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Aortic Valve Disease Flashcards

1
Q

Aortic Valve Disease

  • Aortic stenosis
  • Aortic regurgitation or insufficiency
  • Combined valvular disease
A
  • Aortic stenosis
    • Abnormal thickening & restriction in aortic valve leaflet motion
  • Aortic regurgitation or insufficiency
    • Abnormal retrograde flow across the valve
  • Combined valvular disease
    • Aortic stenosis + aortic regurgitation
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2
Q

Obstruction to LV Outflow

  • Normal aortic valve
  • Subvalvular obstruction
  • Valvular stenosis
  • Supravalvular stenosis
A
  • Normal aortic valve
    • 3 leaflets: right, left, & non-coronary cusps
    • Leaflets are attached to the aortic wall in the sinuses of Valsava
    • Commissure: region where the leaflet edges coapt
    • Cross-sectional area: 3-4 cm2
  • Subvalvular obstruction
    • Abnormal thickening of the intraventricular septum (ex. hypertrophic cardiomyopathy)
    • Congenital subaortic membranes in the left ventricular outflow tract
  • Valvular stenosis
    • Narrowing, stiffening, thickening, fusion or blockage of one or more valves
  • Supravalvular stenosis
    • Muscular ridge or hypoplasia of the ascending thoracic aorta
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3
Q

Hemodynamics of Valvular Aortic Stenosis

  • Normal aortic valve
    • Opens when…
    • Closes when…
    • Pressure gradient
  • Congenital valvular disease
    • General
    • Unicuspid aortic valves
    • Bicuspid aortic valves
  • Acquired valvular disease
    • Rheumatic valve disease
    • Calcific degenerative valve disease
    • Systemic disease
A
  • Normal aortic valve
    • Opens when LV systolic pressure > central aortic pressure
    • Closes when LV pressure < central aortic pressure
    • Normally: no significant gradient across the aortic valve during systolic ejection
  • Congenital valvular disease
    • Congenitally malformed aortic valves
    • Unicuspid aortic valves: present during infancy & childhood
    • Bicuspid aortic valves: present later in life (3rd - 5th decades)
  • Acquired valvular disease
    • Rheumatic valve disease
      • Thickening of the valve leaflet margins w/ commissural fusion & restriction in leaflet motion
      • Long-term sequelae of the valvulitis associated w/ acute rheumatic fever
      • Rarely occurs in the absence of concomitant mitral valve disease, esp in women
    • Calcific degenerative valve disease
      • Abnormal thickening & calcification of valve leaflets w/ age
      • Chornic inflammation + upregulation of neurohormonal mediators
      • Ex. renin-angiotensin system, lipid accumulation, & lymphocytic infiltration of valve surfaces leading to leaflet calcification
    • Systemic disease (uncommon)
      • Rheumatoid arthritis, ankylosing spondylitis, Paget’s disease, & onchronosis
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4
Q

Changes Following Aortic Valve Area Decrease

A
  • LV systolic pressure increases
  • Aortic transvalvular pressure gradient presents throughout systolic ejection
  • Contour of the centrla aortic pressure tracing becomes blunted
  • LV hypertrophy
    • Response to chronic elevation in LV end systolic pressure
    • Increase LV systolic pressure –> increase LV wall tension
    • Replication fo myofibrils –> compensatory thickening of LV wall (hypertrophy)
    • Tries to maintain normal wall tension in the presence of chronically elevated afterload
  • Cencentric LV hypertrophy
    • With little change in LV cavity size
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5
Q

LV Compliance

  • Hypertrophy vs. compliance
  • LV pressure-volume relationship
A
  • Hypertrophy vs. compliance
    • Increase ventricular hypertrophy –> decrease LV compliance
  • LV pressure-volume relationship
    • Upward & leftward shift
    • For any given LV volume, there’s a higher corresponding LVEDP
    • Increase LVEDP –> prominent a-waves on the LA pressure tracing during late diastole w/ atrial contraction (atrial “kick”)
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6
Q

