BASICS OF CONGENITAL

HEART DISEASE
 Fetal Circulation
Pre-condition
 Oxygenated blood from placenta

 Lungs ineffective

 Rt heart has little role

Characteristic of Fetal Circulation

 Oxygenated blood flows through systemic venous

system rt heartleft heart systemic circulation

 Rt heart outflow insignificant

 Rt heart outflow re-directed to systemic circulation

Changes at birth
 Pulmonary vascular resistance decreases
 Systemic vascular resistance increases
 Ductus venosus closes
 ASD closes
 Ductus arteriosus closes
Development of heart
Primitive heart
tube
Atrial Septum
NORMAL HEART
Congenital Heart Disease
 Left/ Rt mixing through a
hole/communication
 Outflow obstruction: atriaventricles
Ventricles great vessels

 Atrio-ventricular mixing through a communication:

defect in valves
CLASSIFICATION

SHUNTS
 L R VSD, ASD, PDA
 R L EISSENMENGER,
TOF
OBSTRUCTION
 Rt sided outflow obstrn: PS , PA
 Lt sided outflow obstrn :
AS, Coarctation

MIXING OF BLOOD DORV, TGA, SV, TAPVC,

Persistent Truncus
Congenital Heart Diseases
L R SHUNTS
 Recurrent RTI
 Large heart
 Pre cordial bulge
 Hyperkinetic heart
 Co-exiting TR/ MR
 Plethoric lung fields
RL SHUNT
 Cyanosis
 With increased pulmonary blood flow
 Pulmonary Arterial Hypertension
 Cardiomegaly
 CCF
 Plethora
 With pulmonary outflow obstruction: see Fallot’s
Physiology
MIXING OF BLOOD
 Cyanosis
 Recurrent RTI
 Large heart
 Pre cordial bulge
 Hyperkinetic heart
OUTFLOW TRACT OBSTRUCTION

 No bulge, no heave, silent heart

 Concentric hypertrophy, later failure
 Rt side obstruction: cyanosis
 Lt side obstruction: dyspnea, fatigue, syncope,
pain
LeftRt Shunt
 Atrial Septal defect
 Ventricular Septal defect
 Patent Ductus Arteriosus
Atrial Septal Defect

 Most common form of ASD

(fossa ovalis)
 In large defects, a
considerable shunt of
oxygenated blood flows
from the left to the right
atrium.
 Mostly asymptomatic
 The 2nd heart sound is
characteristically widely
split and fixed. Secundum
Atrial Septal defect

 LtRt shunt at atrial level

 Rt atrium dilates to accommodate extra blood
 Rt ventricle enlarges
 Large volume blood thru normal tricuspid valve:
delayed diastolic murmur
 Large volume blood thru normal pulm valve:
Ejection systolic murmur
 P2 fixed wide split
Ventricular Septal defect

 Flow of blood from LtRt ventricle from early

systole, continues thru’ out systole. Even after
aortic valve closes (A2) : Pan systolic murmur
 This extra blood passes on into pulmonary artery
during systole. So no Rt ventricular dilatation.
 Pulmonary circulation overloaded Venous return
to Lt Atrium: overload Left Atrial enlargement:
delayed diastolic murmur
 Left ventricular overload LVH
Patent Ductus Arteriosus

 Lt Rt shunt from aorta to pulmonary artery

 Continues through out systole and diastole:
machinery systolo-diastolic murmur
 Left atrial enlargement and LVF
Rt sided Outflow Obstruction
 Pulmonary Stenosis/ Atresia
(Pre-valvar/valvar/post valvar)

 Fallot’s Physiology
 Pulmonary outflow obstruction
 Rt Ventricular pressure increased
 RtLt shunt
 Fallot’s Physiology

Presentation
 Cyanosis

 Normal sized heart/ RVH

 Ejection systolic murmur

Conditions:
 Fallot’s Tetralogy
 TGA with VSD-PS
 Corrected TGA with VSD-PS
 DORV with VSD-PS
 Single Ventricle with PS
 Tricuspid atresia with diminished pulmonary flow
Tetralogy of Fallot
Normal vs Fallots
 Fallots Physiology

TOF Single
Ventricle,
PS

DORV
TGA
Acyanotic CHD

Normal ASD VSD