Supraventricular Tachycardia

(SVT)

MUHAMMAD ALI

Supraventricular Tachycardia (SVT)

SVT is characterized by rapid heart rates, usually 200 to
300 beats/minute, with a QRS complex of normal
duration
Cardiovascular emergency in infant and children
The incidence: 1/25,000-1/250
Early detection and prompt treatment important
Congestive heart failure
Circulatory arrest

Mechanism of SVT

Mechanism of SVT
Automaticity
Reentry

Mechanism of SVT
Automaticity
Acceleration of phase 4
Source:
Atrium
AV junction
His bundle
Ventricle
Pulmonary vein
SVC

Cause

Metabolic disorder
Hypoxia
Hypokalemia
Hypo magnesemia
acidosis

Mechanism of SVT
Reentry
Condition
Two pathway
make closed
circuit
Block in 1
pathway
Antegrad in
normal
conduction
retrograd in
block
pathway

Mechanism of SVT

 The episodes usually start and end abruptly

Wolff-Parkinson-White (WPW) syndrome is
responsible for about 50% of SVT in neonates
Structural heart diseases (such as Ebstein's
Anomaly, Tricuspid Atresia, and cardiac tumors)
are less frequent causes of SVT in neonates
Viral myocarditis and thyrotoxicosis also have
been associated with SVT

Short episodes of tachycardia usually do not harm the patient

Newborns with sustained SVT become restless and

tachypneic with feeding difficulties and eventually develop
signs of CHF and circulatory shock within 12 to 24 hours
after onset
Although rare, SVT diagnosed in utero may present with
severe CHF at birth and has a high mortality rate, requiring
prenatal treatment

Treatment
Adenosine is the treatment of choice, followed by
digitalization
Adenosine is given in a rapid intravenous bolus, starting at
50 g/kg, every 1 to 2 minutes (maximum, 250 g/kg)

If the patient is unresponsive to adenosine and is in CHF,

cardioversion may be performed, followed by digitalization
and diuretics

In SVT of short duration without signs of CHF, digoxin alone

is used

An ice bag applied to the face has been effective in some

neonates

 Vagal stimulatory maneuvers rarely are effective

in neonates
Transesophageal atrial overdrive stimulation
may prove effective
Verapamil and propranolol are not the drugs of
choice
Tried only when other measures fail, and may
produce extreme bradycardia and hypotension
in a newborn; one should administer these drugs
in a step-by-step dosage, monitor the infant
carefully, and be prepared to resuscitate

Short-Term management
of SVT

Delacretaz. NEJM 2006;354:1039-51

ATRIAL FLUTTER
&
ATRIAL FIBRILLATION

MUHAMMAD ALI
PEDIATRIC CARDIOLOGY

ATRIAL
FLUTTER
Description
The pacemaker lies in an 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
beats/minute, a ventricular response with varying
degrees of block (e.g., 2:1, 3:1, 4:1), and normal QRS
complexes

Causes
Possible causes are structural heart disease with dilated
atria, myocarditis, previous surgery involving atria (the
Mustard or Senning procedure, Fontan operation, or
atrial septal defect repair), and digitalis toxicity
Significance
The ventricular rate determines eventual cardiac output;
a too-rapid ventricular rate may decrease cardiac output.
Atrial flutter usually suggests a significant cardiac
pathology.

Management
Digitalization is provided if the arrhythmia is not the result of digitalis
toxicity; digitalis increases the AV block and thereby slows the
ventricular rate. Propranolol (1 to 4 mg/kg per day orally in three or
four doses) may be added to digoxin
Recent reports suggest that amiodarone may be more effective than
digoxin in treating atrial flutter. One can start with a trial of digoxin
and, if digoxin fails, progress to amiodarone
Electric cardioversion may be required. Digitalis should be
discontinued for at least 48 hours before cardioversion.
Anticoagulation with warfarin is recommended before cardioversion
to prevent embolization
Rapid atrial pacing with a catheter in the esophagus or the right
atrium can be effective when cardioversion is contraindicated (e.g.,
digitalized patients)
Quinidine may prevent recurrence.

