Atrial septal defect Ventricular septal defect Persistent ductus arteriosus

Defect  Secundum ASD (80%) 30% of all cases of congenital heart disease In PDA duct fails to close 1month after the ex-
 Partial atrioventricular septal defect AVSD/pri-  Perimembranous ( adjacent to tricuspid pected date of delivery due to defect in constrictor
mum ASD valve) mechanism of the duct.
 Muscular (completely surrounded by muscle) Flow if blood is from the aorta to the pulmonary
According to size:- artery.
 Small VSD (smaller than aortic valve in diam- In preterm infant PDA presence is not from congen-
eter up to 3mm) ital disease
 Large VSD
Symptoms  None Small VSD:
 Recurrent chest infections Asymptomatic
 Arrhythmias(fourth decade onwards) Large VSD
 Heart failure with breathlessness and falter-
ing growth after 1 week old
 Recurrent chest infection

Physical signs  An ejection systolic murmur at upper left ster- Small VSD  Continuous murmur beneath left clavicle/Upper
nal edge, due to increased flow at pulmonary  Loud pan-systolic murmur(lower left sternal left sternal edge, continues into diastole (because
valve, from increased flow across pulmonary edge pressure in pulmonary is always lower than
valve)  Quiet pulmonary second sound aorta)
 Fixed widely split heart sound (due to right ven- Large VSD  Pulse pressure increased, collapsing or bounding
tricular stroke volume being equal in both inspi-  Soft pan-systolic murmur or no murmur pulse
ration and expiration  Apical mid-diastolic murmur (from increased  When duct is large there will be increased blood
 In partial AVSD: Apical pan systolic murmur flow across the mitral valve after blood has flow with heart failure and pulmonary hyperten-
(from atrioventricular valve regurge) circulated through the lungs) sion
 Loud pulmonary second sound P2 (from
raised pulmonary arterial pressure)
 Tachypnea, tachycardia, and enlarged liver
from heart failure
 Active precordium
Chest radiograph  Cardiomegaly  In Large VSD Usually normal
 Enlarged pulmonary arteries  Cardiomegaly  Normal or enlarged heart
 Increased pulmonary vascular markings  Enlarged pulmonary arteries  Enlarged pulmonary arteries
 Increased vascular markings  Increased pulmonary vasculature
 Pulmonary edema
ECG  Secundum ASD  In Large VSD  Usually normal
- partial right bundle branch block Biventricular hypertrophy by 2 months of age  Left ventricular hypertrophy with large left to
- right axis deviation(due to right ventricular right shunt
enlargement)  Right ventricular hypertrophy with pulmonary hy-
 Partial AVSD pertension
- A superior QRS axis
- Negative deflection in AVF
Echocardiography Will delineate he anatomy  In Large VSD Duct readily identified
Demonstrates anatomy of defect
Hemodynamic effects and high pulmonary pres-
sure (due to high flow)
Management If defect is large enough to cause right ventricular  Small VSD At 1 year of age:
dilation. Lesion will close spontaneously but prevention of Closure with a coil or occlusion device, introduced
At 3 years to 5 years (to prevent right heart fail- bacterial endocarditis is important: by maintain- through a cardio catheter Occasionally surgical liga-
ure and arrhythmias) ing good dental hygiene, avoiding body piercings tion is required
 Secundum ASD and tattoos
Cardiac catheratization with insertion of occlusion  In Large VSD
device Surgery performed at 3 month to 6 months of
 Partial AVSD age.
surgical correction  To manage heart failure and faltering growth
 Prevent permanent lung damage from pul-
monary hypertension

Drug therapy is with diuretics often combined

with captopril.
Additional calorie input is required.
Aortic stenosis Pulmonary stenosis Coarctication of aorta