Seminar

On
“Acynotic Heart Disease”

Submitted to: Submitted by:

Submitted on – 09 / 01 / 20

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Name of the Institution : Institute of Liver and Biliary Sciences

Title of the Seminar Topic : Bronchial Asthma

Subject : Clinical Speciality I

Name of the Supervisor : Ms Sarita Ahwal

Group : 1st year M.Sc Nursing

Date and Time :

AV Aids : Power point slides

General objective :

At the end of the class, the students will be able to acquire knowledge on “Bronchial
Asthma” and will be able to apply this knowledge in their day to day teaching practices.

Specific objective :

At the end of the class, the students will be able to

 Describe the anatomy and physiology of respiratory system

 Define bronchial asthma
 Discuss prevalence and epidermiology of bronchial asthma
 Enlist the risk factors and triggers involved in bronchial asthma
 Explain the etiological factors of bronchial asthma
 Discuss the pathogenesis of bronchial asthma
 Explain the pathophysiology of bronchial asthma
 Enumerate the clinical manifestations of bronchial asthma
 Discuss the investigations done for diagnosing bronchial asthma
 Explain the medical management of bronchial asthma, acute severe asthma
 Discuss the nursing management of bronchial asthma
 Discuss its prevention and prognosis
 Summerization
 Conclusion of the topic “Bronchial asthma”.

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TABLE OF CONTENT

LIST OF TABLES

LIST OF FIGURES / DIAGRAMS

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ACYNOTIC HEART DISEASE

INTRODUCTIONl
Acynotic heart defects are congenital cardiac malformations that affect the atrial or
ventricular walls, heart valves, or large blood vessels. Common causes include genetic
defects (e.g., trisomies), maternal infections (e.g, rubella), or maternal consumption of drugs
or alcohol during pregnancy. In these, blood is shunted from the left side of the heart to the
right side of the heart due to a structural defect in the interventricular septum.

ANATOMY AND PHYSIOLOGY OF HEART

EMBRYOLOGY DEVELOPMENT OF HEART

 In human embryos the heart begins to beat at about 22-23 days, with blood flow
beginning in the 4th week.

 The heart begins very early in mesoderm within the trilaminar embryonic disc.

 The heart forms initially in the embryonic disc as a simple paired tube inside the
forming pericardial cavity, which when the disc folds, gets carried into the correct
anatomical position in the chest cavity.

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EARLY DEVELOPMENT
1. Endocardial tubes

 By day 19, an endocardial tube begins to develop in each side of this region.
 These two tubes grow and by the third week have converged towards each other to
merge, using programmed cell death to form a single tube, the tubular heart.
 From splanchnopleuric mesenchyme, the cardiogenic region develops cranially and
laterally to the neural plate.
 In this area, two separate angiogenic cell clusters form on either side and coalesce to
form the endocardial tubes.
 As embryonic folding continues, the two endocardial tubes are pushed into the
thoracic cavity, where they begin to fuse together, and this is completed at about 22
days.
 At around 18 to 19 days after fertilisation, the heart begins to form.
 This early development is critical for subsequent embryonic and prenatal
development.
 The heart is the first functional organ to develop and starts to beat and pump blood at
around day 21 or 22.
 The truncus arteriosus will divide to form the aorta and pulmonary artery; the
bulbuscordis will develop into the right ventricle; the primitive ventricle will form the
left ventricle; the primitive atrium will become the front parts of the left and right
atria and their appendages, and the sinus venosus will develop into the posterior part
of the right atrium, the sinoatrial node and the coronary sinus.
 The two tubes migrate together and fuse to form a single primitive heart tube, the
tubular heart which quickly forms five distinct regions.
 From head to tail, these are the truncusarteriosus, bulbuscordis, primitive ventricle,
primitive atrium, and the sinus venosus.

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2. Heart tube position

 The heart and the pericardial cavity move first to the cervical region and then into the
chest.
 The curved portion of the horseshoe-shaped area expands to form the future
ventricular infundibulum and the ventricular regions, as the heart tube continues to
expand.
 The tube starts receiving venous drainage in its caudal pole and will pump blood out
of the first aortic arch and into the dorsal aorta through its polar head.
 Initially the tube remains attached to the dorsal part of the pericardial cavity by a
mesodermal tissue fold called the dorsal mesoderm.
 This mesoderm disappears to form the two pericardial sinuses the transverse and the
oblique pericardial sinuses, which connect both sides of the pericardial cavity.
 The myocardium thickens and secretes a thick layer of rich extracellular matrix
containing hyaluronic acid which separates the endothelium.
 Then mesothelial cells form the pericardium and migrate to form most of the
epicardium.
 Then the heart tube is formed by the endocardium, which is the inner endothelial
lining of the heart, and the myocardial muscle wall which is the epicardium that
covers the outside of the tube.

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3. Heart folding

 The heart tube continues stretching and by day 23, in a process called morphogenesis,
cardiac looping begins.
 The cephalic portion curves in a frontal clockwise direction.
 The atrial portion starts moving in a cephalic ally and then moves to the left from its
original position.
 This curved shape approaches the heart and finishes its growth on day 28.
 The conduit forms the atrial and ventricular junctions which connect the common
atrium and the common ventricle in the early embryo.
 The arterial bulb forms the trabecular portion of the right ventricle.
 A cone will form the infundibula blood of both ventricles.
 The arterial trunk and the roots will form the proximal portion of the aorta and the
pulmonary artery.
 The junction between the ventricle and the arterial bulb will be called the primary
intra-ventricular hole.
 The tube is divided into cardiac regions along its craniocaudal axis: the primitive
ventricle, called primitive left ventricle, and the trabecular proximal arterial bulb,
called the primitive right ventricle.
 This time no septum is present in heart.

