Valvular Stenosis - Grand Valley State University
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Transcript Valvular Stenosis - Grand Valley State University
Valvular Stenosis
Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)
Radiologic and Imaging Sciences - Echocardiography
Grand Valley State University, Grand Rapids, Michigan
[email protected]
Basic Principles
Approach to Evaluation Valvular Stenosis
Complete echocardiographic evaluation
Diagnostic imaging of the valve to define the etiology of stenosis
Quantification of stenosis severity
Evaluation of coexisting valvular lesions
Assessment of left ventricular systolic function
Response to chronic pressure overload of other upstream cardiac
chambers, and the pulmonary vascular bed
Echocardiographic information integration with pertinent clinical
data
Fluid Dynamics of Valvular Stenosis
High Velocity Jet
Characterized by formation of a laminar, high
velocity jet in the narrowed orifice
Flow profile in cross section of origin is flat (blunt) –
Remains blunt as the jet reaches the narrowest crosssectional area in the vena contracta
Physiologic cross-sectional area < anatomic cross-sectional
area
Fluid Dynamics of Valvular Stenosis
High Velocity Jet
Length of high velocity jet is dependent on:
Orifice geometry
Examples:
Very short jet across a deformed, irregular calcified
aortic valve
Longer jet along smoother tapering symmetric rheumatic
mitral valve
Rheumatic Heart Disease
Heart valves are damaged by a disease process that begins
with a sore throat from streptococcal infection.
Who is at risk of rheumatic heart disease?
Untreated, the streptococcal infection can develop into acute rheumatic fever.
Rheumatic fever is an inflammatory disease that can affect many connective
tissues of the body, especially those of the heart, joints, brain or skin.
Anyone can get acute rheumatic fever, but it usually occurs in children five to
fifteen years old. The resulting rheumatic heart disease can last for life.
What are the symptoms of rheumatic heart disease?
The symptoms vary greatly from person to person. Often the damage to heart
valves is not immediately noticeable.
A damaged heart valve either does not completely close or does not completely
open.
Rheumatic Heart Disease
Mitral stenosis
Progressive fibrosis
Thickening and calcification of valve
Enlargement of LA
Formation of mural thrombi
Funnel shaped “fish-mouthed” mitral valve
MS and MR
AS and AI
Non-dynamic images
Fluid Dynamics of Valvular Stenosis
Relationship between Pressure Gradient and Velocity
Simply stated: Simplified Bernoulli
equation
2
4V
Fluid Dynamics of Valvular Stenosis
Distal Flow Disturbance
Distal to stenotic jet
Flowstream becomes disorganized w/multiple blood
flow velocities and directions
Distance that flow disturbance propagates downstream is
related to stenosis severity
Aortic proximal flow patterns
Proximal to a stenotic valve
Flow is smooth and laminar (organized) with normal flow
velocity
“Flat” flow profile
Fluid Dynamics of Valvular Stenosis
Distal Flow Disturbance
Mitral valve proximal velocities
Left atrial to left ventricular pressure
gradient drives flow passively from the left
atrium abruptly across the stenotic orifice
Proximal flow acceleration is prominent
over a large region of the left atrium
3D velocity profile is curved: flow velocities
are
Faster adjacent to and in the center of a
line continuous with the jet direction
through the narrowed orifice
Slower at increasing radial distances from
the valve orifice
Hemi-elliptical in comparison to a stenotic
semilunar valve
Fluid Dynamics of Valvular Stenosis
Distal Flow Disturbance
Take home message
Stroke volume
Calculated proximal to a
stenotic valve
Based on knowledge of
cross-sectional area of flow
and spatial mean flow
velocity over a period of flow
Aortic Stenosis
Classified as Three Types
1.
2.
3.
Valvular
Subaortic
Supra-valvular
Diagnostic Imaging of the Aortic Valve
Aortic stenosis most often due to:
Calcific aortic stenosis
Congenital valve disease (most often
bicuspid. In rare instances or unicuspid or
quadracuspid)
Rheumatic valve disease
Diagnostic Imaging of the Aortic Valve
Calcific Aortic Stenosis
Most common etiology of aortic stenosis
Degenerative age related calcification
Occurs slowly over many years
Initially presents as “sclerosis” area of
increased echogenicity typically at base of
valve leaflets sans significant obstruction to
left ventricular outflow
Aortic Stenosis
Calcific/Degenerative
Mean age 60 – 70
Clinically significant obstruction occurs typically from
age 70-85 years old
Most common cause of aortic stenosis
10-007 Feigenbaum
Pathologic specimen of a severely stenotic trileaflet
aortic valve, which demonstrates gross nodular
athero-calcific changes on the aortic side of
the leaflets.
