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    PANCE Prep Pearls Valvular Disease

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    kat
    This document discusses aortic stenosis (AS) and its etiologies, pathophysiology, clinical manifestations, diagnosis, and management. AS results from obstruction of blood flow from the left ventricle into the aorta. It is usually caused by degenerative heart disease in those over 70 and congenital heart disease in younger patients. Symptoms occur when the aortic valve area decreases below 1 cm2 and include angina, syncope, and heart failure. Diagnosis involves echocardiogram, EKG, and chest x-ray. Treatment is surgical aortic valve replacement, which is the only effective treatment once patients become symptomatic.

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    PANCE Prep Pearls Valvular Disease

    Uploaded by

    kat
    668 views4 pages
    This document discusses aortic stenosis (AS) and its etiologies, pathophysiology, clinical manifestations, diagnosis, and management. AS results from obstruction of blood flow from the left ventricle into the aorta. It is usually caused by degenerative heart disease in those over 70 and congenital heart disease in younger patients. Symptoms occur when the aortic valve area decreases below 1 cm2 and include angina, syncope, and heart failure. Diagnosis involves echocardiogram, EKG, and chest x-ray. Treatment is surgical aortic valve replacement, which is the only effective treatment once patients become symptomatic.

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    This document discusses aortic stenosis (AS) and its etiologies, pathophysiology, clinical manifestations, diagnosis, and management. AS results from obstruction of blood flow from the left ventricle into the aorta. It is usually caused by degenerative heart disease in those over 70 and congenital heart disease in younger patients. Symptoms occur when the aortic valve area decreases below 1 cm2 and include angina, syncope, and heart failure. Diagnosis involves echocardiogram, EKG, and chest x-ray. Treatment is surgical aortic valve replacement, which is the only effective treatment once patients become symptomatic.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    668 views4 pages

    PANCE Prep Pearls Valvular Disease

    Uploaded by

    kat
    This document discusses aortic stenosis (AS) and its etiologies, pathophysiology, clinical manifestations, diagnosis, and management. AS results from obstruction of blood flow from the left ventricle into the aorta. It is usually caused by degenerative heart disease in those over 70 and congenital heart disease in younger patients. Symptoms occur when the aortic valve area decreases below 1 cm2 and include angina, syncope, and heart failure. Diagnosis involves echocardiogram, EKG, and chest x-ray. Treatment is surgical aortic valve replacement, which is the only effective treatment once patients become symptomatic.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
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    The key takeaways are the etiologies, pathophysiology, clinical manifestations and management of various valvular heart diseases including aortic stenosis, aortic regurgitation, mitral stenosis and mitral regurgitation.

    The main causes of aortic stenosis discussed are degenerative heart disease (calcifications), congenital heart disease (bicuspid aortic valve), and rheumatic heart disease.

    The main clinical manifestations of aortic stenosis discussed are angina, syncope, and congestive heart failure.

    AORTIC

    STENOSIS (AS)

    www.pancepreppearls.com

    AS: obstruction of Left ventricular outflow of blood across the aortic valve

    ETIOLOGIES
    1. Degenerative heart disease: calcifications (ex atherosclerotic/wear & tear) common in patients >70y*
    2. Congenital heart disease: (ex. bicuspid Aortic valve) common in patients <70y*.
    3. Rheumatic heart disease: AS may be accompanied by AR or mitral disease (but may be isolated).

    PATHOPHYSIOLOGY
    Stenosis LV outflow obstruction (fixed CO) afterload (pressure overload) LVH LV failure.

    CLINICAL MANIFESTATIONS
    Most are asymptomatic. Usually becomes symptomatic when aortic valve area <1 cm2 (Normal 3-4 cm2)
    Once symptomatic, patients lifespan becomes significantly shortened if aortic valve replacement not performed.

    1. Angina: (5y mean survival if valve replacement not done). O2 demand (LVH coupled with exertion) +
    O2 supply (2ry to fixed cardiac output) subendocardial ischemia.
    2. Syncope (exertional): (3y survival if valve replacement not done). Exertional peripheral vasodilation
    in the setting of a fixed CO insufficient cerebral perfusion during exercise/exertion.
    3. Congestive Heart Failure: (2y survival if valve replacement not done). Worst prognosis!