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4. Heart chambers

 In the middle of the fourth week, the sinus venosus receives venous blood from the
poles of right and left sinus.
 Each pole receives blood from three major veins: the vitelline vein, the umbilical vein
and the common cardinal vein.
 The sinus opening moves clockwise.
 This movement is caused mainly by the left to right shunt of blood, which occurs in
the venous system during the fourth and fifth week of development.
 When the left common cardinal vein disappears in the tenth week only the oblique
vein of the left atrium and the coronary sinus remain.
 The right pole joins the right atrium to form the wall portion of the right atrium.
 The right and left venous valves fuse and form a peak known as the septum spurium.
 At the beginning, these valves are large, but over time the left venous valve and the
septum spurium fuse with the developing atrial septum.
 The upper right venous valve disappears, while the bottom venous valve evolves into
the inferior valve of the vena cava and the coronary sinus valve.

5. Heart wall
 The main walls of the heart are formed between day 27 and 37 of the development of
the early embryo.
 The growth consists of two tissue masses actively growing that approach one another
until they merge and split light into two separate conduits.
 Tissue masses called endocardial cushions develop into atrioventricular and
conotroncal regions.

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  In these places, the cushions will help in the formation of auricular septum,
ventricular conduits, atrio-ventricular valves and aortic and pulmonary channels.

Atria

 At the end of the fourth week, a crest grows that leaves the cephalic part.
 This crest is the first part of the septum primumWhen the right of the atrium expands
due to the incorporation of the pole of the sinus, a new fold appears, called the septum
secundum.
 At its right side it is fused with the left venous valve and the septum spurium.
 A free opening will then appear, called the foramen ovale.
 The remains of the upper septum primum, will become the valves of the foramen
ovale.
 The passage between the two atrial chambers consists of a long oblique slit through
which blood flows from the right atrium to the left

Ventricles

 Initially, a single pulmonary vein develops in the form of a bulge in the back wall of
the left atrium.
 This vein will connect with the veins of the developing lung buds.
 As development proceeds the pulmonary vein and its branches are incorporated into
the left atrium and they both form the smooth wall of the atrium.
 The embryonic left atrium remains as the trabecular left atrial appendage, and the
embryonic right atrium remains as the right atrial appendage.

Septum formation of the atrioventricular canal

 At the end of the fourth week, two atrioventricularendocardial cushions appear.

Initially the atrioventricular canal gives access to the primitive left ventricle, and is
separated from arterial bulb by the edge of the ventricular bulb.
 In the fifth week, the posterior end terminates in the center part of the upper
endocardial cushion.
 Because of this, blood can access both the left primitive ventricle and the right
primitive ventricle. As the anterior and posterior pads project inwardly, they merge to
form a right and left atrioventricular orifice.

Atrioventricular valves

 When forming intra-atrial septa, atrio-ventricular valves will begin to grow.

 A muscular interventricular septum begins to grow from the common ventricle to the
atrio-ventricular endocardial cushions.
 The division begins in the common ventricle where a furrow in the outer surface of
the heart will appear the interventricular foramen eventually disappears.

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  This closure is achieved by further growth of the muscular interventricular septum, a
contribution of trunk crest-conal tissue and a membranous component

6. Heart rates
 Starting at week 5 the embryonic heart rate accelerates by 3.3 bpm per day for the
next month. Before this, the embryo possesses a tubular heart.
 The embryonic heart begins to beat at approximately the same rate as the mother's,
which is typically 80 to 85 bpm. The approximate fetal heart rate for weeks 5 to 9
(assuming a starting rate of 80):
 Week 5 starts at 80 and ends at 103 bpm
 Week 6 starts at 103 and ends at 126 bpm
 Week 7 starts at 126 and ends at 149 bpm
 Week 8 starts at 149 and ends at 172 bpm
 At week 9 the embryonic heart tends to beat within a range of 155 to 195 bpm.
 By the end of week 9, the embryonic heart has developed septa and valves, and has all
four chambers.
 At this point, the fetal heart rate begins to decrease, and generally falls within the
range of 120 to 160 bpm by week 12

CHAMBERS OF THE HEART

The four chambers of the heart are

 the right atrium

 left atrium
 right ventricle and
 left ventricle.

The atria are the two upper chambers that receive blood from the veins. The ventricles
are the two lower chambers that pump blood into the arteries.

LAYERS

 Epicardium: the outer protective layer of the heart.

The epicardium is composed of loose connective tissue, including elastic fibers and
adipose tissue. The epicardium functions to protect the inner heart layers and also
assists in the production of pericardial fluid.
 Myocardium: muscular middle layer wall of the heart.
It is composed of cardiac muscle fibers, which enable heart contractions. The
myocardium is the thickest layer of the heart wall. The myocardium of the left
ventricle is the thickest, as this ventricle is responsible for generating the power needed
to pump oxygenated blood from the heart to the rest of the body.

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 Endocardium: the inner layer of the heart.
This layer lines the inner heart chambers, covers heart valves, and is continuous with the
endothelium of large blood vessels. The endocardium of heart atria consists of smooth
muscle, as well as elastic fibers. An infection of the endocardium can lead to a condition
known as endocarditis

Definition The circulation of oxygenated blood, de-oxygenated blood, nutritive material

in the fetus is termed as fetal circulation.
Umbilical cord
- 2 umbilical arteries : Return de-oxygenated blood, fecal waste to placenta.
- 1 umbilical vein : Brings oxygenated blood and nutrients to the fetus.
Three shunts in fetal life
- Ductus venosus : connects umbilical vein to inferior vena cava
- Ductus arteriosus : connects pulmonary artery to aorta
- Foramen ovale : opening between right and the left atrium
Blood flow in fetal circulation
Umbilical vein carries oxygenated blood and nutrients from placenta
.
. oxygenated blood passes from inferior vena cava to ductus venosus
oxygenated blood enters the hepatic veins and to the growing liver
receives deoxygenated blood from the portal vein
. through ductus venosus

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 Inferior vena cava
Right atrium of the heart
. through foramen ovale
Left atrium of the heart
Left ventricle of the heart
During ventricular systole

Left ventricular blood . Right ventricular blood

. pumped Pulmonary
ascending aorta and distributed by arteries .
their branches to the heart, head, ductus arteriosus . .
neck, brain, arms. descending aorta

