Week 4: Valvular heart disease Flashcards

1
Q

What are causes of aortic stenosis?

A
  1. Bicuspid instead of tricuspid valve. congenital
  2. Rheumatic: assoc. with mitral involvement, symptoms in 4th and 5th decade
  3. Degenerative calcific changes: most common form in older patients
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2
Q

Describe the pathophysiology of aortic stenosis.

A
  • Chronic course
  • LV compensates via concentric hypertrophy (pressure overload), leading to decreased compliance and increased diastolic LV pressure–>LA hypertrophy
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3
Q

Describe the symptoms of aortic stenosis and the causes behind them.

A
  1. Angina
    - increased O2 demand due to hypertrophy and increased wall stress
    - decreased oxygen supply due to increased diastolic pressure and less coronary perfusion pressure gradient between aorta and myocardium
  2. Syncope
    - LV can’t increase CO during exercise b/c stenotic aorta. Exercise also causes vasodilation of peripheral muscle beds
    - leads to decreased cerebral perfusion
  3. dyspnea/CHF symptoms
    - LV may have contractile dysfxn due to increased after load
    - increased LV diastolic vol and pressure leads to increased LA and pulmonary venous pressure–>congestion
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4
Q

Describe the physical findings of aortic stenosis.

A
  1. sustained LV impulse from LV hypertrophy
  2. weakened and delayed arterial upstroke (carotid artery pulsations) -b/c ventricle pushes against resistance, leads to delay
  3. harsh late systolic ejection murmur
    EKG
    -LVH, LBBB, secondary ST-T
    CXR: cardiomegaly, post-stenotic dilatation, aortic calcification
    doppler and cath: pressure gradient between LV and aorta
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5
Q

What is the treatment for aortic stenosis?

A
  • No medical Rx
  • surgery, aortic valve replacement
  • valvuloplasty/TAVI (transcatheter aortic valve implantation)
  • TAVI balloons native valve against wall, puts in stent, and implants prosthetic valve via catheter
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6
Q

Describe etiology of aortic regurgitation.

A
  1. valve
    -congenital bicuspid
    -rheumatic
    -endocarditis
    -myxomatous degeneration
  2. Aortic root
    -marfans
    -Erdheim’s medial necrosis
    -Ankylosing spondylitis
    -syphilis
    ACUTE ETIOLOGY
    -infectious endocarditis
    -traumatic rupture
    -dehiscence of prosthetic valve
    -dissecting aneurysm
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7
Q

Describe pathophysiology of aortic regurgitation.

A

ACUTE: surgical emergency
-LV normal, volume load increases LV diastolic pressure, transmitted to LA and Pulm circulation, leading to edema and dyspnea
CHRONIC
-regurg occurs during diastole, LV must pump regurg vol+normal volume
-LV adapts to volume and pressure overload–>eccentric hypertrophy
-LV dilation leads to increased compliance
-drop in aortic diastolic pressure since LV accommodates larger regurg vol–>widened pulse pressure
-drop in aortic diastolic press also leads to decreased coronary artery perfusion pressure
-can eventually develop systolic dysfxn/heart failure

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8
Q

What are symptoms of chronic aortic regurgitation?

A
  • pounding pulse-wide pulse pressure with systolic hypertension from increased stroke volume and decreased aortic diastolic press
  • orthopnea, PND from volume overloaded LV
  • Angina/chest discomfort from inadequate coronary perfusion
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9
Q

What are physical findings of chronic aortic regurg?

A

-bounding pulses (increased aortic pulse pressure)
-increased LV stroke volume (impulse)
EKG: LVH, LBBB
CXR: cardiomegaly, apex laterally and downward displaced
Echo-doppler: aortic valve and root morphology and dimensions, regurg area, vena contracta, etc…

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10
Q

What are treatments for chronic aortic regurg?

A
  • medical: asymptomatic patients with preserved LV fxn may benefit from after load reduction via nifedipine
  • Surgery: timing is key issues for aortic valve repair/replacement
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11
Q

Describe etiology for mitral stenosis.