ATRIAL
FIBRILLATION
Description
The mechanism of this arrhythmia is circus movement,
as in atrial flutter. Atrial fibrillation is characterized by an
extremely fast atrial rate (f wave at a rate of 350 to 600
beats/minute) and an irregularly irregular ventricular
response with normal QRS complexes

Causes
Atrial fibrillation usually is associated with structural heart
disease, including dilated atria; myocarditis; digitalis
toxicity; or previous intra-atrial surgery
Significance
The rapid ventricular rate, in addition to the loss of
coordinated contraction of the atria and ventricles,
decreases the cardiac output, as occurs in atrial
tachycardia.
Atrial fibrillation usually suggests a significant cardiac
pathology.

Management
AF > 48 hours, anticoagulation warfarin for 3 weeks to prevent
systemic embolization of atrial thrombus. Anticoagulation is continued
for 4 weeks after the restoration of sinus rhythm. If cardioversion
cannot be delayed, heparin should be started, with subsequent oral
anticoagulation
Digoxin is provided to slow the ventricular rate. Propranolol (1 to 4
mg/kg per day orally in three or four doses) may be added
As a pharmacologic means of conversion, class I antiarrhythmic
agents (e.g., quinidine, procainamide, flecainide) and the class III
agent amiodarone may be used
In patients with chronic atrial fibrillation, anticoagulation with warfarin
should be considered to reduce the incidence of thromboembolism
Quinidine may prevent recurrence.

Congestiv
e Heart
Failure

MUHAMMAD ALI
PEDIATRIC CARDIOLOGY
DIVISION

Definition
Congestive heart failure (CHF) is a clinical syndrome in
which the heart is unable to pump enough blood to the
body to meet its needs, to dispose of venous return
adequately, or a combination of the two.

Cause
CHF may result from congenital or acquired
heart diseases with volume and/or pressure
overload or from myocardial insufficiency.

CONGENITAL HEART DISEASE

CHD with volume or pressure overload is the most
common cause of CHF in the pediatric age group.
Volume overload lesions, such as VSD, PDA and ECD,
are the most common causes of CHF in the first 6
months of life.
Children with TOF do not develop CHF unless they
have received a large aortatopulmonary artery
(PA) shunt procedure (such as the Waterston or
Potts operation), which is no longer performed.

 ASD rarely causes CHF in the pediatric age group,

although it causes CHF in adulthood.
Large L-R shunt lesions, such as VSD and PDA, do not
cause CHF before 6 to 8 weeks of age because the
PVR does not fall low enough to cause a large left-toright shunt until this age.

The onset of CHF resulting from L-R shunt lesions

may be earlier in premature infants (within the first
month) because of an earlier fall in the PVR in these
infants.

ACQUIRED HEART DISEASE

Metabolic abnormalities (severe hypoxia and acidosis,
hypoglycemia and hypocalcemia)
Endocardial fibroelastosis
Viral myocarditis
Acute rheumatic carditis
Rheumatic valvular heart diseases
Dilated cardiomyopathy
Cardiomyopathies associated with muscular dystrophy
and Friedreich's ataxia
Doxorubicin cardiomyopathy

MISCELLANEOUS CAUSES

Supraventricular Tachycardia (SVT)

Complete heart block
Severe anemia
Acute hypertension
Bronchopulmonary dysplasia
Acute cor pulmonale caused by acute airway
obstruction

Physical Examination
The following are compensatory responses to impaired cardiac
function:
Tachycardia, gallop rhythm, and weak and thready pulse
Cardiomegaly
There are signs of increased sympathetic discharges (e.g.,
growth failure; perspiration; cold, wet skin).
Pulmonary venous congestion (left-sided failure) results in the
following:
Tachypnea is common.
Dyspnea on exertion (poor feeding in small infants) is
common.
Orthopnea
Wheezing and pulmonary crackles