    PHYSICAL EXAMINATION
    1. systolic ejection crescendo-decrescendo murmur @ RUSB radiates to carotid (neck)*.
    - murmur c venous return: ex valsalva, standing, inspiration.
    - murmur c venous return (ex squatting, leg raise, expiration); if patient sits & leans fwd.
    - Signs of severity: late peaking murmur, pulsus parvus et tardus, paradoxically split S2, signs of
    LVH: LV heave & loud S4 (due to contraction into stiff ventricle).
    2. pulsus parvus et tardus: small, delayed, carotid pulse*. Narrowed pulse pressure, HTN.

    DIAGNOSTIC STUDIES
    1. Echocardiogram: small aortic orifice L ventricular hypertrophy, thickened/calcified Aov.
    2. EKG: LVH; Nonspecific changes (LAE, LBB, left axis deviation, A fib or ischemic changes).
    3. CXR: Nonspecific changes (poststenotic aortic dilation, AoV calcification, pulmonary congestion)

    MANAGEMENT
    A. SURGICAL THERAPY: Aortic valve replacement only effective treatment (tx of choice)!
    1. AoV replacement (AVR): symptomatic AS, asymptomatic severe AS (EF or AVA <0.6 cm2).
    - mechanical: prolonged durability but thrombogenic (ex. stroke) so must be placed on
    anticoagulation therapy c warfarin (Coumadin).
    - bioprosthetic: less durable but minimally thrombogenic (usually used in patients that
    cant take warfarin). Heterograft (porcine valve); pericardial.
    2. Percutaneous Aortic valvuloplasty (PAV): results in 50% AV area, but 50% restenosis @ 6-
    12 mos, so used as a bridge to AVR, if pt not a surgical candidate or in pediatric pts
    3. Intraortic balloon pump: stabilization, used as a bridge to AVR.

    B. MEDICAL THERAPY no medical treatment truly effective!


    - No exercise restrictions in patients with mild AS.
    - severe AS: because they are dependent on preload to maintain CO avoid physical
    exertion/venodilators (ex. nitrates)/negative inotropes (CCB, -blockers)

    AORTIC REGURGITATION (AR) or AORTIC INSUFFICIENCY (AI)


    ETIOLOGIES
    1. Valve disease: rheumatic heart dz (usually mixed AS/AR); Endocarditis, Bicuspid AoV.
    2. Aortic root disease/dilation: hypertension, Marfan syndrome, syphilis, rheumatoid
    arthritis, systemic lupus erythematosus, aortic dissection, ankylosing spondylitis.
    PATHOPHYSIOLOGY
    Incomplete AoV closure during diastole regurgitation of blood from Ao to LV (in addition to the
    normal antegrade flow from LA to LV) LV volume overload* LV dilation CHF.
    CLINICAL MANIFESTATIONS

    Acute: (ex. acute MI, aortic dissection, endocarditis) pulmonary edema, hypotension
    Chronic: clinically silent while LV dilates LV decompensation CHF.
    PHYSICAL EXAMINATION

    1. Diastolic decrescendo, blowing murmur best at @ left upper sternal border (LUSB)
    -

    murmur intensity c venous return: sitting forward, expiration, handgrip,


    squatting. Severity of AR proportional to duration of murmur (except in
    acute/late disease); displaced PMI, thrill.
    c venous return (valsalva, standing, inspiration) & c afterload (amyl nitrate).

    Austin Flint murmur (mid-late diastolic rumble @ apex 2ry to retrograde regurgitant
    jet mixing c antegrade flow from left atrium into the ventricle).