Hypogastric arteries

Umbilical arteries

Placenta
AT BIRTH
Clamping the cord shuts down low-pressure system
Increased atmospheric pressure cause lungs to inflate with oxygen
Placental blood flow stops and begins respiration
Ductus arteriosus closes by muscular contraction
Increased blood flow in the lungs rises pressure in left atrium
Pressure in right atrium decreases
The septum primumis then apposed to the septum secundum
Foramen ovale closes

Closure of ductus venosus and ductus arteriosus

Forms ligamentum venosum Forms ligamentum arteriosum

SYSTEMIC CIRCULATION
Oxygenated blood is pumped by the heart - the left ventricle into the aorta ,from which it
is distributed to different parts of the body by arteries. The arteries branch and rebranch to
form arterioles and capillaries which distribute blood to the tissues. The capillaries have
only one layer of flat, endothelial cells, the oxygen ,carbon dioxide ,nutrients and waste
products are exchanged in the capillaries.

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The capillaries drains into venules ,they unite to form larger veins . venous blood from the
upper part of the body is drained by a large vein, the superior vena cava, venous blood
from the lower part of the body is drained by the inferior vena cava. These two veins carry
the deoxygenated blood back to the right atrium of the hear. This completes the systemic
circulation.
PULMONARY CIRCULATION
Blood cells enter pulmonary circulation after returning from a trip around the body and
enter the right atrium of the heart through two major veins, the superior and inferior vena
cava. At this point in the journey, the blood cells do not contain any oxygen. From the
atrium, the heart pushes the blood through the tricuspid valve into the right ventricle and
then through the pulmonary valve into the pulmonary artery. The pulmonary artery splits
in two and carries the blood to both lungs where it will receive oxygen.
Now laden with oxygen, the blood cells are sent back towards the heart. The tiny
capillaries segue into pulmonary veins, which merge into ever larger ones until there are
two from each lung. These are referred to as the right superior and inferior pulmonary
veins and the left superior and inferior pulmonary veins. All of them, however, empty into
the left atrium of the heart. With a contraction of the heart muscle, the blood will be
forced through the mitral valve into the left ventricle, and then through the aortic valve
and out the aorta, where it enters the systemic loop to deliver oxygen-rich blood to the
body.
BLOOD SUPPLY
Arteries supply
Arterial supply by right and left coronary artery,
1. The right coronary artery originates from the anterior aortic sinus of the ascending
aorta, immediately above the aortic valve.
After arising from the ascending aorta, the right coronary artery first runs forwards
between the pulmonary trunk and the right auricle, and after that it descends just about
vertically in the right atrioventricular groove (right anterior coronary sulcus) up to the
junction of the right and the inferior borders of the heart. At the inferior border of the
heart, it turns posteriorly and runs in the groove where it ends by anastomosing with the
left coronary artery.
 Right Conus Artery

It supply the anterior surface of the pulmonary conus (infundibulum of the right ventricle).

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  Atrial Branches
They supply the atria. One of the atrial branches – the artery of sinuatrial node (also
referred to as sinuatrial nodal artery) provides the SA node in 60% cases. In 40% of
individuals it originates from the left coronary artery.
 Anterior Ventricular Branches
They’re 2 or 3 and supply the anterior surface of the right ventricle.
The marginal branch is the largest and runs along the lower margin of the sternocostal
surface to make it to the apex.
 Posterior Ventricular Branches
They may be generally 2 and supply the diaphragmatic surface of the right ventricle.
 Posterior Interventricular Artery
It runs in the posterior interventricular groove up to the apex. It supplies the posterior part
of the interventricular septum, atrioventricular node (AV node) in 60% of the cases, and
right and left ventricles. In 10% individuals, the posterior interventricular artery originates
from the left coronary artery
2. Left coronary artery

The left coronary artery originates from the left posterior aortic sinus of the ascending
aorta, immediately above the aortic valve.
After arising from ascending aorta, the left coronary artery runs forwards and to the left
between the pulmonary trunk and the left auricle. It then divides into an anterior
interventricular and circumflex artery. The anterior interventricular artery (left anterior
descending/LAD) runs downwards in the anterior interventricular groove to the apex of
the heart. It then enters posteriorly around the apex of the heart to go into the posterior
interventricular groove to terminate by anastomosing with the posterior interventricular
artery- a branch of the right coronary artery.

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The circumflex artery winds around the left margin of the heart and continues in the left
posterior coronary sulcus up to the posterior interventricular groove where it ends by
anastomosing with the right coronary artery.
 Anterior interventricular artery/left anterior descending (LAD) artery: It
provides (a) anterior part of interventricular septum, (b) greater part of the
left ventricle and part of right ventricle, and (c) a part of left bundle branch
(of His) posterior atrioventricular groove (right posterior coronary sulcus)
up to the posterior interventricular.
 Circumflex artery: It supplies a left marginal artery that provides the left
margin of the left ventricle up to the apex of the heart.
 Diagonal artery: It may originate directly from the trunk of the left
coronary artery.
 Conus artery: It supplies the pulmonary conus.
 Atrial branches: They supply the left atrium.
3. Nerve supply
The heart is supplied by the autonomic nerve fibres. Parasympathetic fibres derived
from both vagus nerves. Sympathetic fibres are derived from sympathetic trunks. Both
these fibres form a network called the cardiac plexus.
4. Venous drainage of the heart
The right side is drain by the anterior veins of right ventricle coronary sinus, small
cardiac vein, right marginal vein, middle cardiac vein.
The left side is drain by great cardiac vein ,anteriorinterventricular vein.

