valve disorders Flashcards
types of valve disorders
tricuspid
pulmonic
mitral
aortic
three thin leaflets open and close properly
healthy aortic valve
narrowing
stenosis
the leaflets become stiff and thickened limiting the amount of blood pumped out to the body
diseased stenotic valve
backflow
regurgitation
what does regurgitation look like
the chordae tendinae become floppy
3 leaflets – aortic and pulmonary
semi-lunar valves
mitral and tricuspid
AV valves
function of valves
- Keep blood moving in one direction through pumping chambers
- Each valve has leaflets that open easily and close fully in response to
pressure changes and muscle contractions produced during systole
and diastole to ensure forward progression of blood through the
heart. - An increase in forward pressure across a valve forces the leaflets to
open. An increase in backward pressure against a valve forces the
leaflets to close. - The valves are stabilized and supported by the fibrous skeleton, a
sheet like structure of dense fibrous connective tissue that separates
the atria from the ventricles and encircles each valve, creating a ring or annulus. The annulus acts as an anchor to the heart muscle.
separates the left ventricle and the aorta
aortic valve
Leaflets close edge-to-edge by a fibrous collagen edge called
commisures
Surrounding the valve, at
the base of each leaflet is
the fibrinous ring, called the
annulus
Two of the sinuses house
the
R and L Ostia of the
coronary arteries
The walls of the aorta bulge
out slightly behind each
leaflet, called a
sinus of valsava
Coronary arteries fill during
diastole
what valves open during ventricular diastole
AV valves
- Acquired
- Calcium deposition (similar to that of athlerosclerotic disease of the coronary arteries)
- 60- 75y/o
- Rare in people younger than 50
degenerative/calcific aortic stenosis
- Born this way
- Symptoms usually occurs around 50 y/o, when
degenerative processes begin to manifest - Younger when stenosis is severe
- Often occurs with
Dilated aortic root
Coarctation of the aorta - Look for it in the family- parent, children
congenital/unicuspid or bicuspid valves
1) Bicuspid or unicuspid,
2) Fibrinous fused
commissures,
Symptoms age 50
congenital aortic stenosis
1) Nodular calcification
1) 3-cusp valve, no
commissural fusion
Limit leaflet movement,
Symptoms age 70
degenerative aortic stenosis
1) Fibrous thickening,
2) 3-cusp valve, mild
calcification, rheumatic
fever history in ½,
fused commisures
Rheumatic Aortic Stenosis
mild valve thickening or calcification
affects normal leaflet motion. As the disease progresses, leaflets become thicker, calcium nodules form, and new blood vessels appear.
calcium nodules located within the layers of the leaflet bulge outward toward the aorta and extend to
the sinuses of Valsalva, causing restricted leaflet motion and obstruction of left ventricular outflow during systole
aortic stenosis pathophysiology
what creates left ventricular hypertrophy
As the aortic valve progresses from sclerosis to stenosis, it creates worsening resistance to LV blood outflow/ejection
The ventricle must generate a higher systolic pressure to eject the blood out.
the left ventricle encounters chronic resistance (over time) to systolic ejection (Increased Afterload)
LHV then causes an increase in the _____________ (best measured at the very end of diastole= LVEDP)… because the space available in the LV is now limited but must hold
the same amount of volume.
diastolic pressure
Cardiac output is maintained… UNTIL… the aortic valve becomes so severely stenosed, left ventricular can no longer generate enough pressure to overcome the afterload. this results in
reduced LV systolic contractility (EF<50%)
Or reduced diastolic volume: the LVH is so big, there is no volume to push out (EF>50%)
Both of these scenarios= Hypoperfusion to other organs
Syncope ( Not enough blood to the brain)
Renal Failure ( Prerenal hypoperfusion RI)
- condition characterized by widespread inflammation affecting a number of organs in the body, including the heart.
It occurs after an infection of the throat caused by the bacterium
Group A streptococcus.
The resulting immune response targets both the bacteria and some
of the body’s own tissues.
rheumatic fever
Rheumatic heart disease results from
persisting inflammation of the
heart after acute or recurrent episodes of rheumatic fever
gold standard for diagnosing aortic stenosis
noninvasive 2-dimensional Doppler echocardiography. (TTE)
peaks in early systole in mild aortic stenosis and progressively later as aortic stenosis becomes more severe.
