ACYNOTIC

HEART
DISEASES
MS. DEVYANI MESHRAM
 CONGENITAL HEART DISEASE

INTRODUCATION
Congenital heart defects are the most common type of birth defect. As
medical care and treatment have advanced, babies with a congenital heart
defects are living longer and healthier lives. These conditions are present at
birth and can affect the structure of a baby’s heart and the way it works. They
can affect how blood flows through the heart and out to the rest of the body.
They can vary from mild (such as a small hole in the heart) to severe (such as
missing or poorly formed parts of the heart). About one in four babies born
with a heart defect has a critical CHD(also known as critical congenital heart
defect).
 DEFINITION:

• Congenital heart diseases is a category of heart disease that

includes abnormalities in cardiovascular structures that occur
before birth.
OR
• Congenital heart disease, also called a defect, refers to one or
more problems with the heart structure that are present at birth.
OR
• Congenital heart disease refers to a problem with the hearts
structure and function due to abnormal heart development
before birth. Congenital means present at birth.
ANATOMY AND PHYSIOLOGY OF HEART
 PREVELANCE OF CONGENITAL HEART
DISEASE:

 Considering a birth prevalence of congenital heart disease as 9/1000, the

estimated number of children born with congenital heart disease in India is
more than 200,000 per year. Of these, about one-fifth are likely to have
serious defect, requiring an intervention in the first year of life.
 6 -8 per 1000 live births.
 1 per 1000 at 10 yrs of age.
 2% of total death is due to CHD
 A Cyanotic heart disorders are more common than cyanotic ones.
 For girls –PDA,ASD
 For boys –Pulmonary Stenosis ,Arterial Stenosis ,transposition and
coarctation are more common.
ACYNOTIC
HEART
DISEASE
 INTRODUCTION:

Acyanotic heart disease is where the blood contains enough oxygen

but it’s pumped abnormally around the body.
Babies born with acyanotic heart disease may not have any apparent
symptoms but, over time, the condition can cause health problems.
In this group of conditions there can be a significant increase in
blood pressure, putting the heart under more strain as it works much
harder. This can weaken the heart, and increases the risk of
developing heart failure, where the muscle is unable to efficiently
pump blood around the body.
 DEFINITION

In acyanotic heart diseases, either there is no abnormal

communication between pulmonary and systemic circulation
or if such connection is present, the pressure forces the blood
from arterial to venous side. The blood supplied in the body
is therefore oxygenated and cyanosis does not occur.
 INCIDENCE

 Congenital heart disease in 0.5-0.8% of live births.

 In stillborn (3–4%)
 Spontaneous abort uses (10-25%), and premature
infants (about 2% excluding [PDA])
 This incidence does not include mitral valve
prolapsed, PDA of preterm infants, and bicuspid aortic
valves (present in 1-2% of adults.
TYPES OF ACYNOTIC HEART DISEASE
 ACYNOTIC
CONGENITA
L HEART
DISEASE

INCREASED OBSTRUCTION TO
PULMONARY BLOOD FLOW FROM
BLOOD FLOW VENTRICLES

1. ARTERIAL SEPTAL DEFECT

2. VENTRICULAR SEPTAL DEFECT
3. PETENT DUCTUS ARTERIOSUS
4. ATRIOVENTRICULAR CANAL
1. PULMONARY STENOSIS
2. AORTIC STENOSIS
3. COARCTATION OF AORTA
INCREASED PULMONARY BLOOD FLOW

I.ARTERIAL SEPTAL DEFECT

DEFINITION :
Atrial septal defects (ASDs) are abnorrmal in the wall separating the
right and left atria.

Incidence:
Atrial Septal Defect Atrial septal defect (ASD) as an isolated anomaly
accounts for 5-10% of all CHD. Atrial septal defects accounts for about
17 % Of all congenital cardiac defects and occurs more frequent in girts
than in boys.
ASD is classified as follows:

Fossa Sinus
ovalis venosus
ASD ASD

Coronary Ostium
sinus primum
ASD ASD
PATHOPHYSIOLOGY of ASD
DIAGNOSTIC EVALUATION:
SURGICAL MANAGMENT
II. Ventricular Septal Defect
(VSD) :
DEFINITION:

Ventricular septal defect (VSD) is an abnormal communication between

the right and left ventricle.
INCIDENCE:

Ventricular septal defects are the most common heart lesions, accounting
for approximately 20% of all congenital heart defects.
 VSD
Atrioventricular
Canal Type
Subpulmonic
VSDs or
VSDs
Posterior
Defects

