Transcript 4-Cardiac Arrhythmiasx

Dr. Talaat Ali Sabeeh
Al-Jarrah
Pediatric Cardiologist
Cardiac Arrhythmias
The normal heart rate varies with age. The younger the 
child, the faster the HR.Therefore, definitions of
bradycardia (<60 bpm) and tachycardia (>100 bpm)
used for adults do not apply to infants and children.
Tachycardia is HR beyond the upper limit of normal
for the pt age, and bradycardia is HR slower than the
lower limit of normal.
I-Rhythms Originating in the Sinus Node
A- Regular Sinus Rhythm is regular, and the
rate is normal for age. The characteristic of
sinus rhythm described previously are
present .This rhythm is normal at any age
B-Sinus Tachycardia 
HR is faster than the upper limit of normal for age. A 
rate greater than 140 bpm in children and greater than
170 bpm in infants may be significant. The heart rate is
usually less than 200 bpm in sinus tachycardia.
Causes:Anxiety, fever, hypovolemia or circulatory 
shock, anemia, congestive heart failure (CHF),
administration of catecholamines, thyrotoxicosis, and
myocardial disease Management:underlying cause.
C-Sinus Bradycardia:HR is slower than the lower limit of normal for the 
age.A rate slower than 80 bpm in newborn infants and slower than 60 bpm
in older children may significant .
Causes: normal individuals and trained athletes. It may occur with vagal 
stimulation, increased intracranial pressure, hypothyroidism,
hypothermia, hypoxia, hyperkalemia, and administration of drugs such as
digitalis and β-adrenergic blockers.
Significance:In some patients, marked bradycardia may not maintain 
normal cardiac output.
Management: The underlying cause is treated.
D-Sinus Arrhythmiais a phasic variation in the heart
rate, increasing during inspiration and decreasing
during expiration. This occurs with maintenance of
characteristics of sinus rhythm
Causes is a normal phenomenon and is due to phasic 
variation in the firing rate of cardiac autonomic nerves
with the phases of respiration.
Significance: it is a normal finding in children. 
Management:No treatment is indicated 
II-Rhythms Originating in the Atrium
Rhythms that originate in the atrium (ectopic atrial 
rhythm) are characterized by :
1-P waves have an unusual contour, caused by an 
abnormal P axis, and/or there is an abnormal number
of P waves per QRS complex.
2-QRS complexes are usually of normal configuration, 
but occasional bizarre QRS complexes caused by
aberrancy may occur .
A-Atrial Flutter 
Description 
The ectopic focus, and “circus movement” in the atrium is the 
mechanism of this arrhythmia. Atrial flutter is characterized by
an atrial rate (F wave with “sawtooth” configuration) of about
300 (range 240 to 360) bpm, a ventricular response with varying
degrees of block (e.g., 2:1, 3:1, 4:1), and normal QRS complexe.
Causes: usually suggests a significant cardiac pathology, 
although fetuses,neonates with AFL frequently have a normal
heart. Structural heart disease with dilated atria, acute infectious
illness, myocarditis or pericarditis, previous surgery involving
atria ( Senning procedure, Fontan operation, or ASD repair),
digitalis toxicity,and thyrotoxicosis are possible causes.
Significance:The ventricular rate determines eventual COP; a 
too-rapid ventricular rate may decrease COP. Thrombus
formation may lead to embolic events. Uncontrolled flutter may
precipitate heart failure. The flutter may associated with
syncope, presyncope, or chest pain.
Management: 
divided into acute conversion, chronic suppression of the arrhythmia, 
control of ventricular rate, prevention of recurrences, and refractory
cases.
