The lecture has been given on May 19th, 2011 by Dr. Jamal.

1. Cardiac Arrhythmias
"C. A."
Abnormal rate and rhythm of the heart can be physiological or pathological, congenital or
acquired, transient or chronic, self-limited or life threatening. For all of which ECG is
essential to make a diagnosis.
I. Tachyarrhythmia (increased H.R.):
1) Sinus tachycardia: a physiological compensatory mechanism due to rapid discharge
from S.A. node in response to:
a. Certain physiological events as crying, pain, anxiety and exercise.
b. Certain pathological events as fever, shock, hypoxia, H.F. , anemia or
c. Due to certain drugs as atropine, adrenaline or theophylline.
ECG shows tachycardia with normal "P", normal 1:1 AV conduction and normal QRS.
2) Supra ventricular tachycardia "S.V.T."; the discharge is from an abnormal mechanism
proximal to the bifurcation of "His" bundle. It is of 3 types:
a. Paroxysmal S.V.T.: caused by "Re-entery" phenomenon through the AV
node or through other conducting pathways. SVT affects all ages from
fetal life onward.
The paroxysm occurs suddenly without an event cause or follows an
infection or a physical factor and usually occurs at rest. The H.R. is
between 180 and 300 /min. short attacks for minutes or hours may be
tolerated but prolonged and severe forms may lead to C.C.F.
The attack may spontaneously terminate as suddenly as it began. Polyuria
may occur due to release of atrial nitriuretic peptide.
Maneuvers that increase vagal tone (unilateral carotid sinus massage,
valsalva maneuver, abdominal pressure, pressure on the eye ball [not in
young infants] and ice pack on the face) may successfully terminate the
attack.
SVT may be precipitated by nasal decongestants (sympathomimetics).
ECG reveals a very fast rate, normal "P", normal 1:1 AV conduction and
normal QRS.
Some patients with SVT have WPW syndrome and are at higher risk for
sudden death from WPW syndrome.
During the paroxysm the ECG misses WPW picture which is in the form
of short P-R and slow upstroke QRS (delta wave).
If the above measures fail I.V adenosine 0.05 mg/kg bolus repeated every
2 min for several times.
When available DC cardioversion
Other drugs used in SVT include; Phenylphrine, Edrophonium,
Amiodarone, Quinidine, Procainamide, propranolol and Verapamil (not
used in infants).
After cessation of the acute paroxysm maintenance drugs as Digoxin (not
in presence of WPW), Propranolol, Amiodarone, Verapamil, etc….should
be used for 1 year.
Recurrences are common in older children and may indicate for
radiofrequency ablation therapy.

2. b. Atrial flutter: a very uncommon form of tachyarrhythmia, caused by an
abnormal atrial focus discharging at a very high rate (300-500/min)
producing atrial "sawtooth" flutter waves on ECG.
As the AV node can not transmit all these impulses a degree of AV block
occurs.
ECG shows a regular sawtooth "P" waves and a regular QRS complexes
but there is one QRS for each 2 or 3 P waves.
This conduction is rare in normal heart.
Treatment includes vagal maneuvers, adenosine and synchronized DC
cardioversion.
c. Atrial fibrillation: mostly seen in older children with chronic rheumatic
heart disease, usually mitral stenosis. Thyrotoxicosis may be the cause. It
is characterized by irregular discharges from atrial foci resulting in an
irregular disorganized atrial rate of 350-600/min. patients are liable to have
thromboemboli and stroke.
The ventricular response is variable, resulting in a very irregular beating.
ECG shows:
 Absent "P" waves (irregular base lines)
 Irregular P-R intervals (irregular ventricular contractions)
 Normal shapes QRS complex.
Treatment is by digitalization which restores the ventricular rate to normal
although the atrial fibrillation usually persists, followed by Amiodarone±
Warfarin.
3) Ventricular tachyarrhythmia: the rapid heart rate originates from abnormal ventricular
mechanisms.
Two main forms are known:
o Ventricular tachycardia; a serious condition which may change to fatal
ventricular fibrillation, predisposed by myocarditis, cardiomyopathy,
digoxin toxicity, hypoxia or severe electrolyte imbalance.
Clinically there is tachycardia ± syncope and sudden death may occur.
ECG shows rapid wide QRS not preceded by P waves.
I.v. lidocaine is essential to prevent fibrillation and death.
o Ventricular fibrillation: a potentially fatal dysrhythmia which cause
death within few minutes unless immediate resuscitative measures ere
provided.
Clinically the patient suddenly loses consciousness with no detectable
heart beat and the ECG shows total disorganization with absent QRS.
Immediate cardiac massage, i.v. amiodarone or lidocaine,intracardiac
adrenaline and artificial ventilation + cardioversion when available.