Membranous
Muscular VSDs
VSDs

TYPES
PATHOPHYSIOLOGY OF VSD
Systematic to pulmonary circulation connection

Left to right shunting of blood

Increased Pulmonary blood flow

Irreversible pulmonary vascular resistance

Right to left shunting of blood

Hypoxia and erythrocytosis

DIAGNOSTIC
EVALUATION
SURGICAL MANAGEMENT:
III. PETENT DUCTUS
ARTERIOSUS
 DEFINITION

Patent ductus arteriosus (PDA) is a communication between the pulmonary

artery and the aorta. The aortic attachment of the ductus arteriosus is just
distal to the left subclavian artery. The ductus arteriosus closes functionally
and anatomically soon after birth; its persistence is called PDA.
OR
Petent ductus arteriosis is a heart problem that is usually noted in the first few
weeks or month after birth . It is Characterized by a connection between the
aorta and the pulmonary artery which allow oxygen- rich (red) blood that
should go to the body to recirculate though the lungs.
PATHOPHYSIOLOGY
 CLINICAL MANIFESTATIONS

 Patients with PDA may become symptomatic in early life and develop
congestive cardiac failure around 6—10 weeks of age. Older children give
history Of effort intolerance, palpitation and frequent chest infections.
 Patients are usually asymptomatic when the ductus is small.
 Exertional dyspnea may be present in children with a large-shunt PDA.
 A large-shunt PDA may cause a lower respiratory tract infection, atelectasis, and
CHF (accompanied by tachypnea and poor weight gain).
 Tachycardia and tachypnea may be present in infants with CHF.
 A grade 1 to 4/6 continuous (“machinery”) murmur is best audible at the left
infraclavicular area or upper left sternal border.
 If pulmonary vascular obstructive disease develops, a right-to-left ductal shunt
results in cyanosis only in the lower half of the body.
DIANOSTIC EVALUATIONS
SURGICAL MANAGMENT
IV. ATRIOVENTRICULAR SEPTAL
DEFECTS
DEFINITION

Atrioventricular
Septal Defects are
characterized by
complete absence
of AV septum
 INCIDENCE

 AVSDs account for 4% to 5% of congenital heart disease

 New England Regional Infant Cardiac Program - 0.118/1000
livebirths
 Baltimore-Washington Infant study defined a prevalence of 0.362
 The Alberta Heritage study the prevalence was 0.203 and 0.242 per
1000 live births using invasive or noninvasive methodology for the
diagnosis respectively
 Gender distribution is approximately equal or may show a slight
female preponderance.
 CLINICAL MANIFESTATION

 Dyspnea
 Mild Cyanosis
 A newborn baby will show signs of heart failure such
as edema, fatigue, wheezing, sweating and irregular
heartbeat
 Characteristic Murmur
 Difficulty
Irregular or
breathing or Excessive
rapid
rapid sweating
heartbeat
breathing
Bluish Swelling in
discoloratio the legs,
COMPLETE Wheezing
n of the lips ankles and
DEFECT and skin feet (edema)

Pale skin
Fatigue
color

Lack of Poor weight

appetite gain
PARTIAL DEFECT
Abnormal
heartbeat
(arrhythmia)

Shortness of
Heart failure
breath

High blood
pressure in the
Heart valve
lungs
problems
(pulmonary
hypertension)
DIAGNOSTIC EVALUATION
SURGICAL CORRECTIONS
B. OBSTRUCTION TO BLOOD FLOW
FROM VENTRICLE

I. PULMONARY STENOSIS
 DEFINITION OF PULMONARY STENOSIS

Narrowing of the pulmonary

valve which controls the
outflow of blood from right
ventricle to the pulmonary
artery is known as pulmonary
stenosis. It is an obstructive
lesion that interferes with blood
outflow from the right ventricle.
TYPES OF PULMONARY STENOSIS

a. Sub valvular

b. Valvular

c. Supravalvular
 Due to Etiological factor
PATHOPHYSIOLOGY pulmonary wall is obstructed by fusion of cups
Resistance to blood flow from right ventricle to
pulmonary artery
Increase pressurein right ventricle

Increase pulmonary stenosis

Blood is backed up into the right atrium

Reopening of the foraman ovale

shunting of un-oxygenated blood to the left atrium

shunting of blood from aorta to pulmonary artery
and to lungs
No cyanosis
 CLINICAL MANIFESTATION

 Symptoms vary according to the degree of obstruction..