Aortic Stenosis
Calcific/Degenerative
Systolic leaflet excursion of less than 15 mm by 2D or
M-mode
Severe obstruction is reliably excluded
Again 10-007 Feigenbaum
Aortic Stenosis
Calcific/Degenerative
Planimetry of aortic valve is possible in
some patients
Interpretation with caution due to complex
3D anatomy of the orifice in calcific
degenerative stenosis
Ensure image plane is aligned at narrowest
orifice of the valve
2D represents anatomic valve area –
Doppler data reflects functional valve area
Planimetry
10-006b Feigenbaum
Aortic Stenosis - Bicuspid Valve
Severe calcification: difficult to differentiate
between bicuspid and tricuspid aortic valve
http://info.med.yale.edu/intmed/cardio/echo_atlas/
entities/aortic_stenosis_senile.html
Aortic Stenosis - Bicuspid Valve
Average age of onset of calcific stenosis
symptom is younger: usually 45 to 65
years old
http://info.med.yale.edu/intmed/cardio/echo_atlas/entities
/aortic_stenosis_senile.html
Aortic Stenosis - Bicuspid Valve
Can be identified best in parasternal shortaxis view
Football shaped opening
Long-axis: “dome-like” appearance
Typically leaflets are unequal in size
If anterior-posterior opening: anterior leaflet is larger
If lateromedial opening: rightward leaflet is larger
Aortic Stenosis - Bicuspid Valve
Often have raphae (seam-like line or ridge) in
the larger leaflet: closed valve appears trileaflet
Identify as trileaflet only in systole
18-34a & b Feigenbaum
Aortic Stenosis – Unicuspid
Valve
http://www.med.yale.edu/intmed/cardio/chd/c_unic_aov/index.html
Aortic Stenosis - Rheumatic
Rheumatic valvular disease preferentially
involves mitral valve
Rheumatic aortic stenosis occurs concurrently with
rheumatic mitral valve disease
Results in commissural fusion of the aortic
leaflets similar to rheumatic mitral disease
Appears similar to calcific aortic stenosis (if
mitral involved suspect aortic stenosis due to
rheumatic disease)
Summary
Aortic Stenosis - Congenital
Usually diagnosed at childhood
May not become symptomatic until young adulthood
May be resultant from re-stenosis after surgical
valvotomy
Aortic Stenosis
Differential Diagnosis
Left ventricular outflow tract obstruction
Fixed valvular obstruction
Dynamic subaortic obstruction
Subaortic membrane or a muscular subaortic stenosis
Hypertrophic cardiomyopathy
Supravalvular stenosis
Aortic Stenosis
Differential Diagnosis
Aortic Stenosis
Differential Diagnosis
Fixed valvular obstruction
Subaortic membrane
Suspect when valve anatomy is not clearly stenotic
even though Doppler velocity and color flow indicates
stenosis
TTE vs TEE
10-027 Feigenbaum
Subaortic Membrane – Fixed
Subvalvular Stenosis
18-30 Feigenbaum
Dynamic Subvalvular Stenosis
19-29a Feigenbaum
Supravalvular stenosis in a 30 year old with
familial hypercholesterolemia
Non-dynamic
Aortic Stenosis
Quantitation of Stenosis Severity
Measurement of maximum aortic jet velocity
Calculation of mean and maximum gradient
Determination of continuity equation valve area
Ratio of outflow tract to aortic jet velocity
Aortic Stenosis
Quantitation of Stenosis Severity
Dependence of pressure gradients on volume
flow rate
Coexisting aortic regurgitation = high transaortic
pressure gradient
Depressed ejection fraction/coexisting mitral
regurgitation = low transaortic pressure
Coexisting conditions common in adults with aortic
stenosis
Aortic Stenosis
Quantitation of Stenosis Severity