Aortic Stenosis Physical Findings

  • PMI
  • Carotid pulse contour
A
  • PMI
    • Inferolaterally displaced
    • Sustained
      • Prolonged LV systolic ejection –> prolonged apical impulse
    • Presystolic heave
      • LV end diastolic pressure increases –> prominent atrial “kick” during late diastolic atrial contraction
  • Carotid pulse contour: pulsus parvus et tardus
    • Decreases in amplitude
    • Delay of carotid upstroke
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7
Q

Aortic Stenosis Cardiac Auscultation

A
  • Turbulent flow across a stenotic valve –> rhomboid shaped SEM
    • Heard at the caridac base
    • Can radiate to the suprasternal notch & LV apex
  • Restricted but pliable valves (ex. bicuspid aortic valves) –> early systolic ejection sound (“click”)
    • Heard in the suprasternal notch or apex
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8
Q

Severe Aortic Stenosis Auscultatory Findings

  • SEM peaking
  • S2 splitting
  • S2 splitting (other)
  • SEM intensity
  • Extra heart sounds
A
  • Late peaking SEM
    • Narrowing aortic valve –> delay in time to peak systolic ejection
  • Narrowed S2 splitting
    • May –> paradoxical splitting
    • Normally: A2 closes before P2
      • Inspiration: negative pressure –> increased venous return –> increased pulmonary vascular bed capacitance –> prolonged RV systolic ejection time –> widened separation b/n A2 & P2 –> widened S2 split
      • Expiration: narrowed separation b/n A2 & P2 –> narrowed S2 split
    • Worsening aortic stenosis: LV ejection time increases –> delayed A2 closure –> A2 moves closer to P2 –> diminished / more singular S2
  • Reversed splitting of S2 w/ paradoxical movement w/ respiration
    • S2 split narrows w/ inspiration & widens w/ expiration
    • Worsening aortic stenosis –> prolonged systolic ejection time –> A2 occurs after P2
  • Decreased SEM intensity
    • LV fails –> decrease SV –> decrease SEM intensity
  • S4
    • Increase LV hypertrophy –> decrease ventricular compliance
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9
Q

Natural History of Aortic Stenosis

  • Symtpom development
  • Cardinal symptoms
  • Avg survival after developing a cardinal symptom
A
  • Patients typically have a failry long latent period before developing symptomatic disease
  • Cardinal symptoms
    • Angina
    • Syncope
    • Dyspnea & congestive heart failure
  • Avg survival after developing a cardinal symptom
    • Angina: 5 years
    • Syncope: 3 years
    • Congestive heart failure: 2 years
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10
Q

Angina

  • Angina
  • Severe aortic stenosis
  • LVEDP vs. myocardial blood flow
A
  • Angina
    • Occurs when there’s a mismatch b/n myocardial oxygen supply & demand
  • Severe aortic stenosis
    • Chronic elevation in LV systolic pressure
    • Myocardial oxygen demand increases in response to increased myocardial wall tension
  • Chronic elevation in the LVEDP can compromise myocardial blood flow
    • Coronary blood noramlly flows form the epicardial to endocardial surfaces of the myocardium
      • Driven by the pressure gradient b/n the aorta & LV
    • Aortic stenosis –> decrease MAP –> increase LVEDP –> decrease transmyocardila perfusion pressure gradient –> mismatched myocardial supply & demand –> angina
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11
Q

Syncope

A
  • Results from cerebral hypoperfusion
  • May be exacerbated by physical exertion, bradyarrhythmias, or tachyarrhythmias
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12
Q

Congestive Heart Failure

  • Mild aortic stenosis
  • Worsening aortic stenosis
  • Ongoing disease progression
A
  • Mild aortic stenosis
    • Increase LV systolic pressure & aortic transvalvular gradients
    • Normal to mildly elevated LVEDP
    • Normal CO & systemic BP
  • Worsening aortic stenosis
    • Increase LV outflow tract obstruction + decrease LV compliance –> increase LVEDP –> increase pressure in pulmonary vascular bed
    • –> pulmonary hypertension, interstitial pulmonary edema, & congestive heart failure
  • Ongoing disease progression
    • LV systolic dysfunction –> decrease forward flow across aortic valve –> decrease transvalvular gradients –> increase pulmonary arterial pressure –> worsen CHF
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13
Q