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DEFINITION
Acyanotic Heart Disease is the common congenital heart disease present at birth. It’s
prevalence is mostly unknown. It is a congenital heart disease with structural malformation of the
heart or great vessels. In this mostly the cyanosis is not seen hence known as acyanotic heart
disease.
INCIDENCE /PREVALENCE /EPIDEMIOLOGY
 Approximately 5 to 8 per 1000 live births
 About 2 or 3 in 1000 infants will be symptomatic during the first year of life with
significant heart diseases that will require treatment.
 CHD is the major cause of death in the first year of life.
 There are more than 35 well recognized cardiac defects the most common heart
anomaly is VSD

It is estimated that over 180,000 children in India are born with CHD every year and the
majority of CHD cases (58%) diagnosed were between 0 and 5 years of age. The prevalence
of CHDs in adults was 2.4 per 1000 individuals in this.About 66.74% of patients were
diagnosed with acyanotic and 33.26% with cyanotic type. The most common CHD was
ventricular septal defect (VSD) (30.01%) followed by atrial septal defect (20.70%), tetralogy
of fallot (TOF) (16.05%), and patent ductusarteriosus (10.23%).

According to a large hospital based study from India, the incidence of congenital heart
disease is 3.9/ 1000 live births. In community based studies from India ,the prevalence of
CHD ranges from 0.8 – 5.2/1000 patients

RISK / ETIOLOGY FACTOR

 Maternal age ˃ 30 years old

 Paternal age - Offspring having paternal age >25 years had increased risk of CHDs in
comparison to those with paternal age <25 years
 Not proper intake of multivitamin containing folic acid
 Febrile illness during first trimester
 Bad obstetric history
 Pregestational diabetes
 The exact cause is unknown
 Heredity and consanguineous marriage are important etiology factors
 Genetic disorder and chromosomal aberration(Trisomy 21,Turner’s syndrome) are
also known to predispose congenital heart disease.
 Others associated factors include responsible for CHD include fetal and maternal
teratogenicinfection(rubella),teratogenic drug(thalidomide) intake,alcohol intake by
the mother and irradiation in first trimester of pregnancy, and maternal IDDM.

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 CLASSIFICATION

Congenital Heart Disease (CHD)

Acynotic Cyanotic

 Tetralogy of fallot
 Tricuspid atresia
Left - to - Right Outflow  Transposition of great
shunts obstructions vessels
 Truncus arteriosus
 Ventricular  Pulmonary  Total anomalous pulmonary
septal defect stnosis venous return
(VSD)  Aortic stenosis  Ebstein’s anomaly
 Atrial septal  Coarctation of
defect (ASD) aorta (COA)
 Patent ductus
arteriosus (PDA)

1. Atrial septal defect

It is an abnormal opening between right and left atria resulting left to right shunting of blood,
it account for 9 percent of all congenital heart disease.

Definition
An atrial septal defect (ASD) is a hole in the wall (septum) between the two upper chambers
of the heart (atria). The condition is present at birth (congenital).

This defect allows oxygen-rich blood to leak into the oxygen-poor blood chambers in the
heart.

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What causes it ?
Every child is born with an opening between the upper heart chambers. It’s a normal fetal
opening that allows blood to detour away from the lungs before birth. After birth, the opening
is no longer needed and usually closes or becomes very small within several weeks or
months.

Sometimes the opening is larger than normal and doesnot close after birth.

How does it affect the heart ?

Normally, the left side of the heart only pumps blood to the body, and the right side of the
heart only pumps blood to the lungs. In a child with ASD, blood can travel across the hole
from left upper heart chamber (left atrium) to the right upper chamber (right atrium) and out
into the lung arteries.

If the ASD is large, the extra blood being pumped into the lung arteries makes the heart and
lungs work harder and the lung arteries can become gradually damaged.

If the hole is small, it may not cause symptoms or problems. Many healthy adults still have a
small left over opening in the wall between the atria, sometimes called a Patent Foramen
Ovale.

Types
ASD are classified by their different location and development :

 Ostium secundum
An abnormal opening in the middle of the atrial septum presents due to abnormal
development of the septum secundum
 Ostium primum
It presents as an abnormal opening at the bottom of the atrial septum due to improper
development of the septum primum.
 Sinus venosus
It is an abnormal opening at the top of the atrial septum.there may be increase
association with partial anomalous pulmonary venous connection.
 Coronary sinus ASD
It occurs when there is a defect in the wall between coronary sinus and left atrium.

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Pathology
1. ASD (> 9 mm)
. result in
left-to-right shunt (blood shunts from the left atrium to the right atrium)
. causing
volume overload of both the right atrium and the right ventricle
. if untreated
. this condition can result in .
. . enlargement of the right side of the heart
.
. .
. ultimately heart failure.

2. The left-to-right shunt

. increases
. the filling pressure of the right heart (preload)
. forcing the right ventricle
. to pump out more blood than the left ventricle.

. this constant overloading of the right side of the heart .

. causes .
. an overload of the entire pulmonary vasculature
. eventually, 
. . pulmonary hypertension may develop
. causing
. the right ventricle to face increased afterload.
(Hypertension increases the pressure that the left ventricle has to generate to open the aortic
valve during ventricular systole, and coronary artery disease which increases the stiffness of

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the left ventricle, thereby increasing the filling pressure of the left ventricle during
ventricular diastole

3. The right ventricle is forced to generate

.
. higher pressures to try to overcome the pulmonary hypertension .
. leading to 
. right ventricular failure (dilatation and decreased systolic function of the right ventricle).

4. If the ASD is left uncorrected,

.
. the pulmonary hypertension progresses
the pressure in the right side of the heart becomes
greater than the left side of the heart
. causing
. the shunt to reverse - a right-to-left shunt.
. this phenomenon is known as  . .
. Eisenmenger's syndrome.

Once right-to-left shunting occurs,

. a portion of the oxygen-poor blood gets shunted . . .
. to the left side of the heart
. and
. ejected to the peripheral vascular system
. causing
. signs of cyanosis.

The flow of oxygenated blood

. from
. higher pressure left atrium
. to
. lower pressure right atrium across the ASD
. results in
. volume overload to right ventricles and right ventricular dilation
. thus increasing
. blood flow to lungs leads to elevated pulmonary artery pressure.

Clinical manifestation
 Shortness of breath
 Fatigue
 Dyspnea on exertion
 Fast breathing

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  Heart palpitation
 Chest pain
 Slow growth
 Recurrent lower respiratory tract infection
 Murmur (noise heard with a stethoscope)
 Heart arrhythmias
 Hypertension

Diagnostics

 Echocardiogram –
To check the heart chambers and their pumping strength, heart valves and signs of
heart defects.

