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93 Cards in this Set
- Front
- Back
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acute rheumatic fever def
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- inflammatory condition that 1* involves heart (carditis all layers), skin and CT
-complication of URI caused by group A streptococci = 3% pts with acute streptococcal pharyngitis develop ARF 2-3 weeks after mainly children, young adults - rare today (penicillin, improvement in general HC, less overcrowding) |
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chronic rheumatic heart disease
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most devestating sequelae of ARF
10-30 years after ARF permenant deformity and impairment of one or more cardiac valves 50% will develop mitral stenosis 25% will also develop aortic stenosis or regurg Tricuspid involvement rare |
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Aschoff body
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histopath finding of ARF
area of focal fibrinoid necrosis surrounded by inflamm cells - lymphocytes, plasma cells, macrophages later resolves to form fibrous scar tissue |
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most common presenting symptoms of ARF
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chills
fever fatigue migratory arthralgias * Jones criteria |
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Carey-Coombs murmur
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mid-diastolic murmur at cardiac apex
sometimes present in acute episode of ARF |
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treatment acute episode ARF
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high-dose aspirin - inflamm
penicillin - strep therapy for complications (CHF, pericarditis) ** recurrences can cause more damage therefore low-does penicillin prophylaxis until early adulthood |
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Jones Criteria
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diagnosis ARF requires evidence of strep (antistreptolysin 0 Ab, positive throat culture) and 2 major or 1 major + 2 minor
Major: Carditis Polyarthritis Sydenham chorea Erythema marginatum subcutaneous nodules Minor: Migratory arthralgias Fever ^ acute phase reactants (ESR, CRP, leuks) Prolonged PR interval EKG |
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sydenham chorea
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involuntary movements
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erythema marginatum
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skin rash with advancing edge and clearing center
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causes of mitral stenosis
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50% due to ARF
rest are rare: - congenital stenosis - prominent calcification extending from mitral annulus onto leaflets (elderly) - endocarditis w v large vegetations |
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pathologic features rheumatic mitral stenosis
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fibrous thickening and calcification of valve leaflets
fusion of commissures thickening and shortening of chordae tendineae due to inflammation |
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cross-sectional area of normal mitral valve orifice and mitral stenosis
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4-6 cm2
<2 cm2 = hemodynamically significant MS = mild 1.1 -1.5 cm2 = moderate MS <1.0 cm2 = severe MS calculate with Echo or cardiac cath |
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abnormal heart sounds of mitral stenosis
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diastolic opening snap (opening mitral valve)
decresendo murmur presystolic accentuation: crescendo of murmur just before S1 (^ pressure gradient when LA contracts) |
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passive vs reactive pulm HTN in mitral stenosis
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Passive: backward transmission of elevated LA P into pulm vasculature; "obligatory" increase in pulm artery P to preserve forward flow
reactive (40%): medial hypertrophy and intimal fibrosis of pulm arterioles; "beneficial" by reducing pressure in pulm capillaries BUT ^ RV P |
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Cardiac pathophys in mitral stenosis
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high LA pressure passively transmitted to pulm circulation
- transudation in interstitum and alveoli = dyspnea, CHF symptoms rupture of bronchial vein = hemoptysis passive or reactive pulmonary HTN - RS HF LA enlargement - atrial fibrillation from stretched fibers? = decreased CO predisposition to inter-atrial thrombus formation |
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conditions and activities that increase HR and cardiac blood flow
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exercise
fever anemia hyperthyroidism pregnancy rapid arrhythmias - exercise, emotional stress, sexual intercourse |
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signs of advancing/more serious mitral stenosis
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dyspnea occurs even at rest
orthopnea PND signs of RS HF: - jugular venous distension - hepatomegaly - ascites - peripheral edema |
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signs on physical examination of mitral stenosis
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right ventricular "tap" on palpitation of L anterior chest
auscultation= loud S1 early (late stages reduced from thickening, calcification, immobility) = high pitched opening snap = low freq decrescendo murmur (diastolic rumble) |
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test results in mitral stenosis
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EKG:
- LA enlargement - RV hypertrophy if pulm HTN - atrial fib Chest xray: - LA enlargement - pulm vascular redistribution - Kerley B lines - RV hypertrophy and ^ prominence pulm arteries with pulm HTN ** Echo: - thickened mitral leaflets - abnormal fusion commuissures - LA enlargment - intra-atrial thrombus - mitral valve area calculated |
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treatment of mitral stenosis
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Diuretics: vascular congestion
if A fib: - Beta blocker - Ca2+ channel antagonist w negative chronotropic properties (verapamil, diltiazem) -digoxin Chronic anticoagulation therapy mechanical correction: - percutaneous balloon mitral valvuloplasty - open mitral commissurotomy - mitral valve replacement |
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open mitral commissurotomy
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operation where stenotic commissures are seperated under direct visualization (vs balloon)
restenosis occurs in fewer than 20% over 10-20 year follow up |
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percutaneous balloon mitral valvuloplasty
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via femoral vein
requires creating small atrial septal defect rapidly inflated balloon "cracks open" fused commissures most effective w/o complications such as: -mitral regurgitation - extensive calcifications - atrial thrombus 5% left with ASD 67-76% event-free survival 7 years post |
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etiology mitral regurgitation
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require normal closure of mitral valve during systole, coordinated action of each component
Mitral annulus: annular calcification Leaflets: myxomatous degeneration, rheumatic disease, endocarditis, systolic anterior motion chordae tendineae: idiopathic rupture, endocarditis papillary muscles: dysfunction, rupture left ventricle cavity dilation (interputs spatial arrangments) |
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direct cardiac consequences of mitral regurgitation
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1) elevation of LA volume and pressure
2) reduction of forward CO 3) volume-related stress on LV from regurgitated blood returns to LV with normal pulm venous return Frank-Starling = LV SV must rise |
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regurgitant factor in mitral regurgitation
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volume of MR/ Total LV stroke volume
ratio rises whenever resistance to aortic outflow increases eg ^ systemic BP, aortic stenosis |
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factors severity of mitral regurgitation depends on
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1) size mitral orifice in regurg
2) systolis pressure gradient bw LA and LV 3) systemic vascular resistance opposing forward LV flow 4) LA compliance 5) duration regurg in each systole |
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acute mitral regurgitation pathophys
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ie sudden rupture chordae tendineae
LA compliance has little change = rapid pulm congestion and edema = medical emergency! (get prominent v wave (aka cv bc can merge) compensatory ^ LV SV (F-S) |
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chronic mitral regurgitation pathophys
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ie rheumatic valve disease
LA compensation to lessen effects on pulm circ = LA dilation = LA ^ compliance = ^ volume w/o substantial ^ pressure BUT now "low pressure sink", decreasing forward CO = weakness, fatigue, A fib! LV = gradual compensatory dilation (eccentric hypertrophy) = F-S compensation for SV eventual HF |
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test results of mitral regurgitation
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Xray: acute MR: may display pulm edema
chronic asymp MR: LV and LA enlargement - no pulm congestion (may see calcification of mitral annulus if that is the cause) EKG: LA enlargement, LV hypertrophy Echo: ID structural cause, grade severity, LV size and fn Cardiac cath and angio: ID coronary ischemic disease, grade severity MR (large v wave on PCW tracing) |
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auscultation of mitral regurgitation
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chronic MR: apical holosystolic murmur past S2 radiating to axilla, best heard at apex, high pitched and "blowing"
exceptions: ischemic papillary dysfunction interfers w valve closure may hear at L sternal edge or aortic area **confuse w aortic stenosis! ** pt clench fists = severity MR murmur will intensify, not AS (bc ^ systemic vascular resistance) severe acute MR: decrescendo chronic MR: S3 |
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treatment acute mitral regurgitation
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- intravenous diuretics to relieve pulm edema
- vasodilators to reduce resistance to forward flow (IV Na nitroprusside) |
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treatment chronic mitral regurgitation
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mitral valve repair (reconstruction of part of valve responsible for regurg) to prevent eventual heart failure
2-4% operative mortality (5-7% for mitral replacement; more often in elderly w more extensive valve pathology) |
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myxoma
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a soft tumor made up of gelatinous connective tissue resembling that found in the umbilical cord
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mitral valve prolapse
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common
usually asymptomatic billowing of mitral leaflets into LA during LV systole aka floppy mitral valve myxomatous mitral valve Barlow syndrome inherited (auto dom) Marfan syndrome Ehlers-Danlos syndrome |
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pathological changes creating MVP
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valve leaflets enlarged
