Cardiac notes for B.Sc Nurisng students..BY Jayesh Soni Sir

1. Mr. Jayesh Soni
HOD Pediatrics
VCN Udaipur

2. 1. Umbilical arteries :- umbilical ligament (2 to 3
months)
2. Umbilical vein :- ligamentum teres
3. Ductus venosus :- ligamentum venosum
4. Ductus arteriousus :- ligamentum arteriosum
(1- 3 months)
5. Foramen ovale :- functional closure soon after
birth but anatomical closure occurs in about 1
year time (fossaovalis)

5. INCIDENCE:-
 Approximately 8 to 12 childern in 1000
are born with a congenital heart defect.
 Heart defects are among the most
common birth defect and are the
leading cause of birth defect-related
deaths.
 Right sided lesions are more common
in female, & left sided in males

6. ETIOLOGY:-
 90 % of cases is unknown.
 Heredity
 Consanguinous marriage
 Chromosomal abnormality – Trisomy 21(Down
syndrome), - Turner syndrome
 Other associated factors
- Teratogenic infections (Rubella)
- Teratogenic drug (thalidomide)
- Alcohol intake
- Radiation in 1st trimester of pregnancy
- Maternal IDDM
- High altitude
- Fetal hypoxia
- Birth asphyxia

7. CLASSIFICATION OF CHD :-
Obstruction of
blood from
ventricles
Increased pulmonary
blood flow
•Aortic stenosis
•Coarctation of aorta
•Pulmonary stenosis
•ASD
•VSD
•PDA
•AVC DEFECT
Acyanoti
c

8. CLASSIFICATION OF CHD :-
Mixed blood flow Decreased
pulmonary blood flow
• TGA
• Total anomalous
pulmonary venous
return
• Truncus arterious
• Hypoplastic left heart
syndrome
•TOF
•TA
Cyanotic

10. ACYANOTIC HEART DISEASES
If there is no abnormal communication
between pulmonary & systematic circulation
Or
If such connection is present, the pressure
forces the blood from arterial to venous side.
The blood supplies in the body is therefore
oxygenated & caynosis does not occurs.

12. ASD:
Atrial Septal defects are abnormal opening in
wall separating the right & left atria
….
More common in females, approx 17% of all
cases in congenital cardiac defects..

13. TYPES :-
1. Ostium primum - opening at lower
end of septum
2. Ostium secundum - opening at
centre of septum
3. Sinus venosus - opening at top of
septum

15. PATHOPHYSIOLOGY:-
Shunting b/w Lt to Rt
Volume overload in Rt
side
Rt heart enlargement
Overload on pulmonary
vasculature
Pulmonary HTN RVF

16. CLINICAL MANIFESTATIONS
• Frequent chest infection
• Effort intolerance
• dyspnoea
• Bulging of chest
• Congestive heart failure
• Cardiac enlargement

17. DIAGNOSIS
• Physical examination: systolic murmur
• Chest x ray: RA & RV hypertrophy
• Echocardiography
• ECG

18. MANAGEMENT :-
Medical management
• Treatment of chest infection & infective
endocarditis
• Interventional therapy
- Percutaneous ASD closure
Surgical management
• Mostly by simple suture closure
• In larger defects pericardial or prosthetic
patch

20. PERCUTANEOUS ASD CLOSURE

21. NURSING MANAGEMENT :-
 Closely monitor vital signs, central venous
and intra-arterial pressures, and intake and
output.
 Watch for atrial arrhythmias.
 Give an antibiotic and an analgesic, as
ordered.
 Provide range-of-motion exercises and
coughing and deep-breathing exercises.

22. COMPLICATIONS
• Pulmonary hypertension
• Heart failure
• Atrial fibrillation
• Stroke from embolization
• Eisenmenger syndrome (reversal of the
shunt into a right-to-left shunt)
• Infective endocarditis
• Surgical complication

23. VENTRICULAR SEPTAL DEFECT
Accounts for 25 %of
all congenital heart
lesions. Also called
 Roger’s disease
 Interventricular
septal defect

24. Types of VSD:-
1. Membranous VSD 2. Muscular VSD

25. PATHOPHYSIOLOGY :-
Shunting of blood from Lt to Rt
Rv to pulmonary artery
Volume overload in the Rt side
Pulmonary HTN
Eisenmenger’s syndrome and hypertrophy of
muscle

26. SIGNS & SYMPTOMS :-
 Palpitation
 Frequent chest infection
 Feeding difficulties
 Tachycardia
 Excessive sweating associated with feeding
 Poor weight gain
 Failure to thrive
 Biventricular hypertrophy
 Congestive heart failure

27. DIAGNOSTIC EVALUATION
•Auscultation of heart sounds – harsh
systolic murmur sound.
•Chest X-ray :- enlargement of heart.
•ECG = biventricular hypertrophy.
•2-D-echocardiogram with colour
Doppler study.

28. MANAGEMENT OF VSD:-
• SMALL VSD
- all close spontaneously
* 50% by 2yrs
* 90% by 6yrs
* 100% during school yrs
Surgical intervention is usually
not necessary

29. • MODERATE TO LARGE VSDs :-
1. Medical Management:
a. CHF management: digoxin and diuretics
b. Avoid oxygen; oxygen is a potent pulmonary
vasodilator and will increase blood flow into the PA.
c. Increase caloric intake
2. Cardiac catheterization for placement of a
ventricular occlusion device for muscular defects

30. INDICATIONS for SURGERY
• Basic Indications for surgical closure
– Mid-large shunt
– Failure to thrive
– Continued CHF or
– Recurrent pulmonary infections
• SURGERY:- (Usually repaired before age 1)
a. One-stage approach: preferred surgical plan; patch closure
of VSD (an oval patch of knitted dacron by mattress suture
posteriorly).
b. Two-stage approach: first surgery is to band the PA to
restrict pulmonary blood flow; second surgery is to patch close
the VSD and remove the PA band.

31. Surgical
correction has
to be done
before
irreversible
damage to
pulmonary
vasculature
occurs.

33. COMPLICATIONS
• Congestive cardiac failure
• Infective endocarditis on rt.ventricular side
• Complete heart block
• Delayed growth & development in infancy
• Damage to electrical conduction system
during surgery (causing arrythmias)
• Pulmonary hypertension
• Eisenmenger's syndrome.