Valvular Heart Disease Flashcards
congenital aortic stenosis
- 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
Acquired aortic stenosis
- 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
- Calcific – leaflets become sclerotic (we don’t know why)
pathophysiology of aortic stenosis
- 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
- Diastolic dysfunction – ventricle doesn’t relax as much because its so hypertrophied
- 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
symptoms of aortic stenosis
- 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
signs of aortic stenosis
- 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
- Thrill – palpable murmur, theres nothing different between murmur and thrill except that one is heard and one is felt
- 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
diagnosis of aortic stenosis
- 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
Echo findings in aortic valve area with aortic stenosis
- 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.
use of cardiac cath in aortic stenosis
- 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
Aortic stenosis tx
- 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
aortic stenosis valvuloplasty
- 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)
aortic stenosis valve replacement
- 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
Aortic regurgitation: etiology (chronic)
- 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
aortic regurgitation etiology (acute)
- Aortic Dissection
- Endocarditis
- Trauma
- Valve prosthesis
- Rupture of sinus of Valsalva aneurysm
- Rheumatic fever
Aortic regurgitation pathophysiology
- 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
Aortic regurgitation sxs
- CHF
- Palpitation
- Increased stroke volume
- Arrhythmia
aortic regurgitation signs
- 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
Acute, severe aortic regurgitation
- 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!
diagnosis of aortic regurgitation
- 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
natural history of aortic regurgitation
- 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
treatment of aortic regurgitation
- 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
Mitral regurgitation etiology
- Coronary disease: papillary m. malfunction
- LV dilatation, any cause
- Endocarditis
- Myxomatous degeneration/prolapse – MVP
- Rheumatic
- Other connective tissue, incl. inflam. dis.
- Congenital
Acute mitral regurgitation
- Chordal rupture: myxomatous, endocarditis, trauma
- Papillary rupture: infarction, trauma
- Acute papillary ischemia (usually circumflex)
- Valve perforation: endocarditis
pathophysiology of mitral regurgitation
- 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
symptoms of mitral regurgitation
- Left CHF
- Secondary right CHF – from chronic elevation of pressure
- Symptoms of primary disease, e.g.
- Angina
- Fever
signs of mitral regurgitation
- 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
diagnosis of mitral regurgitation
- 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
- Semi-quantitative MR estimation
- 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
treatment of mitral regurgitation
- 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
- Timing was the hardest issue, now easier
- Catheter based
- Repair with clips and/or annular rings
- MitraClip is approved
- Replace the valve
- Repair with clips and/or annular rings
- Numerous valves that can be delivered on a catheter are under development
Tricuspid regurgitation etiology
- 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)
- Pulmonary hypertension
- Endocarditis, especially IV drug users
- Rheumatic: very rare as primary lesion
Tricuspid regurgitation signs and symptoms
- 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
Tricuspid regurgitation treatment
- 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
-
Must treat the primary lesion (e. g. mitral)