normal dense collagen and elastin replaced with myxomatous CT more severe: elongated or ruptured chordae annular enlargement thickened leaflets |
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auscultation of mitral valve prolapse
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midsystolic click: sudden tensing of involved leaflet or chordae as leaflet forced back toward LA
late systolic murmur heard best at cardiac apex: regurgitant flow sudden squat = ^ venous return = delay sudden stand = decrease volume blood in LV = prolapse occurs more readily = occur earlier |
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complications of mitral valve prolapse
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eventual development mitral regurgitation
rupture of myxomatous chordae = sudden, severe regurgitation + pulm edema infective endocarditis peripheral emboli (microthrombus behind redundent valve) atrial or ventricular arrhythmias |
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test results of mitral valve prolapse
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echo: posterior displacement of one or both mitral leaflets into LA in systole
EKG: usually normal* Xray: usually normal* *unless chronic mitral regurg = LA and LV enlargement |
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auscultation of tricuspid stenosis
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- opening snap
- diastolic murmur heard closer to sternum intensifies on inspiration bc of ^ right heart blood flow |
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physical signs of tricuspid stenosis
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auscultation: opening snap and diastolic murmur
distended neck veins large a wave abdominal distention, hepatomegaly (passive venous congestion) |
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treatment of tricuspid regurgitation
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directed at conditions responsible for elevated RV size or pressure
diuretics surgical repair in severe cases |
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most common signs of tricuspid regurgitation
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prominent v waves in jugular veins
pulsatile liver systolic murmur at lower-left sternal border (louder on inspiration bc ngve intrathoracic P), high pitched and blowing |
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tricuspid regurgitation
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usually functional rather than structural
most commonly results from RV enlargement (either pressure or volume overload) rather than primary valve disease 20% of pts w rheumatic mitral stenosis also have TR, 80% of those functional, 20% from rheumatic involvement |
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which type of valve prosthesis to use?
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1) patient's expected lifespan in comparison to valve
2) risk-versus-benefit considerations of chronic anticoagulation therapy 3) patient and surgeon pref mechanical: younger pts; pts tolerant of and compliant with anticoag bioprosthetic: 65yo+ ; pts w contraindications to chronic coagulation |
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pros and cons of valve types
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mechanical: durable >30yrs
BUT foreign thrombogenic sufrace = lifelong coagulation bioprosthetic: limited durability (failure up to 50% in 15 yrs; leaflet tears and calcification) BUT low rate of thromboembolism both have risk of infective endocarditis mortality and complication rates are similar for first 10 years after replacement |
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types of bioprostheses
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glutaraldehyde-fixed porcine valves secured in support frame
bovine pericardium human homograft (aortic valves from cadavers) |
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types of bioprostheses
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glutaraldehyde-fixed porcine valves secured in support frame
bovine pericardium human homograft (aortic valves from cadavers) |
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infective endocarditis
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infection of endocardial surface of heart including cardiac valves
can lead to extensive tissue damage often fatal (6 mnth mortality rate 20-25%) |
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classification infective endocarditis
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1) clinical course: ie acute bacterial, subacute bacterial
2) host substrate: naive valve (60-80%), prosthetic valve, IV drug abuse (R sided) 3) specific infecting microorganism |
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acute bacterial endocarditis
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acute
fulminant - high fever, shaking chills Staphylococcus aureus |
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subacute bacterial endocarditis
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more insidious clinical course
- low-grade fever, nonspecific constitutional symp (fatigue, anorexia, weakness, myalgia, night sweats) **hx important!** less virulent organism - steptococci viridans most often in individuals with prior underlying valvular damage |
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conditions for pathogenesis of endocarditis
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1) endocardial surface injury (typically turbulent blood flow from pre-existing valvular disease)
2) thrombus formation at site of injury (vegetation) 3) bacterial entry into circulation 4) bacterial adherence to injured endocardial surface 1 & 2 provide environment favourable to infection 3 & 4 permit implantation organism on endocardial surface |
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vegetation
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a sterile thrombus from fibrin deposition