Evaluation of Aortic Stenosis

  • Echocardiography (cardiac ultrasound)
  • Cardiac catheterization lab
  • EKG
  • Chest X-ray
A
  • Echocardiography (cardiac ultrasound)
    • Noninvasive
    • 2-D echo provides info about LV function & valvular anatomy
    • Doppler interrogation of the aortic valve provides quantitative info about…
      • Valve gradients
      • Orifice area
      • Valvular regurgitation
      • Pulmonary arterial pressure
  • Cardiac catheterization lab
    • Invasive
    • Calculate aortic valve area from CO, systolic ejection time, & aortic valve gradients
    • Used to verify inconsistent data in hemodynamic info from noninvasive tests
    • Coronary angiography: evaluates coronary anatomy prior to surgical aortic valve replacement
    • Coronary artery bypass grafting (CABG): performed at the time fo aortic valve replacement if coronary artery disease is identified
  • EKG
    • LVH
    • LA enlargement
    • LAD
  • Chest X-ray
    • Cardiomegaly
    • Aortic valve calcification
    • Aortic dilation
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14
Q

Medical Management of Aortic Stenosis

  • Drugs
  • What to avoid
A
  • Diuretics
    • Manage intravascular volume overload
  • Digoxin
    • Enhances myocardial contractility to treat congestive heart failure
  • Intravenous inotropes
    • DA & dobutamine are used for acute management of more criticall ill patients
  • Avoid vasodilators in severe aortic stenosis
    • Patients may not be able to adequately augment CO in response to peripheral vasodilation
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15
Q

Surgical Management of Aortic Stenosis

  • When to use surgery vs. medicine
  • Aortic valve replacement
  • Bioprosthetic or metallic valve prosthesis
  • Percutaneous balloon valvuloplasty
    • Limited use
    • Peri-procedural complications
  • Percutaneous transcatheter aortic valve replacement (TAVR)
A
  • Symptomatic severe aortic stenosis is pirmarily a surgical disease
  • Aortic valve replacement
    • In symptomatic patients w/ moderate to severe aortic stenosis
  • Bioprosthetic or metallic valve prosthesis
    • Variety of variables taken into consideration when choosing the appropriate valve for a patient
  • Percutaneous balloon valvuloplasty
    • Limited use in long-term management of severe aortic stenosis
      • Used primarily as a bridge to aortic valve replacement
      • Exception: congential aortic stenosis in peds
    • Peri-procedural complications
      • Death
      • Severe aortic regurgitation
      • Myocardial perforation
      • Infarction
      • Recurrent aortic stenosis at 6 months
  • Percutaneous transcatheter aortic valve replacement (TAVR)
    • For patients who arent’ candidates for traditional surgical valve replacement
    • Femoral arterial catheters are advanced across the aortic valve in a retrograde fashion
    • Aortic valve is pre-dilated w/ a balloon tipped catheter
    • Catheter implantation of a bioprosthetic valve
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16
Q