    2. Bounding pulses*: 2ry to stroke volume (SV). Laterally displaced PMI.



    3. Wide pulse pressure (classic signs); Seen in chronic AI only.
    Classic Signs of WIDENED PULSE PRESSURE in AR/AI (seen ONLY with chronic AR/AI)
    DESCRIPTION
    Corrigans (Water Hammer) pulse rapidly swelling & fall of radial pulse accentuated c wrist elevation
    Hills sign
    Popliteal artery systolic pressure > brachial artery by 60mmHg (most sensitive)
    Duroziezs sign
    Gradual pressure over femoral artery systolic and diastolic bruits
    Traubes sound (pistol shot)
    Double sound heard @ femoral artery c partial compression of femoral artery
    De Mussets sign
    Head-bobbing c each heartbeat (low sensitivity)
    Mllers sign
    Visible systolic pulsations of the uvula
    Quinckes pulses
    Visible fingernail bed pulsations with light compression of fingernail bed
    SIGN

    4. Pulsus Bisferiens: seen c AR + AS together or severe AR. Double pulse carotid upstroke.


    DIAGNOSTIC STUDIES
    1. Echocardiogram: regurgitant jet seen with Doppler flow.
    2. EKG: nonspecific: ( LVH, LAD). CXR: nonspecific: cardiomegaly (due to LV dilation).

    MANAGEMENT
    Variable progression. CHF 2 year mean survival. Monitor for sx onset or progression of AR.
    A. Surgical therapy: acute or symptomatic AR; asymptomatic AR c LV decompensation (LV
    ejection fraction <55%). Although 55% is a within normal LVEF range, patients with AR
    need a hyperdynamic ventricle to maintain CO. Aortic valve replacement preferred.

    B. Medical therapy: afterload reduction c vasodilators (ACEI, ARBs, nifedipine, hydralazine)
    b/c afterload reduction improves ventricular performance by increasing forward flow.

    MITRAL STENOSIS (MS)


    ETIOLOGIES
    1. Rheumatic heart disease (RHD): almost always caused by rheumatic heart disease*.
    fish mouth valve. MC in 3rd/4th decade
    2. Congenital, left atrial myxoma, thrombus, valvulitis (SLE, amyloid, carcinoid).

    PATHOPHYSIOLOGY
    Obstruction of flow from LA to LV 2ry to narrowed mitral orifice blood backs up into the L atrium
    L atrial pressure/volume overload pulmonary congestion pulmonary HTN* CHF.

    CLINICAL MANIFESTATIONS
    Slow progression until symptoms. When symptoms occur, it is then associated c rapid progression.
    1. Pulmonary sx: Dyspnea (MC sx), pulmonary edema, hemoptysis, cough, frequent
    bronchitis, pulmonary HTN.
    2. Atrial fibrillation*: secondary to atrial enlargement embolic events (esp CVA).
    3. Right-sided heart failure: (due to prolonged pulmonary hypertension).
    4. Mitral facies = ruddy (flushed) cheeks c facial pallor (chronic hypoxia).
    5. Signs of left atrial enlargement: dysphagia (esophageal compression), hoarseness

    PHYSICAL EXAMINATION
    1. PROMINENT (LOUD) S1: due to delayed forceful closure of mitral valve. split S2.

    2. OPENING SNAP (OS)*: high-pitched early diastolic sound of the opening of stenotic valve.
    Valve area proportional to S2-OS interval (tighter valve shorter S2-OS interval).
    Severity of MS: shorter S2-OS interval & prolonged diastolic murmur

    3. Early-mid diastolic rumble @ apex (low pitched) esp in LLD position: (preceded by OS)
    - murmur intensity: venous return (Valsalva, standing, inspiration).
    - murmur intensity: venous return (lying down, squatting, expiration), exercise,
    placing patient in left lateral decubitus position.

    DIAGNOSTIC STUDIES
    1. Echocardiogram: narrowed mitral valve (normal LV function usually, LA pressure,
    pulmonary HTN).
    2. EKG: left atrial enlargement (LAE/P mitrale); A fib or RVH (pulmonary HTN).
    3. CXR: nonspp. LAE (straightening of L heart border, L mainstem bronchus elevation).