 Chest X-ray

 Electrocardiogram –
To identify heart rhythm problems.

 MRI -
This uses a magnetic field and radio waves to create 3D images of the heart and other
organs and bodily tissues.

 CT scan -
This uses a series of X-rays to create detailed images of your heart. It can be used to
diagnose an atrial septal defect and related congenital heart defects if
echocardiography hasn't definitely diagnosed an atrial septal defect.

Medical management
Medications won't repair the hole, but they may be used to reduce some of the signs and
symptoms that can accompany an atrial septal defect. Drugs may also be used to reduce the
risk of complications after surgery. Medications may include those to keep the heartbeat
regular (beta blockers) or to reduce the risk of blood clots (anticoagulants).

Surgical management
Surgery isn't recommended if patient has severe pulmonary hypertension because it might
make the condition worse.
For adults and children, surgery involves sewing closed or patching the abnormal opening
between the atria. Surgeon will evaluate patients condition and determine which of two
procedures to use:

 Cardiac catheterization. 
A thin, flexible tube (catheter) is inserted into a blood vessel in the groin and is guided
to the heart using imaging techniques. Through the catheter, a mesh patch or plug is
placed to close the hole. The heart tissue grows around the mesh, permanently sealing

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 the hole.
This type of procedure is used to repair only the secundum type of atrial septal defects.
 Open-heart surgery. This type of surgery is done under general anesthesia and
requires the use of a heart-lung machine. Through an incision in the chest, surgeons use
patches to close the hole. This procedure is the only way to repair primum, sinus
venosus and coronary sinus atrial defects.

This procedure can be done using small incisions (minimally invasive surgery) and with
a robot for some types of atrial septal defects.

Follow-up care

 Repeated echocardiograms are done after hospital discharge, one year later and then
as requested by your or your child's doctor.

 For simple atrial septal defects closed during childhood, only occasional follow-up
care generally is needed.

 Adults who've had atrial septal defect repair need to be monitored throughout life to
check for complications, such as pulmonary hypertension, arrhythmias, heart failure
or valve problems.

 Follow-up exams are typically done yearly.

Lifestyle

 Exercise. Having an atrial septal defect usually doesn't restrict you from activities or
exercise. If a patient has complications, such as arrhythmias, heart failure or pulmonary
hypertension, he/she might be counseled to avoid some activities or exercises.

If a patient has an unrepaired defect, doctor will likely advise you to avoid high-altitude
climbing.

 Preventing infection. Some heart defects and the repair of defects create changes to
the surface of the heart that make it more prone to infection (infective endocarditis).
Atrial septal defects generally aren't associated with infective endocarditis, though
doctor will likely recommend preventive antibiotics for about six months after closure
whenever you have dental work done.

But if a patient has other heart defects besides an atrial septal defect, or atrial septal
defect repair within the last six months, patient might need to take antibiotics before
certain dental or surgical procedures.

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 2. Patent Ductus Arteriosus
It is the persistent vascular connection the pulmonary artery and the aorta.Functionally,the
closure of ductusarteriosus occurs soon after birth. When ductusarteriosus remains patent and
open after birth, the blood flows in the ductus from the aorta to the pulmonary artery due to
higher pressure in the aorta.

Aorta Patent Ductus Arteriosus

Epidemiology
• Incident 1 : 2500-5000 birth

• Genesis PDA approximately 12 % of all congenital heart defects

• Premature babies is a high risk of PDA and a higher incidence , in the event of respiratory
distress

• Male : female = 3 : 1

Risk factors
• Prematurity conjunction with respiratory distress syndrome

Chromosomal abnormalities (e.g. Down syndrome)

• Children born in the highlands like mountain . Because the O ₂ plateau levels lower

• Mother of rubella infection during pregnancy

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Types of PDA
The Krichenko classification system (Appearance on Angiography)

Type A Conical – Well-defined aortic ampulla and constriction near pulmonary insertion

Type B Window – Short with narrowing near aortic insertion

Type C Tubular – Tubular duct without constriction

Type D Complex - Multiple constrictions

Type E Elongated - Long PDA with conical appearance and multiple constrictions

Pathophysiology
Because of the failure to close the ductus arteriosus

the aorta and the pulmonary artery are interconnected

There is left to right shunt as blood flows from aorta (higher pressure)
. to . .

. pulmonary artery(lower pressure)

. leading to .
. pulmonary overload

Thus oxygenated blood of systemic circulation

. flows back to . .
. pulmonary circulation
. resulting in . .
. increased vascular pressure in the pulmonary tree . .
. and volume load on
. left heart
. Because aortic pressure is higher than the pulmonary artery blood flow
. from the aorta to the pulmonary artery

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. Blood flow increases in pulmonary artery .
. when the pressure is
. higher than the aorta
.
. there is pulmonary hypertension
. and
. increased pulmonary vascular resistance ( left - right shunt )
.
. which leads to Eisenmenger syndrome.

Clinical manifestation
 Dyspnea
 Rapid breathing (tachypnea)
 Tachycardia
 Heart murmur
 Cardiomegaly
 Left subclavian thrill
 Bounding pulse
 Widened pulse pressure
 Increased cardiac output
 Increased systolic pressure
 Poor growth
 Cyanosis

Diagnosis
 Echocardiography  
Sound waves are used to capture the motion of the heart and
associated Doppler studies are the primary methods of detecting PDA. 
 Electrocardiography (ECG)
Electrodes are used to record the electrical activity of the heart.
Large PDA with normal pulmonary resistance à atrial and left ventricular hypertrophy
Large PDA with pulmonary hypertension à right ventricular hypertrophy
 Chest X-ray 
Reveals overall heart size (as a reflection of the combined mass of the cardiac
chambers) and the appearance of blood flow to the lungs.
A small PDA most often accompanies a normal-sized heart and normal blood flow to
the lungs.
A large PDA generally accompanies an enlarged cardiac silhouette and increased
blood flow to the lungs.