The crescendo-decrescendo late-peaking murmur is heard best at the upper right sternal boarder at the second intercostal space and may radiate to the carotid arteries.
In older patients, the murmur may be less intense and may radiate to the apex of the heart rather than to the base
In severe AS a palpable LV heave or thrill can present
systolic ejection murmur
what valves does rheumatic heart disease affect
the mitral and aortic valves. Chronic inflammation may cause narrowing of the valves resulting in decreased blood flow through the heart or
leakage of the valves causing blood to flow in the wrong direction
how to diagnose AS
- EKG-
Show LVH - Chest Xray-
Cardiomegaly (Enlarged cardiac silhouette)
Aortic Valve Calcification
Aortic Root Dilation or Calcification - Echocardiogram
Visualize the Aortic valve leaflets, commissures, opening/closing
Severity of LV thickness
Overall ventricular function
Aortic valve gradient
Valve area estimation - Cardiac Catheterization
Measure pressures and gradients from inside the heart, and across the aortic valve
Anatomy or coronary arteries
Aortic stenosis is graded:
mild, moderate, or severe.
Grading is based on 3 hemodynamic
parameters measured by using Doppler echocardiography:
Aortic jet velocity
Mean aortic valve pressure gradient
Aortic valve area
Aortic stenosis is considered hemodynamically important when the :
Valve area is less than 1.0 cm (per TTE or TEE) or
Aortic jet velocity >4m/s (per TTE) or
Mean gradient >40mmHg (per TTE or Cath)
aortic stenosis treatment
aortic valve replacement
how to treat cardiovascular risk factors
control:
Hypertension (No Beta blockers - depress myocardial function and can induce left ventricular failure)
diabetes mellitus
smoking tobacco
high cholesterol levels
Overweight
lack of exercise.
what is important to consider in AS treatment
Having patients compare current activity level with past activity level may indicate if usual activity has been altered to avoid signs and symptoms
what is the choice of replacement device of age <60 years
Mechanical prosthesis
Must be on anticoagulation!
13% in men and 8.5% in women with most being trace or mild; a prevalence of 15.6% was reported in African-Americans.
Prevalence increases with Age in both genders.
Of asymptomatic people >55 years of age, 13% have moderate or severe echocardiographic AR
with a total prevalence of 29% (including mild AR).
The prevalence of AR appears to be similar across racial populations in the United States, although internationally there is significant
variation in the prevalence of predisposing conditions, such as rheumatic heart disease.
epidemiology of aortic valve insufficiency/regurgitation
what is the choice of replacement device of Age >60 years
Porcine or bovine pericardial tissue bio-prosthetic grafts
Last for average 10-15 years
Avoid the need for anticoagulation
The diastolic leakage of blood from the aorta into the left ventricle.
It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease
or dilation of the aortic root
aortic valve insufficiency/regurgitation
medical emergency with high mortality
Most commonly it results from aortic dissection or endocarditis and, in rare cases, trauma.
NO LV dilatation
End-diastolic pressure in the left ventricle rises sharply. The heart tries to compensate by increasing the heart rate and increasing the contractility (Starling’s law) to keep up with the increased preload, but this is insufficient to maintain the normal stroke volume and fails
acute AR
Developed countries:
Congenital bicuspid aortic valve
Aortic root dilation
Developing countries:
Rheumatic Fever
AI etiology
the most common
congenital -the most common cause of isolated AR
Most patients remain asymptomatic for decades, as the left ventricle maintains forward stroke volume with compensatory
chamber enlargement and hypertrophy. Eventually, the left ventricular systolic dysfunction supervenes and left ventricular
end-diastolic pressure rises resulting in symptomatic congestive heart failure.
Timing AVR before irreversible myocardial dysfunction develops is of critical importance.
chronic/progressive AR
Wide Pulse Pressure goes with
chronic AR
Symptoms: most patients remain asymptomatic for years
Exertional dyspnea and fatigue
May not worsen with exertion in the early stages due to compensatory tachycardia with shortened diastole
Palpitations
Chest pain
Paroxysmal Nocturnal Dyspnea/ Pulmonary Edema
Sudden cardiac death
This is uncommon (< 0.2% per year) in asymptomatic patients with preserved LV functi
chronic AI
Sudden, severe shortness of breath
Rapidly developing heart failure
Chest pain if myocardial perfusion pressure is decreased (hypoperfusion ischemia) or an aortic dissection is present
acute AI
caused by the regurgitant flow causing vibration of
the mitral apparatus, is lower pitched and short in duration
Austin flint murmur
AI PE
Diastolic Decrescendo Murmur, usually as a high-pitched sound that is loudest at the
left sternal border.