from endocardial surface injury and platelet response = nonbacterial thrombotic endocarditis = more hospitable to microbes 1) easier adherence 2) fibrin covers organisms = protection from host defenses |
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factors that determine an organism's ability to induce infective endocarditis
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1) access to bloodstream (dental, IV drug use)
2) survival in circulation 3) adherence of bacteria to endocardium 90% are gram-positive organisms 1* staphylococci 2* streptococcal (greater in rural communities w lower IV drug use) |
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complication of infective endocarditis
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1) mechanical cardiac injury: local infection
2) thrombotic or septic emboli: dislodging of vegetation, to CNS, kidneys, spleen 3) immune injury mediated by Ag-Ab deposition: glomerulonephritis, arthritis, vasculitis |
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peripheral stigmata of endocarditis
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skin findings resulting from septic embolism or immune complex vasculitis
- petechiae - splinter hemorrhages - Janeway lesions (palms and soles; rarely encountered) - Osler nodes (pulp space fingers and toes) - Roth spots (retina) |
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Roth spots
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emboli to retina = microinfarctions
white dots surrounded by hemorrhage peripheral stigmata of endocarditis |
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Splinter hemorrhages
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subungal microemboli
small, longitudinal hemorrhages beneath nails peripheral stigmata of endocarditis |
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laboratory findings of infective endocarditis
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elevated WBC count
- leftward shift (neutrophils and immature granulocytes) elevated ESR or C-reactive protein elevated serum rheumatoid factor 50% of cases |
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physical findings of infective endocarditis
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- fever
- preexisting or new murmur - peripheral stigmata - splenomegaly |
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Echo for infective endocarditis
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used to visualize:
- vegetations - valvular dysfunction - associated abscess formation TTE: useful in detecting large vegetations, noninvasive, easy specificity high sensitivity <60% TEE sensitivity >90% for detection of small vegetations |
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Duke criteria
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for diagnosis of infective endocarditis
2 major; 1 major 3 minor; 5 minor |
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infective endocarditis treatment
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4-6 weeks high-dose IV antibiotics
initially empiric broad-spectrum directed therapy preferable surgical intervention if: - persistant bacteremia - severe valvular dysfunction - myocardial abscesses - recurrent thromboembolic events |
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prevention of infective endocarditis
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prophylactic antibiotics to *susceptible individuals before invasive procedures likely to result in bacteremia
1) turbulent flow 2) artificial valves etc 3) site of entry possible contamination into blood 30-60min b4 tx Standard: Amoxicillin PO Adults: 2.0g Children: 50mg/kg |
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Etiology aortic stenosis
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1* age related degenerative calcific changes
Under 65, usually calcifications of congenitally deformed valve (bicuspid; unicuspid v young presentation) Also rheumatic valve disease |
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Pathophys aortic stenosis
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Chronic increase in pressure/ force needed to eject blood
= LV concentric hypertrophy = decreased compliance = LA hypertrophy (to fill LV) (^ proportion contribution to SV - AFib -> marked clinical deterioration!) |
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Major manifestations of aortic stenosis
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1) angina (imbalance bw O2 demand and supply)
2) exertional syncope (hard to ^CO; vasodilation peripheral muscle beds) 3) CHF Increasingly ominous prognosis |
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Aortic valve cross-sectional area
Norm and AS |
Normal: 3-4cm^2
Mild AS < 2cm^2 (pressure gradient bw LV and aorta first appears) Moderate AS: 1.5-1.0cm^2 Severe AS: <1.0cm^2 |
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Key physical features of advance AS
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1) coarse, late-peaking systolic ejection murmur
2) pulsus parvus et tardes of carotid artery 3) S4 4) reduced intensity or complete absence of S2 |
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Test results in Aortic Stenosis
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EKG: LVH
Echo: ^LV wall thickness; transvalvula pressure gradient ^, aortic valve area Cardiac cath: can be used to confirm AS severity; concurrent CABG often needed |
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Treatment of aortic stenosis
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Indicated when develop symptoms or evidence LV dysfunction
Aortic valve replacement W/o tx 1 yr survival 57% w tx, 10yr survival 60% No valvuloplasty: 50% restenosis in 6mnths No slowing progression, but v slow progression! In 20years, only 20% will progress to symptoms Research on statins if used early... |
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Causes of aortic regurgitation
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Abnormalities of valve leaflets:
- congenital (bicuspid) - endocarditis - rheumatic Dilation of aortic root: - aortic aneurysm - aortic dissection - annuloaortic ectasia - syphilis |
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Annuloaortic ectasia
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dilatation of the proximal ascending aorta and aortic annulus. It may cause aortic regurgitation, thoracic aortic dissection, aneurysm and rupture
- often associated with Marfan syndrome - can also be a complication due to tertiary syphilis. |
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Factors affecting severity of aortic stenosis
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1) size regurgitant aortic orifice
2) pressure gradient across aortic valve during diastole 3) duration of diastole |
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Acute aortic regurgitation
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LV normal size and noncompliant
- increase in volume during diastole = increase pressure = reflected back into LA and pulmonary circulation = dyspnea and pulmonary edema Usually a surgical emergency, valve replacement |
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Chronic aortic regurgitation
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LV compensation - Frank-Starling to augment SV, dilation from volume overload, but also some thickening; reduces P transmitted into LA
BUT get drop in diastolic P in aorta and systemic (from LV compliance) = widened pulse pressure = decreased coronary perfusion -> angina Over years, gradual remodeling results in LV systolic dysfunction -> HF |
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Common symptoms of chronic aortic regurgitation
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- dyspnea on exertion
- fatigue - decreased exercise tolerance - uncomfortable sensation of forceful heartbeat associated w high pulse pressure |
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Austin Flint murmur
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Low hz mid-diastolic rumbling at cardiac apex in severe AR
- turbulence through mitral valve during diastole from downward displacement of mitral ant leaflet by regurgitant stream |
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Test results in Aortic regurgitation
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X-ray: enlarged LV silhouette (not in acute, see pulmonary vascular congestion instead)
Doppler echo: identify and quantify degree AR and cause Cardiac cath: evaluate LV fn, degree AR, assess coexisting CAD |
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Physical exam signs of aortic regurgitation
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Bounding pulse
Many stigmata of wide pulse pressure Hyper dynamic LV impulse Blowing murmur in early diastole along L sternal border (best heard leaning forward and on exhalation) Austin Flint murmur |
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Bisferiens pulse
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Double systolic impulse in carotid or brachial artery
Associated with widened pulse pressure of AR |
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Corrigan pulse
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"water-hammer" pulse with marked distension and collapse
Associated with widened pulse pressure of AR |
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de Musset sign
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Head-bobbing with each systole
Associated with widened pulse pressure of AR |
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Duroziez sign
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To-and-fro murmur heard over femoral artery with light compression
Associated with widened pulse pressure of AR |
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Hill sign
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Popliteal systolic pressure more than 60mmHg greater than brachial systolic pressure
Associated with widened pulse pressure of AR |
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Muller sign
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Systolic pulsations of the uvula
Associated with widened pulse pressure of AR |
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Quincke sign
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Capillary pulsations visible at lip or proximal nail beds
Associated with widened pulse pressure of ARc |
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Traube sign
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"pistol-shot" sound auscultated over femoral artery
Associated with widened pulse pressure of AR |
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Treatment of aortic regurgitation
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Slow progression in asymptomatic Chronic AR and normal LV- monitor, echo
After load reducing vasodilators when HTN - CCB - ACE inhibitor Symptomatic or severe with EF < 0.50: offer surgical correction |
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Pulmonic stenosis
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Rare; almost always congenital deformity
Tx w transcatheter balloon valvuloplasty |
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Pulmonic.regurgitation
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Most commonly develops in setting of severe pulmonary HTN
- dilation valve ring by enlarged pulmonary artery High-pitched decrescendo murmur at L eternal border (often indistinguishable from AR until Doppler echo) |
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Classic presentation of pulmonary edema from high pressures
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Hemoptysis
- high pulmonary vascular P may rupture a bronchial vein into lung parenchyma |
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Neural cause of hoarseness
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Compression of recurrent laryngeal nerve by enlarged pulmonary artery or LA
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