Flashcards in Valvular Heart Disease Deck (106):
What are the 3 main conditions that cause aortic stenosis?
1. Dystrophic calcification (degeneration)
2. Rheumatic heart disease
3. Bicuspid valve
The 3 leaflets of the aortic valve open during _______ to allow blood to flow from the ________ to the _________.
The leaflets open during systole to allow blood to flow from the LV to the aorta.
When does aortic valve opening occur?
When does it close?
It opens when LV pressure exceeds aortic pressure.
It closes when the aortic pressure exceeds LV pressure at the end of ejection (systole).
During systole, the aortic valve area normally is what?
What is the pressure gradient between LV and aorta?
The area is 2.5-4 cm squared and there is only a trivial pressure gradient between LV and aorta
In a normal heart, what is the only heart sound that should be associated with the aortic valve?
What does the sound mark the beginning of?
A2 of the second heart sound when the valve closes after ejection (systole) and aorta pressure > LV pressure. This sound marks the beginning of diastole.
Abnormality of aortic valve structure and function can results in ______________during systole or __________ during diastole.
Aortic stenosis (obstruction of LV outflow at the valve level) during systole
Aortic regurgitation/insufficiency (backward leakage of aortic blood into LV) during diastole
Aortic stenosis leads to __________ overload of the LV with resultant ____________________ resembling that seen with severe hypertension.
PRESSURE overload of the LV with resultant LV hypertrophy resembling that seen in severe hypertension.
Aortic regurgitation leads to _______ overload of the LV with resultant ___________.
VOLUME overload of the LV that results in LV chamber dilation (cor bovinum)
Who is mainly affected by dystrophic calcification of aortic valves?
Elderly because this is the result of years of atherosclerotic material and calcific deposits on the aortic cusps and commissures.
They do not have clinically relevant evidence of AS until 70-80 years old
When do patients with tricuspid valves present with degenerative AS?
With a bicuspid valve?
normal valve- over 70 years old
bicuspid valve - 40 to 50 years old
How does the deposition product differ between rheumatic heart disease and degenerative AS?
Degenerative- calcific and atherosclerotic deposits
Rheumatic- fibrosis and calcification of the mitral AND aortic valve.
Is AS an acute or chronic problem with the valve?
Chronic- gradual asymptomatic progression of aortic valve obstruction over many years.
0.1cm sq a year in patients diagnosed with AS.
How is flow across a valve calculated? Explain what this means for aortic stenosis.
Flow = area x velocity
The goal is to maintain constant flow to tissues.
In AS, the area is decreased, so you need to increase velocity.
To increase velocity you need to convert potential energy (pressure) to kinetic (velocity) at the valve orifice.
This leads to a pressure decrease just down stream from the valve.
Peripheral autoregulation maintains BP in the aorta to perfuse tissue, so LV pressure has to increase as a result to maintain a pressure gradient over the valve.
What are the pathological changes in heart as a result of the increased LV pressure due to AS?
1. compensatory hypertrophy and increased wall thickness of the LV.
2. This increases the stiffness, diastolic pressure rises and leads to pulmonary congestion.
3. systole fails due to hypertrophy and increased work for ejection
What is the prognosis for someone with AS that has symptoms of:
1. 2 years
2. 3 years
3. 5 years
What are the 3 main presenting symptoms of someone with aortic stenosis?
1. Angina (with exertion due to hypertrophied heart)
2. syncope (related to or post exertion)
3. CHF (first at exertion then proceeding to rest)
What is heard on auscultation for AS?
What component of the sound tells you it is worse?
1. a systolic ejection murmur that peaks in mid-to-late systole.
2. S4 gallop due to hypertrophy
3. ejection click early in systole (opening)
4. paradoxical splitting and diminished A2
The later the peak, the worse the prognosis.
Where do murmurs from aortic stenosis radiate to?
When you palpate this area what do you notice?
It radiates to the carotids.
The carotid pulse will be diminished in amplitude and delayed in time (PULSUS PARVUS EN TARDUS)
Why is it difficult to appreciate pulsus parvus en tardus in the elderly?
They have stiff, atherosclerotic carotid arteries
What does the CXR show in someone with AS?
Are the finding specific and diagnostic?
1. calcification of aortic valve
2. post-stenotic dilation of ascending aorta
4. pulmonary congestion
These findings are non-specific and thus not diagnostic
What is seen on the EKG for AS?
Is this diagnostic and specific?