A

-sequelae of rheumatic fever: most common cause, 90% of cases
-rare causes: congenital, myxoma, large vegetations, massive mitral annulus calcification
ACUTE
-endocarditis, chordal tear, papillary muscle rupture, ischemia or infarct.

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12
Q

Describe the pathophysiology of mitral stenosis.

A
  • emptying of LA to LV is impeded. Results in increased LA pressure
  • high LA pressure transmitted to pulm circulation–>congestion
  • becomes significant when valve area leads than 2cm2
  • reactive pulmonary HTN in severe cases can lead to right heart failure
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13
Q

Describe the symptoms of mitral stenosis.

A

-dyspnea
-orthopnea
-decreased exercise capacity
(from pulmonary HTN)
-palpitations
-hemoptysis (dilated bronchial veins, rupture, not common)
COMMONLY found in pregnant women who were previously asymptomatic

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14
Q

Describe physical findings/signs of mitral stenosis.

A

-Loud S1 (mitral valve closure, high pressure gradient forces valve leaflets widely separate during diastole)
-opening snap - after S2- sudden tensing of chord tendinae and stenotic valves)
-RV lift, Loud P2 (w/ pulm HTN)
-diastolic rumble/murmur -turbulent flow
-atrial fib -commonly developed
EKG: LAE, RVH, Afib
CXR: LAE, double contour R lower border, widening of carina, L atrial appendage prominent main pulm artery, RVE, pulm venous congestion
-doppler: fish mouth appearance, two leaflets stuck together

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15
Q

Describe treatment for mitral stenosis.

A
  • Medical: slow rate, anti coagulate with Afib, SBE antibiotic prophylaxis
  • valvuloplasty
  • surgery
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16
Q

Describe etiology of mitral regurg.

A
  • inflammatory: rheumatic, SLE valvulitis, anoretic drugs
  • degnerative myxomatous MVP, marfans, ehlers-danlos
  • secondary to annulus dilation
  • congenital
17
Q

Describe pathophysiology of mitral valve regurgitation.

A

Consequences of MR
1. increased left atrial volume and pressure
2. decreased forward CO
3. volume-related stress on LV
ACUTE
-compliance in LA changes little, increased pressure prevents more regurg but transmits backwards to pulmonary congestion and edema
CHRONIC
-LA dilates and increases compliance to accommodate increase in volume, but results in decreased forward CO (LA becomes low pressure sink vs. higher impedance aorta)
-LA and pulmonary venous pressure is somewhat normal due to dilation
-LV also undergoes compensatory dilation in response to increased volume

18
Q

Describe symptoms of mitral regurg.

A

ACUTE: pulmonary edema symptoms
CHRONIC
-fatigue and weakness due to decreased CO
-decreased exercise capacity
-dyspnea (severe MR, with LV contractile dysfunction)

19
Q

What are physical findings/signs of mitral regurg.?

A
  • PMI laterally displaced (LVE)
  • holosystolic murmur, max at apex radiating to axilla
  • S3 occasionally
  • in acute MR: short systolic murmur with S4 (high LA pressure and non compliant non dilated LV and LA)
  • EKG: LAE, LVenlargement
  • CXR: cardiomegaly, pulmonary congestion
  • Echo/doppler: mechanism of MR
20
Q

What is the treatment for mitral regurg.?

A
CHRONIC
-surgery for MV repair/replacement
-CHF: digoxin, diuretics, ACE I
-Afib: anticoagulant
-SBE antibiotic prophylaxis
ACUTE
-IV vasodilator
-intra aortic balloon bump
-urgent mitral valve repair/replacement
21
Q

Describe mitral valve prolapse.

A

-billowing of mitral valve leaflets into LA during ventricular systole
-usually enlarged posterior leaflet
-often asymptomatic
-some have chest pain, palpitations, lightheadedness, fatigue
PE findings
-mid systolic click (sudden tensing of involved mitral leaflet as leaflet forced backwards)
-late systolic murmur (regurg flow through valve)
-tend to be tall, thin, hyperdistensible joints, thoracic cage abnormalities
RX: nothing, sometimes beta blockers