1-Acute situation: a)Adenosine does not convert the arrhythmia to 
sinus rhythm.
b)Immediate synchronized DC cardioversion is the treatment of choice 
for A FL of short duration, if the infant or child is in severe CHF.
c)Temporary transvenous or transesophageal pacing may be used 
d)In children, IV amiodarone (class III) or IV procainamide (class IA) 
2-For chronic cases: For long-standing AFL or fibrillation (of 24 to 48 
hours) or those with unknown duration, thrombus formation, so TTE
&Anticoagulation with warfarin is started and cardioversion delayed for
2 to 3 weeks. After conversion to sinus rhythm, anticoagulation is
continued for an additional 3 to 4 weeks.
3-For rate control: For control of ventricular rate, calcium channel 
blockers appear to be the drug of choice. Propranolol equally effective.
4-For prevention of recurrences: Class I and class III antiarrhythmic 
drug or Amiodarone .
5-For refractory cases: Antitachycardia pacing or radiofrequency 
ablation may be indicated.
B-Atrial Fibrillation
less common than A Fl in children. The mechanism is 
circus movement, is characterized by an extremely fast atri
al rate (f wave at a rate of 350 to 600 bpm and an irregularly 
irregular ventricular response with normal QRS complexes
.Causes: usually associated with structural heart diseases
with dilated atria( rheumatic heart disease, Ebstein's
anomaly, tricuspid atresia, atrial septal defect, AV valve
regurgitation, or previous intra-atrial surgery).
Thyrotoxicosis, pulmonary emboli, and pericarditis should
be suspected in a previously normal child who develops
atrial fibrillation.Management: is similar to atrial flutter
C-Supraventricular Tachycardia 
HR is extremely rapid and regular (usually 240 ± 40 bpm). The P wave 
is usually invisible.The QRS duration is usually normal, but
occasionally, aberrancy increases the QRS duration, making
differentiation from ventricular tachycardia difficult .the most
common tachyarrhythmia seen in the pediatric age group.Patients with
accessory pathways frequently have WPW preexcitation
Causes 
1)No heart disease is found in about half of patients. This idiopathic 
type of SVT occurs more commonly in young infants than in older
children.2)WPW preexcitation is present in 10% to 20% of cases, which
is evident only after conversion to sinus rhythm.3)Some CHD (e.g.,
Ebstein's anomaly, single ventricle, congenitally corrected TGA) are
more susceptible.4)may occur following cardiac surgeries
Significance: If SVT is sustained for 6 to 12 hours, signs of CHF usually 
happened. Older children :chest pain, palpitation, shortness of breath,
lightheadedness, and fatigue.
Management 
1)Vagal stimulatory maneuvers (unilateral carotid sinus massage, gagging, 
pressure on an eyeball), effective in older children rarely effective in infants.
ice-water bag on the face (for up to 10 seconds) is often effective in infants (by
diving reflex).
2)Adenosine is considered the drug of choice. 
3)If the infant is in severe CHF, emergency treatment is immediate 
cardioversion. The initial dose of 0.5 joule/kg is increased in steps up to 2
joule/kg.
4)Esmolol, other β-adrenergic blockers, verapamil, and digoxin have also 
been used with some success.
5)For postoperative SVT(which requires rapid conversion), IV amiodarone 
6)Overdrive suppression (by transesophageal pacing or by atrial pacing) may 
be effective in children who have been digitalized.
7)Radiofrequency catheter ablation or surgical interruption of accessory 
pathways
Prevention of Recurrence of SVT 
1-In infants without WPW, oral propranolol for 12 months is effective. 
Verapamil can used causiousioly in patients with poor LV function and in
young infants.
2-In infants in CHF and ECG evidence of WPW, start with digoxin (just to treat 
CHF),switched to propranolol when the infant's heart failure improves.
III-Rhythms Originating in the Atrioventricular Node
Rhythms that originate in the AV node are 
characterized by :1) P wave may be absent, or inverted
P waves may follow the QRS complex.2) QRS complex
is usually normal .
A-NODAL PREMATURE BEATS. 
B-NODAL ESCAPE BEATS. 
C-NODAL OR JUNCTIONAL RHYTHM 
D-NODAL TACHYCARDIA (JUNCTIONAL ECTOPIC 
TACHYCARDIA).