Continuity Equation
Stroke volume proximal to valve = transvalvular
stroke volume
CSA
LVOT
X VTI
LVOT
= CSA
Ao
X VTI
Ao
Aortic Stenosis
Aortic Valve Index
Effect of body size into account
AVA index = AVA/BSA
Aortic Stenosis
Technical Considerations and Pitfalls
Continuity equation valve areas: well validated in
comparison with Gorlin formula
Continuous wave Doppler needed d/t high
velocities
Use of non-imaging transducer learning curve
Parallel to flow: utilize several windows
Outflow tract diameter: measure in mid-systole
(inner edge to leading edge)
Aortic Stenosis
Coexisting Valvular Disease
Approximately 80% of patients with
predominate aortic stenosis have
coexisting aortic regurgitation
Regurgitation does not alter continuity
calculation valve area calculations
Aortic Stenosis
Response of the Left Ventricle to Valvular Aortic Stenosis
Chronic overload
Concentric left ventricular hypertrophy
LV systolic function typically preserved
until late in disease course
Dysfunction due to increased afterload and
often reversible post repair
Aortic Stenosis
Response of the Left Ventricle to Valvular Aortic Stenosis
Female vs. male
Female:
More hypertrophy
Smaller ventricles
Preserved systolic function
Male:
Less hypertrophy
More left ventricular dilation
Higher prevalence of systolic dysfunction
Aortic Stenosis
Clinical Applications in Specific Patient Populations
Symptomatic Aortic Stenosis
Doppler evaluation
Aortic jet maximum velocity: simplest and most
quantitative
>4 m/sec considered surgical
May have >4 m/sec and coexisting MR = not surgical
<3 m/sec significant aortic stenosis unlikely; valve
replacement unnecessary
Caution: parallel to flow and systolic dysfunction
Aortic Stenosis
Clinical Applications in Specific Patient Populations
Asymptomatic Aortic Stenosis: Disease Progression
and Prognosis
Reproducibility
Recording variability
Measurement variability
Intercept angle, wall filters, signal strength, acoustic window
Identification of the maximum velocity, outflow tract
diameter
Physiologic variability
Interim changes in heart rate, stroke volume, or pressure
gradient
Aortic Stenosis
Clinical Applications in Specific Patient Populations
Asymptomatic Aortic Stenosis: Disease Progression and
Prognosis
Doppler echocardiography
Prognosis depends o presence or absence of clinical symptoms
and not on hemodynamics severity
Rate of hemodynamic progression is variable from patient to
patient
On average:
Increase of 0.3 m/sec per year
Increase of mean pressure of 7 mmHg per year
Valvular size decrease of 0.1 cm2 per year
Concurrent decrease in volume flow rate may obscure disease
progression resulting in no change in jet velocity
2D Criteria
Aortic Stenosis
Systolic “doming” and diastolic prolapse represent congenital
features
Usually thickened valve leaflets with restricted motion. Doming
during early systole.
Concentric left ventricular hypertrophy with normal LV cavity
size. LA size will be increased (late in course of AS)
http://www.med.yale.edu/intmed/cardio/chd/e_as/index.html
Aortic Stenosis
Dobutamine Echocardiography
Dobutamine is a drug used to increase stroke volume across the
stenotic valve.
Mild to moderate stenosis valve leaflets will open wider with
increase in stroke volume.
True severe stenosis
Valve will not open wider
Dobutamine infusion will increase the maximum velocity of
both the outflow tract and the jet proportionally.
