Valvular Heart Disease Flashcards

1
Q

congenital aortic stenosis

A
  • Bicuspid – MC
    • Person born with two leaflets instead of three
    • Theres a strong correlation between bicuspid valve and marfan system which affects the medial layer of the aorta and dissection of the thoracic aorta
      • Aortic dissection = MCC death in bicuspid
  • Membranous subvalvar – can be very tricky to determine where problem is – occurs a lot in kids
  • Fused leaflets with doming – they are flexible but because of the fusion, they dome upward due to the left ventricular systole
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2
Q

Acquired aortic stenosis

A
  • Acquired – much more common than congenital
    • Calcific – leaflets become sclerotic (we don’t know why)
      • You can see in renal disease where they have a lot of calcium phosphate
    • Hypertrophic subaortic – this is not actually stenosis of valve, but rather beneath it
    • Rheumatic – rheumatic fever typically affects the mitral valve
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3
Q

pathophysiology of aortic stenosis

A
  • Increased systolic ventricular pressure – this is like a body builder working out – muscle hypertrophies
    • First thing that happens is NOT loss of strength
  • Left ventricular hypertrophy
    • Diastolic dysfunction – ventricle doesn’t relax as much because its so hypertrophied
      • Only later does the ventricle poop out because its tired
  • Systolic decompensation
  • Low pulse pressure, hypotension – if the ejection is impeded, the systolic doesn’t rise as high and because the vessels in the periphery are so constricted, the diastolic doesn’t fall as much
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4
Q

symptoms of aortic stenosis

A
  • Angina (triad #1) – pain in chest from inadequate coronary blood flow
    • Theres no obstruction in coronary artery
    • There is more demand for oxygen from the hypertrophied ventricle
    • EXERTIONAL angina
  • Congestive heart failure – constellation of signs and symptoms
    • Diastolic – most common presentation with aortic stenosis – the muscle is so hypertrophied that for the ventricle to fill, the left atrial pressure rises and backs up into the lungs
    • Systolic
  • Presyncope and syncope (Stokes-Adams attacks) – refers to presyncope and syncope caused by hypotension when the left ventricle cant maintain systolic pressure
    • Peripheral vasculature for muscles being utilized are still dilated, but as person slows down, there is a dip in blood pressure or loss in consciousness
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5
Q

signs of aortic stenosis

A
  • Systolic murmur
    • Thrill – palpable murmur, theres nothing different between murmur and thrill except that one is heard and one is felt
      • If you feel a thrill, because aorta is anterior, you can be pretty sure it is aortic stenosis
  • Soft second heart sound
  • Delayed arterial upstroke – normally the ventricle has ejected most of the blood, but now it takes longer to get all the blood out
    • If you can feel artery filling under your fingertips, that could be an indication of a delayed upstroke
  • Narrow pulse pressure
  • Rales and other signs of CHF
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6
Q

diagnosis of aortic stenosis

A
  • Symptoms
  • Examination
  • Echocardiogram
    • Increased leaflet thickness and echodensity with decreased excursion on structural views
    • Increased systolic velocity of blood flow (gradient) with reduced valve area on Doppler
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7
Q

Echo findings in aortic valve area with aortic stenosis

A
  • If you think about cars in a racetrack (oval), the rate of cars crossing past any point in that oval has to be the same or cars would be piling up
  • Continuity principle: flow rate is constant regardless of where it is measured
  • Flow rate in an orifice is equal to area multiplied by velocity
    • A(cm x cm) x V (cm/sec) = CO (cm­3/sec)
    • Outflow tract flow = Aortic valve flow
    • Aortic area X vel. = Outflow area X vel.
    • Aortic area = (Outflow area X vel.)/aortic vel.
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8
Q

use of cardiac cath in aortic stenosis

A
  • Aortic stenosis and coronary atherosclerosis often go hand in hand
  • Systolic gradient across valve
  • With cardiac output, valve area is calculated
  • Echocardiogram superior to cardiac cath for above
  • Cardiac cath primarily to evaluate coronaries: CAD frequently accompanies AS
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9
Q

Aortic stenosis tx

A
  • CHF from diastolic dysfunction may be treated with medication: diuretics
    • ONLY diastolic numbers are off – for any of the other classical triad, you have a mechanical problem with imminent trouble
  • For any of the classical triad of angina, CHF (from systolic dysfunction), or Stokes-Adams attacks, mechanical intervention:
    • Valve replacement – THE SOLUTION
    • Balloon valvuloplasty – makes the valve a little more flexible – if you can increase valve area by 50%, results in a huge difference! But, this is not a permanent cure
      • Mostly for people who need urgent surgery but have aortic stenosis
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10
Q

