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Atrial Septal Defect (ASD)

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


Fossa Ovalis

2 flaps of muscles should overlap to close to fossa

Right Atrium

Left Atrium

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Ventricular Septal Defect (VSD)

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

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Patent Ductus Arteriosus (PDA)

90% occur as isolated anomalies (common in babies whose mothers had rubella) Rough machine-like murmur (S4) on auscultation Permanent closure of the DA is usually complete by 8 weeks after birth o Patency due to failure to contract and become fibrotic in response to arterial oxygen o Large caliber of the ductus incomplete closure should be closed as early in life as feasible o Pulmonary HPN o Shunt reversal o Cardiac hypertrophy Adaptation to workload eventually leads to heart failure o Dilated pulmonary artery

Complications PDA

Left Pulmonary Artery Patent Ductus Arteriosus

Aorta (take note of the 3 branches)

Pulmonary Artery

Left Pulmonary Artery

Patent Ductus Arteriosus (w/ probe)

Aorta (Opened)

Pulmonary Artery (Opened)

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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

Stenotic Pulmonary Artery


RV hypertrophy

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Pulmonary Hypertension in Congenital HD w/ Left and Right Shunts

Grade I Medial Hypertrophy (Reversible) Tunica Adventitia External Elastic Membrane Tunica Intima Single layer of Endothelial cells (simple squamous) Internal Elastic Membrane Hypertrophied Tunica Media

Grade II Intimal Hyperplasia (Reversible) Internal Elastic Membrane

Intimal Hyperplasia External Elastic Membrane Hypertrophied Tunica Media

Grade III Intimal Fibrosis (Irreversible)

Fibrous tissue in the Tunica Intima (Occlusion of the lumen)

Hypertrophied Tunica Media

Grade IV Plexiform Lesions (Irreversible)

Fibrous Tissue

Newly formed Capillaries

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Rheumatic Heart Disease

cardiac involvement in rheumatic fever Rheumatic Fever: immunologic hypersensitivity rxn to Strep antigens (NO BACTERIA present) o Ig & complement demonstrable in myocardial fiber membrane o Cross reacting Ab against Strep protein and myocardial sarcolemma in patients sera Ab w/c supposedly should be specific for Strep antigen will also attack the tissue of the heart due to similarity of the hearts antigen to the strep antigen Jones Criteria: 2 major or 1 major + 2 minor Major Criteria Minor Criteria Carditis RHD or previous rheumatic fever Polyarthritis Athralgia Chorea Fever Subcutaneous nodules Elevated esr Erythema marginatum Postive CrP Leukocytosis Prolonged PR interval on ECG

Acute Lesion Pancarditis (all layers)

Pericarditis fibrous type Endocarditis verrucae along lines of closure of valve leaflets Myocarditis Aschoff bodies in granulomatous stage (histologic hallmark of rheumatic activity)

Pericarditis (Gross)

Fibrous type (Bread and Butter Pericarditis)

Pericarditis (Microscopic)

Fibrin deposits

Epicardial layer

Myocardial fibers

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Rheumatic Heart Disease

Endocarditis (Gross)

Mitral Valve (Translucent = Normal)

Verucae (Vesicle like structures)

Thickened Papillary Muscles

Endocarditis (Microscopic)

Fibrin deposits

Neutrophilic infiltrations

Aschoff Bodies in Myocarditis

special type of interstitial inflammation a perivascular focus of swollen eosinophilic collagen surrounded by lymphocytes, monocytes and plasma cells

Three Stages 1. Exudative stage 2. Granulomatous stage 3. Healed Stage

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Blood Vessel Lumen

Exudate with Neutrophilic infiltrations

Cardiac Muscles

Granulomatous Stage

Granuloma formation (with epithelial histiocytes and macrophages)

Healed Stage
Fibrosis around the BV

Blood Vessels

Myocardial layer

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Rheumatic Heart Disease

Chronic Lesion
commisures fused; cusps thickened and fibrotic; chordae tendinae thickened, shortened and fused Most commonly involved valve- mitral, alone or in combination with others

Deformed orifice (Fish Mouth Deformity) Fibrotic and smooth mitral valve

Fused Commisures

Short, thickened and fused together Chordae tendinae

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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


Complications: Sepsis Cardiac valve insufficiency, myocardial abscess Embolic Renal embolic infarction, focal glomerulonephritis, abscesses

Aortic Valve

Bulky Vegetations



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Mitral Valve Prolapse (Floppy Valve)

Degenerative change, in 6% of population, young women Accumulation of mucopolysaccharides in valve leaflet causing ballooning of the valve Myxomatous degeneration of spongiosa layer, degeneration & attenuation of fibrosa layer Complications Mitral Insufficiency Chordal rupture o Due to stretching Infective endocarditis

Three Layers of the Valve 1. Auricularis layer (from atrium) 2. Ventricularis layer (from ventricles) 3. Spongiosa layer thickens

Abundant amount of tissue (Bulging appearance)

Thin Ventricularis layer

Thin Auricularis layer

Thick Spongiosa layer Myocardial layer

Bulging Valve

Ruptured Chordae Tendinae Stretched Chordae Tendinae HEC B5MD2011

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Ischemic Heart Disease

Syndromes resulting from imbalance between supply and demand of the heart for oxygenation 1. Increased demand (increased heart rate) 2. Diminished oxygen transport (sever anemia, congenital heart disease) 3. Diminished coronary blood flow Coronary atherosclerosis is the most common cause of diminished blood flow 1. 75% narrowing is significant 2. Stenosis within 2cm of left anterior descending and circumflex artery Ischemic syndromes 1. Angina pectoris 2. Myocardial infarct 3. Sudden cardiac death

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

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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)

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Myocardial Infarct
to 1 hr After Myocardial Infarct

Wavy myocardial fibers

<12 hr After Myocardial Infarct

Early Coagulation Necrosis

3-7 days After Myocardial Infarct

Full Blown Coagulation Necrosis (Inflammatory cells to take up the dead myocardial fibers)

7th week After Myocardial Infarct

Fibrosis (Disappearance of dead myocardial cells)

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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


Rupture of the infarct part of the heart collection of blood in the pericardial sac causing cardiac tamponade

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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

Fibrous tissue (between the fibers)

Hypertrophy Fibrous tissue (between the fibers)


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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


Thick Septum

Bulge prevents blood flow to Aorta Left Ventricle Right Ventricle

Right Atrium enlargement

Subaortic stenosis due to thick septum

Asymmetric Septum

Disorganized myocardial fibers

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Restrictive Cardiomyopathy

Decreased compliance of the ventricular muscle, increased resistance to filling, and cardiac failure Many cases are due to cardiac amyloidosis

Mitral Valve (translucent = normal)

Overwhelming deposits (Obscured Trabeculae Carnae)

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


Endocardial Fibrosis (whiteness of the wall)

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Slides Review (taken from different sources)

Acutely Injured Heart Granulation Tissue (Trichome)

Removal of Dead Myocardial cells

Healed Infarct (Trichome)

Clearance of Dead Tissues Hypertrophy with Healed Infarct

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Hypertrophy with Healed Infarct

Purulent Pericarditis

Coronary Atherosclerosis


Purulent Pericarditis


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