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CONGENITAL HEART DISEASE.

Congenital heart disease (CHD) affects 0.5-0.8% of live births and is the leading cause of pediatric mortality. Its etiology is often multifactorial, with genetic factors and environmental influences playing significant roles. Common types include atrial septal defects (ASD), ventricular septal defects (VSD), and patent ductus arteriosus (PDA). Clinical features vary widely, from asymptomatic cases to severe symptoms like cyanosis and heart failure. Diagnosis involves imaging and echocardiography, while treatment may include medications, catheterization, or surgery.

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CONGENITAL HEART DISEASE.

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  1. CONGENITAL HEART DISEASE. SADATH ALI KHAN.

  2. Epidemiology • Prevalence:0.5-0.8% of live births (8/1000).Leading cause ofdeath in children with CHD. • Etiology:Unknown,multifactorial inheritance,genetic factors implicated,high incidence in first degree relatives. • 3% have a single gene defect,13% have associated chromosomal abnormalities. • 2-4% are associated with environmental or maternal conditions & teratogenic influences. • Gender differences:ASD,VSD,PDA & Pulmonic stenosis more common in girls,left sided lesions in boys.

  3. Acyanotic:according to the predominant physiologic load placed on the heart. Volume load:L-R shunts-ASD,VSD,PDA. Pressure load:Ventricular outflow obstruction Pulmonary,aortic valve lesions,aortic coarctation & pulmonary stenosis. Cyanotic:based on pathophysiology. Decreased pulmonary bloodflow:TOF,Pulmonary atresia,Tricuspid atresia,Single ventricle with pulmonic stenosis. Increased pulmonary blood flow:Transposition of great vessels,Truncus arteriosus. Classification

  4. ATRIAL SEPTAL DEFECT. • Sinus venosus defect:high in the septum. • Ostium secundum defect:midseptum. • Ostium primum defect:low in the septum. • Pathophysiology:L-R shunt-increased flow across Rt heart-RV & PA enlargement. • Clinical features:asymptomatic,slow wt gain,frequent LRTI. • Diagnosis:Rt ventricular heave,systolic murmur,fixed wide split S2.

  5. Investigations: • CXR:enlarged heart & PA,increased vascularity. • ECG:Rt axis in secundum defect,hallmark of primum defect is extreme Lt axis,RVH. • ECHO:RVH,valve anatomy,flow direction. • Treatment:closure during cardiac cathetrization,surgical closure.

  6. VENTRICULAR SEPTAL DEFECT. • Most common CHD (26%),may be single or multiple. • Pathophysiology:Lt-Rt shunt as long as pulmonary vascular resistance is lower than systemic resistance,if reverse shunt reverses • Large defects lead to pul.hypertension-Eissenmenger syndrome. • Clinical features: depend on size,asymptomatic,growth failure,recurrent LRTI,congestive heart failure,SOB,cyanosis • Diagnosis:pansystolic murmur,loud p2.

  7. Investigations • CXR:cardiomegaly,enlarged LA&LV. • ECG:extreme lt axis is charecteristic,biventricular hypertrophy. • ECHO:chamber size & pressures. • Cardiac catheter:O2 content,PA pressure,size & no of defects. • Treatment:Endocarditis prophylaxis,digoxin,diuretics. • Surgical closure before pulmonary vascular changes become irreversible.

  8. PATENT DUCTUS ARTERIOSUS. • Connection between PA & descending aorta • 10% of CHD. • Pathophysiology:Lt-Rt shunt,reverses if pulmonary resistance increases-RV enlargement.If PDA is large Eissenmenger syndrome can develop. • Clinical features:depend on size & direction of flow,slow growth,LRTI,SOB,cyanosis. • Diagnosis:bounding pulse,continous murmur,loud S2.

  9. Investigations • CXR:cardiomegaly,increased pul vascularity. • ECG:Lt or biventricular hypertrophy. • ECHO:2D visualises PDA,doppler shows turbulance. • Cardiac catheter:PA pressures & O2 sats. • Treatment:Endocardial prophylaxis as long as patent,Indomethacin. • Surgical:ligation is curative.

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