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Neonatal Congenital Heart Diseases Guide

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0% found this document useful (0 votes)
48 views73 pages

Neonatal Congenital Heart Diseases Guide

Uploaded by

hemlata
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

NEONATAL HEART

DISEASES

Presented by :
Ms. Hemlata
Tutor
CON,AIIMS Jodhpur
INTRODUCTION

Congenital Heart Diseases


• They are serious and have significant
impact on morbidity and mortality.
• Its incidence is 8/1000 live birth
Globally

• It is a general term for a


range of birth defects that
affect the normal way the
heart works
ANATOMY OF THE HEART

• The Heart Valves Four


types of valves regulate
blood flow through your
heart:

1. The tricuspid valve

2. The pulmonary valve

3. The mitral valve

4. The aortic valve


FETAL CIRCULATION
ETIOLOGY
• Unknown in most cases
• Genetic factors - single gene defect
• Chromosomal abnormality- down syndrome
• Maternal infections- rubella
• Smoking, Alcohol and statins or acne
medicines
• Diabetes in pregnancy
Clinical Classification

Acynotic Heart Cyanotic Heart


Ma. Tosca Cybil A. Torres,
Disease Disease
RN
DEFINITION
A congenital disorder
manifested with left to
right shunting and left
sided obstructive lesions.

Clinical signs are not always


apparent at birth, they
manifest anytime during
infancy or early childhood.
PATHOPHYSIOLOGY

Normal circulation is impaired

Increased pressure in left side of heart

Shunting of blood from left side to right side

Since the left side blood is oxygenated , does not


cause cyanosis

ACYNOTIC HEART DISEASE


ARTERIAL SEPTAL
DEFECT

VENTRICULAR
PATENT
SEPTAL
DUCTUS
DEFECT
ARTERIOSUS

ATRIO-VENTRICULAR
SEPTAL DEFECT
Coarctation
of aorta

Congenital Left-sided
Interrupted
aortic obstructive
aortic arch
stenosis lesions

Mitral
stenosis
ARTERIAL SEPTAL DEFECT
• Hole in the wall(septum)
between right and left
atria.

• Commonest type of
CHD(30-40%)

• 1Child/1500 Live births


PATHOPHYSIOLOGY

During fetal development, a foramen ovale left open

To allow blood bypass the lungs and take maternal circulation

Due to force from either side of atrium, it closes

If failed , and left open called

ATRIAL SEPTAL DEFECT


TYPES
TYPES
Sign and Symptoms
• Fatigue
• Tired
• Shortness of breath
• Fluid And blood in the lungs
• Fluid in feet, ankles and legs
• Sweating
• Rapid breathing
• Poor growth
ALTERED HEMODYNAMICS

Increased Enlarge
blood flow Increased
Left to right
through Pulmonary
right Atrium
ASD Blood
shunting and right
Flow
Ventricle
DIAGNOSTIC EVALUATION
MANAGEMENT

THERAPEUTICS MANAGEMENT
• Elective Surgical Repair (2-5 years of age)
MEDICAL MANAGEMENT
Atrial dysrythmias (anti-dysrythmics
SYMPTOMATIC CASES
SURGICAL TREATMENT

• Surgical closure using either sutures or a pericardial


prosthetic patch is performed on an elective basis early
in childhood. This is an open heart procedure, through
a sternal incision.
VENTRICULAR SEPTAL DEFECT
A hole in the wall
between the two
lower chambers is
called a ventricular
septal defect.

25% In all CHD


PATHOPHYSIOLOGY

During fetal development, muscular ridge from apex


grows upward

While , membranous region grows downward from


endocardia cushion

Form 2 different chambers called right and left


ventricles

If failed to fuse form a defect, called

VENTRICULAR SEPTAL DEFECT


ALTERED HEMODYNAMICS

Pulmonary Pulmonary
Increased vascular hypertension and
blood circulation pulmonary
L R flow receives vascular
Shunt through increased diseases(EISONM
VSD pulmonary ERGER’S
blood flow SYNDROME)
TYPES
C/F OF VSD
• Poor growth and poor weight gain
• Tachycardia, tachypnoea, and
hepatomegalyy
• Pneumonia
• Sweating
• Frequent cough
DIAGNOSTIC EVALUATION
MANAGEMENT

20-80% closes spontaneously /


no surgery
Antibiotic prophylaxis
ACE inhibitors to reduce after
load
Nutritional supplement to
increase calorie intake (infant
formula)
Prevent respiratory infections
SURGICAL MANAGEMENT

PLACING THE PATCH OVER THE DEFECT


THROUGH RA PATCH PLACED, TO AVOID
RV INCISION
Congestive Heart
Failure

Growth failure

Irregular rhythm

Pulmonary
hypertension
PATENT DUCTUS ARTERIOSUS

The vessel does not close


and remains "patent"
resulting in irregular
transmission of blood
between two of the most
important arteries close to
the heart, the aorta and the
pulmonary artery