    MANAGEMENT
    A. Surgical Management:
    1. Mitral valve repair or replacement: symptomatic MS, pulmonary HTN. Mechanical
    better than porcine (porcine not as suitable in replacement).
    - percutaneous balloon valvuloplasty/valvotomy: best treatment of younger
    patients*, symptomatic isolated severe MS, asymptomatic patients with
    moderate to severe MS & good valve morphology, noncalcified valves.
    - Open valvotomy: if percutaneous is not successful or not possible.
    - mitral valve replacement: if unable to perform valvotomy
    B. Medical Management: does not alter natural history nor delay need for surgery.
    - Congestion (loop Diuretics & Na+ restriction); blockers; digoxin (if A fib).

    MITRAL REGURGITATION
    ETIOLOGIES
    1. Leaflet abnormalities: mitral valve prolapse MC cause*, rheumatic heart disease,
    endocarditis, valvulitis, any cause of LV dilation (ex. Marfan syndrome).
    2. Papillary muscle dysfunction: ischemia/infarction, displacement 2ry to cardiomyopathy.
    3. Ruptured chordae tendinae: collagen vascular disease, dilated cardiomyopathy, MVP
    PATHOPHYSIOLOGY
    Retrograde blood flows from the LV into the LA (but the refluxed blood in LA returns to LV during
    diastole) LV volume overload LA dilation as blood backflows to lungs (LA/pulmonary
    pressures) CO due to diminished effective forward flow.

    CLINICAL MANIFESTATIONS
    1. Acute: pulmonary edema (rapid volume overload on LA), hypotension. Dyspnea, fatigue.
    2. Chronic: A fib, progressive Dyspnea on exertion, fatigue, CHF, pulmonary HTN, hemoptysis.

    PHYSICAL EXAMINATION
    1. Blowing holosystolic (pansystolic) murmur @ apex c radiation to axilla (high pitched).
    - (diminished) murmur: venous return (valsalva, standing) inspiration; amyl nitrate
    - (augmented) murmur: venous return (squatting, laying down, inspiration) & handgrip,
    left lateral decubitus position
    2. Widely split S2 (LV ejection time results in early A2, pulmonary HTN results in delayed P2).
    3. Laterally displaced PMI, thrill, S3 (LV dysfunction), decreased S1 if severe.

    DIAGNOSTIC STUDIES
    1. Echocardiogram: regurgitant jet, hyperdynamic LV (EF <60% = LV impairment)
    2. ECG: nonspecific: LAE (P mitrale), LVH, A fib
    3. CXR: nonspecific: cardiomegaly (dilated LA/LV), pulmonary congestion

    MANAGEMENT
    A. Surgical:
    1. Indications: acute or symptomatic MR; asymptomatic MR c LV decompensation/dilation (EF
    <55-60%). IABP for stabilization/bridge to surgery. Repair preferred over replacement.
    B.

    Medical: indicated if not operative candidate. Vasodilators to afterload (ACEI, hydralazine/nitrates);


    preload (amount of MR diuretics, nitrates); antiarrhythmics or digoxin to control A fib.

    MITRAL VALVE PROLAPSE (MVP)


    Etiologies: myxomatous degeneration of the MV apparatus, assoc c connective tissue diseases (ex
    Marfans, Ehlers-Danlos). MC in young women.
    CLINICAL MANIFESTATIONS: most are asymptomatic! Autonomic dysfunction: anxiety, atypical
    chest pain, panic attacks; arrhythmias causing palpitations, syncope, dizziness, fatigue
    sx assoc with MR progression: fatigue, dyspnea, PND, CHF. stroke, endocarditis.
    PHYSICAL EXAM: narrow AP diameter, low body weight, hypotension, scoliosis, pectus excavatum.

    Mid-systolic click* best heard @ apex mid-late systolic murmur. Any maneuver, which makes
    the LV smaller (ex. valsalva, standing) results in earlier click & longer murmur duration (2ry
    to increased prolapse of abnormal valve c normal valve).

    DIAGNOSIS: echocardiogram shows posterior bulging leaflets (with tissue redundancy).
    MANAGEMENT: reassurance (good prognosis). Beta blockers for autonomic dysfunction*.

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