11/14/24, 10\:41 AM Tetralogy of Fallot

Tetralogy of Fallot

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Tetralogy of Fallot (TOF)\: most common cyanotic congenital heart disease presenting after neonatal period; accounts for
7-10% of all congenital cardiac defects; includes four defects\: ventricular septal defect (VSD), pulmonary stenosis,
overriding aorta, right ventricular hypertrophy.
Genetic associations\:
Down's syndrome (trisomy 21)\: 40% have congenital heart disease, including TOF.
DiGeorge syndrome (22q11.2 deletion)\: cardiac abnormalities, abnormal facies, thymic aplasia/hypoplasia, cleft palate,
hypocalcaemia/hypoparathyroidism.
CHARGE syndrome\: caused by CHD7 mutation; features include coloboma, heart defects, atresia choanae, restricted
growth, ear abnormalities/deafness.
VACTERL association\: vertebral defects, anal atresia, cardiac defects, tracheoesophageal
abnormalities.
Associated congenital defects\: right aortic arch, abnormal coronary artery anatomy, pulmonary atresia, aorticopulmonary
collateral vessels, patent ductus arteriosus, atrioventricular septal defect, atrial defect, absent pulmonary valve.
Pathophysiology\:
Ventricular septal defect\: failure of truncus arteriosus to divide.
Pulmonary stenosis\: narrowing of pathway from right ventricle to pulmonary artery.
Overriding aorta\: aorta enlarged and extends over right ventricle out
Right ventricular hypertrophy\: due to increased afterload.
Risk factors\: family history of congenital heart disease, parental history of TOF or DiGeorge syndrome, foetal exposure to
teratogens (e.g., alcohol, warfarin), poorly controlled maternal diabetes, maternal intake of retinoic acid, congenital rubella
infection, increased maternal age (>40 years).
Clinical features\:
TOF with mild pulmonary stenosis\: asymptomatic at birth, cyanosis develops around 1-3 years.
TOF with pulmonary atresia\: presents within
TOF with absent pulmonary valve\: marked dysplasia and regurgitation of pulmonary valve, presents within
with cyanosis and respiratory distress.
Examination
systolic murmur (pulmonary area), ejection click, single S2, continuous murmur (if patent ductus arteriosus).
Di
Pulmonary Venous Drainage, Hypoplastic Left Heart Syndrome, VSD with Eisenmenger syndrome).
Investigations\:
Bedside\: pulse oximetry, ECG (right axis deviation, right ventricular hypertrophy).
Laboratory\: genetic testing if a syndrome is suspected.
Imaging\: chest X-ray (boot-shaped heart, reduced pulmonary vascular markings), cardiac MRI, cardiac catheterisation.
Management\:
Surgical intervention\: within
Bridging procedures\: Blalock-Taussig shunt, right ventricle to pulmonary artery conduit, pulmonary artery band.
Complete repair\: performed under cardiopulmonary bypass, involves resection of right ventricle out
artery stenosis, VSD closure, possible pulmonary valve repair.
Complications\:
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Post-surgical\: pulmonary regurgitation, right ventricular dilatation, arrhythmias (e.g., ventricular tachycardia, atrial
atrial
Cyanotic ('tet') spells\: sudden episodes of cyanosis and hypoxia; managed by positioning knees to chest, oxygen,
morphine, IV
Other\: heart failure, infective endocarditis, stroke, polycythaemia, cardiac transplant, death.
Prognosis\: 90% of children with repaired TOF survive into adulthood; prognosis depends on severity; lifelong follow-up
required.
Article 🔍
A comprehensive topic overview

Introduction

Tetralogy of Fallot (TOF) is the most common cyanotic congenital heart disease (CHD) presenting after the neonatal
period 1,2 3
. It accounts for between 7% to 10% of all congenital cardiac defects.
The word 'tetralogy' refers to something made up of four parts. Therefore, Tetralogy of Fallot is characterised by four
defects. Three of the defects are anatomical\: ventricular septal defect (VSD), pulmonary stenosis and an overriding aorta.
The fourth defect is a physiological adaptation which is right ventricular hypertrophy.
Tetralogy of Fallot is sometimes referred to as ‘blue baby syndrome ’
.

