5. Lead II has the most positive deflection compared to leads I and III Lead III has the most positive deflection and lead I should be negative
•Lead I has
the most positive deflection.
•Leads II and III are negative.
6.
7.
8. Width can be described as NARROW (< 0.12 seconds) or BROAD (> 0.12
seconds):
9. ST-elevation is significant when it is greater than 1 mm (1 small square) in 2 or
more contiguous limb leads or >2mm in 2 or more chest leads
ST depression ≥ 0.5 mm in ≥ 2 contiguous
leads indicates myocardial ischaemia
10.
11. Normal Sinus Rhythm and Sinus Node
Dysfunction
Sinus node small, epicardial structure, at the posterior junction of the superior
vena cava and right atrium.
Balance of sympathetic and parasympathetic inputs determines the underlying
heart rate at any given moment
With normal cardiac anatomy, sinus bradycardia or sinus tachycardia are usually
physiologic findings
in newborns, the resting heart rate is typically 90 and 160 bpm, with intermittent
decreases to as low as 70 bpm during rest or sleep
12. Sinus bradycardia
<60 bpm (valid for infants and childrens)
Generally physiologic
Can be secondary to increased vagal tone
Increased intracranial pressure,
an acute abdominal process (e.g., necrotizing enterocolitis),
suctioning of an endotracheal tube,
gastric reflux,
apnea of prematurity, or
medications
13. Evaluation
1. Electrocardiogram (ECG) to evaluate for
atrioventricular (AV) block
any cardiac channelopathy
24-hour cardio scan monitor (Holter) to evaluate the infant’s heart rate variability
Rarely used - a vagal nerve antagonist Atropine administration
Increased HR bradycardia is secondary to vagotonia
minimal or no heart rate increase primary sinus node dysfunction.
14. Treatment
Rarely required
Cases of episodic bradycardia to be evaluated.
If no hemodynamic compromise no intervention
If persistent hemodynamically significant Very rare, but pacemaker may be placed
15. Sinus tachycardia
sinus rate above 160-180 bpm
physiologic response to anemia, hyperthyroidism, fever, agitation, infection, or
medications
rarely - primary cardiac etiology ( cause leading to myocarditis).
important to differiantiate from supraventricular tachycardia (SVT).
16. findings that suggest a pathologic mechanism
1. The lack of heart rate variability
2. Abnormal P-wave morphology or axis (normally upright in leads I and aVF) on ECG
3. Prolongation of PR interval
4. Very rapid increases or decreases in heart rate
5. Abnormal cardiac function on echocardiogram
17. Evaluation
ECG to rule out pathologic arrhythmia
24-hour Holter
Treatment
treat the underlying cause
Note - Neonates with high resting heart rates generally do not require any
treatment but should be closely evaluated to make sure they do not have a
secondary cause such as infection or anemia
18. Sinus Arrhythmia
a/k/a respiratory sinus arrhythmia
phasic variations in heart rate seen with an increase in heart rate during inspiration
and a decrease in heart rate with expiration
by the so-called Bainbridge reflex (baroreceptor reflex)
Appropriate ECG interpretation is helpful if the diagnosis is in question
variation in the rate
no change in the appearance of the P-wave morphology or axis
no treatment or follow-up required.
19.
20. Arrhythmias
Arrhythmias in the neonatal period are not uncommon
A normal heart or in with structural heart disease
incidence of neonatal arrhythmia is 1%–5% in all neonates
Congenital heart disease (CHD) not only affects the anatomical defect but also
causes electrical changes, that induce various arrhythmias.
Surgical correction may also be related to the cause of arrhythmia in patients with
CHD.
21. Classification
Classified as either benign or non benign.
Benign arrhythmias
sinus arrhythmia, premature atrial contraction (PAC), premature ventricular contraction
(PVC), and junctional rhythm;
these arrhythmias have no clinical significance and do not need therapy.
Non-benign arrhythmias
Supraventricular tachycardia (SVT), ventricular tachycardia (VT), atrioventricular (AV)
conduction abnormalities, and genetic arrhythmias such as congenital long-QT
syndrome (LQTS)
24. 1. Premature Atrial Contractions
Common in the neonatal period and manifest as irregular heartbeats.
Types Of PAC
A premature P wave superimposed on the previous T wave can cause deformation of the
T wave.