 Growth and development are usually normal with moderate
pulmonary stenosis. However, during the first 2 to 3 years of life they
may develop dyspnea on exertion and easy fatigability. Symptoms of
severe stenosis are:
 Poor exercise tolerance
 Exertional dyspnea due to poor or insufficient blood flow to lungs.
 Fatigability
 Strenuous exercise in these children results in syncope or sudden
death.
DIAGNOSTIC EVALUATION
SURGICAL MANAGMENT
II. AORTIC STENOSIS
DEFINITION

Aortic valve stenosis is narrowing of the orifice between

the left ventricle and aorta. In adults, stenosis often is a
result of degenerative calcifications.
 CAUSES
 Calcifications may be caused by proliferative and inflammatory
changes that occur in response to years of normal mechanical stress,
similar to changes that occur in atherosclerotic arterial disease.
 Age, diabetes, hypercholesterolemia, hypertension, smoking, and
elevated levels of low-density lipoprotein cholesterol may be risk
factors for degenerative calcific changes of the valve.
 Congenital leaflet malformations or an abnormal number of leaflets
(i.e., one or two rather than three) may be involved.
 Rheumatic endocarditis may cause adhesions or fusion of the
commissars and valve ring, stiffening of the cusps, and calcific
nodules on the cusps.
 PATHOPHYSIOLOGY
Aortic valve obstruction

Increase intraventricular pressure

Left ventricle hypertrophy

Increase left ventricle end diastolic pressure

Progressive valvular obstruction and increasing wall stress

Increased filling pressure, ventricular dilation, and contractile

dysfunction, ischemia

Angina, syncope, dyspnea

 CLINICAL MANIFESTATIONS

 patients usually first have exertional dyspnea, caused by

increased pulmonary venous pressure due to left ventricular
failure Orthopnea, PND, and pulmonary edema also may occur.
 Reduced blood flow to the brain may cause dizziness and
syncope.
 Angina pectoris is a frequent symptom: it results from
increased oxygen demand of the hypertrophied left ventricle
with decreased blood supply due to decreased blood flow into
the coronary arteries and decreased time in diastole for
myocardial perfusion.
DIGNOSTIC EVALUATION
 SURGERY:

one or two-balloon
percutaneous valvuloplasty
procedures
III. MITRAL VALVE STENOSIS
 CAUSES:
 At congenital level
 Thick or stiff valve flaps, also called leaflets.
 Deformed leaflets or leaflets that join together. Your provider may say they
are fused.
 Problems with the cords that support the valve. They might include missing
cords, short and thick cords, or cords attaching to the heart muscle near the
mitral valve.
 Heart tissue or heart muscle problems near the mitral valve.
 More than one opening in the area of the mitral valve. This is called a double-
orifice valve.
 PATHOPHYSIOLOGY:

Mitral valve stenosis

Gradient between left atrium and
left ventricle increases
Left atrial pressure rises

pulmonary venous congestion

Pulmonary edema and pulmonary
hypertension
 CLINICAL MANIFESTATIONS:

 Shortness of breath, especially with activity or when you lie down

 Fatigue, especially during increased activity
 Swollen feet or legs
 Sensations of a fast, fluttering or pounding heartbeat
 Dizziness or fainting
 Irregular heart sound, also called a heart murmur
 Fluid buildup in the lungs
 Irregular heart rhythms
 Chest discomfort or chest pain
 Coughing up blood
 DIAGNOSTIC EVALUATION

 Echocardiogram.
 Electrocardiogram.
 Chest X-ray.
 Exercise stress tests.
 Cardiac CT.
 Cardiac MRI.
 SURGICAL REPAIR:

1.Balloon valvuloplasty
2.Open-heart surgery to
repair the valve.
3.Mitral valve
replacement.
IV. COARCTATION OF AORTA
DEFINITION

Coarctation of aorta is a discrete

narrowing of aortic arch, usually in
juxta ductal position (in the region
of ductus arteriosus and left
subclavian artery).
 CLINICAL MANIFESTATIONS

There are two groups of patients with coarctation:

I. Those who are symptomatic in infancy.

II.Those who remain asymptomatic and are
diagnosed during routine physical examination in
later years.
 DIAGNOSTIC EVALUATION

 Cardiac examination: The first and second heart sounds are usually normal.
There may be no murmurs present or a systolic murmur may be heard along
the left mid to upper sternal border that radiates to the back.
 Electrocardiogram: Left or right ventricular hypertrophy is seen on ECG in
the infant with coarctation. The older child may have left ventricular
hypertrophy or a normal ECG.
 Echocardiogram: The presence of a coarctation and the degree of narrowing
as well as presence of other cardiac defects may be determined by the
echocardiogram.
 MRI and cardiac catheterization are useful in clearly defining the area and
extent of narrowing.
SURGICAL CORRECTIONS
C. MALPOSITION AND MALCONNECTION