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Medical management
Treatments for patent ductus arteriosus depend on the age of the person being treated.
Options might include:

 Watchful waiting. In a premature baby, a PDA often closes on its own. The doctor
will monitor baby's heart to make sure the open blood vessel is closing properly. For
full-term babies, children and adults who have small PDAs that aren't causing other
health problems, monitoring might be all that's needed.

 Medications. In a premature baby, nonsteroidal anti-inflammatory drugs (NSAIDs)

— such as ibuprofen (Advil, Infant's Motrin, others) or indomethacin (Indocin) —
might be used to help close a PDA. NSAIDs block the hormonelike chemicals in the
body that keep the PDA open. NSAIDs won't close a PDA in full-term babies, children
or adults.

Indomethacin stimulates the muscles inside the PDA to tighten. This closes the . . . ..
.. connection. To help the heart and lungs work better, sometimes diuretics are pescribed.
. . Diuretics help the kidneys remove extra fluid from the body. This may be needed
when . the heart is not working well. Or it may be needed if the blood vessels in the lungs
have . to make room for more blood flow, as with a PDA.

 Surgical closure. If medications aren't effective and your child's condition is severe
or causing complications, surgery might be recommended. A surgeon makes a small cut
between child's ribs to reach your child's heart and repair the open duct using stitches or
clips.

After the surgery, child will remain in the hospital for several days for observation. It
usually takes a few weeks for a child to fully recover from heart surgery. Occasionally,
surgical closure might also be recommended for adults who have a PDA that's causing
health problems. Possible risks of the surgery include hoarseness, bleeding, infection
and a paralyzed diaphragm.

 Catheter procedures. Premature babies are too small for catheter procedures.

However, if a baby doesn't have PDA-related health problems, the doctor might
recommend waiting until the baby is older to do a catheter procedure to correct the
PDA. Catheter procedures can also be used to treat full-term babies, children and adults.

In a catheter procedure, a thin tube (catheter) is inserted into a blood vessel in the groin
. and threaded up to the heart. Through the catheter, a plug or coil is inserted to close the .
. ductus arteriosus.

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 Nutrition
Premature infants or those infants with large PDAs may get tired when feeding. They may
not be able to eat enough to gain weight. Nutrition choices include:
 High-calorie supplements. Special nutritional supplements may be added to formula
or pumped breastmilk to increase the number of calories. Your baby can drink less and still
have enough calories to grow correctly.
 Supplemental tube feedings. Supplemental feedings are given through a small,
flexible tube. The tube passes through the nose, down the food pipe (esophagus), and into the
stomach. The feedings can either be added to or take the place of bottle-feedings. Infants who
can drink part of their bottles, but not all, may be fed the rest through the feeding tube. Babies
who are too tired to bottle-feed may get all of their formula or breastmilk through the feeding
tube.

Complications of PDA
If not treated, PDA may lead to long-term lung damage. It can also damage the blood vessels
in the lungs. But this is not common because most children will have been treated for their
PDA before the lungs and blood vessels get damaged.

3. VENTRICULAR SEPTAL DEFECT

A ventricular septal defect is an abnormal opening in the septum between right and left
ventricles. The ventricular septum consists of an inferior muscular and superior membranous
portion and is extensively innervated with conducting cardiomyocytes.

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RISK AND ETIOLOGY FACTORS

 Maternal age ˃ 30 years old

 Paternal age - Offspring having paternal age >25 years had increased risk of CHDs in
comparison to those with paternal age <25 years
 Not proper intake of multivitamin containing folic acid
 Febrile illness during first trimester
 Bad obstetric history
 Pregestational diabetes
 The exact cause is unknown
 Heredity and consanguineous marriage are important etiology factors
 Genetic disorder and chromosomal aberration(Trisomy 21,Turner’s syndrome) are
also known to predispose congenital heart disease.
 Others associated factors include responsible for CHD include fetal and maternal
teratogenic infection(rubella),teratogenic drug(thalidomide) intake,alcohol intake by
the mother and irradiation in first trimester of pregnancy, and maternal IDDM

TYPES

 Large Size is >75% of aortic annulus, flow velocity less than 1 m/s, VSD resistance
index < 20 u/m2
 Moderate Size 33- 75% of aortic annulus, flow velocity 1-4 m/s,
 Small Size <33% of aortic annulus, flow velocity > 4 m/s, VSD resistance index more
than 20 u/m2

ANATOMIC PHYSIOLOGIC CLASSIFICATION OF VSD:

TYPE 1 (RESTRICTIVE VSD)

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Resistance that limits the left to right shunt resides at the level of VSD.

 Normal PVR
 Normal PA pressure and RVSP
 LV pressure > RV pressure
 Produces a significant pressure gradient between the left ventricle and the right
ventricle
 Pulmonary-to-aortic systolic pressure ratio < 0.3 3. Small (≤1.4 : 1) shunt.
 Less than 5mm, or defect size <=25% of annulus diameter
 Normal PA and branches
 Normal LV, LA size
 A restrictive VSD may close spontaneously during childhood or may go unnoticed as
it hardly produces symptoms or may lead to infective endocarditis.

TYPE 2 (MODERATELY RESTRICTIVE VSD)

 Higher than normal RV AND PA pressure but with low and variable PVR
 LV pressure > RV pressure
 Qp/Qs of 1.4 to 2.2 2. pulmonary-to-aortic systolic pressure ratio less than 0.66.
 Diameter of defect >25% <75% of annulus size or 5-10 mm
 RVP,PAP normal or near normal
 Mild to moderate PA,LA,LV dilation

TYPE 3 ( NON RESTRICTIVE VSD):

 Large left to right shunt, identical LV to RV pressure

 RV and LV behave as single chamber with direction of flow determined by resistance
in pulmonary and systemic circulation
 PVR is high but subsystemic.
 Qp/Qs > 2.2 2. pulmonary-to-aortic systolic pressure ratio greater than 0.66. 3. Defect
diameter >75% of aortic diameter
 PH in less than 2years
 Ventricular volume overload early in life leading to CHF in childhood. Progressive
rise in pulmonary artery pressure . A fall in left-to-right shunting. Finally the reversal
of shunt

TYPE 4 (VSD WITH REVERSAL OF SHUNT):

 Identical RV and LV pressure

 Suprasystemic PVR and reversal of shunt across VSD.
 PAP/systolic pressure ratio of 1
 Qp/Qs less than 1 : 1

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  Net right-to-left shunt and cyanosis.