Nonconduction of PACs can sometimes occur and be misdiagnosed as sinus
bradycardia in neonatal intensive care units.
the aberrant conduction of PACs causes a different QRS morphology
Isolated PACs in neonates are associated with electrolyte abnormalities,
hypoglycemia, hypoxia, and hyperthyroidism.
PACs are generally benign and usually do not need treatment
25. Premature
Atrial
Contraction
Conducted
Not
conducted
Aberrantly
conducted
• Usually happens
• P wave followed by
normal looking QRS
wave
• a/k/a “blocked” PAC
• AV node or bundle of
His is refractory
• P wave not followed
by QRS
• clinically bradycardia
• If either the right or left
bundle branch is
refractory
• P wave will be followed
by a wide QRS
(aberrant ventricular
conduction).
26.
27. 2. Atrial Ectopic Tachycardia
Three or more consecutive PACs and rate >120 beats per minute
increased automaticity of atrial myocardium (abnormal firing foci)
Direct stimulation - arterial catheter with the tip in the atrium
On ecg – different P-wave morphology
Evaluation
ECG and Holter monitoring
2d echo to rule out CHD
Electrolyte Disturbances - should be corrected
28. Treatment
Medications
beta blockers (propranolol),
sodium channel blockers (flecainide)
class III antiarrhythmic medications (sotalol, amiodarone).
Spontaneous resolution - in the first 6 months
refractory atrial tachycardia Cardiac - Radiofrequency ablation (RFA)
29. 3. Atrial Flutter
a/k/a atrial reentry tachycardia.
the circuit for reentry is myocardium around tricuspid valve
typical atrial rate b/w 300 and 600 beats per minute
ventricular rate much less decremental properties of the AV node
conduction to the ventricles is in ratio 2 : 1, 3 : 1, or 4 : 1
Evalution
ECG - continuous sawtooth pattern (adenosine administerd sometimes for easy
identification of the sawtooth pattern
P waves are masked by QRS complexes or T waves.
31. 4. Atrial Fibrillation
Exceptionally rare dysrhythmia
A/w –
severe structural congenital heart disease (such as Ebstein anomaly of the tricuspid valve)
an accessory pathway (Wolff-Parkinson- White)
cardiac channelopathies
ECG - Irregular tachycardia with disorganized atrial activity
Distinguish from Chaotic atrial tachycardia (or multifocal atrial tachycardia)
Treatment –
synchronized cardioversion
Pediatric cardiology consultation should be obtained
32. 5. Chaotic atrial tachycardia
a/k/a multifocal atrial tachycardia
ECG - irregular tachycardia with disorganized atrial activity (Same as Afib)
Occur in short bursts with sinus beats interspersed
May or may not respond to cardioversion
medical treatment with antiarrhythmic medications needed (alone or in
combinations)
beta blockers
flecainide,
sotalol
amiodarone,
34. Most common form of SVT in neonates
Mechanism –
two distinct conducting pathways linked around an area of nonconducting tissue.
Failure to conduct in one of these pathways (block) causes the impulse to turn around in
the other pathway, creating an electrical loop that causes tachycardia reentrant
mechanisms
Pathways
1. Accessory pathway (m/c) (Manifest OR Concealed)
2. Through atrioventricular node a/k/a atrioventricular nodal reentry tachycardia
35. Accessory Pathway
accessory pathway additional conduction pathway
Conduction
Bidirectional
Unidirectional – Antegrade Atria to ventricle OR Retrograde Ventricle to atria
Retrograde conducting accessory pathway
a/k/a concealed accessory pathway
baseline ECG will appear normal
Antegrade conducting cessory pathway
manifest accessory pathway
preexcitation on the baseline ECG (Wolff-Parkinson- White).
36.
37. Wolff-Parkinson- White
Antegrade conducting acessory pathway
ECG - delta wave short PR interval and widened QRS complex
normal physiologic delay does not exist with accessory pathway and ventricular
myocardium activates before it would normally be activated resulting in a delta
wave on the ECG
A/w underlying structural heart disease (most commonly Ebstein anomaly)
atrial fibrillation as wide complex tachycardia or sudden cardiac death
Adenosine should be used in a very controlled environment
digoxin relatively contraindicated
38.
39.
40. Presentation
rapid increase in heart rate (Any Sinus rate > 220 bpm – possibility)
Ventricular rates - 200 -300 bpm
Narrow complex tachycardia on ECG.