DescriptionIf the SA node consistently fails, the AV 
node may function as the main pacemaker of the
heart, producing a relatively slow rate (40 to 60 bpm).
characterized by no P waves or inverted P waves after
QRS complexes and normal QRS complexes with a rate
of 40 to 60 bpm.
IV-Rhythms Originating in the Ventricle 
Rhythms that originate in the ventricle (ventricular 
arrhythmias) are characterized by the
following:1)Bizarre and wide QRS complexes.2)waves
pointing in directions opposite to QRS
complexes.3)QRS complexes randomly related to P
waves, if visible.
B-Ventricular Tachycardia 
1)VT is a series of three or more PVCs with HR of 120 to 200 bpm. QRS 
complexes are wide and bizarre, with T waves pointing in opposite directions.
2)The onset may be paroxysmal (sudden) or nonparoxysmal.. 
Causes 
1)VT may occur in patients with structural heart diseases such as tetralogy of 
Fallot (TOF), aortic stenosis (AS), hypertrophic or DCM or MVP.
2)Postoperative CHDs (such as TOF, TGA, or double-outlet right ventricle). 
3)Myocarditis, pulmonary hypertension, arrhythmogenic RV dysplasia , 
Brugada syndrome Chagas' disease (trypanosomiasis, in South America),
myocardial tumors, myocardial ischemia, and infarction are other possible
causes of VT.
4)Metabolic causes include hypoxia, acidosis, hyperkalemia, hypokalemia, and 
hypomagnesemia.
5)Mechanical irritation-intraventricular catheter. 
6)Pharmacologic or chemical causes include catecholamine infusion, digitalis 
toxicity, cocaine, and organophosphate insecticides. Most antiarrhythmic
drugs (especially classes IA, IC, and III) are also proarrhythmic.
7)VT may occur in healthy children who have a structurally& functionally 
normal heart.
Significance: 
1)VT may signify a serious myocardial dysfunction 2)sudden cardiac death. 
3)the rhythm may deteriorate to ventricular fibrillation. 
Management 
1-Synchronized DC cardioversion. 
2)Rarely, if the patient is conscious, an IV bolus of lidocaine followed by an IV 
drip of lidocaine .
3)Treatment of reversible of VT (e.g., hypokalemia, hypoxemia) 
4)IV amiodarone is used in patients with drug-refractory VT, 
5)Virtually all classes of AAD including all class I and III drugs, with varying 
levels of success.
6)IV injection of magnesium sulfate is reportedly effective and safe treatment 
for torsades de pointes in adults (2 g in an IV bolus).
7)Recurrence may be prevented with administration of propranolol, atenolol, 
phenytoin sodium, or quinidine .
8)Patients with long QT syndrome are treated with β-blockers, which alleviate 
symptoms in 75% to 80%.
9)Some incessant VTs need surgical or radiofrequency ablation. 
10)ICD has become the established standard treatment 
C-Ventricular Fibrillation 
is rare in the pediatric population. QRS bizarre ,of 
varying sizes and configurations. The rate is rapid and
irregular,VF due to multiple reentrant circuits make
portions of the myocardium are depolarizing
constantly.
Causes All the causes listed for VT can cause 
ventricular fibrillation
Significance: 
It is usually a degeneration of VT and is terminal arrhythmia because it 
results in ineffective circulation. Immediate resuscitation must be
provided.
Management 
1-Acute care: 
a)Immediate cardiac and pulmonary resuscitation (CPR), 
b)Defibrillation with 2 joule/kg. 
c)Administration of epinephrine by the IV or intraosseous (IO) 
d)One should identify and treat causes, including metabolic 
environment (hypoxia, acidosis).
e)One of the following antiarrhythmic agents may be used: 
Amiodarone,Lidocaine ,Magnesium sulfate for torsades de pointes or
hypomagnesemia
2-A child with susceptibility to ventricular fibrillation and those 
resuscitated from the arrhythmia should have a comprehensive
pediatric electrophysiology evaluation.