PATHOPHYSIOLOGY
Pressure in the left ventricle is higher than the right ventricles

Blood flow through abnormal opening from left ventricle to right ventricle

Mixing up of blood in the right ventricle and it is enters into the pulmonary artery

Pulmonary hypertension

Regurgitation of blood into right atrium

Hypertrophy of right side of the heart

Increased pulmonary vascular resistance

Left to right shunt reduced and right to left shunt started

Decreased amount of blood for purification

Unoxygenated blood is supplied by aorta to the body

Cyanosis, Eisenmenger syndrome

CLINICAL PRESENTATION

Small VSD

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  may be asymptomatic
 Pan systolic murmur

Moderate breathing difficulty

 slow to gain weight

 Respiratory infection
 Sign of LV failure
 Mid systolic murmur

Large VSD

 Hepatomegaly &oliguria
 Systolic murmur with thrill
 Failure to thrive
 Biventricular hypertrophy and CCF
 Feeding difficulty
 Poor Weight Gain
 Failure to cry
 Increased sweating
 Palpitation
 Dyspnoea
 Cyanosis

Others

 Pale
 Tachycardia
 Cough
 Irritability

DIGNOSTIC TEST

 History of illness and physical examination

 Infant cough and fatigue after feeding, sweats excessively and become restless
when recumbent,
sleeps poorly
 Dyspnoea and irritability are most pronounced when the infant is supine and
get improved when infant is held upright
 Feeding patterns are typical: a hungry infant awakes from fretful sleep and
feeds vigorously only to stop due to dyspnoea, then falls to sleep to be awaken
due to hunger due to effort exhaustion

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  ARTERIAL PULSE- nonrestrictive VSD with large left to right shunt and
congestive heart failure are associated with diminished arterial pulse and
pulsusalternance.
 JUGULAR VENOUS PULSE :non restrictive VSD with congestive heart
failure are associated with raised JVP with increase in A and V waves.

 poor growth and development

 cachexia in infants due to catabolic effects of chf.
 cyanosis due to reversal of shunt
 clubbing
 harrisons grooves are due to thoracic retractins caused by chronic dyspnoea
 Chest x-ray

Shows enlargement of the heart and increased pulmonary vascular marking.

 ECG

Reveals biventricular hypertrophy

Nonrestrictive VSD: . Right atrial or combined atrial P wave abnormality in lead 2 and
V1 and V2. QRS axis shift moderately towards right. Biventricular hypertrophy : large R
wave in V1, large R wave in V5,V6, tall T waves in V5 V6.

 ECG 2D

In this test, sound waves produce a video image of the heart. Doctors may use this test to
diagnose a ventricular septal defect and determine its size, location and severity. It may
also be used to see if there are any other heart problems

 Cardiac catheterization.

In this test, a thin, flexible tube (catheter) is inserted into a blood vessel at the groin or
arm and guided through the blood vessels into the heart. Through cardiac catheterization,
doctors can diagnose congenital heart defects and determine the function of the heart
valves and chambers.

 Pulse oximetry. A small clip on the fingertip measures the amount of oxygen in the
blood.

MANAGEMENT

Medical management

 Diuretics: Furosemide decreases the amount of fluid in the pulmonary and systemic
circulation, relieving pulmonary congestion. To minimise potassium loss,
Spironolactone can be added.

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  Angiotensin-Converting Enzyme (ACE) inhibitors: These are second stage medical
treatment and reduce the left to right shunt by reducing mainly the systemic arterial
pressures (afterload reduction) and allowing more blood to flow through the aortic
valve and less through the VSD.

 Digoxin: Used to treat congestive heart failure. It increases heart muscle strength,
helps to maintain a normal heart rhythm, and removes excess water from the body.
This may be indicated if diuresis and afterload reduction do not adequately relieve
symptoms.

preoperative care

 Admission history and physical examination

The medical and nursing theories are obtained so that an individualized plan of
surgical management and preoperative and postoperative nursing intervention can be
formulated.

Previous history of fever , duration, and onset should be collected

Sign of dehydration, and also sign and symptoms of the disease should be assessed
during the time of admission.

 Baseline vital signs.

This are obtained so that the child intraoperative and postoperative status can be
evaluated.

 Height and weight measurement

These measurement are obtained because they form the basis for calculating fluid
replacement volumes and medication dosages throughout the hospitalization.
 Others like ,the child normal cycle activity and rest are determine ed from the nursing
history and are observed during the preoperative period.

Surgical procedure

 Surgical repair: This is open heart surgery. It is performed under cardiopulmonary

bypass via median sternotomy. A patch material or stitches are used to close the hole.
 Catheter procedure: This procedure is less common than open heart surgery, as most
defects are not suitable for transcatheterclosure.A catheter is inserted into the femoral
artery through the groin and is guided into the heart, under general anaesthesia. A
specially sized mesh device is deployed to close the hole.
 Hybrid approach: The surgeon creates a small access through the left ventricle for the
interventional cardiologist to deploy the closing device

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Postoperative care

 Cardiopulmonary functioning
- Immediately after surgery vitals sign should be check for the first every 15 minutes
for 24 hours.
- Additional heat loss must be prevented
- Heart rate should be assessed and recorded properly and strictly
- Proper measurement of CVP should be done.
- Onserve for complication such as infection,bloodloss,airemboli,arterial thrombosis.
- Administering of oxygen
- Postural drainage should be maintained properly by every 3-4 hours
 Gastrointestinal and renal functioning
- Fluid by mouth is fully restricted for 24 hours followed after post operation
- Nasogastric tube can be inserted to prevent aspiration
- All the intake and output are measured accurately
- The clinical manifestation of the degree of hydration are assessed frequently by
examining the child skin tugors and dryness of the mucous membrane.
 Central nervous system functioning
- This should be assessed because brain tumour may occurred during open heart open.
- Chld orientation should be assessed by asking question
Like how are you?
- Identify the abnormal reflexes on both hands and arns
- Teching of family members for discharge

PROGNOSIS

After a successful surgical repair of the VSD, the two ventricles are entirely separate from
each other and the circulation of the blood within the heart is normal. If the heart was
enlarged, it can return to a more normal size. The high pressure in the pulmonary artery
should also begin to resolve. If the child's growth had slowed, the child usually catches up
within a year or two. Long-term follow-up is required. The long-term prognosis is usually
excellent.