3. II. Bradyarrhythmia:
Bradycardia is considered to be present when the heart rate is less than the lower normal
limit for age.
The lower limit of heart rate in awake state is:
}
− Newborn 90/min.
− Infant 100/min.
− Young children 80/min. Some what less during sleep
− Older children 60/min.
Bradyarrhythmias include:
1) Sinus bradycardia (S.B.); characterized by abnormally slow heart rate caused
by discharge from S.A. node.
Sinus bradycardia may be physiological (during sleep and in athletes),
pathological (syncope or raised intra cranial pressure) or caused by drugs
(Digoxin or propranolol)
Clinically there is bradycardia which increases with exertion (crying), a
point which differentiates sinus bradycardia from AV block.
ECG shows a slow rate but normal P-QRS-T complexes.
2) Atrioventricular block; it is of three types:
a. First degree AV block: prolonged P-R interval but all the atrial impulses
are conducted to the ventricle.
b. Second degree; failure of conduction of some of the atrial impulses to
the ventricle.
It is subdivided in to two forms:
− Mobitz type I (wenckebach); in which the P-P interval remains
constant, but there is progressive increase of the P-R interval
until a "P" wave is not conducted. After this dropped beat the
cycle starts again with a short P-R interval.
− Mobitz type II; P-R interval remains constant, but an occasional
atrial beat does not conduct to the ventricle. Syncope may occur
and the conduction may change to complete AV block.
c. Third degree (complete heart block): no atrial impulse reaches the
ventricles.
The cause may be;
− Congenital, usually associated with maternal SLE.
− Acquired; digixin, post cardiac surgery, or bacterial endocarditis.
Clinically; most are asymptomatic, heart rate is around 50/min,
may increase by 10-20 on exercise or atropine.
Symptoms include fatigue, exercise intolerance, syncope (stokes-
Adams attacks) and rarely sudden death may occur.
Systolic murmurs are commonly heared. Cardiomegaly and
elevated blood pressure may be detected.
ECG: QRS duration may be prolonged.
Prognosis of the congenital complete heart block is good. Some
who have exercise intolerance,progressive cardiomegaly or
Stokes-Adams attacks need implantation of the permanent
cardiac pace maker.

4. 3) Sick Sinus Syndrome "SSS"
This form of Bradyarrhythmia usually follows cardiac surgery, myocarditis,
myocardial ischemia or cardiomyopathy. SSS is characterized by profound unresponsive
sinus bradycardia with or without periods of tachycardia (bradycardia- tachycardia
syndrome) manifests as dizziness and syncope. In symptomatic cases drugs as digoxin or
ventricular pacemaker are necessary.
4) Asystole; complete cessation of cardiac contraction, (flat ECG) may follow
bradycardias or results from sever hypoxia, acidosis, shock, hypothermia,
electrolyte disturbances or hypovolemia. Stressful procedures as lumber
puncture, intubation or intra venous canulation may cause cardiac arrest.
Extrasystoles (premature beat): these are mostly benign and occur in normal children.
They may also accompany various organic (inflammation, ischemia, fibrosis) heart
disease or be drug induce (digoxin)
They result from isolated discharge from an ectopic atrial or ventricular focus.
The atrial extrasystoles are shown on ECG as;
− Abnormally shaped "P" wave
− Normal QRS
− No compensatory pause
The ventricular extrasystoles are shown on ECG by:
− Wide bizarre QRS, inverted "T" and a compensatory pause.
Long Q-T Syndrome
"LQTS"
This is a rare condition characterized by prolonged QT interval, syncopal attacks. Nerve
deafness, hemiplegia, petit-mal may be present. LQTS may be a cause of SUIDS.
There may be an abnormality in the sympathetic innervation of the myocardium.
LQTS may be familial (both A.R. and A.D. are known) or acquired due to:
− Drugs as phenothiazine
− Hypokalemia, hypocalcemia or hypomagnisemia
− Hypothermia
− Cerebrovascular diseases
− Neck surgery.
Treatment includes propranolol, di-phenyl hydantoin and left satellate ganglionectomy.
The mortality is high (75%) without treatment.