Heard best with the patient leaning forward in full expiration in a quiet room
It is one of the cardiac murmurs most commonly missed.
An Austin-Flint murmur, which is caused by the regurgitant flow causing vibration of
the mitral apparatus, is lower pitched and short in duration.
Auscultation may reveal an S3 gallop if LV dysfunction is present
characterized by narrowing of
the mitral valve orifice
mitral stenosis
usually as a high-pitched sound that is loudest at the
left sternal border.
Heard best with the patient leaning forward in full expiration in a quiet room
Diastolic Decrescendo Murmur,
chronic aortic regurgitation PE
The murmur of AR occurs in diastole, usually as a high-pitched sound that is loudest at the left sternal border.
Manifestations of severe chronic AR are often the result of widened pulse pressure.
Corrigan pulse (“water-hammer” pulse) - Abrupt distention and quick collapse on palpation of the peripheral arterial
pulse
Quincke sign - Visible pulsations of the fingernail bed with light compression of the fingern
The PMI or Apical Pulse is prominent, laterally displaced, hyperdynamic, and may be
sustained
AI PE
AI diagnosis
Transthoracic echocardiography
- Chordal Fusion
- Papillary muscle malposition (Too close together
congenital mitral stenosis
AI treament
Surgical replacement
Mechanical vs. bioprosthetic
Anticoagulation
Age
TAVR
- Rheumatic Fever- Thickening of the leaflets, fusion of the commissures, retraction, thickening of the Chordae, calcium deposition
in the valve - Inner to outer deposits/commissures to
annulus - Mitral annular calcification (Old age and Dialysis)
- Outer to inward deposits/ annulus to commissure
acquired mitral stenosis
what is the most common cause of mitral stenosis
rheumatic fever
Mitral stenosis presents 20 to 40 years after an episode of rheumatic fever.
more common in females.
onset usually between the third and fourth decade of life
rheumatic mitral stenosis
There are several risk factors which support calcific degeneration such as ageing,
hypertension and mechanical stress, diabetes, atherosclerosis and systemic inflammation,
kidney disease and mineral disorders
mitral annular calcifications
MS pathophysiology
The normal mitral orifice area is 4 to 6 square centimeters.
The mitral valve opens during left ventricular diastole to allow blood to flow from the
left atrium to the left ventricle.
The pressure in the left atrium and the left ventricle during diastole are equal.
The left ventricle gets filled with blood during early ventricular diastole. There is
only a small amount of blood that remains in the left atrium.
With the contraction of the left atrium (the “atrial kick”) during late ventricular
diastole, this small amount of blood fills the left ventricle.
Mitral valve areas < 2 square centimeters causes an impedimence to the
blood flow from the left atrium into the left ventricle.
Mitral valve area less than 1 square centimeter = increase in
left atrial pressure. This left atrial pressure is transmitted to the pulmonary
vasculature resulting in pulmonary hypertension.
As left atrial pressure remains elevated, the left atrium will increase in size. As the
left atrium increases in size, there is a greater chance of developing atrial fibrillation.
If atrial fibrillation develops, the atrial kick is lost.
Thus, in severe mitral stenosis, the left ventricular filling is dependent on the
atrial kick/contraction.
With the loss of the atrial kick, there is a decrease in cardiac output and
sudden development of congestive heart failure.
- Mitral stenosis with a measured valve area <1cm2 = Severe
- Severe MS causes severe pulmonary hypertension
- And further… then causes Right heart failure
MS pathophysiology
MS most common cause of death
CHF
Exertional dyspnea and/or decreased exercise tolerance, Fatigue, proportional to the severity of the stenosis
Chest pain – Pulm HTN
Hemoptysis
Palpitations – Atrial Fibrillation
Thromboembolism- Atrial Fibrillation
Orthopnea
Paroxysmal nocturnal dyspnea
Right Sided Heart Failure Symptoms- ascites, edema, and hepatomegaly
MS symptoms
A low pitched mid-diastolic rumbling murmur with presystolic accentuation is heard after
the opening snap.
It is best heard with the bell of the stethoscope at the apex.
