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26 Cards in this Set

  • Front
  • Back
Acute rheumatic fever
Inflammatory condition
-all 3 layers

Group A Strep
-2-3 weeks after throat infection
-does not involve direct bacterial infection of heart

Histopathologic
-Aschoff body (focal fibrinoid necrosis surrounded by inflammatory cells)
-Fibrous scar tissue

Valvular symptoms may not manifest for 10-30 years later
-most often mitral valve stenosis followed by aortic stenosis

Presenting symptoms: chills, fever, fatigue, migratory arthralgias (Jones criteria)

For those who have already experienced ARF
-low dose penicillin prophylaxis until early adulthood
Mitral stenosis: etiology, pathology
Rheumatic fever

Fibrous thickening and calcification of valve leaflets
Fusion of commissures
Mitral stenosis: pathophysiology
Emptying of LA is impeded and there is an abnormal pressure gradient between LA and LV
LA pressure is higher than normal
Increased pulmonary venous and capillary pressures
-dyspnea and other symptoms of CHF
-hemoptysis
Chronic elevation of right ventricular pressure leads to hypertrophy and dilation of that chamber and ultimately to right sided heart failure
Chronic pressure overload of the LA in MS leads to left atrial enlargement
-atrial fibrillation (could lead to stroke, requires anticoagulation)
Mitral stenosis: presentation
Mild:
Dyspnea upon exertion
Decompensation with hyperthyroidism, pregnancy, exercise

Severe:
Dyspnea at rest
Orthopnea
Paroxysmal nocturnal dyspnea
Signs of right sided heart failure
Compression of recurrent laryngeal nerves may cause hoarseness
Mitral stenosis: examination
Loud S1
-in early stages
-in late stages, leaflets might be immobile

Opening snap
-follows S2
-interval between S2 and OS relates inversely to severity of MS

Diastolic rumble
-low frequency decrescendo murmur after OS with presystolic accentuation
-duration relates to severity

Chest radiograph reveals LA enlargement, pulmonary vascular redistribution, interstitial edema, Kerley B lines

Echocardiography: thickened mitral leaflets and fusion of commissures
Mitral stenosis: treatment
Diuretics

If atrial fibrillation:
B blocker, CCB, or digoxin to slow rapid ventricular rate and improve diastolic LV filling.
Chronic anticoagulation

Percutaneous balloon mitral valvuloplasty
-complications: cerebral emboli, cardiac perforation, mitral regurgitation

Open mitral commissurotomy

Mitral valve replacement
Mitral regurgitation: etiology
Myxomatous degeneration of valve
Infective endocarditis
Rheumatic fever
Hypertrophic obstructive cardiomyopathy
Calcification of mitral annulus
-can occur with normal aging but more common among HTN, diabetes, end-stage renal disease
Primary rupture of chordae tendineae
Ischemic heart disease
LV enlargement
Fen-phen
Mitral regurgitation: pathophysiology
Forward cardiac output into aorta is less than LV total output (some going into LA)

Elevation of LA volume and pressure
Reduction of forward cardiac output
Volume related stress on LV

Affected by systemic vascular resistance opposing forward LV flow
-increases regurgitant fraction

Left atrial compliance
Left atrial compliance and mitral regurgitation
Acute MR
-no compliance yet
-rapid pulmonary congestion and edema
-prominent v wave

Chronic MR
-LA dilates and compliance increases
-Prevents significant increases in pulmonary vascular pressures (at cost of reduced forward cardiac output)
-Low forward cardiac output leads to weakness and fatigue
-chronic LA dilation predisposes to Afib
-LV undergoes gradual compensatory dilation through eccentric hypertrophy
Mitral regurgitation: examination
Apical holosystolic murmur
Clench fists
-murmur intensifies

Severe acute MR
-decrescendo murmur

S3
Laterally displaced PMI
Large v wave
Mitral regurgitation: treatment
Medical therapy involves augmenting forward cardiac output while reducing regurgitation into LA and relieving pulmonary congestion

Diuretics
Vasodilators

Mitral valve surgery should be done before chronic MR results in LV contractile impairment
-Mitral valve repair
-Mitral valve replacement
Mitral valve prolapse
Common, usually asymptomatic

Midsystolic click
Aortic stenosis: etiology
Age related degenerative calcific changes (>65)
Congenitally deformed aortic valves (<65)
Aortic stenosis: pathology
Common etiology with atherosclerotic vascular disease
Aortic stenosis: Pathophysiology and presentation
Significant elevation of LV pressure

Chronic

Concentric hypertrophy
-reduces ventricular wall stress
-reduces compliance
-elevates diastolic LV presure causes LA to hypertrophy to fill "stiff LV"

May cause angina
-imbalance between myocardial oxygen supply and demand

May cause syncope during exertion

May cause symptoms of heart failure
-elevation of LA and pulmonary venous pressures

Once angina, syncope, and CHF develop, they confer a significantly decreased survival
Aortic stenosis: exam
Late peaking systolic ejection murmur
Weaking parvus and delayed tardus

S4

Reduced intensity or complete absence of A2
Aortic stenosis: natural history and treatment
Natural history of severe symptomatic uncorrected AS is poor
-effective treatment requires replacement of valve

Aortic valve replacement
-severe, symptomatic
-LVEF almost always increases after replacement

Percutaneous valvuloplasty disappointing
-high rates of restenosis

Mild, asymptomatic has slow rate of progression
-avoid hypotension
Aortic regurgitation: etiology
Disease of aortic leaflets
Dilation of aortic root
Aortic regurgitation: pathophysiology
Acute
-LV noncompliant and diastolic pressure rises
-Transmitted to LA and pulmonary circulation
-Dyspnea and pulmonary edema
-Therefore, usually a surgical emergency

Chronic:
-LV compensation
-Chronic dilation (eccentric), eventually results in systolic dysfunction
-Widened pulse pressure
-Angina
Aortic regurgitation: examination
Bounding pulses
Hyperdynamic LV impulse
Blowing murmur in early diastole

CXR shows enlarged LV silhouette (chronic)
Pulmonary vascular congestion (acute)
Aortic regurgitation: treatment
Clinical progression is normal and slow

Asymptomatic:
Vasodilators
ACEI (when HTN present)

Symptomatic:
-surgical (death soon if not corrected)
Tricuspid stenosis
Rare
Long term consequence of rheumatic fever
OS
Diastolic murmur intensifies on inspiration
Neck veins distended and show large a wave
Tricuspid regurgitation
Functional rather than structural (results from RV enlargement)
Rare cause is carcinoid syndrome

Prominent v waves and pulsatile liver

Systolic murmur louder on inspiration
Pulmonic stenosis
Almost always congenital deformity of valve
Pulmonic regurgitation
Severe pulmonary hypertension
Prosthetic valves
Mechanical:
Require lifelong anticoagulation
Younger

Biological:
Don't require long term anticoagulation
Older