Aoritc Regurgitation Etiologies

  • Aortic regurgitation
  • Congenital
    • Aortic valves
    • Sinus of Valsalva aneurysms
    • Subaortic membranes
    • Subaortic ventricular septal defects (VSDs)
  • Acquired
    • Rheumatic valvular disease
    • Endocarditis
    • Aortic root disease
      • Acending thoracic aortic aneurysm
      • Aortic dissection
    • Systemic diseases
      • Connective tissue diseases
      • Vasculitides
A
  • Aoritc regurgitation
    • Abnormal retrograde flow of blood across the aortic valve from the aorta into the LV
  • Congenital
    • Bicuspid (& quadricuspid) aortic valves
    • Sinus of Valsalva aneurysms
      • Dilation of the aortic annulus
      • Prolapse of an aortic leaflet into the LVOT
    • Subaortic membranes
      • Damage to the aortic valve form chronic turbulent flow through the subaortic membrane
    • Subaortic ventricular septal defects (VSDs)
      • Prolapse of an aortic valve leaflet through the VSD
  • Acquired
    • Rheumatic valvular disease
      • Inflammation fo the valve leaflets from rheumatic fever
      • Chronic fibrosis & retraction of hte leaflet tips
      • Incomplete leaflet coaptation & secondary regurgitation
      • Uncommon to see rheumatic aortic valve disease w/o concomitant mitral valve disease (esp in women)
    • Endocarditis
      • Bulky vegetations
      • Leaflet destruction & perforation
      • Complications from perivalvular abscesses
    • Aortic root disease
      • Acending thoracic aortic aneurysms
        • Dilation of the aortic valve annulus w/ incomplete coaptation fo the aortic valve leaflets
        • Risk factor: chronic hypertension
        • Bicuspid aortic valves are associated w/ a primray aortopathy which increases the risk for developing aortic aneurysms
      • Aortic dissection
        • Retrograde extension of a dissection flap into the aortic valve annulus
        • Spontaneous or from trauma
    • Systemic diseases (rare)
      • Connective tissue diseases
        • Lupus
        • Rheumatoid arthritis
        • Ankylosing spondylitis
      • Vasculitides
        • Takayasu’s arteritis
17
Q

Hemodynamics of Aortic Regurgitation

  • Chronic regurgitation
    • Chronic LV volume overload –>
    • LVEDV & LVEDP
    • Hypertrophy
    • Cardiomegaly
    • Increase LV wall thickness –>
  • Chronic severe regurgitation
    • Aortic pulse pressure
    • Forward SV
    • End diastolic pressure
  • Aortic regurgitation
    • Preload & compensatory time
    • LV compliance
    • LV filling pressure
    • Regurgitation
A
  • Chronic regurgitation
    • Chronic LV volume overload –> LV remodeling
    • LVEDV & LVEDP increase
    • Eccentric hypertrophy
      • Increase LV diastolic wall stress –> sarcomere replication –> myocyte elongation –> LV cavity dilation
    • Cardiomegaly
      • Increase LV size –> compensatory increase wall thickness to restore normal LV wall stress
      • Untreated –> enlared heart –> increase myocardial mass –> cardiomegaly
    • Increase LV wall thickness –>
      • Increase LV wall stress, increase afterload mismatch, & LV systolic dysfunction
  • Chronic severe regurgitation
    • Widened aortic pulse pressure
    • Increase LVEDV –> increase forward SV
    • Rapid diastolic run-off from aorta to LV –> equalized aortic & LV pressure at end of diastole –> abnormally low end diastolic pressure
  • Acute regurgitation
    • Abrupt increase LV preload + insufficient time for compensatory LV remodeling
    • Unchanged LV compliance –> normal ventricle can’t accommodate large increases in LV volume
    • Increase LV filling pressure –> pulmonary edema
    • Acute aortic regurgitation w/ endocarditis, aortic dissection, & trauma
18
Q

Changes in LV Pressure-Volume Relationships

  • Acute aortic regurgitation
  • Chronic aortic regurgitation
A
  • Acute aortic regurgitation
    • Upward LV pressure-volume curve shift
    • Increase LV volume –> greater increase in LV pressure
  • Chronic aortic regurgitation
    • Ventricular remodeling –> new pressure-volume relationship
    • Significantly increase LV volume –> minimally increase LV pressure
    • LV systolic dysfunction: increase LV volume –> significantly increase LV pressure –> congestive heart failure
19
Q

Chronic Moderate to Severe Aortic Regurgitation Physical Findings

  • PMI
  • Quincke’s sign
  • Corrigan’s or water hammer pulse
  • Deroziez’s sign
  • Hill’s sign
A
  • Laterally displaced PMI
    • Due to cardiomegaly
  • Quincke’s sign
    • Vascular pulsations in the capillary beds of fingernails
    • Augmented by shining a light through the fingertip & compression of the distal finger
  • Corrigan’s or water hammer pulse
    • Peripheral artery rapid distension & collapse in the contour of the pulse
  • Deroziez’s sign
    • Systolic femoral murmur w/ compresison of the proximal femoral artery
    • Diastolic femoral murmur w/ compression of the distal femoral artery
  • Hill’s sign
    • >60 mmHg differential in teh brachial & popliteal systolic pressure
20
Q