Aetiology

Causes of Tetralogy of Fallot

There is no single cause for Tetralogy of Fallot. Instead, the development of TOF is multifactorial. However, Tetralogy of
Fallot is associated with various genetic conditions.
Down's syndrome
Down's syndrome (trisomy 21) is a genetic disorder caused by a third copy of chromosome 21.
Down's syndrome causes delays in physical growth, intellectual disability, and characteristic facial features. About 40% of
those with Down's syndrome are born with a form of congenital heart disease. Lesions include Tetralogy of Fallot, atrial
septal defect and ventricular septal defects.
4
DiGeorge syndrome
syndrome.
DiGeorge syndrome is caused by a microdeletion on the long arm of chromosome 22. It is also known as 22q11.2 deletion
DiGeorge syndrome is autosomal dominant and occurs in about 1 in 4000 people.
3
The salient features of DiGeorge syndrome are summarised as CATCH-22\:
Cardiac abnormalities (commonly Tetralogy of Fallot)
Abnormal facies (cleft palate, hypertelorism and short philtrum)
Thymic aplasia/hypoplasia
Cleft palate
Hypocalcaemia/hypoparathyroidism
CHARGE syndrome
CHARGE is a complex syndrome with a wide range of mental and physical disabilities. It is caused by a mutation of CHD7
on chromosome 8 in 80 to 90% of cases. CHARGE syndrome occurs in 1\:10 000 to 1\:15 000 live births.
6
Clinical features of CHARGE syndrome include\:
Colomba
Heart defects
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Atresia choanae (bone blocking the nasal passage which causes di
Restriction of growth and development
Ear abnormalities and deafness
VACTERL association
VACTERL association is a condition that is characterised by the presence of a group of congenital malformations.
7
The exact cause is unknown but microdeletions of the FOX gene cluster at 16q24.1 have been reported to cause VACTERL
associations. 8
It occurs in 1 per 10000 to 40000 live births.
Patients need to have at least three of the following characteristics to make a diagnosis of VACTERL association\:
Vertebral defects
Anal atresia
Cardiac defects
Tracheoesophageal
Renal anomalies
Limb abnormalities
Associated congenital defects
Tetralogy of Fallot can be associated with the presence of other congenital cardiac abnormalities\:
9
Right aortic arch (25%)
Abnormal coronary artery anatomy (5 to 10%)
Pulmonary atresia
Aorticopulmonary collateral vessels
Patent ductus arteriosus
Atrioventricular septal defect
Atrial defect
Absent pulmonary valve

Pathophysiology

There are four components of Tetralogy of Fallot (Figure 1)\:
Ventricular septal defect
Pulmonary artery stenosis
Overriding aorta
Right ventricular hypertrophy
Figure 1. Tetralogy of Fallot diagram.
Development of Tetralogy of Fallot
The development of Tetralogy of Fallot begins in utero and is caused by a single developmental error.
14
Normally, the primitive truncus arteriosus is split in two by the evolving spiral septum. However, in Tetralogy of Fallot, the
truncus arteriosus fails to divide. Therefore, the spiral septum cannot fuse with the growing muscular ventricular septum
causing a ventricular septal defect.
There is narrowing of the pathway from the right ventricle to the pulmonary artery which causes pulmonary artery
stenosis.
In addition, the aortic root is enlarged and extends over the right ventricle out
Finally, right ventricular hypertrophy occurs as a physiological adaptation to increased afterload in the heart. A right-
sided aortic arch, coronary artery abnormalities and additional VSDs are associated abnormalities.
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Fetal circulation
When the fetus is in the womb, its lungs are not in use. This is because circulating blood bypasses the lungs. Fetal blood is
oxygenated at the feto-maternal interface and shunted from the right atrium to the left atrium via the foramen ovale. The
oxygenated blood moves from the left atrium to the left ventricle and into the aorta to the rest of the body.
When deoxygenated blood returns from the foetal body it enters the right atrium and
In an adult, blood would then