CONGENITALLY CORRECTED
TRANSPOSITION

OF THE GREAT ARTERIES

 PATHOPHYSIOLOGY

The most common clinical sequelae and/or complications with CCTGA

include right ventricular dysfunction, tricuspid regurgitation, residual
left ventricle outflow obstruction, and complete heart block. Progressive
right ventricle dysfunction resulting in heart failure is associated with
increasing age, typically in the fifth decade, as the morphological right
ventricle begins to fail as the systemic ventricle. Complete heart block,
if not present at birth, is likely to develop at a rate of 2% per year, due
to the unusual location and course of the atrioventricular node. In
patients without associated lesions, it is expected that up to 27% are in
need of a pacemaker. This percentage increased up to 45% in patients
with associated heart defects.
 CLINICAL MANIFESTATIONS

Adults with CCTGA present as one of two groups:

(1) those diagnosed and repaired in infancy and now
present with residual defects associated with a VSD or
pulmonic stenosis, or
(2) those with no associated lesions who have essentially
remained asymptomatic but now have developed symptoms
related to progressive right ventricle dysfunction or to
atrioventricular valve regurgitation.
DIAGNOSTIC EVALUATION
SURGICAL MANAGMENT
 HEALTH
EDUCATION
 NURSING RESPONSIBILIY:

Nurses play a crucial role in caring for patients with

acyanotic heart disease, which refers to congenital heart
defects that do not cause cyanosis, a bluish discoloration
of the skin and mucous membranes due to low oxygen
levels in the blood. Nursing care for these patients
involves a combination of assessment, monitoring,
education, and emotional support. Here is a detailed
overview of the nursing role in caring for acyanotic
heart disease patients:
Nursing Care Plan for Child with
Congenital Heart Disease:
RESEARCH
EVIDANCE:
 Article :
Nurses' Perceptions of a Novel Rooming-in Program for Infants With Critical
Congenital Heart Disease

AUTHORS: Jenna Shackleford , Jennifer Nelson , Susan Brasher

Abstract
Background: The transition to home for infants who require complex care
can be overwhelming for caregivers. Infants with critical congenital heart
disease (CCHD) require advanced care management, so their caregivers
must acquire extensive training before the infants are discharged home.
Rooming-in programs have improved patient outcomes in other settings,
such as the postpartum period. However, little research has examined a
rooming-in program in a pediatric cardiac acute care setting.
Objective: To describe nurses' perceptions of a novel rooming-in
program implemented in a pediatric cardiac acute care unit.
Methods: A qualitative descriptive research design was used to
describe nurses' perceptions of the rooming-in program for infants with
CCHD. Three focus groups were conducted with a convenience sample
of 13 registered nurses who cared for infants with CCHD during the
rooming-in program. Four trained independent coders performed
qualitative thematic analysis.
Results: Nurses provided critical insight into the rooming-in program. Three
themes were identified: improved nursing and family outcomes, leading the way
through collaboration, and room for improvement.

Conclusions: Infants with CCHD have complex needs, and caregivers must
acquire advanced skills to adequately care for these infants. This study is the first
to explore nurses' perceptions of a rooming-in program for infants with CCHD.
The findings could improve rooming-in programs in the pediatric acute care
setting, which can translate to better patient outcomes.
SUMMARY
CONCLUSION:
 BIBLIOGRAPHY

1. Janice L. Hinkle and Kerry h. Cheever, Brummer & Suddharth’s Textbook of Medical
– Surgical Nursing, Volume II, Edition 13, Wolter Kluwers publications, page no. 1379
2. Joyce M. Black, Jane Hokanson Hawks, Medical Surgical Nursing, Clinical
management for positive outcome, Volume- II, Edition 8, Elsevier Publication page no
1312-1325
3. Rimple Sharm, Essentials of Pediatric Nursing, Jaypee brothers medical publishers,
page no. 407-413
4. Vinod K Paul Arvind Bagga, GHAI Essential Pediatrics, Ninth Edition, CBS
Publishers & Distributors Pvt Ltd, 409-419
5. Woods susan, Textbook of cardiac nursing, Wolter kluver publications, 6 th edition,
page no. 723-737
6. https://pubmed.ncbi.nlm.nih.gov/36587000/
7. https://www.heart.org/en/health-topics/congenital-heart-defects/about-congenital-
heart-defects
THANK YOU !