1. R wave >11mm in aVL
2. R wave in V4-V6 >25mm
3. S in V1 + R in V6 or V5 >35mm
Not specific for AS so, not diagnostic.
What is the most useful non-invasive test for AS?
What exactly is evaluated?
2. ventricle chamber size and function
3. quantitative aortic valve area
What is the continuity equation and what does it allow you to calculate?
It measures the velocity and cross-sectional area of the LV outflow tract proximal to the aortic valve.
The product (VxCSA) is divided by velocity of flow at the stenotic valve to yield the valve area.
What technique allows you to see the direction and speed of RBCs to calculate pressure gradients and aortic valve velocity?
What are the two main techniques used to measure aortic valve area?
What is a normal aortic valve area?
What is the area for mild stenosis, moderate and severe stenosis?
1. Doppler Echo
2. Cardiac catheterization
Normal is 2.5 -4 cm sq
Mild is 1.5 to 2 cm sq
moderate is 1.0 to 1.5 cm sq
Severe is less than 1cm sq
What is done in elderly patients with AS to assess the presence of CAD prior to aortic valve surgery?
What is the main determinant for whether or not to do surgery for someone with AS?
Symptoms (angina, syncope, CHF) NOT valve area
It was found using Doppler echo, that even if a patient has "severe" stenosis (less than 1cmsq), if they are asymptomatic, their risk of mortality is 3-4% (which is less than the risk for surgery)
Who has a higher risk of mortality after aortic valve replacement surgery:
1, an 70 year old who also needs coronary artery bypass
2. a 95 year old
The 70 year old has a higher risk of mortality.
There is not significant risk associated with age but there is a positive relationship between concomitant bypass surgery and valve surgery and mortality.
Describe the structure of the normal mitral valve leaflets.
How are they attached to the LV endocardium?
It has 2 leaflets (anterior and posterior)
Anterior is larger but posterior has a longer circumference (covers 2/3 of the annulus).
they are attached to the LV endocardium by chordae tendineae (avascular) attached to anterolateral and posteromedial papillary muscles
Describe the annulus of the mitral valve.
The posterior annulus is rigid and fibrous while the anterior annulus is thin and continuous with the aortic annulus.
What is the normal area of:
1. aortic valve
2. mitral valve
3 pulmonary valve
4. tricuspid valve
A= 2.5 to 4 cmsq
M = 4 to 6 cmsq
P = ?
T = 6 to 10 cmsq
When does the mitral valve open? When does it close?
The mitral valve opens early in diastole when the LV has relaxed enough that it has less pressure than the LA. Once the valve is open the pressure gradient is trivial (LA pressure = LV pressure)
The mitral valve closes when the LV pressure > LA pressure
Why does blood flow from LA to LV in diastole?
LV pressure when the mitral valve opens is subzero and acts as a vacuum creating suction to fill the LV.
The mitral valve drifts closed during filling, opens again when the atrium contracts in late diastole and then closes shortly after LV contraction starts.
In a normal heart, what sound is associated with mitral closing?
It is a component of S1 (with the tricuspid valve closing)
What is the main cause of mitral stenosis?
What areas of the valve are affected?
Rheumatic heart disease- causes fibrosis and calcification that fuses the valve commissures and narrows the valve orifice. It can also affect the annulus and chordae tendineae
Symptoms of mitral stenosis occur 10-30 years after the GABHS infection
What is the normal valve area for the mitral valve area?
At what area is there a measurable pressure gradient?
Normal valve = 4 to 6 cmsq
measurable pressure gradient at 2cmsq
What are the pathological changes in the heart due to a narrowed mitral valve?
(what happens to LA? LV?)
The LA has increased pressure to keep the gradient to increase velocity to maintain flow across the valve.
The increased pressure dilates the LA (atria don't generally hypertrophy) and can cause atrial fibrillation.
The pressure in the LA causes increased pulmonary artery pressure
The LV is underfilled and has a diminished stroke volume (although systole can be normal)
Why is the LA so sensitive to HR?
LV fills during diastole. If the HR increases, there will be less time in diastole and this less time to fill. The blood remains in the LA and causes increased pressure.
What exacerbates the symptoms of a person with MS?
What are some of the symptoms?
1. The patients will develop symptoms during exercise, stress or arrhythmia because these cause increased HR which decreases diastolic filling time and makes LA pressure worse.
2. pulmonary congestion
3. fatique (low CO)
What are the ausculatory findings of mitral stenosis?