Some times - wide complex tachycardia (a/w left bundle branch block)
Persistent tachycardia can cause depressed myocardial function
a/w generalized symptoms - poor feeding and irritability
tachycardia with preexcitation on ECG – s/o WPW
41.
42. Treatment
Consider - hemodynamically stable or unstable
Anticipate - intubation, cardioversion, and resuscitation
adenosine or direct current cardioversion.
intravenous pressors and even ECMO can be needed
cardioversion - 0.5 and 1 joule per kilogram (larger doses may be required)
If QRS complex generating a pulse - synchronized cardioversion
43. First line –
vagal stimulation
small bag or glove filled with ice over the entire face for 10-15 seconds)
Holding a child upside down
Gagging, ocular pressure, and anal stimulation should be avoided
adenosine administration
IV adenosine (dose is 0.1 mg/kg per dose, if the arrhythmia persists, then 0.2 mg/kg per dose)
rapid IV push followed by a 5-10 cc bolus normal saline
IV amiodarone refractory cases of SVT (as per pediatric cardiologist)
Second-line
sotalol, flecainide, or amiodarone (only under pediatric cardiologist recommendation)
44.
45.
46.
47. Long term –
60%-80% resolve spontaneously within the first year of life
Beta blockers (propranolol 1 mg/ kg /dose Q 6 H)
cardiac catheterization and ablation drug-refractory tachycardias
Digoxin (fetal tachycardias 4-5 μg/kg per dose given twice a day)
48. Junctional reciprocating tachycardia
(PJRT)
Tachycardia present immediately after birth
P waves before each QRS complex, which may be mistaken for sinus rhythm
deeply negative clearly visible P waves in the inferior leads II, III, and aVF
tachycardia-induced cardiomyopathy if left untreated
spontaneous termination or spontaneous reinitiation
Treatment
antiarrhythmics.
Flecainide - treatment of choice
an ablation if does not resolve
49.
50. Junctional Ectopic Tachycardia
Increased automaticity is focus of tachycardia present in
bundle of His (most commonly)
proximal bundle branches (very rarely)
On ECG - tachycardia with no association b/w P waves & QRS complexes (VA
dissociation),
Ventricular(narrow QRS) rate being faster than the atrial rate.
51. Acquired JET
Commonly after cardiac surgeries for CHDs
Mechanism - swelling/edema, electrolyte imbalances, catecholamine surges,
vasopressors
resolves within 3-5 days after surgical repair
heart rate in range of 150-170
hemodynamically stable
no specific treatment
hemodynamically unstable
Treat fever and/or cool the patient.
Decrease/wean all catecholamines.
Initiate atrial pacing at rates faster than the JET rate to restore AV synchrony.
Administer amiodarone or procainamide intravenously for at least 48 hours.
52. Congenital JET
Rare
life-threatening tachycardia in fetuses, neonates, and infants less than 6 months
tachycardia-induced cardiomyopathy
mortality rate of greater than 50%
Usually not respond to any form of intervention
Conservative
remove additional catecholamines
initiate amiodarone or procainamide
Adenosine - minimal response to tachycardia, used for AV disassociation
55. Premature ventricular contractions
Relatively uncommon compared with PACs
On ECG
No preceding P wave
different morphology of premature QRS complex
Common causes CHD, cardiomyopathy, inflammatory myocardial disease, metabolic
disease, electrolyte disturbance and LQTS
frequent PVCs are defined as >60 beats/hr in a child
Causes of frequent PVCs immaturity of cardiac conduction tissue and autonomic
nerve system
Isolated PVCs usually resolve spontaneously, and no treatment is required a normal
heart
asymptomatic frequent PVCs in newborns have a good long-term prognosis
56.
57. Ventricular tachycardia (VT)
When rhythm disturbance is below the bifurcation of bundle of His
Typical - wide complex rhythm (QRS > 80 ms)
Ventricular tachycardia rhythm – Bening Form
idioventricular rhythm (accelerated ventricular rhythm)
rate no more than 20% faster than the underlying sinus rate
patient is asymptomatic and hemodynamically stable
requires no intervention
58. Structurally normal hearts
Automatic focus is cause
the outflow tract (RV Outflow is m/c) or one of the fascicles in the left ventricle
Cardiac tumors or myocardial hamartomas
rare, causes
extremely difficult to control with medications
May require surgical resection.
poor ventricular function
myocarditis / structural cardiac disease
59.
