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Incomplete closure of the fossa ovalis allowing inter-arterial communication Often a mild disease not detected until adult life o Due to pressure and volume handled by the atria level is lower compared to the systemic level Pulmonary flow is increased to about twice the systemic output o Pressure (Left > Right) o blood preferentially goes from Left Right atrium = Pulmonary blood flow RV is dilated and hypertrophied o Adaptation of the right ventricle to the workload(hypertrophy) dilatation
Complication o Pulmonay HPN o RV failure (due to dilatation) death also from CHF (due to arrhythmia) and IHD o Shunt reversal (Late cyanosis) pressure from right side to left Mixing of unoxygenated blood from right side to the left Types: 1. Fossa or Ostium seccundum (most common) 2. Outlet (Primum SD) 3. Sinus Venosus defect 4. Coronary sinus defect
to systemic circulation
ASD
Fossa Ovalis
Right Atrium
Left Atrium
HEC B5MD2011
Most common cardiac anomaly in children (recognized early) incomplete closure of ventricular septum left to right interventricular communication o inadequate growth or absent fusion of embryologic septal components Increases risk for infective endocarditis Functional disturbance depends on the size of the defect o defect = disturbance and vice versa o Small defects can sometimes close spontaneously as the heart enlarges o Surgery (1st year) to prevent irreversible obstructive pulmonary vascular disease Large VSDs result in overload of both ventricles o Similar to ASD (movement is from L R) o Right ventricle carries the initial burden
Complications Eisenmenger syndrome o Pulmonary HPN o shunt reversal o cyanosis (Late cyanosis) VSD
Supraventricularis Defect
Muscle band
Muscle band
Infraventricularis Defect
HEC B5MD2011
Complications PDA
Pulmonary Artery
Aorta (Opened)
HEC B5MD2011
Tetralogy of Fallot
Most common cyanotic congenital anomaly Four Components: o Large VSD o Stenosis of pulmonary outflow tract Narrowing of the lumen due to subpulmonic muscle block o Biventricular origin of the aorta (overrides the right ventricle) septal defect is below overriding aorta receives blood from the RV and LV EARLY cyanosis o Right ventricular hypertrophy 0.6-1cm thick (normal 0.5cm) results from anterosuperior & leftward displacement of the infundibular septum Left to Right Shunt Tetralogy of Fallot Initial L R Shunt VSD PDA ASD PTA No Shunt Coartaction of the aorta Pulmonary stenosis Aortic stenosis
Complications o Heart failure o Polycythemia o risk for thrombosis o risk for infective endocarditis
Stenosis VSD
RV hypertrophy Aorta
VSD
RV hypertrophy
HEC B5MD2011
Fibrous Tissue
HEC B5MD2011
Pericarditis (Gross)
Pericarditis (Microscopic)
Fibrin deposits
Epicardial layer
Myocardial fibers
HEC B5MD2011
Endocarditis (Microscopic)
Fibrin deposits
Neutrophilic infiltrations
HEC B5MD2011
Cardiac Muscles
Granulomatous Stage
Healed Stage
Fibrosis around the BV
Blood Vessels
Myocardial layer
HEC B5MD2011
Deformed orifice (Fish Mouth Deformity) Fibrotic and smooth mitral valve
Fused Commisures
HEC B5MD2011
Infective Endocarditis
Invasion of the heart by microbiologic agent (friable vegetations laden with organisms) Predisposing factors: o Rheumatic heart disease (valves become fibrotic), congenital heart disease, calcific stenosis, artificial valves, immunodeficiency/ immunodepression, IV drug abuse ACUTE virulent organisms affects previously normal valve highly destructive bulkier vegetations valve perforation common SUBACUTE low virulence superimposed on damaged valves; less destructive smaller vegetations
Types:
Complications: Sepsis Cardiac valve insufficiency, myocardial abscess Embolic Renal embolic infarction, focal glomerulonephritis, abscesses
Aortic Valve
Bulky Vegetations
Vegetations
Perforation
HEC B5MD2011
Three Layers of the Valve 1. Auricularis layer (from atrium) 2. Ventricularis layer (from ventricles) 3. Spongiosa layer thickens
Bulging Valve
Calcium deposits (make vessel more brittle) Large deposits of Atheromatous plaques
Narrowed lumen
Blood clot (complete occlusion) BP injures the surface of the blood vessel coagulation cascade thrombus formation blood clot
HEC B5MD2011
Myocardial Infarct
Transmural necrosis of full thickness of the LV wall, associated with occlusive thrombi in 90% Subendocardial necrosis limited to inner 1/3, diffuse coronary atherosclerosis, no thrombus
Infarct (Left Main CA) Full Thickness of the Ventricle (Anterior wall, anterior 2/3 of septum and lateral ventricular wall)
Infarct (Left Main CA and Right CA) (Anterior wall, anterior 2/3 of septum, lateral ventricular wall and posterior wall)
HEC B5MD2011
Myocardial Infarct
to 1 hr After Myocardial Infarct
Full Blown Coagulation Necrosis (Inflammatory cells to take up the dead myocardial fibers)
HEC B5MD2011
Myocardial Infarct
Complications Cardiac arrhythmias Left ventricular failure with pulmonary edema o Decreased hydrostatic pressure Cardiogenic shock o Failure of the heart as a pump Myocardial rupture Thromboembolism o Relaxation of the muscle wall during an infarct stasis of blood promotes coagulation o Coagulation mural thrombosis (fragile) fragmented and turns into an embolus
Infarct
Rupture of the infarct part of the heart collection of blood in the pericardial sac causing cardiac tamponade
HEC B5MD2011
Congestive Cardiomyopathy
Failure of the ventricle to empty in systole Increased ventricular end-systolic and diastolic volumes biventricular dilatation and failure Non-specific histologic features irregular hypertrophic and atrophic myocardial fibers with progessive fibrosis No detectable cause associated with alcoholism, delayed pregnancy, hypo and hyperthyroidism
Normal Carotid Sinus Normal Aortic Valve Normal Mitral Valve Normal Chordae Tendinae Dilated Ventricle Everything is normal except the biventricular dilatation
Hypertrophy
HEC B5MD2011
Hypertrophic Cardiomyopathy
Marked hypertrophy of the ventricular muscle with resistance to diastolic filling 20-30% are familial, autosomal dominant inheritance pattern Greater thickening of ventricular septum than the LV free wall Histology: disorganized myocardial fibers
Aorta
Thick Septum
Asymmetric Septum
HEC B5MD2011
Restrictive Cardiomyopathy
Decreased compliance of the ventricular muscle, increased resistance to filling, and cardiac failure Many cases are due to cardiac amyloidosis
Obliterative Cardiomyopathy
Marked subendocardial fibrosis encroachment of the lumen, decreased ventricular filling and cardiac failure Endocardial fibroelastosis collagen and elastic tissue is laid down beneath the endocardium in infancy Endomyocardial fibrosis, common in Africa
Thrombus
HEC B5MD2011
HEC B5MD2011
Purulent Pericarditis
Coronary Atherosclerosis
Atrophy
Purulent Pericarditis
Atrophy
HEC B5MD2011