Where are these finding best heard?
2. opening snap at the beginning of diastole (heard with the diaphragm at the left lower sternal border)
3. low pitch diastolic murmur (heard best with the patient in left lateral decubitus position with the bell over the apical impulse)
4. Increased P2 intensity b/c of pulmonary hypertension
Which ausculatory finding can tell you the severity of mitral stenosis?
the time between A2 and the opening snap of the mitral valve is the A2-OS interval.
Higher LA pressure shortens this interval so the shorter A2-OS, the more severe the mitral stenosis.
What accentuates the diastolic murmur of MS?
IT is accentuated by the atrial contraction in late diastole
What does the EKG show for mitral stenosis?
1. LA overload
2. atrial fibrillation
What does the CXR show for mitral stenosis?
1. enlarged LA
2. straightening of left heart border
3. upward displacement of bronchus on the left
What is seen on echo for mitral stenosis?
What is pathognomonic?
1. Hockey stick deformity of the anterior mitral leaflet
** this is pathognomonic
2. LA size
3. LV function
What are the two main goals of treatment for people with MS?
1. alleviate symptoms
2. reduce the risk for stroke (bc afib can cause emboli. since its left it goes to cerebral vasculature)
What 4 drugs are generally used to treat someone with symptomatic MS?
1. b-blocker (because symptoms are exacerbated by increased HR)
2. diuretic (decrease pulmonary congestion)
3. amiodarone as anti-arrhythmia (anti-afib)
4. Anticoagulation if they have Afib to reduce stroke risk
What criteria of patients with MS is used to determine if they need pharmacological therapy or procedural?
What are the 2 procedural options?
If the valve is less than 1.2cmsq and they are symptomatic, they are considered for:
1. surgery (replacement or open commissurotomy)
2. balloon mitral valvuloplasty
What is more preferred, open commissurotomy or balloon mitral valvuloplasty? Why?
Balloon is preferred because is does not require cardiopulmonary bypass or sternotomy.
Both are preferable to mitral valve replacement surgery.
What technique and criteria determines whether someone is a good candidate for balloon mitral vavuloplasty?
What are the contraindications?
Echocardiography is used to show if they have:
1. pliable leaflets
2. minimal thickening/calcification
3. little subvalvular involvement
1. thrombus in LA appendage
2. moderate mitral regurgitation
What is the cause of the majority of cases of pulmonic stenosis?
Congenital - leaflet fusion during intrauterine development
The valve should be 3 leaflets, but the defect makes it 2.
Acquired is very rare (rheumatic, carcinoid, tumor)
What are the hemodynamic effects of pulmonic stenosis?
F= axv and the area is decreasing so velocity must increase. This makes a pressure gradient.
Pressure increases in the RV which if severe can lead to RV failure.
What classifies PS as mild?
A gradient less than 80mmHg
What are classic symptoms of PS?
1. exertional dyspnea (RV cant pump blood to lungs efficiently so tissue cant get oxygenated blood )
5. cyanosis (again due to lack of oxygenation)
What is heard on auscultation of a PS?
Where is the murmur heard?
Where does the murmur radiate?
1. Harsh systolic ejection murmur (heard at upper left sternal border with a thrill..Radiates to the axilla) GETS LOUDER WITH INSPIRATION
What physical exam finding shows you that there may be RHF associated with PS?
Jugular venous distention because the RV is backed up to RA which backs up to JV
What does the EKG show for PS?
Right axis deviation and RV hypertrophy.
What does the CXR show for PS?
Post-stenotic dilation of pulmonary arteries and dilated right sided heart chambers
What is the indication for surgery and what is the surgery of choice for PS?
symptomatic patients can get balloon valvuloplasty.
What is the main cause of tricuspid stenosis?
It is almost always associated with rheumatic mitral stenosis.
(other causes = large vegetations, endomyocardial fibrosis, intracardiac tumor)
What are the hemodynamic disturbances associated with TS?
pressure gradient develops across the valve and the RA pressure increases leading to systemic venous congestion/edema and low CO.
What are the 4 main clinical signs of TS?
2. peripheral edema
3. low cardiac output-fatigue
4. congestion of the liver can cause ascites/abdom discomfort
What are the 2 general categories of pathology that cause aortic regurgitation?
2. Annulus and Ascending aorta
What are the abnormalities that affect aortic leaflets and cause AR?