1 in 2000 live births


PATHOPHYSIOLOGY
During fetal development, Ductus arteriosus
vessel connects the pulmonary artery and
Arota

It closes after birth and become ligament


arteriosus

If fails to close, become patent

PATENT DUCTUS ARTERIOSUS


ALTERED HEMODYNAMICS

Pulmonary
Increased vascular
L R blood flow circulation Pulmonary
through receives
Shunt PDA increased hypertension
pulmonary
blood flow
SIGN AND SYMPTOMS
DIAGNOSTIC EVALUATION
MANAGEMENT

 Prostaglandin
inhibitor

orally 0.2
mg/kg TDS at an
interval of 12 to
24 hours
SURGICAL
MANAGEMENT
ATRIO-VENTRICULAR CANAL
DEFECT
• Complete absence of AV septum
– A common atrioventricular ring
– A five leaflet valve that guards
the common AV orifice
– An unwedged left ventricular
outflow tract
– LV mass characterized by
longer distance from apex to
aortic valve than from apex to
left AV valve
ENDOCARDIAL CUSHION
DEFECT
• AVSDS account for 4% to 5% of congenital heart
disease
PATHOPHYSIOLOGY

A hole or abnormality in septum of atrium and


ventricles

Leads to increase blood flow to lungs cause


high blood pressure

Pulmonary hypertension

EISENMENGERS SYNDROME
TYPES OF AVSD
• Asymptomatic
Partial • Dysnoea
AVSD • Growth retardation

• Tachypn a
Complete • Pulmonary vascular
AVSD obstructive disease
SIGN & SYMPTOMS
• Blue or gray skin color due to low oxygen levels
• Difficulty breathing or rapid breathing
• Excessive sweating
• Fatigue
• Irregular or rapid heartbeat
• Lack of appetite
• Poor weight gain
• Swelling in the legs, ankles and feet
• Wheezing
DIAGNOSTIC EVALUATION
MANAGEMENT
EISENMENGER’S SYNDROME
SIGN AND SYMPTOMS
• asymptomatic or have only
mild dyspnea
• Reduced exercise capacity
• Dyspnea and fatigue
develop gradually as
pulmonary blood flow
decreases
• hypoxemia increases due to
bidirectional shunting
DIAGNOSTIC EVALUATION
MANAGEMENT
Transplantation is an effective choice of treatment
HEART
DEFECTS
TATRALOGY OF FALLOT

1. Ventricular septal
defect
2. Pulmonary
stenosis
3. Overriding aorta
4. Right ventricular
hypertrophy
PATHOPHYSIOLOGY
The blood normally returns from the systemic
circulation to the right atrium and right ventricles

The outflow of blood from the right ventricles is


resisted by the pulmonary stenosis so that the blood
flows through the ventricular septal defect in to the
aorta

There is right to left shunt. Hypertrophy of the right ventricles


occurs as a result of the pressure exerted against the
pulmonary stenosis.

CYANOSIS
CLINICAL MANIFESTATION
DIAGNOSTIC EVALUATION

ON AUSCULTATION A loud
harsh systolic murmur may be
heard at the left middle to
lower sturnal border.
MANAGEMENT
SURGICAL
MANAGEMENT
COMPLETE REPAIR PALLIATIVE SHUNT
TRICUSPID ATRESIA
• Failure of the tricuspid
valve to develop
consequently no
communication form right
atrium to right ventricle

• complete mixing of
unoxygenated and
oxygenated blood in the
left side of the heart.
CLINICAL MANIFESTATION
MANAGEMENT
TRANSPOSITION OF THE GREAT
ARTERIES
Aorta arising
from the right
ventricle and
pulmonary
artery from the
left ventricle.
SIGN & SYMPTOMS
PATHOPHYSIOLOGY
Aorta has its origin in the right ventricles and pulmonary artery
has its origins in the left ventricles.

aorta carries unoxygenated blood to the systemic circulation and


the pulmonary circuit carries oxygenated blood back to the lungs

The pulmonary venous return is to the left atrium and the


systemic veins returns to the right atrium

There is two separate circulatory systemic exist, one pulmonary


and one systemic.

CYANOSIS
DIAGNOSTIC EVALUATION
MANAGEMENT
• CONTROL TO CCF

• Blalock Hanlon
procedure -surgical
creation or enlargement
of an existing arterial
septal defect.
• Rash kind operation –
enlargement of an
existing arterial septal
defect.
NURSING DIAGNOSIS
1. Decreased cardiac output related to structural
defect
2. Activity intolerance related to imbalance between
oxygen supply and demand.
3. Altered growth and development related to
inadequate oxygen, nutrients to tissue and social
isolation
4. High risk for infection related to debilitated
physical status.
5. Altered family process related to having a child
with a heart condition.
6. High risk for injury (complications) related to
cardiac condition and therapies
CONCLUSION
TAKE HOME MESSAGE
THANK YOU……..

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