The murmur accentuates in the left lateral decubitus position and with isometric exercise
MS physical exam
MS diagnosis
-(Kerly B lines)
TTE (Echo)- Transthoracic Echocardiogram annually
Mean gradient (mmHg) less than 10
Pulmonary artery systolic pressure (mmHg) greater than 50
Valve area (cm2) less than 1.0
MS severe
MS treatment
Currently, no medical therapy can relieve a fixed obstruction of the mitral valve.
Medical therapy is focused on preventing endocarditis, decreasing new cases of rheumatic fever,
improving symptoms, and decreasing the thromboembolic risk.
MS treatment high risk patients
Endocarditis prophylaxis should only be given to high-risk patients before dental procedures that involve manipulation of gingival tissue or perforation of the oral mucosa.
High-risk patients are those patients with a prosthetic heart valve or prosthetic material used for valve
repair, previous history of infective endocarditis, and cardiac valvuloplasty
MS treatment rheumatic fever prophylaxis
Benzathine penicillin is the primary prevention treatment in
patients with streptococcal pharyngitis
MS treatment if the rhythm is normal sinus
Diuretics are utilized to help relieve pulmonary congestion. Beta-blockers and/or calcium channel
blockers help with exertional symptoms associated with elevated heart rate.
MS treatment if rhythm is atrial fibrillation
Ventricular rate control using AV node blocking agents such as beta blockers, calcium channel blockers,
and/or digitalis, to help with symptoms
Anticoagulation to prevent stroke/embolus.(Warfarin/Coumadin)
In an unstable patient, perform direct current cardioversion. If you cannot convert atrial fibrillation to
normal sinus rhythm, then the primary goal is rate control.
MS treatment
Anticoagulation prevents thromboembolic events.
Anticoagulation is indicated in patients with mitral stenosis and atrial fibrillation
(paroxysmal, persistent, or permanent), previous embolic events, and the presence of left
atrial thrombus.
At present, Warfarin is the anticoagulation of choice. Warfarin should be monitored using
international normalized ratio (INR) to target 2.0-3.0.
The development or presence of symptoms or evidence of pulmonary hypertension
is the indication for intervention
MS treatment intervention options
Percutaneous mitral balloon valvuloplasty (PMBV)
Valve Replacement Surgery –> symptomatic patients
Affects a functional component of the valve apparatus
often referred to as organic MR - (leaflets, chordae tendineae, papillary muscles, and/or annulus)
Thus the valve component is responsible for the regurgitation
primary (degenerative) causes of mitral valve insufficiency/regurgitation
In the developed world, the most common etiologies of MR are
degenerative disease with
mitral valve prolapse (a primary cause) and coronary heart disease (a secondary cause).
left ventricular (LV) dysfunction such LV dilation, or a cardiomyopathy (often caused by ischemic
heart disease), trauma, infective endocarditis
Thus the valve is structurally normal but the regurgitation is caused by annular enlargement, papillary
displacement, leaflet tethering, or a combination
Functional MR: refers specifically to LV dilation with incomplete coaptation of the mitral valve leaflets
secondary causes of mitral valve insufficiency/regurgitation
A. Mitral leaflets are the most common structures involved
B. Rheumatic heart disease can manifest itself as mitral stenosis,
insufficiency or both (years later)
D. Rheumatic process includes:
1) leaflet thickening, calcification and retraction
2) periannular calcification with limitation of annular motion
3) leaflet fusion (esp. at the commussural regions) and “fish-mouthing”
4) chordal thickening , shortening, and fusion
5) papillary muscle inflammation
rheumatic fever
a connective tissue disorder characterized by
thickening and elongation of the mitral leaflets and chordae and by dilatation of the
mitral annulus
primarily affects the chordae and leaflets in older patients
Causes redundancy of anterior and posterior mitral leaflets and the chordae
Chordae elongate leading to MV regurgitation
Myxomatous degeneration with prolapse is a common cause for mitral valve operation
myxomatous degeneration
leaflet tissue is commonly involved resulting in vegetations and destruction of leaflet
may result in annular or periannular abscess
destruction of leaflets, chordae, or papillary muscle may result in rupture and massive MV
regurgitation
annular involvement of one valve may result in involvement of the other valve (aortic)
endocarditis
A. myocardial ischemia from coronary artery disease affects
mitral valve function in many ways
1) ischemia leads to loss of contractility which affects mitral valve
competence
2) lateral ventricle wall and papillary muscle dysfunction
a) anterior papillary muscle is supplied usually by the LAD but can be
from a diagonal, ramus or proximal marginal arteries
b) posterior papillary muscle is usually supplied by RCA or distal CX
c) ischemia in these distributions can lead to papillary muscle
dysfunction
3) papillary muscle necrosis and rupture leads to acute cardiac
decompensation
4) left ventricular aneurysm may lead to valvular incompetence
5) the chordae tendinea and valve leaflets are avascular and not
directly affected by ischemia
6) annular dilatation can lead to MV incompetence
a) up to 20% of patients undergoing surgery for CAD will have some
MV regurgitation
b) often with correction of underlying CAD with improve MV
regurgitation
ischemic mitral valve disease
most common form off valvular heart disease
mitral valve prolapse
It is characterized by typical fibromyxomatous changes in the mitral leaflet tissue with superior
displacement of 1 or both leaflets into the left atrium
mitral valve prolapse
More common in women between ages of 15-30yrs.