1. Infective endocarditis
2. Bicuspid valves
3. Rheumatic Heart disease
5. ankylosing spondylitis
7. myxomatous degeneration
What are common causes of AR with dilated, expanded, or unsupported annulus?
2. aortoannular ectasia (big aorta stretches annulus)
4. aortic dissection- raised intimal flap
5. osteogenesis imperfect
6. Takayasu's arteritis/giant cell arteritis
Regurgitant flow from the aortic valve does what to the LA and LV?
It causes a diastolic volume load on the LV which increases diastolic pressure in the LV which transmits passively to cause congestion in pulmonary venous circulation.
In acute aortic regurgitation, the rapid volume and pressure increase in the LV leads to the sudden onset of ______________.
shortness of breath
What are the pathological changes seen with chronic severe AR?
LV dilates to accommodate regurgitant volume while maintaining normal filling pressure. There is a normal stroke volume but an increased afterload
How does the left ventricle enlarge in aortic regurgitation?
What does this allow it to maintain?
The increased volume causes it to enlarge by adding new sarcomeres and developing increased muscle mass WITHOUT increasing thickness.
This allows it to maintain stroke volume but results in an increased afterload (volxpres/wall thickness)
What physical exam finding characterizes severe chronic AR?
Widened pulse pressure (PP= sys-diastolic)
When do the coronary arteries flow?
Low aortic diastolic pressure = less flow.
The low diastolic aortic pressure leads to myocardial ischemia
What are the 3 major symptoms associated with acute severe AR?
Why does each occur?
1. Tachycardia- less blood pressure in aorta stimulates reflex tachycardia
2. pulmonary edema- flow back into the ventricle increases volume (dilation) and pressure in the LV which increases pulmonary vein pressure which backs up into the pulmonary circulation
3. hypotension- less blood is pumped out to tissue because some is regurgitant
What would a typical blood pressure be for someone with chronic severe AR?
What does this do to the pulse?
180/40... The LV will have dilated to accommodate the increased volume due to regurgitation while maintaining near normal filling pressures.
The pulse will be a "waterhammer pulse" (Corrigan) with rapid filling and abrupt collapse.
What are the major physical exam findings characteristic of chronic AR? (6)
1. Corrigans pulse (waterhammer)
2. Traube's sign - pistol over femoral artery
3. de Musset - head bob with heartbeat
4. Muller- uvula pulsation
5. Quincke's - capillary pulse in fingernails
6. Duroziez sign- sys. murmur when proximal femoral artery is compressed and diastolic murmur distally
Describe the heart sounds associated with AR.
1. laterally displaced apical impulse
2. No S2
3. S3 gallop
4. midsystolic ejection murmur
5. decrescendo diastolic murmur
6. Austin Flint murmur that starts late diastole
Where is it best to listen for AR heart sounds? Where do they radiate?
With diaphragm at upper right sternal border radiating down to the left lower sternal border.
Austin flint component is best heard with the bell over the apex
What on auscultation determines the severity of an AR murmur?
The length of the murmur
What is an Austin Flint murmur?
Where can it be heard?
What can it be mistaken for?
It is a late diastolic murmur heard at the apex of the heart (using the bell of the stethoscope)
It is due to the aortic regurgitation flow vibrating off the anterior mitral leaflet.
It can be mistaken for mitral stenosis.
What does the chest X-ray show for AI?
cardiomegaly (for chronic severe)
Pathology of ascending aorta
size of LV at end-diastole
size of LV end-systole
image the amount of regurgitation
Flow of regurgitation
LV end diastolic pressure
coronary artery assessment
Which patients with acute severe AR should receive surgery?
1. All acute aortic regurgitation with symptoms
2. Asymptomatic with progressive LV dilation on serial echo BEFORE EF is below 55 or LV end-systolic dimension increases by 5.5cm.
What are the 4 major mechanisms by which MR can develop?
1. papillary muscle dysfunction (myocarditis, ischemia, infarct, infiltrate)
2. Chordae tendineae changes (myxomatous degeneration)
3. Leaflets (RHD, infiltrative, myxomatous, endocarditis, trauma, etc)
4. Annular dilation secondary to LV dilation (functional/secondary MR)
What are the 2 main causes of ACUTE MR?
1. Papillary rupture after acute MI
2. flail leaflet due to chordal rupture/endocarditis
Why is LV function supranormal in acute MR?