3-ICDs are often indicated in patients who survived ventricular 
fibrillation..
V-Long QT Syndrome 
is a disorder of myocardial repolarization characterized by a prolonged QT 
interval on the ECG and ventricular arrhythmias, usually torsades de pointes,
that may result in sudden death. Patients with LQTS may present with
complaints of syncope, seizures, or palpitation during exercise or with
emotion. The first manifestation may be cardiac arrest.The QT prolongation
may be congenital or acquired.
1- Congenital LQTS is caused by mutations of cardiac ion channel 
genes.Romano-Ward syndrome(AD,NO DEAFNESS)& Jervell- Lange-Nielsen
syndrome(AR, DEAFNESS) are identified.
2-Acquired prolongation of the QT interval can be caused by a number of 
drugs, electrolyte disturbances, and other underlying medical conditions .
Clinical Manifestations1)The family history is positive in 60% of patients, 
and deafness in 5% .
2)Presenting symptoms: syncope (26%), seizure (10%), cardiac arrest (9%), 
presyncope, or palpitation (6%).
Ppt factor occur during exercise or with emotion. 
Diagnosis A)The ECG shows :1) prolonged QT interval with a QTc usually 
greater than 0.46 second the upper limit of normal is 0.44 second. 2)Abnormal
T-wave morphology (bifid, diphasic, or notched) is frequent.B)Holter
monitoring :QTc interval on Holter monitor may be longer than standard ECG
.C)family history. D) exercise testing,(TMT). E) electrophysiology study,
F)Genetic testing identify genotypes of the LQTS. Although it is not widely
available.
MANAGEMENT 
A)Treat risk factors for sudden death:1)Bradycardia for age 2) 
extremely long QTc interval (>0.55 second),3)Symptoms at
presentation (syncope, seizure, cardiac arrest),4)Young age at
presentation (<1 month), and 5)Documented torsades de pointes or
ventricular fibrillation.
B)General measures:Avoid:1) medications that prolong the QT 
interval 2) Catecholamines and sympathomimetic drugs should be
avoided because trigger torsades de pointes 3)competitive sports policy
applies.4)poor compliant with their medications.
C)Treatment of Congenital LQTS: aimed at1) interrupting 
sympathetic input to the myocardium with β-blockers. 2)cardiac
pacemaker & ICD.3)Surgical approach to interrupting sympathetic
input to the heart (through left cardiac sympathetic denervation
surgery) is no longer frequently used.4)Targeted pharmacologic
therapy(sodium channel blocker- e.g mexiletine-,or Potassium
supplementation might improve repolarization abnormalities or Gene
therapy).
PROGNOSIS very poor in untreated patients, with annual mortality as 
high as 20% and 10-year mortality of 50%. β-Blockers may reduce
mortality to some extent, but they do not completely protect patients
from sudden death. The ICD appears promising in improving
prognosis.
VI-Disturbances of Atrioventricular Conduction 
disturbance in conduction between normal sinus impulse& eventual 
ventricular response.
A-First-Degree Atrioventricular Block 
Description:PR interval is prolonged beyond the upper limits of normal for
the patient's age and HR .
Causes:1)healthy children and young adults, particularly in 
athletes.2)congenital heart diseases (such as endocardial cushion defect,
atrial septal defect, Ebstein's anomaly),3) infectious disease,
4)inflammatory conditions (rheumatic fever),5) cardiac surgery,6)certain
drugs (such as digitalis, calcium channel blockers).
Significance:does not produce HDD. It sometimes progresses to a 
more AV block.Management:No treatment is indicated, except when
the block is caused by digitalis toxicity
B-Second Degree Atrioventricular Block
Some, but not all, P waves are followed by a QRS (dropped beats.
1-MOBITZ TYPE I:PR interval progressively prolonged until one QRS
complex is dropped completely .Causes 1)otherwise healthy children.