Increased familial incidence for some
Varies in clinical presentation
Most patients are asymptomatic and remain so
Most common cause of isolated MR in North America
Mid or late systolic “click”
Generated by chordae tendinea tensing or prolapsing leaflet
High pitched, mid-late systolic crescendo-decrescendo murmur which is occasionally
“whooping” or “honking” heard best at the apex
MR- MVP
Acute pulmonary edema
Due to sudden increase in LA pressure
Acute dyspnea
Chest pain
Pan-systolic Murmur heard best at the
Apex
acute MR
Can be asymptomatic if mild to moderate isolated
MR for years
Fatigue
Orthopnea
SOB, DOE
CHF
Pulmonary congestion
Leads to R sided HF – ascites, ankle edema,
distended neck veins from
LA enlargement/ LV enlargement
Pan-systolic Murmur heard best at the Apex
Listen for mid systolic CLICK
chronic MR
Left ventricular enlargement- MPI!!!
High pitched apical pansystolic murmur that radiates to the axilla
Holosystolic murmurs = severe MR
Murmur intensity will vary with ischemia and papillary muscle dysfunction
Right LV failure in advanced disease
LA pressure and volume, backed up the pulmonary system. Pulmonary Congestion backs up
the Right ventricle= RV failure!
Ascites
Hepatomegaly
DOE
MR PE
MR diagnosis
ECHO/TTE- mainstay of mitral valvular pathology diagnosis
1) reveals leaflet thickening and abnormal excursion
2) doppler ECHO can estimate transvalvular gradient
3) detection of atrial thrombi and valvular vegetations
MR treatment medical
Depends upon the cause to a degree
Atrial Fibrillation – place on Coumadin, INR goal 20-3
Treatment of heart failure
Diuretics
BB
ACE
Digitalis
MR treatment: indications for operation
Indications for operation are more complex than mitral stenosis
Endocarditis and acute ischemic mitral regurgitation are clear indications= YES! SURGERY!