In milder forms of stenosis, increase in velocity of the left
ventricular outflow tract will be much greater than that of the jet
(due to the increase in valve area)
Limitation of zero change in velocity results
Aortic Stenosis
Dobutamine Stress Echocardiography
10-022 Feigenbaum
Additional Information
http://www.echoweb.com/asp/samples/sample5.asp
Mitral Stenosis
Mitral Stenosis
Diagnostic Imaging of the Mitral Valve
Evaluate:
Valve anatomy, mobility and calcification
Mean transmitral pressure gradient
2D echo mitral valve area
Doppler pressure half-time area
Pulmonary artery pressures
Coexisting mitral regurgitation
Technical Considerations
Accurate pressure gradient calculations depend
on accurate velocity measurements
PW Doppler signals may show better definition
of the maximum velocity and early diastolic
slope than CW Doppler
Better signal-to-noise ratio
Mitral Valve Area-2D
Simpler planimetry than with aortic valve
Well validated compared with valve area at surgery
and catheterization-determined valve areas
Shape of inflow region similar to a funnel
Important to perform planimetry at leaflet tips
Begin at apex and scan toward leaflet tips and low gain
Technical Considerations
Direct planimetry of mitral valve area on
2D shown to be a valid technique in most
clinical situations
Size may be underestimated if gain is too low
(and vice versa)
Image at leaflet tips
Mitral Valve Area
Pressure Half-Time
Rate of pressure decline across the stenotic mitral orifice
is determined by the cross-sectional area of the orifice
Smaller the orifice, the slower the rate of decline
Image right: maximum velocity and
diastolic slope are identified. Pressure
half-time of 226 ms corresponds to valve
area of 1 cm2. No a-wave d/t atrial
fibrillation
Mitral Valve Area
Pressure Half-Time
Influence of atrial and ventricular compliance is
assumed to be negligible
Assumption not always warranted especially after
percutaneous commissurotomy
Mitral Stenosis
Differential Diagnosis
Includes other grounds of pulmonary congestion
Standard echocardiography evaluation
LV systolic function
Aortic valve disease
Presence of mitral regurgitation
Diastolic LV function
Rare case of atrial myxoma or other atrial tumor
obstruction to LV inflow
Rare case of cor triatriatum
Mitral Stenosis
Rheumatic Disease
Predominately affects mitral valve
Most common cause of mitral stenosis
Characterized by commissural fusion
Results in bowing or doming of the valve
leaflets in diastole
Base and midsections of leaflets move
toward ventricular apex
Rheumatic Heart Disease
Mitral Stenosis
Rheumatic Disease - continued
Motion of the leaflet tips is restricted due
to fusion of the anterior and posterior
leaflets along the medial and lateral
commissures
Thickening of leaflet tips occurs frequently
May have normal thickening of base and
midportions
Often calcification and fibrosis of chordae
tendinae
Mitral Stenosis
Rheumatic Disease
11-011 Feigenbaum
Mitral Annular Calcification (MAC)
Common finding in elderly patients
Mild MAC appearance
Isolated area of calcification on the left ventricular side of the posterior annulus,
near the base of the posterior mitral leaflet
Area of fibrous continuity between aortic root and anterior mitral leaflet is rarely
involved
MAC may result in mid-to-moderate MR d/t increased rigidity of mitral annulus
Occasionally MAC extends into based of mitral leaflets resulting in functional mitral
stenosis (MS) due to narrowing of inflow area
Mitral Annular Calcification
Degenerative process seen frequently in
older patients
MAC can vary from very mild to very
severe
Precise cause of MAC is not fully known
Mitral Annular Calcification
Theory
Natural step in the degeneration of the
cardiovascular fibrous tissue that occurs in
the older population
Predisposing factors include: Advanced
Age, Female Gender, Diseases that
Increase Stress on Mitral Valve Apparatus
Mitral Annular Calcification
MAC May Contribute to
the Following:
Conduction
Disturbances
Stroke
Infective Endocarditis
11-089 Feigenbaum
Mitral Stenosis:
Left Atrial Enlargement and Thrombus
Chronic pressure overload
Gradual enlargement of left atrium
Stasis of blood due to low volume rate
Results in thrombi
Preferential to left atrial appendage
May occur in body of atrium as protruding or as laminated
thrombus along atrial wall or interatrial septum