The descending aorta connects to the umbilical arteries and the deoxygenated blood
The deoxygenated blood is oxygenated again in the feto-maternal interface at the level of the placenta. The oxygenated
blood travels across the placenta into the foetus’s right atrium. The cycle repeats.
Figure 2. Normal fetal circulation.
Right to left shunt and cyanosis
When a baby takes its
right ventricle. The ductus arteriosus and foramen ovale close as they are not required. The baby’s circulation is now the
same as an adult’s circulation.
However, in Tetralogy of Fallot, this is not the case. Firstly, the ventricular septal defect allows the mixing of oxygenated
and deoxygenated blood.
This means deoxygenated blood enters the aorta and is pumped to the rest of the body. The tissues receive poorly
oxygenated blood resulting in cyanosis.
Secondly, the overriding aorta means that the aortic valve is placed further to the right than normal, above the VSD. The
aorta is also enlarged. When the right ventricle contracts and pumps blood upwards, the aorta is in the direction of travel
of that blood. Therefore, more deoxygenated blood enters the aorta from the right side of the heart.
Thirdly, pulmonary stenosis means there is greater resistance to the
pulmonary artery.
Instead of deoxygenated blood
the aorta. The pulmonary stenosis along with the overriding aorta causes deoxygenated blood to be shunted from the
right to the left side of the heart causing cyanosis.
Fourthly, the right ventricle is pumping blood into the pulmonary artery under great resistance due to pulmonary stenosis,
and due to pressures from the left ventricle being directly transmitted to the right ventricle because of the open VSD. This
puts increased strain on the right ventricle causing right ventricular hypertrophy.
The degree of cyanosis is related to the severity of the pulmonary stenosis.
Figure 3. Comparison of Tetralogy of
Fallot with a normal heart.
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Risk factors

Risk factors for ToF include\:
13
1st-degree family history of congenital heart disease
A parent with Tetralogy of Fallot
A parent with DiGeorge syndrome
Foetal exposure to teratogens in utero (e.g. alcohol, warfarin and trimethadione)
Poorly controlled maternal diabetes
Maternal intake of retinoic acid
Congenital Rubella infection
Increased maternal age (over 40 years old)

Clinical features

Clinical features will vary depending on the subtype of TOF.
There are three major subtypes of TOF\:
15
1. TOF with a milder form of pulmonary stenosis
2. TOF with pulmonary atresia
3. TOF with absent pulmonary valve

TOF with a milder form of pulmonary stenosis

Children born with mild pulmonary stenosis are usually asymptomatic at birth. As the child and the heart grows, the
symptoms develop. Around the age of 1 to 3 years, the child develops cyanosis.

TOF with pulmonary atresia

Children who are born with moderate to severe pulmonary stenosis will present within the
cyanosis and respiratory distress.

TOF with absent pulmonary valve

This is caused by TOF with pulmonary atresia or TOF with an absent pulmonary valve.
In TOF with an absent pulmonary valve, the pulmonary valve is markedly dysplastic and is e
moderate or severe degree. This causes enlargement of the branch pulmonary arteries as well as the right ventricle.
The branch pulmonary arteries enlarge so much sometimes that they may obstruct the tracheal tree and there may be
associated tracheo or bronchomalacia as a result.
The deoxygenated blood can only
respiratory distress within the

Clinical examination

Typical
Central cyanosis
Clubbing (Figure 4)
Respiratory distress
Typical cardiovascular examination may include\:
Thrill
Heave (due to right ventricular hypertrophy)
An ejection systolic murmur loudest in the 2 nd
intercostal space, upper left sternal edge (pulmonary area)
Ejection click due to the closure of the dilated aortic valve in diastole
Single S2 due to closure of the aortic valve in diastole with reduced pulmonary valve closure due to PA stenosis
Continuous murmur at the left upper sternal edge if there is a patent ductus arteriosus
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Figure 4. Digital clubbing with cyanotic
nail beds in an adult with tetralogy of
Fallot