60. Treatment
Idioventricular rhythm and Asymptomatic
no therapy required
normal ventricular function
beta blockers (propranolol)
flecainide, sotalol or amiodarone
Decreased ventricular function
rapid control - important
IV Amiodarone or sotalol
61. Long-term therapy
Many resolve spontaneously (in first several months)
refractory tachycardia
Radiofrequency ablation
Hamartoma or tumor
surgical excision
poor ventricular function
Implantable cardioverter-defibrillator (ICD) therapy
62. Genetic Arrhythmia Syndromes
Inherited disorders causing cardiac dysrhythmias and even death
Channelopathies (m/c)
Disruptions in myocardial ion channels (e.g., sodium, potassium, calcium)
altered electrical depolarization and repolarization
atrial and/or ventricular arrhythmias.
Examples of channelopathies
long QT syndrome (major culprit)
catecholaminergic polymorphic ventricular tachycardia (CPVT),
Brugada syndrome
short QT syndrome
63. Long QT Syndrome
ECG - prolongation of the corrected QT interval (QTc)
torsades de pointes - lethal form of cardiac arrhythmias
polymorphic ventricular tachyarrhythmia
leading ventricular fibrillation sudden death
Pathophysiology
reduced cardiac output during the arrhythmia brain hypoperfusion true seizures
(recurrent syncopal episodes or seizure episodes )
64. Inherited Types are LQT1, LQT2, and LQT3 syndromes
Other causes
Drug Induced (methadone, erythromycin, albuterol, etc.)
Can cause lifethreatening ventricular arrhythmias (esp. if QTc is >500 msec)
Electrolyte disturbances (hypocalcemia, hypokalemia)
65. LQTS presentation
incidentally on an ECG
pseudo or pure AV block (QT interval must be evaluated)
As ventricular arrhythmias
Sudden death (SIDS)
Torsades de pointes (LQTS should be suspected)
66. Evaluation
Measured in leads II and V5 on the ECG
If QTc intervals between 450 and 500 msec (Normal < 450 msec
67. Treatment
avoid QTc prolonging medications
Start nonselective beta blocker (typically nadolol or propranolol)
Pediatric cardiologist consultation
Pacing if AV block caused by LQTS
Sympathectomy (new modality)
Treatment of Torsades de Pointes
Discontinue any potential offending drug. Avoid amiodarone
Magnesium bolus and continuous infusion
Isoproterenol can be used if magnesium is unsuccessful.
72. Supraventricular tachycardia (SVT), a tachyarrhythmia that originates proximal to
the bundle of His, can occur in infants who have underlying congenital heart
defects. Of the following, the most common congenital heart disease that
predisposes to SVT is:
A. Coarctation of the aorta.
B. Ebstein anomaly of the tricuspid valve.
C. Pulmonary atresia with intact ventricular septum.
D. Tetralogy of Fallot.
E. Total anomalous pulmonary venous return.
73. A term newborn has recurrent episodes of tachycardia that began at 12 hours of
age. During one such episode, the heart rate is 280 beats/min.
Electrocardiography reveals inverted P waves, most of which follow QRS
complexes; normal QRS pattern; and P-R intervals that exceed R-P intervals. The
infant is hemodynamically stable, has no echocardiographic evidence of congenital
heart disease, and has no indwelling vascular catheters. Vagal maneuvers and
intravenous adenosine are unsuccessful in restoring normal heart rhythm. Of the
following, the next pharmacologic agent recommended, according to the algorithm
for management of neonatal supraventricular tachycardia, is:
A. Amiodarone.
B. Digoxin.
C. Esmolol.
D. Procainamide.
E. Propafenone
74. In neonatal cases of supraventricular tachycardia nonresponsive to a single
pharmacologic agent, a combination of medications may be tried. Of the following,
the combination of medications most successful in controlling refractory
supraventricular tachycardias is:
A. Amiodarone and propranolol.
B. Digoxin and amiodarone.
C. Digoxin and propranolol.
D. Flecainide and amiodarone.
E. Flecainide and sotalol.
75. Take Home Message
Neonates can experience all forms of arrhythmias
Atrial flutter common in newborns, treatment is synchronized cardioversion.
supraventricular tachycardia IV adenosine is treatment of choice
60 – 80 % supraventricular tachycardias resolve by 1 year of age