aortic stenosis valvuloplasty

A
  • Only for calcific or rheumatic AS of trileaflet valves
  • Respite is temporary, therefore use limited:
    • Palliation of nonsurgical candidates
    • Stabilization of patients requiring urgent major noncardiac surgery
    • Possible reduction of operative M&M during AVR in patients with poor LV contractility (theoretical)
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11
Q

aortic stenosis valve replacement

A
  • Mechanical: Indefinite durability at the price of chronic anticoagulation
  • Heterograft: anticoagulation not necessary (in the absence of AF); durability finite
    • From another species – from a pig or constructed using pig endocardium
  • Homograft: at one time more durable; rarely used now
  • TAVR: Percutaneous delivery of a heterograft valve mounted on a balloon, supported by a stent
    • Transcutaneous aortic valve replacement
    • Tissue valve is sewn into metallic stent – stent is crimped onto a catheter with balloon on the end – inserted into femoral artery and up to the heart, balloon is expanded, valve is in place
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12
Q

Aortic regurgitation: etiology (chronic)

A
  • Hypertension (& other root dilatation) – the leaflets no longer coapt during diastole
  • Arteriosclerosis
  • Aortic stenosis – leaflets are so stiff that they often don’t come together well – results in some regurgitation
  • Prosthesis: leaflet vs. perivalvular
    • Leaflet – in a mechanical valve, soft tissue can start to grow into the valve region
    • Endocarditis can eat through a leaflet or a tear in the leaflet
    • Perivalvular – if there is difficulty in surgery, there might be leakage around where the valve was sewn in
  • Endocarditis
  • Connective tissue diseases, e. g. Marfan’s
  • Inflammatory diseases, e. g. RA, SLE
  • Congenital disease
    • Bicuspid – can become frozen in open position
    • VSD – sometimes the jet from the septal defect can affect the aortic valve and cause leaflet malformation
    • Sinus of Valsalva aneurysm – the three pouches that are created by the shape of the aortic valve – sometimes they dilate and rupture – most common on right side of the heart
  • Aortitis – can cause dilation and regurgitation
  • Rheumatic – can stiffen the leaflets into a position where they can’t coapt
  • Syphilis
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13
Q

aortic regurgitation etiology (acute)

A
  • Aortic Dissection
  • Endocarditis
  • Trauma
  • Valve prosthesis
  • Rupture of sinus of Valsalva aneurysm
  • Rheumatic fever
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14
Q

Aortic regurgitation pathophysiology

A
  • Blood regurgitates into LV in diastole
  • LV maintains net stroke volume by dilating – the stroke volume can double and that is how CO is maintained
  • Acute decompensation: pulmonary congestion – the decrease in LV volume has not occurred
    • Diastolic pressure rises so high from the leakage, suddenly someone is in CHF (pulmonary edema)
  • Chronic decompensation: LV systolic failure – has maintained normal stroke volume but when it tires out and ejection fraction falls, the decompensation occurs
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15
Q

Aortic regurgitation sxs

A
  • CHF
  • Palpitation
    • Increased stroke volume
    • Arrhythmia
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16
Q

aortic regurgitation signs

A
  • Large stroke volume
    • Rapid upstroke
    • Wide pulse pressure
    • Displaced PMI with LV lift
  • Low diastolic pressure
  • High pitched early diastolic decrescendo murmur radiating to LSB and apex
  • Systolic flow murmur, usually louder than diastolic – not because the valve is obstructing flow, but because of the volume of flow through the dilated aortic root which was not meant to handle such a large volume
  • CHF
17
Q

Acute, severe aortic regurgitation

A
  • Severe decompensation: Often pulm. edema because LV cannot handle the load
  • Normal heart size – most people with HF have enlargement of at least one chamber of the heart
  • Murmur may be inaudible: low output, wide open valve, noisy respiration
  • LV diastolic pressure very high
    • Diastolic BP not low – because the two places that will allow it to drop cant allow this
    • S1 absent: mitral valve is closed
  • The one clue = even if diastolic murmur is hard to hear, you should be able to heart the first heart sound because the ventricle is contracting hard – S1 here is missing!
18
Q

diagnosis of aortic regurgitation

A
  • Symptoms and signs
  • CXR: cardiomegally, CHF
  • Echo-Doppler
    • Regurgitation by Doppler
    • Structural abnormalities, e. g. vegetation, dilated root, etc.
    • LV size and function
  • Transesophageal: vegetation, abscess, aortic dissection
  • Cardiac catheterization
    • Not needed for diagnosis
    • Can help estimate severity by aortography – echocardiogram has taken over
    • Assesses hemodynamic compromise
      • LVEDP
      • Cardiac output
      • Pulmonary pressures – when LV pressure rises, LA pressure rises, pulmonary pressure rises
    • Defines other disease, e. g. coronary
19
Q

natural history of aortic regurgitation

A
  • Long period of compensation without symptoms
  • Gradual LV enlargement with normal systolic function
  • Symptoms and/or LV dysfunction associated with rapid deterioration
  • LV systolic dysfunction w/o symptoms rare
20
Q

treatment of aortic regurgitation

A
  • Medical
    • Afterload reducton
    • CHF treatment
    • Antibiotic prophylaxis
  • Surgical
    • Acute, severe AR is an emergency
    • Chronic AR
      • Symptoms
      • Systolic dysfunction
      • Progressive LV dilatation (e.g. end systolic diameter greater than 55mm) a relative indication
    • AVR with endocarditis is often successful
21
Q

