensatory pause.
Long Q-T SyndromeLong Q-T Syndrome
"LQTS""LQTS"
This is a rare condition characterized by prolonged QTThis is a rare condition characterized by prolonged QT
interval, syncopal attacks. Nerve deafness, hemiplegia,interval, syncopal attacks. Nerve deafness, hemiplegia,
petit-mal may be present. LQTS may be a cause of SUIDS.petit-mal may be present. LQTS may be a cause of SUIDS.
There may be an abnormality in the sympatheticThere may be an abnormality in the sympathetic
innervation of the myocardium.innervation of the myocardium.
LQTS may be familial (both A.R. and A.D. are known) orLQTS may be familial (both A.R. and A.D. are known) or
acquired due to:acquired due to:
Drugs as phenothiazine ,Hypokalemia, hypocalcemia orDrugs as phenothiazine ,Hypokalemia, hypocalcemia or
hypomagnisemia ,Hypothermia ,Cerebrovascular diseaseshypomagnisemia ,Hypothermia ,Cerebrovascular diseases
or Neck surgery.or Neck surgery.
 TreatmentTreatment includes propranolol, di-phenyl hydantoin andincludes propranolol, di-phenyl hydantoin and
left stellate ganglionectomy.left stellate ganglionectomy.
 The mortality is high (75%) without treatment.The mortality is high (75%) without treatment.

22. Cardiomyopathy “CMPCardiomyopathy “CMP””
This entity means myocardial dysfunction, which could be familialThis entity means myocardial dysfunction, which could be familial
or results from different other diseases like muscle dystrophy,or results from different other diseases like muscle dystrophy,
glycogen storage disease , hemochromatosis etc.glycogen storage disease , hemochromatosis etc.
C.M.P is of 3 distinctive forms :C.M.P is of 3 distinctive forms :
1. Congestive (dilated) C.M.P ; characterized by CCF ,arrhythmias ,1. Congestive (dilated) C.M.P ; characterized by CCF ,arrhythmias ,
mitral or tricuspid murmurs and emboli.mitral or tricuspid murmurs and emboli.
X-ray shows cardiomegalyX-ray shows cardiomegaly
Prognosis is bad.Prognosis is bad.
2. Restrictive C.M.P: also presents as C.C.F. with cardiomegaly ,2. Restrictive C.M.P: also presents as C.C.F. with cardiomegaly ,
distant heart sounds , but usually no murmurs .distant heart sounds , but usually no murmurs .
ECG shows low voltage, arrhythmias, ST and T changes.ECG shows low voltage, arrhythmias, ST and T changes.
3. Obstructive : characterized by obstruction to left ventricle and3. Obstructive : characterized by obstruction to left ventricle and
interventricular septum.interventricular septum.It is also termed Idiopathic HypertrophicIt is also termed Idiopathic Hypertrophic
Subaortic Stenosis (IHSS)Subaortic Stenosis (IHSS)
30 % of cases of IHSS are familial but usually appears after30 % of cases of IHSS are familial but usually appears after
childhood.childhood.

23. Management :Management :
 In general there is no specific treatment for C.M.P.In general there is no specific treatment for C.M.P.
 Anti failure (vasodilator , Diuretics and ACE inhibitor )Anti failure (vasodilator , Diuretics and ACE inhibitor )
 Anticoagulant when emboli are suspectedAnticoagulant when emboli are suspected
 Beta blockers are used for hypertrophic CMPBeta blockers are used for hypertrophic CMP
 Anti arrhythmic agent.Anti arrhythmic agent.
 Surgical myotomy in some forms of localized obstruction.Surgical myotomy in some forms of localized obstruction.
 Repair or replacement of mitral valve may be needed.Repair or replacement of mitral valve may be needed.
 Cardiac transplant in terminal cases.Cardiac transplant in terminal cases.

24. MyocarditisMyocarditis
Causes of which are numerous including:Causes of which are numerous including:
 Different virusesDifferent viruses
 Bacterial toxinsBacterial toxins
 Parasitic infection.Parasitic infection.
 Fungal infection.Fungal infection.
 Collagen vascular diseases.Collagen vascular diseases.
 Metabolic and nutritional diseases.Metabolic and nutritional diseases.
 Neuromuscular disorders.Neuromuscular disorders.
 IEMIEM
 Blood disorders.Blood disorders.
 Drugs.Drugs.
 Corornary artery damage.Corornary artery damage.

25.  Viral myocarditis is, however the most common form,Viral myocarditis is, however the most common form,
symptoms of which are usually abrupt especially insymptoms of which are usually abrupt especially in
neonates with unexplained breathlessness, gallop rhythm,neonates with unexplained breathlessness, gallop rhythm,
shock ,C.C.F. &arrhythmia. ECG shows ; low voltage , STshock ,C.C.F. &arrhythmia. ECG shows ; low voltage , ST
and T changes , X-ray shows cardiomegaly.and T changes , X-ray shows cardiomegaly.
Treatment :Treatment :
 O2O2
 Bed restBed rest
 Anti failureAnti failure
 Steroid especially in presence of cardiovascular collapseSteroid especially in presence of cardiovascular collapse
and conduction disturbance.and conduction disturbance.