Di

Di
Transposition of the Great Arteries (TGA)
Total anomalous pulmonary venous drainage (TAPVD)
Hypoplastic left heart syndrome (HLHS)
VSD with Eisenmenger syndrome
Cyanotic congenital heart disease\: 6Ts
The '6Ts' can be used to recall the di
Tetralogy of Fallot
Transposition of great arteries
Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid valve abnormalities
Ton of others – hypoplastic left heart, double outlet right ventricle, pulmonary atresia
For more information, see the Geeky Medics guide to congenital heart disease.

Investigations

Many cases of Tetralogy of Fallot are identi
A foetal echocardiogram can be used to identify Tetralogy of Fallot. 16
ventricular septal defect or an overriding aorta on ultrasound.
17
Foetuses with Tetralogy of Fallot can present with a
During a newborn baby check, an ejection systolic murmur caused by pulmonary stenosis may be heard.

Bedside investigations

Relevant bedside investigations include\:
Pulse oximetry
ECG\: to detect heart chamber enlargement and arrhythmia. TOF may present with right axis deviation and right
ventricular hypertrophy

Laboratory investigations

Relevant laboratory investigations include\:
Genetic testing\: if a genetic syndrome is suspected (e.g. Down's syndrome, DiGeorge syndrome)

Imaging investigations

Relevant imaging investigations include\:
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Chest X-ray\: to visualise the structure of the heart and the lungs. Findings may include a boot-shaped heart (due to RVH)
or reduced pulmonary vascular markings (due to reduced pulmonary blood
Cardiac MRI\: used to determine the anatomy of the lesion and the cardiac function
Cardiac catheterisation\: to evaluate the structure and haemodynamic physiology of the heart and help to plan for
surgery. Cardiac catheterisation may also be used to deliver therapy such as stent angioplasty of the ductus arteriosus,
or stent angioplasty to the right ventricular infundibulum in babies who exhibit hypercyanotic spells.

Management

Surgical intervention typically occurs within the
complete repair of the Tetralogy of Fallot.
18
In some infants, a prostaglandin infusion is given to maintain a patent ductus arteriosus. This allows blood to
the aorta back to the pulmonary arteries thereby maintaining the blood
necessary when there is not enough forward

Surgical bridging procedures

Bridging is used in infants who have poor pulmonary artery anatomy or co-morbidities who are not suitable to undergo
surgical repair immediately. Bridging procedures help relieve cyanosis and defers the need for complete surgical repair.
Blalock-Taussig shunt
A Blalock-Taussig (BT) shunt is placed as a form of intermediate management until a complete repair can be conducted.
It allows babies to grow so they are better suited for their complete repair. A BT shunt is usually performed in the
weeks of life.
The BT shunt mimics a patent ductus arteriosus and increases pulmonary blood
performed. There are two ways of performing a BT shunt\:
1. Anastomosis of the subclavian artery to the pulmonary artery\: this allows more blood to be oxygenated by the lungs as
the high-pressure arterial system forces blood through the lungs. It also promotes the growth of the pulmonary arteries
which will make the complete repair easier
2. Modi
There are other forms of bridging including a right ventricle to pulmonary artery conduit (to bypass the right ventricle
out

Surgical repair

The timing of the repair will depend on the severity of the symptoms, but the usual rule is no younger than 3 months and
no older than 4 years. Children must be
The complete repair is performed under cardiopulmonary bypass. A midline sternotomy incision is performed. The right
ventricle out
a patch.
The pulmonary valve may also be repaired (surgeons make an e
called valve preserving surgery).
After surgery children are looked after in a cardiac intensive care unit (CICU).

Complications

Complications of surgical repair

Despite surgical repair of a Tetralogy of Fallot patients can still experience long-term complications.
The most common late complication is signi19
This leads to right ventricular dilatation
and dysfunction. The enlarged right ventricle may interact with the left ventricle and disrupt left ventricular
systolic function.
Some patients can also experience arrhythmias such as ventricular tachycardia, atrial
19
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In addition, pulmonary artery stenosis may persist due to incomplete resection of the obstruction, or it may recur as
muscle bundles in the right ventricular infundibulum hypertrophy over time.