Chronic non-ischemic severe MR
Once symptomatic due to CHF – Persistent NYHA Class III - IV
New onset AF
Pulmonary HTN - PAP > 50mmHg at rest and/or >60mmHg w/exercise
EF <60%
A. low incidence of thromboembolism
B. average durability is 10-15 years
C. porcine valves may be chosen in
females who desire to become
pregnant
D. glutaraldehyde-preserved stented
porcine tissue valves are the most
common
E. bovine pericardial valves were
found to degenerate rapidly
H. some recommend patients should
receive 3 months of anticoagulation
therapy until endocardial healing is
completed
bioprosthetic valves
A. durable with valve life up to 20 years
B. requires anticoagulation (INR 2.5 -3.0)
C. usually indicated in young patients or patients with chronic atrial fibrillation
D. bileaflet (St. Jude, Carbomedics) most common mechanical valve used in the U.S.
E. Higher risk on thromboembolism in the mitral position
mechanical valves
A. Septal, posterior and anterior leaflets
B. Annulus- sphincter-like function
C. Septal annulus- fixed
D. Dilatation only in anterior and posterior
annulus
tricuspid valve anatomy
Less common
Rheumatic in origin in developing
countries
In US, due to carcinoid disease or
previously placed prosthetic failure
Women >Men
Does NOT occur in isolation
Usually associated with MS
Echocardiogram is diagnostic
tricuspid stenosis
Usually masked by MS symptoms – due to MS proceeding TS
Pulmonary congestion
Fatigue
Severe Tricuspid Stenosis
Blood congested in the Venous system
Hepatomegaly, ascites, edema
Can result in cirrhosis
Physical Exam
Murmur has many qualities of MS – best heard along the left sternal border and over xiphoid
process; Mid-diastolic rumble with presystolic accentuation (worse with inspiration)
Opening snap
JVD and giant a-wave
tricuspid stenosis
EKG
RA enlargement, tall peaked P waves in Lead II and upright P waves in lead V1
Afib
CXR
Prominence of the RA and SVC w/o enlargement of the PA
Echo
Valve is thickened and domes in diastole
Valve area < 1.0cm2
RA and IVC are enlarged
Cardiac cath - not routinely necessary
diagnosis for tricuspid stenosis
TS treatment
Decreased Right sided HF symptoms with Diuretics to relieve fluid congestion
Surgery is not terrible effective, because it often causes TR as a consequence.
Secondary to dilation of the annulus from RV enlargement due to PA HTN. NOT
primary valve disease.
Secondary to pacemaker lead placement
Late stages or Rheumatic Fever or Congenital heart disease
Cardiomyopathies
Infarction of the papillary muscles
TVP
Carcinoid heart disease
Infective endocarditis
Leaflet trauma
tricuspid regurgitation
Often due to other underlying cause
Fatigue
DOE
Cervical pulsations
Abdominal fullness
Diminished appetite
Muscle wasting
TR symptoms
R sided HF
Distended neck veins
Marked hepatomegaly, ascites, pleural effusions, edema
Blowing holosystolic murmur along the lower left sternal margin – which may be
intensified during inspiration and reduced during expiration or the Valsalva maneuver
Atrial Fibrillation
TR physical
TR diagnosis
Echo
RA dilation
RV volume overload with abnormal interventricular wall movement
Prolapsed leaflet
TR treatment
Medical
Diuretics – for Right sided heart failure Sx
Treatment of pulmonary HTN
Indications for Surgery
Tricuspid regurgitation
1) Clinical decision- improvement with repair of left-
sided lesion
2) Moderate to severe TR or any structural TR
3) RV volume overload
4) Right-sided heart failure
5) Repair vs replacement
Endocarditis
1) Severe TR
2) Persistent sepsis
3) Recurrent PE
4) Excision vs replacement vs repair
- Uncommon
- Congenital etiologies (vast majority)
- Adult acquired
A. Endocarditis, rheumatic
B. Secondary to previous procedures
A. Congenital (Tetralogy of Fallot)
B. Adult (Ross)
pulmonary valve disease
dynamic or fixed anatomic obstruction to flow from
the right ventricle (RV) to the pulmonary arterial vasculature.
Commonly pediatric patients
Female greater than male
Isolated PS - 10% of all congenital heart disease.
the valve commissures are partially fused and the 3 leaflets are thin and pliant, resulting in a
conical or dome-shaped structure with a narrowed central orifice.
10-15% of individuals have dysplastic pulmonic valves.
These valves have irregularly shaped, thickened leaflets, with little, if any, commissural
fusion, and they exhibit variably reduced mobility.
A bicuspid valve is found in as many as 90% of patients with tetralogy of Fallot
pulmonary stenosis
Symptoms
1) Infants have less symptoms than neonates
2) Older than 1 year–murmur only
3) Second, third, and fourth decade of life chronic right heart failure
4) 30-40% with severe pulmonary stenosis are asymptomatic when first examined
5) Dyspnea of exertion is most common
Signs
A. Loud, Harsh systolic murmur, radiates towards the left shoulder, decreased with
inspiration
B. With a possible thrill in the left 2nd and 3rd intercostal space
C. Ejection click
D. Right ventricular lift due to RVH
pulmonary stenosis
PS diagnosis
ECHO
diagnostic TTE
PS treatment
percutaneous balloon valvuloplasty
Most patients are asymptomatic.
Mild to moderate
PA HTN usually dominates the picture.
Symptoms:
Right heart volume overload and RHF symptoms
Signs: Murmur
High pitched, decrescendo diastolic murmur hear along the
left sternal border, may become louder with inspiration.
Diagnosis:
TTE for diagnosis
pulmonic regurgitation
PR treatment
Surgical repair is rare
Focuses on the underlying cause
Reduce PA vascular resistance/Pulm HT