Most often occurs in conjunction with atrial fibrillation but may
occur in NSR
Br Heart J. 1975 December; 37(12): 1281–1285
Mitral Stenosis:
Left Atrial Enlargement and Thrombus
TTE
High specificity for detection of left atrial
thrombus
Low sensitivity <50%
Challenge is imaging left atrial appendage
TEE
High specificity >99%
High sensitivity >99%
Non-dynamic
Mitral Stenosis:
Left Atrial Enlargement and Thrombus
21-40a Feigenbaum
Mitral Stenosis:
Left Atrial Enlargement and Thrombus
21-41 Feigenbaum
Pulmonary Hypertension
Left atrial
pressure leads
to
Pulmonary
venous
hypertension
leads to
Pulmonary
artery
hypertension
Pulmonary Hypertension
Chronic
Irreversible changes in the pulmonary
vascular bed occur
Elevated pulmonary vascular resistance and
persistence of pulmonary hypertension even after
relief of mitral stenosis
Pulmonary Hypertension
Suspect pulmonary hypertension in mitral
stenosis when there is existing:
Mid-systolic partial closure (“notching” of pulmonic
valve m-mode
Short interval between onset of flow and maximum
velocity
Severe pulmonary hypertension
2D echocardiographic finding
RVH and RVE
Paradoxic septal motion
Tricuspid regurgitation secondary to annular dilation
Mitral Stenosis with Mitral
Regurgitation
Coexisting regurgitation common in
patients with mitral stenosis
Mitral regurgitation will be covered in next
lecture material
Mitral Stenosis with Co-Existing
Other Valvular Disease
Rheumatic disease may also affect
Aortic valve (second in frequency to mitral valve)
Stenosis and/or regurgitation
Aortic regurgitation may complicate assessment of mitral
stenosis due to merging of two diastolic jets
Tricuspid valve (less commonly)
Tricuspid stenosis due to rheumatic disease difficult to
appreciate on 2D imaging
TR may also be caused by mitral stenosis resultant
pulmonary hypertension
Mitral Stenosis –Left Ventricular
Response
Left ventricle
Small with normal wall thickness and normal
systolic function
Diastolic dysfunction is impaired due to mitral
inflow restriction
Presence of dilation suggests coexistent
Mitral or aortic regurgitation
Primary myocardial dysfunction (cardiomyopathy
or ischemic disease)
Pre- and Postpercutaneous Commissurotomy
Balloon mitral balloon valvotomy/
commissurotomy
Echo Doppler evaluation important for patient
selection in terms of
Predicted hemodynamic results
Risk of procedural complications
May use qualitative assessment, an additive
scoring system or quantitative measurements
of leaflet mobility (see Textbook written by
Otto on Valvular Stenosis)
Pre- and Postpercutaneous Commissurotomy
Best hemodynamic results
Thin, mobile leaflets that have commissural fusion but little
calcification or subchordal thickening
Patients with most heavily calcified and deformed
valves
More likely to suffer procedure-related morbidity and mortality
Contraindicated in conjunction with moderate or severe
mitral regurgitation
Left atrial thrombi dislodgement by catheters during
procedure possibility
TEE indicated prior to procedure
Pre- and Postpercutaneous Commissurotomy
Post procedure
Echo identification of complications and
baseline for future assessments
Complications
Increase in severity of mitral regurgitaiton
Presence of an atrial septal defect at the
transseptal catheter puncture site
Mitral Stenosis and Pregnancy
Symptoms due to MS often initially occur
during pregnancy due to
Increased metabolic demands and volume
flow rate
Tricuspid Valve Stenosis
Tricuspid Stenosis
Narrowing of the Tricuspid Valve Orifice
Uncommon in adults
Tricuspid Valve Stenosis
<2.0 cm2 : severe tricuspid
stenosis
Tricuspid Stenosis - Etiologies
Rheumatic Heart Disease – nearly all
cases in association with rheumatic mitral
involvement
Systemic lupus erythematosus
Loeffler’s endocarditis
Metastatic melanoma
Congenital heart disease
Carcinoid
Right atrial tumor/thrombus
Whipple’s Disease
Fabry’s Disease
Infective Endocarditis
Endocardial fibroelastosis
Methysergide therapy
Prosthetic valve
Symptoms
Dyspnea
Fatigue
Right upper quadrant pain
Physical Examination
Jugular venous distention
Quiet precordium
Hepatomegaly
Ascities
Jaundice
Peripheral edema without pulmonary
congestion
Signs and symptoms of mitral stenosis
Carvallo’s Sign
Jose’ Manuel Rivero Carvallo (Mexican cardiologist 1905-1993)
The increase in the intensity
of the pansystolic murmur of
tricuspid regurgitation during
inspiration.