1. increased preload (regurgitant volume + normal forward stroke volume)
2. decreased afterload (ejecting blood into low pressure LA)
This give it an increased ejection fraction
Why is stroke volume in MR decreased despite an increased LV ejection fraction?
Stroke volume is the volume of blood going into the aorta. Despite the fact that the ejection fraction is larger, a great deal of the blood goes into the low pressure LA.
This leads to pulmonary edema.
Why would MR show an elevated V wave on the atrial/venous waveform?
How is this pressure wave measured?
V is the filling of the atrium in atrial diastole (ventricular systole).
Because extra volume is getting ejected into the atrium from the LV, there will be an elevated V wave.
This can be measured with capillary wedge pressure tracing or LA pressure tracing
What is the compensated phase of MR?
What happens in decompensation?
When the regurgitation is slow and chronic, the LV will dilate gradually to accommodate the volume while maintaining low filling pressures.
1. Increased preload
2. decreased afterload
When the dilation reaches a certain point, the wall tension will increase which will raise wall tension, afterload and decrease LV systolic function
In acute MR what would you see in terms of:
1. ejection fraction
2. stroke volume
3. LA pressure
1. increased (because of high preload and low afterload)
2. decreased because some of the ejected blood goes back to LA instead of forward to aorta
3. Increased because of increased volume of regurgitated blood
In compensated chronic MR what would you see in terms of:
1. ejection fraction
2. stroke volume
3. LA pressure
1. increased (because of high preload, low afterload)
2. decreased but almost normal
3. increased slightly (less than acute because LA has dilated a little)
In decompensated MR what would you see in terms of:
1. ejection fraction
2. stroke volume
3. LA pressure
What is the cardiac output for someone with severe MR? What symptoms will this manifest as?
They will have decreased CO and will be lightheaded, fatigued, and weak.
Because some of the EF goes to the LA, they will have pulmonary congestion and shortness of breath
What are the ausculatory finding in mitral regurgitation?
What aspect of the murmur keys you in to the severity of the murmur?
The apical impulse will be hyperdynamic (and if late chronic--displaced)
There will be a holosystolic murmur at the apex of the heart that radiates to the axilla (or back)
The intensity of the murmur does NOT relate to the severity (flail leaflets may have wide communication and NO murmur!)
What is the best technique for assessing MR?
Echocardiography (especially transesophageal) which can show
1. structural abnormalities of the valve
2. LV function and size
Color Doppler can assess:
1. severity of MR by assessing RBC velocity and flow back through the valve
Who is considered for surgery for MR?
a strong trend is emerging toward earlier consideration for surgery because techniques like:
are showing lower mortality
1. MR symptoms
What predicts the ability to repair the mitral valve when assessing for surgery?
Why is repair preferred to replacement with mitral valves?
In the past, chordae to the posterior mitral leaflet were damaged and there was LV spherical remodeling after the surgery decreasing LV function.
Repair ensures the chorda are preserved and LV function does not decline
Survival from mitral valve replacement is much better if surgery is done before EF falls below _______ and before NYHA class ___________ symptoms develop AND before end-systolic dimension reaches ________.
What is the most common cause of pulmonic regurgitation?
dilation of the annulus due to pulmonary hypertension.
(other causes - endocarditis, congenital, trauma)
What are the hemodynamic consequences of pulmonic regurgitation?
Increased volume load on the RV
What are the clinical manifestations of TR?
What sounds are heard on auscultation?
If the cause of the valve regurgitation was pulmonary hypertension (most common) they will present with right-sided heart failure.
1. soft decrescendo murmur during diastole along the upper left sternal border that increases with inspiration
2. may become high-pitched if there is pulm. hypertension
When is surgery recommended for pulmonic regurgitation?
Almost never except when there is infective endocarditis that can't be cleared with antibiotics
What is the main cause of Tricuspid regurgitation?
secondary to RV dilation with pulm. hypertension
What are the hemodynamic consequences of TR?
1. volume overload on RV -->dilation and failure
2. right sided heart failure
What would be seen on physical exam of someone with TR?
What would you hear on auscultation?
You would see;
elevated jugular veins
fatigue due to low CO
On auscultation you would hear a holosystolic murmur that increases intensity with inspiration
What wave is elevated when assessing jugular veins in both mitral and tricuspid regurgitation?
V wave because there will be increased pressure in the LA and RA due to regurgitant volume
Why is tricuspid valve replacement reserved for only very severe cases?
The tricuspid valve is so large (6-10cm) that its replacement almost always gives the patient some mitral stenosis.