Other causes include 2)myocarditis, cardiomyopathy,3) myocardial
infarction,4) congenital heart defect, 5)cardiac surgery, and6) digitalis
toxicity.SignificanceIt usually does not progress to complete heart
block. It occurs in individuals with vagal dominance.
Management The underlying causes are treated
 2-MOBITZ TYPE II
DescriptionThe AV conduction is “all or none” .i.e it is either normal or
completely blocked
Causes: are the same as for Mobitz type I.
SignificanceThe block is at the level of the bundle of His. It is more
serious than type I block because it may progress to complete heart
block, resulting in Stokes-Adams attack.
Management: treat underlying causes. Prophylactic pacemaker therapy
may be indicated
C- Third-Degree Atrioventricular Block 
CHB: atrial & ventricular activities are entirely independent of each other
1)In congenital complete heart block,a) duration of the QRS 
complex is normal because the pacemaker for the ventricular complex
is at a level higher than the bifurcation of the bundle of His. b)The
ventricular rate is faster (50 to 80 bpm) than that in the acquired type,
and c) the ventricular rate is somewhat variable in response to varying
physiologic conditions.
2)In surgically induced or acquired complete heart block,a) the QRS 
duration is prolonged because the pacemaker for the ventricular
complex is at a level below the bifurcation of the bundle of His ,B)The
ventricular rate is in the range of 40 to 50 bpm (idioventricular rhythm)
and c)the ventricular rate is relatively fixed.
Causes:
Congenital Type :TGA, or maternal SLE, Sjögren's syndrome, or
other connective tissue disease.
Acquired Type: 1)Cardiac surgery most common . Other rare
causes include 2) severe myocarditis.3) Lyme carditis, 4)acute
rheumatic fever,5) mumps,6) diphtheria,7) cardiomyopathies,
8)tumors in the conduction system,9) overdoses of certain
drugs, and 10) myocardial infarction. These causes produce
either temporary or permanent heart block.
Significance:1)Congestive heart failure, may develop in infancy,
particularly when there are associated congenital heart defects.
2)Patients with isolated congenital heart block who survive infancy
are usually asymptomatic and achieve normal growth and
development for 5 to 10 years. Chest x-ray films may show
cardiomegaly.
3)Syncopal attacks (Stokes-Adams attacks) may occur with a heart
rate below 40 to 45 bpm. A sudden onset of acquired heart block
may result in death unless treatment maintains the heart rate in
the acceptable range.
Management 
1)Atropine or isoproterenol is indicated in symptomatic children 
2)A temporary transvenous ventricular pacemaker is indicated 
3)No treatment is required for children with asymptomatic 
congenital complete heart block with acceptable rate, narrow
QRS complex, and normal ventricular function.
4)Pacemaker therapy is indicated in patients with congenital 
heart block:
a)If the patient is symptomatic or develops CHF. Dizziness or 
lightheadedness may be an early warning sign of the need for a
pacemaker.
b)If an infant has a ventricular rate less than 50 to 55 bpm or if 
the infant has a congenital heart defect with a ventricular rate
less than 70 bpm.
c)If the patient has a wide QRS escape rhythm, complex 
ventricular ectopy, or ventricular dysfunction.
d)A permanent artificial ventricular pacemaker is indicated in
patients with surgically induced heart block that is not expected
to resolve or persists at least 7 days post surgery.
VII- Cardiac Pacemakers and Implantable CardioverterDefibrillators in Children
A pacemaker is a device that delivers battery-supplied electrical stimuli
over leads to electrodes that are in contact with the heart. It primarily
treats bradycardia.
An implantable cardioverter-defibrillator (ICD) is a
multiprogrammable antiarrhythmic device for treating ventricular
tachycardia and ventricular fibrillation. The ICD also possesses
pacemaking capability to treat bradycardia. The electrical leads are
either placed directly over the epicardium or inserted transvenously
into the cardiac chambers. Electronic circuitry regulates the timing and
characteristics of the stimuli. The power source is usually a lithiumiodine batter.
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