COMPLICATION

 Recurrent respiratory infection

 Infective endocarditis
 Pulmonary stenosis
 Eisenmengers syndrome

4. AORTIC STENOSIS

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Aortic stenosis is the narrowing of the exit of the left ventricle of the heart (where the aorta
begins), such that problems result.

In aortic valve stenosis the opening is narrowed, the heart must work much harder to try and
deliver enough blood to the body and can become overworked. As a result of all this strain on
your heart, this in turn leads to increased demand for blood and oxygen from the heart and
possibly leads to subsequent angina, irregular heart rhythms or heart failure. Arrhythmias
such as atrial fibrillation are often precipitated by the changes to the left ventricle

Clinical manifestation
 Exercise intolerance
 Dizziness and syncope
 Tachypnea
 Faint peripheral pulse
 Poor perfusion
 Poor capillary refill
 Cold skin
 Poor feeding and metabolic acidosis.
 Chest pain on exertion
 Decreased exercise tolerance

5. PULMONARY STENOSIS

Pulmonary valve stenosis (PVS) is a heart valve disorder. Blood going from the heart to the
lungs goes through the pulmonary valve, whose purpose is to prevent blood from flowing
back to the heart. In pulmonary valve stenosis this opening is too narrow, leading to a
reduction of flow of blood to the lungs.

36
Symptoms
 Heart murmur
 Cyanosis
 Dyspnea
 Dizziness
 Upper thorax pain
 chest pain, pressure, or discomfort (called angina or angina pectoris).

6. COARTATION OF AORTA

Coarctation of the aorta — or aortic coarctation — is a narrowing of the aorta, the large
blood vessel that branches off your heart and delivers oxygen-rich blood to your body. When
this occurs, your heart must pump harder to force blood through the narrowed part of your
aorta.

37
Clinical manifestation
 tachypnea
 poor perfusion
 acidosis and absent femoral pulses
 fatigue
 cramps
 headache
 weakness and exertionaldyspnea
 the condition may be complicated with hypertension,CCF, cerebral haemorrhage,
encephalopathy and bacterial endocarditis.

7. ATRIOVENTRICULAR CANAL DEFECT

Atrioventricular canal defect is a combination of heart problems resulting in a defect in the

center of the heart. Atrioventricular (AV) canal defect is a large hole in the center of the
heart. It's located where the wall (septum) between the upper chambers (atria) joins the wall
between the lower chambers (ventricles). This septal defect involves both upper and lower
chambers. Also, the tricuspid and mitral valves that normally separate the heart's upper and
lower chambers aren't formed as individual valves. Instead, a single large valve forms that
crosses the defect in the wall between the two sides of the heart.The condition occurs when
there's a hole between the heart's chambers and problems with the valves that regulate blood
flow in the heart.
Atrioventricular canal defect allows extra blood to flow to the lungs. The extra blood forces
the heart to overwork, causing the heart muscle to enlarge.

How does it affect the heart?

Normally, the left side of the heart only pumps blood to the body, and the heart's right side
only pumps blood to the lungs. In a child with AV canal defect, blood can travel across the
holes from the left heart chambers to the right heart chambers and out into the lung arteries.
The extra blood being pumped into the lung arteries makes the heart and lungs work harder
and the lungs can become congested.

38
Symptoms
Atrioventricular canal defect can involve only the two upper chambers of the heart (partial) or
all four chambers (complete). In either type, extra blood circulates in the lungs.

Complete atrioventricular canal defect

Signs and symptoms usually develop in the first several weeks of life. These signs and
symptoms are generally similar to those associated with heart failure and might include:

 Difficulty breathing or rapid breathing

 Wheezing
 Fatigue
 Lack of appetite
 Poor weight gain
 Pale skin color
 Bluish discoloration of the lips and skin
 Excessive sweating
 Irregular or rapid heartbeat
 Swelling in the legs, ankles and feet (edema)

Partial atrioventricular canal defect

Signs and symptoms might not appear until early adulthood and might be related to
complications that develop as a result of the defect. These signs and symptoms can
include:

 Abnormal heartbeat (arrhythmia)

 Shortness of breath
 High blood pressure in the lungs (pulmonary hypertension)
 Heart valve problems
 Heart failure

Management
An AV canal can be fixed. Open-heart surgery is needed to repair the defect. Unlike some
other types of septal defects, the AV canal defect can't close on its own. Medicines may be
used temporarily to help with symptoms, but they don't cure the defect or prevent permanent
damage to the lung arteries.

In an infant with severe symptoms or high blood pressure in the lungs, surgery must usually
be done in infancy. During the operation, the surgeon closes the large hole with one or two
patches. Later the patch will become a permanent part of the heart as the heart's lining grows
over it. The surgeon also divides the single valve between the heart's upper and lower
chambers and makes two separate valves. These will be made as close to normal valves as
possible.

39
If an infant is very ill, or has a defect that may be too complex to repair in infancy, a
temporary operation to relieve symptoms and high pressure in the lungs may be needed. This
procedure (pulmonary artery banding) narrows the pulmonary artery to reduce the blood flow
to the lungs. When the child is older, an operation is done to remove the band and fix the AV
canal defect with open-heart surgery.

40