Distinguishes tricuspid from
mitral involvement
Best heard over left sternal
border
Complications
Increased risk of infective endocarditis
Decreased cardiac output
Cardiac Auscultation
Opening snap (may occur later than
mitral valve opening snap)
Diastolic rumble best heard along the
lower left sternal border
Higher frequency than mitral stenosis rumble
May be accentuated with inspiration
Presystolic click with atrial contraction
Both the opening snap and the diastolic
rumble may be accentuated with
inspiration
Absence of normal respiratory splitting
of S2
Tricuspid regurgitation murmur
Chest X-Ray (CXR)
Right atrial enlargement
Biatrial enlargement
Atrial fibrillation
Right ventricular hypertrophy
Suggests coexisting mitral stenosis with pulmonary
hypertension
Cardiac Catheterization
Increased mean diastolic pressure
gradient between the right atrium and
right ventricle
Increases with inspiration
Increased right atrial pressure
Persistence of end diastolic gradient between
right atrium and right ventricle
Aids in differentiating tricuspid stenosis from
tricuspid regurgitation
M-Mode Criteria for Tricuspid
Stenosis
Thickened tricuspid valve leaflets
Decreased EF slope of the
anterior tricuspid leaflet
Anterior motion of the posterior
valve leaflet
Decreased/absent A wave of the
anterior tricuspid valve leaflet
Steep A-C slope of the tricuspid
valve
Pulmonary hypertension
Due to coexisting mitral valve
disease
2D Criteria for Tricuspid
Stenosis
Thickened tricuspid valve leaflets, especially at leaflet tips and
chordae tendinae with restricted motion
Diastolic “doming” of the tricuspid valve with commissural fusion of
the leaflets
Right atrial dilatation
Dilated inferior vena cava and hepatic veins
Leftward protrusion of the interatrial septum
Pulmonary hypertension (due to coexisting mitral valve disease)
TV Stenosis Doppler
Surgical Treatment
Surgical/Balloon commisurotomy
Valve repair/valve replacement
Stenosis Tricuspid Valve
Rheumatic Heart Disease
Rheumatic Tricuspid Stenosis
Isolated rheumatic tricuspid almost never occurs
Significant tricuspid stenosis occurs in roughly 35% of patients with rheumatic heart disease
Rheumatic fever affecting the tricuspid valve is
<6% and has a preponderance to females
The tricuspid valve is in rheumatic heart disease
is usually not as thickened or calcified as
compared to mitral valve stenosis
M-Mode Criteria for Rheumatic
Tricuspid Stenosis
Diminished EF slope
Anterior displacement of the posterior
leaflet
Thickening of valve leaflets and apparatus
Caveats of M-Mode Criteria for
Rheumatic Tricuspid Valve
Stenosis
Accuracy is far lower than dx for mitral stenosis with Mmode
Frequently concurrent pulmonary hypertension and right
ventricular hypertrophy, which also lead to a diminished
EF slope
Anterior displacement of the posterior leaflet cannot
always be well visualized and is therefore not a reliable
finding
Therefore, 2D is a more reliable technique in dx of
rheumatic tricuspid stenosis
2D Criteria for Rheumatic
Tricuspid
Valve Stenosis
Doming of tricuspid valve leaflets in diastole,
typically more toward the tips of the leaflets
Thickening and reduced excursion of the
posterior or septal leaflets, or both
Reduced tricuspid orifice diameter relative to the
diameter of the tricuspid annulus in the same
scan plane
RVIT Rheumatic Stenosis
Note the thickening of the leaflets, which is maximal at
the tips and chordae, and the preserved mobility of the
mid portion of the leaflets in the real-time image
12-028 Feigenbaum
Tricuspid Stenosis
Important to Note
Tricuspid stenosis is pressure of the right
atrium, which will eventually produce
peripheral edema and reduced cardiac
output
Tricuspid stenosis almost never occurs as
an isolated lesion; it generally
accompanies mitral stenosis, so evaluate
for mitral, aortic, and pulmonic valve
disease due to rheumatic fever
Pulmonic Stenosis
Pulmonary Stenosis
Pathophysiology
Systolic pressure overload leads to RVH
Regional hypertrophy may lead to infundibular stenosis
Commonly associated with other congenital
malformations (VSDs, ASDs, tetrology of Fallot)
RV chamber size usually normal, RA will enlarge
Increased risk of endocarditis
Pulmonic Stenosis
Etiology
Congenital (most common)
Rheumatic (rare)
Carcinoid
Peripheral (PPS-junction of the R and L
PAs)
Infundibular (subvalvular)
Prosthetic valve dysfunction
Physical Signs of PS
Dyspnea on exertion
Systolic ejection murmur (LUSB)
Pulmonary ejection sound, decreased/delayed P2
Sustained RV impulse at mid-lower LSB
Echo Findings
M-mode may show an increase in the pulmonic
“a” dip of more than 7 mm (useful for severe PS
only)
Valvular thickening and systolic doming (2D)
Right ventricular hypertrophy
Post-stenotic dilatation of the PA
Narrowing of RVOT in infundibular PS
Pulmonary Stenosis
M-Mode and 2D
Mild pulmonary stenosis
No abnormality is
detectable either by Mmode or twodimensional
echocardiography.
