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CONGENITAL HEART DISEASE.

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 عبد المهدي عبد الرضا حسن الشحماني 7/15/2011 10:19:29 AM
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 CONGENITAL HEART DISEASE   
الدكتور عبد المهدي عبد الرضا حسن                                                                                                                                
كلية التمريض / جامعة بابل                                                                                                                                       

PhD, pediatric & Mental Health Nursing                                                                                                             
  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. Classification ? 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. 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. 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. 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. 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. 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. 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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