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Pathology Cardiovascular Practicals Reviewer Page 1 of 20
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 to systemic circulation
ASD
Types: 1. Fossa or Ostium seccundum (most common) 2. Outlet (Primum SD) 3. Sinus Venosus defect 4. Coronary sinus defect
HEC B5MD2011
Fossa Ovalis 2 flaps of muscles should overlap to close to fossa
Left Atrium Right Atrium
Pathology Cardiovascular Practicals Reviewer Page 2 of 20
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
HEC B5MD2011
Complications
• Eisenmenger syndrome o Pulmonary HPN o shunt reversal o cyanosis (Late cyanosis)
VSD
Muscle band
Muscle band
Infraventricularis Defect
Supraventricularis Defect
Pathology Cardiovascular Practicals Reviewer Page 3 of 20
HEC B5MD2011
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 Complications
PDA o Pulmonary HPN o Shunt reversal o Cardiac hypertrophy
Adaptation to ↑ workload eventually leads to heart failure
o Dilated pulmonary artery
Pulmonary Artery
Aorta (take note of the 3 branches)
Patent Ductus Arteriosus
Left Pulmonary Artery
Left Pulmonary Artery
Patent Ductus Arteriosus (w/ probe)
Pulmonary Artery (Opened)
Aorta (Opened)
Pathology Cardiovascular Practicals Reviewer Page 4 of 20
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 Complications Left to Right Shunt Initial L R Shunt No Shunt
Tetralogy of Fallot VSD PDA ASD PTA
Coartaction of the aorta Pulmonary stenosis Aortic stenosis
o Heart failure o Polycythemia o ↑ risk for thrombosis o ↑ risk for infective
endocarditis
Aorta
Stenotic Pulmonary Artery
VSD
RV hypertrophy
VSD
Stenosis
RV hypertrophy
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 5 of 20
Pulmonary Hypertension in Congenital HD w/ Left and Right Shunts
HEC B5MD2011
Tunica Adventitia
Grade IV – Plexiform Lesions (Irreversible)
Newly formed Capillaries
Fibrous Tissue
Grade III – Intimal Fibrosis (Irreversible)
Hypertrophied Tunica Media
Fibrous tissue in the Tunica Intima (Occlusion of the lumen)
Grade II – Intimal Hyperplasia (Reversible)
Hypertrophied Tunica Media
Internal Elastic Membrane
External Elastic Membrane
Intimal Hyperplasia
External Elastic Membrane
Internal Elastic Membrane
Tunica Intima Single layer of Endothelial cells (simple squamous)
Hypertrophied Tunica Media
Grade I – Medial Hypertrophy (Reversible)
Pathology Cardiovascular Practicals Reviewer Page 6 of 20
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 patient’s sera
Ab w/c supposedly should be specific for Strep antigen will also attack the tissue of the heart due to similarity of the heart’s antigen to the strep antigen
• Jone’s Criteria: 2 major or 1 major + 2 minor Major Criteria Minor Criteria
Carditis Polyarthritis Chorea Subcutaneous nodules Erythema marginatum
RHD or previous rheumatic fever Athralgia Fever Elevated esr 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)
HEC B5MD2011
Fibrous type (Bread and Butter Pericarditis)
Pericarditis (Microscopic)
Fibrin deposits
Epicardial layer
Myocardial fibers
Pathology Cardiovascular Practicals Reviewer Page 7 of 20
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
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 8 of 20
Exudative Stage
Exudate with Neutrophilic infiltrations
Blood Vessel Lumen
Cardiac Muscles
Granulomatous Stage
Granuloma formation (with epithelial histiocytes and macrophages)
Healed Stage
Myocardial layer
Blood Vessels
Fibrosis around the BV
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 9 of 20
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
Fused Commisures
Fibrotic and smooth mitral valve
Deformed orifice (Fish Mouth Deformity)
Short, thickened and fused together Chordae tendinae
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 10 of 20
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
Types:
ACUTE SUBACUTE virulent organisms affects previously normal valve highly destructive bulkier vegetations valve perforation common
low virulence superimposed on damaged valves; less destructive smaller vegetations
Complications:
• Sepsis • Cardiac – valve insufficiency, myocardial abscess • Embolic • Renal – embolic infarction, focal glomerulonephritis, abscesses
Bulky Vegetations
Aortic Valve
Vegetations
Perforation
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 11 of 20
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
Three Layers of the Valve
1. Auricularis layer (from atrium) 2. Ventricularis layer (from ventricles) 3. Spongiosa layer thickens
Complications • Mitral Insufficiency • Chordal rupture
o Due to stretching • Infective endocarditis
HEC B5MD2011
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
Pathology Cardiovascular Practicals Reviewer Page 12 of 20
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
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 13 of 20
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
HEC B5MD2011
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)
Pathology Cardiovascular Practicals Reviewer Page 14 of 20
HEC B5MD2011
Pathology Cardiovascular Practicals Reviewer Page 14 of 20
HEC B5MD2011
yocardial Infarct M
Wavy myocardial fibers
½ to 1 hr After Myocardial Infarct
Early Coagulation Necrosis
<12 hr After Myocardial Infarct
Full Blown Coagulation Necrosis (Inflammatory cells to take up the dead myocardial fibers)
3-7 days After Myocardial Infarct
Fibrosis (Disappearance of dead myocardial cells)
7th week After Myocardial Infarct
Pathology Cardiovascular Practicals Reviewer Page 15 of 20
Myocardial Infarct
HEC B5MD2011
plications • 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
Com
Infarct
Rupture of the infarct part of the heart collection of blood in the pericardial sac causing cardiac tamponade
Pathology Cardiovascular Practicals Reviewer Page 16 of 20
HEC B5MD2011
opathy • Failure of the ventricle to empty in systole
ased ventricular end-systolic and diastolic volumes – biventricular dilatation and failure ic features – irregular hypertrophic and atrophic myocardial fibers with
holism, delayed pregnancy, hypo and hyperthyroidism
Congestive Cardiomy
• Incre• Non-specific histolog
progessive fibrosis • No detectable cause • associated with alco
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)
Fibrous tissue (between the fibers)
Hypertrophy
Hypertrophy
Pathology Cardiovascular Practicals Reviewer Page 17 of 20
HEC B5MD2011
y le with resistance to diastolic filling
ized myocardial fibers
Hypertrophic Cardiomyopath• Marked hypertrophy of the ventricular musc• 20-30% are familial, autosomal dominant inheritance pattern • Greater thickening of ventricular septum than the LV free wall • Histology: disorgan
Thick Septum
Aorta
Bulge prevents blood flow to Aorta
Left Ventricle
Right Ventricle
Subaortic stenosis due to thick septum
Right Atrium enlargement
Asymmetric Septum
Disorganized myocardial fibers
Pathology Cardiovascular Practicals Reviewer Page 18 of 20
HEC B5MD2011
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
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)
Thrombus
Endocardial Fibrosis (whiteness of the wall)
Pathology Cardiovascular Practicals Reviewer Page 19 of 20
HEC B5MD2011
t sources) Slides Review (taken from differen Acutely Injured Heart Removal of Dead Myocardial cells
Clearance of Dead Tissues
Granulation Tissue (Trichome)
Healed Infarct (Trichome)
Hypertrophy with Healed Infarct
Pathology Cardiovascular Practicals Reviewer Page 20 of 20
HEC B5MD2011
ypertrophy with Healed Infarct Purulent PericarditisH
Coronary Atherosclerosis
Purulent Pericarditis
Atrophy
Atrophy