More severe obstruction,
May be possible to detect
right ventricular
hypertrophy,
Echocardiography is not a
very sensitive method for
diagnosing this.
Pulmonary Stenosis M-Mode
Another sign that has been
reported, confined to patients
with severe obstruction, is
an exaggerated "a-dip" on the
pulmonary valve
echocardiogram.
“a-dip” or “diving W”
Hypertrophied right atrium forcefully
injects blood into an already full and
stiff right ventricle during atrial
systole.
Pulmonary artery pressure is low,
Sudden increase in right ventricular
pressure is sufficient to partially open
the pulmonary valve
Doppler Findings
Increased velocity and turbulence at level of
obstruction (valvular, subvalvular, or supravalvular)
Use pulsed/color flow Doppler to locate level of
obstruction
Check for coexisting pulmonic regurgitation
Measure peak and mean gradients (PSAX-Ao and
RVOT are best)
Pulmonic Stenosis Doppler
CW Doppler spectral recording from PSAX-Ao view in a patient with mild
pulmonic stenosis and mild pulmonic stenosis.
Turbulent diastolic and systolic flows are noted with a slight increase in the
peak systolic velocity to 1.4 m/s (normal < 1 m/s)
Subvalvular Stenosis
Note the presence of muscle
bundles in the area of the right
ventricular outflow tract (arrow).
18-21 Feigenbaum
Pulmonic Valve Stenosis
18-24PV Feigenbaum
A basal short-axis view demonstrates a
thickened pulmonary valve (arrow).
Doppler imaging demonstrates a peak
gradient of 35 mm Hg.
Dysplastic Pulmonary Valve Stenosis
An example of dysplastic (Any abnormal development of tissues or organs.
In pathology, alteration in size, shape, and organization of adult cells)
pulmonary valve stenosis is provided.
A: The pulmonary valve (arrow) is markedly thickened and immobile.
Doming during systole is present.
B: A maximal pressure gradient of approximately 65 mm Hg is
demonstrated. PA, pulmonary artery; RVOT, right ventricular outflow tract.
18-24 Feigenbaum
Complication
Right Heart Failure
An example of right
ventricular pressure
overload is shown due to
pulmonary hypertension
and consequentially
infundibular hypertrophy.
The right heart is severely
dilated, and there is global
right ventricular
hypocontractility.
07-058a Feigenbaum
Complication
Right Heart Failure
The short-axis view
demonstrates marked
flattening of the
septum that was
maintained in both
systole and diastole.
07-058b Feigenbaum
Sources
Feigenbaum H, Armstrong W. (2004). Echocardiography. (6th
Edition). Indianapolis. Lippincott Williams & Wilkins.
Goldstein S., Harry M., Carney D., Dempsey A., Ehler D., Geiser E.,
Gillam L., Kraft C., Rigling R., McCallister B., Sisk E., Waggoner A.,
Witt S., Gresser C.. (2005). Outline of Sonographer Core Curriculum
in Echocardiography.
Otto C. (2004). Textbook of Clinical Echocardiography. (3rd Edition).
Elsevier & Saunders.
Reynolds T. (2000). The Echocardiographer's Pocket Reference.
(2nd Edition). Arizona. Arizona Heart Institute.