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CONGENITAL HEART DISEASE.

CONGENITAL HEART DISEASE. SADATH ALI KHAN. 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.

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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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