Mitral regurgitation etiology

A
  • Coronary disease: papillary m. malfunction
  • LV dilatation, any cause
  • Endocarditis
  • Myxomatous degeneration/prolapse – MVP
  • Rheumatic
  • Other connective tissue, incl. inflam. dis.
  • Congenital
22
Q

Acute mitral regurgitation

A
  • Chordal rupture: myxomatous, endocarditis, trauma
  • Papillary rupture: infarction, trauma
  • Acute papillary ischemia (usually circumflex)
  • Valve perforation: endocarditis
23
Q

pathophysiology of mitral regurgitation

A
  • Blood regurgitates into left atrium in systole
  • LV compensates by enlarging
  • Acute decompensation: congestion – CHF because LA pressure suddenly rises and atrium gets bigger to accept all the extra blood
  • Chronic decompensation: LV systolic failure
24
Q

symptoms of mitral regurgitation

A
  • Left CHF
  • Secondary right CHF – from chronic elevation of pressure
  • Symptoms of primary disease, e.g.
    • Angina
    • Fever
25
Q

signs of mitral regurgitation

A
  • Systolic murmur
    • Typically holosystolic – aortic stenosis is a crescendo decrescendo
    • Can be late systolic if starts in mid systole
      • Papillary dysfunction
      • Prolapse after a click
  • Left ventricular enlargement (PMI), if chronic
  • Typical CHF signs
26
Q

diagnosis of mitral regurgitation

A
  • ECG
    • LAA – characteristic p wave change
    • LVH
    • Atrial fibrillation – atrium is being stretched and provoked with high pressure
  • CXR
    • LA enlargement
    • LV enlargement
    • CHF
  • Echocardiogram
    • Semi-quantitative MR estimation
      • Depth and width of jet
      • Volume of left atrium filled
    • Quantitative
      • Orifice area, analogous to aortic stenosis
    • Etiology
    • LV function & other consequences
  • Cardiac catheterization
    • Etiology and/or other disease, e. g. CAD
    • Angiographic presence of MR and semi-quantitative severity confirmed, but echo better
    • Large “V” wave in pulmonary wedge pressure – put a catheter into a vein and thread it down the pulmonary artery until its jammed – you are then looking then at a reading in left atrium
    • LV size and contractility confirmed, equivalent to echo
    • Hemodynamic effects: output & RH pressures
27
Q

treatment of mitral regurgitation

A
  • Medical: Analogous to AR
    • Treat the underlying disease
    • Endocarditis prophylaxis
    • Afterload reduction
    • Other treatment for CHF prn
    • Arrhythmias prn
  • Surgical
    • Timing was the hardest issue, now easier
      • Certainly when symptomatic despite medication
      • Before LV deteriorates: post-op afterload is higher
    • Valve repair is increasingly common
      • Shorten or reattach chords
      • Tuck leaflets
      • Reduce annular diameter with a ring
    • Its important to do surgery before the ejection fraction becomes abnormal – if you correct after the ejection fraction is affected, then you will actually make it worse
  • Catheter based
    • Repair with clips and/or annular rings
      • MitraClip is approved
    • Replace the valve
  • Numerous valves that can be delivered on a catheter are under development
28
Q

Tricuspid regurgitation etiology

A
  • Right ventricular failure or dilatation
    • Pulmonary hypertension
      • Primary: rare
      • Secondary: LV failure, mitral disease, lung disease, Eisenmenger syndrome (end stage volume overload, e. g. atrial or ventricular septal defect)
  • Endocarditis, especially IV drug users
  • Rheumatic: very rare as primary lesion
29
Q

Tricuspid regurgitation signs and symptoms

A
  • If its pure right sided tricuspid regurg not secondary to anything, then you have true right sided HF
  • Right sided CHF
    • Edema
    • Ascites
    • Reduced exercise tolerance
  • Large “V” waves in the jugular veins
  • Usually a murmur is not audible
  • Primary disease, e. g. COPD or endocarditis
30
Q

Tricuspid regurgitation treatment

A
  • Medical
    • Underlying condition
    • Diuretics – use for CHF
    • When these fail, surgical approach is necessary
  • Surgical
    • Must treat the primary lesion (e. g. mitral)
      • Sometimes that is enough
    • Tricuspid annuloplasty with ring
    • Valve replacement is uncommon