Cyanotic ('tet') spells

A cyanotic or ‘tet’ spell is a complication of an unrepaired Tetralogy of Fallot. A ‘tet’ spell is a sudden episode of profound
cyanosis and hypoxia and can be fatal.
20
They tend to occur in young children between the ages of 2 months and 2 years. During the ‘tet spell’ the child will become
cyanotic, dyspnoeic, and irritable. In severe cases, a ‘tet spell’ can cause reduced consciousness, seizures and potentially
death.
There are several causes of a ‘tet’ spell\:
1. Decrease in oxygen saturations (e.g. crying, or other forms of emotional or physical distress or defecating)
2. Decrease in systemic vascular resistance (e.g. playing)
3. Increase in pulmonary vascular resistance
4. Tachycardia
5. Hypovolaemia
It is thought that an increase in right to left shunting and a fall in arterial oxygen saturations causes a cyanotic spell.
After the initial drop in arterial oxygen saturation, there is an increase in right ventricular out
increase in pulmonary vascular resistance and/or a decrease in systemic resistance.
This creates a vicious cycle which stimulates the respiratory centre. This causes hyperpnea and an increase in adrenergic
tone with circulating catecholamines.
The increase in circulating catecholamines causes increased contractility which leads to increased out
obstruction.
On auscultation of the heart during a tet spell, there will be a reduced/absent murmur due to decreased pulmonary
blood
How to manage a ‘tet spell’
Children with Tetralogy of Fallot will manage a ‘tet spell’ themselves by squatting or bringing their knees to their
chest. Squatting increases the systemic vascular resistance which pushes blood into the pulmonary vessels.
Management should include\:
20
1. Position the child with their knees at their chest
2. Oxygen
3. Morphine\: decreases respiratory drive
4. Intravenous
5. Beta-blockers (propranolol)\: relaxes the right ventricle infundibulum and improves the
pulmonary vessels
6. Phenylephrine infusion\: increases systemic vascular resistance
7. Emergency ventricular out
8. Sodium bicarbonate if there is metabolic acidosis

Arrhythmias

Adults with Tetralogy of Fallot can experience arrhythmias. Atrial and ventricular enlargement as well as the scars caused
by surgical intervention form the substrate for arrhythmias. Atrial and atrial
Sinus rhythm can be restored by medications, catheter ablation or electrical cardioversion. In the case of ventricular
tachyarrhythmias, an implantable cardioverter-de

Other complications

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Other complications of Tetralogy of Fallot include\:
Heart failure
Infective endocarditis
Stroke
Polycythaemia
Cardiac transplant
Death

Prognosis

Around 90% of children with a surgically repaired Tetralogy of Fallot survive into adulthood. 21
Tetralogy of Fallot depends on the severity. Without surgical treatment the prognosis is poor.
However, the prognosis of
Patients with Tetralogy of Fallot require lifelong follow-up (including ECGs, echocardiography and exercise testing). Further
procedures (e.g. stenting for pulmonary stenosis) may be required into adulthood.

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Image references

Figure 1. LadyofHats. T e t r a l o g y o f F a l l o t . License\: [Public domain]
Figure 2. OpenStax. F e t a l C i r c u l a t o r y S y s t e m . License\: [CC BY]
Figure 3. LadyofHats. B l u e b a b y s y n d r o m e . License\: [Public domain]
Figure 4.Herbert L. Fred, MD and Hendrik A. van Dijk. D i g i t a l c l u b b i n g w i t h c y a n o t i c n a i l b e d s i n a n a d u l t w i t h t e t r a l o gy o f
F a l l o t . License\: [CC BY-SA]
in

Reviewer

Dr Gruschen Veldtman
Consultant in Adult Congenital Cardiology

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Contents

Introduction
Aetiology
Risk factors
Clinical features
Di
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