Aortic Regurgitation Auscultation

  • Chronic aortic regurgitation
    • Murmur
    • Heard
    • Morphology
  • Aortic regurgitation related to aortic root dilation
    • Harvey’s sign
    • Severity of chronic aortic regurgitation
    • Forward SV
    • Austin-Flint murmur
  • Severe acute aortic regurgitation
    • Murmur
    • Physical findings
    • Peripheral findings
A
  • Chronic aortic regurgitation
    • High pitched diasotlic murmur
    • Heard w/ diaphragm in 3rd or 4th intercostal space at LSB
    • Decrescendo morphology: decreases intensity as retrograde flow decelerates w/ narrowing LV & aortic pressures
  • Aortic regurgitation related to aortic root dilation
    • Harvey’s sign
      • Regurgitant murmur heard along the RSB
      • Augmented by listening at the end of expiration w/ the patient leaning forward
    • Severity of chronic aortic regurgitation
      • Correlates more w/ duration than intensity of diastolic murmur
    • Incresaed forward SV –> systolic murmur
      • Differentiated from a murmur related to coexisting aortic stenosis by palpation of the contour of the carotid pulse
    • Austin-Flint murmur
      • Low frequency diastolic murmur consistent w/ mitral stenosis but in the absence of mitral stenosis
      • Occurs due to impairment of mitral valve diastolic excursion from torrential flow related to aortic regurgitant jet
  • Severe acute aortic regurgitation
    • Regurgitant murmur
      • Attenuated due to rapid near equalization of aortic & LV pressures
    • Physical findings
      • Cardoigenic shock w/ tachycardia, hypotension, & pulmonary edema
    • Peripheral findings
      • Not present
21
Q

Evaluation of Aortic Regurgitation

  • Symptoms
  • Valve replacement
  • Echocardiogrpahy
    • Evaluates…
    • Asymptomatic patients w/ mild to moderate aortic regurgitation & normal LV function
    • Asymptomatic patients w/ moderate to severe aortic regurgitation & normal LV function
  • If it’s unclear if a patient is asymptomatic
A
  • Symptoms
    • Patients w/ aortic regurgitation tend to have long latent periods before developing symptoms as long as LV systolic function remains normal
    • Once LV dysfunciton develops, symptoms progress rapidly
  • Valve replacement
    • Should occur prior ot the onset of symptoms, LV dysfunciton, or cardiomegaly
  • Echocardiography
    • Evaluates & follows-up w/ aortic regurgitation, LV size, & LV function
    • Asymptomatic patients w/ mild to moderate aortic regurgitation & normal LV function: echo every 1-2 years
    • Asymptomatic patients w/ moderate to severe aortic regurgitation & normal LV function: echo every 6-12 months
  • If it’s unclear if a patient is asymptomatic
    • Exercise can be helpful
    • Cardiac catheterization can be helpful but isn’t necessary
22
Q

Treatment of Chronic Severe Aortic Regurgitation

  • Asymptomatic patients w/ normal LV function
  • Patients w/ preserved LV systolic function & diastolic hypertension
  • Before patients develop significant symptoms
  • Patients w/ confomitant aortic pathology
  • Patients w/ severe aortic regurgitation
A
  • Asymptomatic patients w/ normal LV function
    • No treatment
    • Followed w/ serial exams & echoes
  • Patients w/ preserved LV systolic function & diastolic hypertension
    • Diuretics, sodium restriction, & vasodilator therapy
    • Nifedipine or ACE-inhibitors may alleviate mild symptoms & slow progression
  • Before patients develop significant symptoms, LV dilation, or LV systolic dysfunction
    • Surgical aortic valve replacement w/ a metallic or bioprosthetic valve
  • Patients w/ confomitant aortic pathology
    • Aortic root replacement
  • Patients w/ severe aortic regurgitation
    • Intra-aortic baloon pump (IABP) is contraindicated b/c diastolic inflation fo the IABP will worsen aortic regurgitation

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