.Systemic venous congestion (right-sided

failure) results in the following:

- Hepatomegaly
- Puffy eyelids
- Distended neck veins and ankle edema
- Splenomegaly

X-ray Studies
The presence of cardiomegaly should be
demonstrated by chest x-ray films. The absence of
cardiomegaly almost rules out the diagnosis of CHF
Electrocardiography
ECGs help determine the type of defect but are not
helpful in deciding whether CHF is present
Echocardiography
Echo may confirm an enlarged chamber or impaired
left ventricle (LV) function (decreased fractional
shortening or ejection fraction, increased left
preejection period/left ventricular ejection time).

Management
The treatment of CHF consists of:
(1) elimination of the underlying causes
(2) elimination of the precipitating or contributing
causes (e.g., infection, anemia, arrhythmias, fever)
(3) control of heart failure state by the use of multiple
drugs, usually inotropic agents, diuretics, and
afterload-reducing agents.

GENERAL MEASURES
A cardiac chair or infant seat is used to relieve respiratory
distress
Oxygen (40% to 50%) with humidity is administered to infants
with respiratory distress
Sedation with morphine sulfate (0.1 to 0.2 mg/kg per dose
subcutaneously every 4 hours as needed) or phenobarbital (2 to 3
mg/kg per dose by mouth or intramuscularly every 8 hours as
necessary)
In older children, salt restriction (<0.5 g/day) and avoidance of
salty snacks (chips, pretzels) and table salt are recommended
Daily weight measurement
Predisposing factors, such as fever, anemia, and infection, are
eliminated
Underlying causes such as hypertension, arrhythmias, and
thyrotoxicosis are treated.

DRUG THERAPY
Three major classes of drugs are used in the treatment of CHF
in children: inotropic agents, diuretics, and afterload-reducing
agents.
Rapidly acting inotropic agents (dopamine, dobutamine) are used
in critically or acutely ill infants and children.
Digoxin is used in all noncritically ill patients. The use of digoxin
is contraindicated in hypertrophic cardiomyopathy, complete
heart block, or cardiac tamponade.
Diuretics are almost always used with inotropic agents.
Afterload-reducing agents have gained popularity because they
can increase cardiac output without increasing myocardial
oxygen consumption.

HEART
TAMPONADE

MUHAMMAD ALI
PEDIATRIC CARDIOLOGY
DIVISION

BLOOD

BLOOD
CLOTH

GAS

HEART TAMPONADE

EFFUSION
FLUID

PUS

DECREASE OF VENTRICULAR FILLING

HAEMODYNAMIC PROBLEMS
LIFE TREATENING

RAPID RESPONS
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ETILOGY:
-MALIGNANCY 30% 60%

-UREMIA 10% 15%

- IDIOPATIC PERICARDITIS 5% 15%
-INFECTION 5% 10%

-SIGN & SIMPTOM:

-DYSPNEA

-CHEST PAIN
-DISTANT / MUFFLE HEART SOUNDS
-PERICARDIAL FRICTION RUB
-TACHYCARDIA
-TACHYPNEA
-PERIPHERAL VASOCONTRICTION

40

 CHEST X-RAY: CARDIOMEGALY WATER BOTTLE

ECG: TACHYCARDIA, LOW QRS VOLTAGE

ECHOCARDIOGRAM: CONFIRM PERICARDIAL
EFFUSION & THE SIZE OF THE EFFUSION
PERICARDIAL TAP: CONFIRM THE DIAGNOSIS OF
MALIGNANT EFFUSION / TO DIFFERENTIATE IT FROM
OTHER CAUSES OF PERICARDIAL EFFUSION

-TREATMENT
-PERCUTANEOUS
PERICARDIOCENTESIS

-SURGICAL TUBE
DRAINAGE

42

COMPLICATIONS:
-HEART LASERATION
-CORONARY OR LUNG LASERATION
-PNEUMOTORAX
-SUDDENT DEATH

THANK YOU

GAMBAR OPERASI PERICARDIAL WINDOW

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