Congenital heart disease. By Dr Saima Ali Professor of pediatrics
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1 Congenital heart disease By Dr Saima Ali Professor of pediatrics
2 What is the most striking clinical finding in this child?
3 Learning objectives By the end of this lecture, final year student should be able to Classify different types congenital heart disease. Discuss the pathophysiology of congenital heart disease. Interpret the CXR and ECG of acynotic heart disease. Manage a child with acyanotic heart disease and refer appropriately whenever needed.
4 Lets
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7 Fetal circulation Three cardiovascular structures unique to the fetus are important for maintaining this parallel circulation: the ductus venosus, foramen ovale, and ductus arteriosus.
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9 prevalence v Congenital heart disease occurs in % of live births. v When two 1st-degree relatives have congenital heart disease, the risk for a subsequent child may reach 20 30%.
10 classification CHD is divided into Acyanotic heart disease (L-R shunt lesion) cyanotic heart disease (R-L shunt lesion)
11 Acyanotic heart disease L-R shunt lesions: Atrial Septal Defect ventricular Septal Defect Patent ductus arteriosus Obstructive Lesions Pulmonary stenosis Aortic stenosis Coarctation of aorta Regurgitant Lesions Pulmonary regurgitation Aortic regurgitation Mitral valve prolapse
12 Ventricular Septal Defect Is the most common congenital heart disease. VSD may be supracristal perimembranous or muscular
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14 P a t h o p h y s i o l o g y
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16 CLINICAL MANIFESTATIONS Clinical finding depends upon ü Size of the defect ü pulmonary blood flow and pressure
17 CLINICAL MANIFESTATIONS dyspnoea, feeding difficulties, poor growth, profuse perspiration, recurrent pulmonary infections, and cardiac failure in early infancy
18 Precordium exam ü palpable parasternal lift, ü a laterally displaced apical impulse, ü a systolic thrill. ü The holosystolic murmur of grade 4 or above ü increased intensity of pulmonic component of the 2nd heart sound ü mid-diastolic, low-pitched rumble at the apex
19 When would be the 2 nd heart sound loud on auscultation of precordium?
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21 DIAGNOSIS. ü CXR ü ECG ü ECHO
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23 Interpretation of CXR?
24 Interpretation of CXR?
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26 TREATMENT WHICH TYPE OF VSD IS MOST LIKELY TO CLOSE? FOR HOW LONG SHOULD WE WAIT FOR VSD TO CLOSE SPONTANOUSLY?
27 TREATMENT CAN LARGE VSD CLOSE SPONTANOUSLY?
28 TREATMENT OF SMALL VSD an isolated, small, hemodynamically insignificant VSD is not an indication for surgery Prophylactic antibiotics,
29 TREATMENT OF large VSD Medical management has two aims: to control heart failure and to prevent the development of pulmonary vascular disease
30 Indications for surgery patients at any age with large defects in whom clinical symptoms and failure to thrive cannot be controlled medically; infants between 6 and 12 mo of age with large defects associated with pulmonary hypertension, even if the symptoms are controlled by medication; patients older than 24 mo with a Qp : Qs ratio greater than 2 : 1. Patients with supracristal VSD of any size
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32 Atrial septal defect
33 ASD sinus venosus defect: high in septum Ostium secundum defect: midseptum Ostium primum defect: low in septum
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39 CLINICAL MANIFESTATIONS dyspnea, easy fatigability, palpitations, sustained atrial arrhythmia heart failure.
40 CLINICAL MANIFESTATIONS A right ventricular systolic lift A loud 1st heart. Wide fixed splitting of the 2nd heart sound A short, rumbling mid-diastolic murmur produced by the increased volume of blood flow across the tricuspid valve Ejection systolic murmur at the upper left sternal border
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42 CXR ECG ECHO
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48 complications pulmonary hypertension, atrial dysrhythmias, tricuspid or mitral insufficiency, and heart failure infective endocarditis
49 treatment ASDs detected in term infants may close spontaneously Surgical or transcatheter device closure is advised for all symptomatic patients and also for asymptomatic patients with a Qp : Qs ratio of at least 2 : 1. The timing for elective closure is after the 1st yr and before entry into school
50
51 Patent ductus arterious
52 Patent ductus arterious Functional closure of the ductus normally occurs soon after birth, but if the ductus remains patent, aortic blood is shunted into the pulmonary artery. PDA persisting beyond the 1st few weeks of life in a term infant rarely closes spontaneously
53 PATHOPHYSIOLOGY As a result of the higher aortic pressure, blood shunts left to right through the ductus, from the aorta to the pulmonary artery In extreme case, 70% of the left ventricular output may be shunted through the ductus to the pulmonary circulation
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56 Displaced and heaving apex beat Machinery or rolling thunder murmur at left upper sternal border.
57 diagnosis CXR ECG: LVH
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59 treatment Irrespective of age, patients with PDA require surgical or catheter closure
60
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