Cardiac valves and skeleton & With applied aspects -final 1.pptx

CARDIAC VALVES AND
SKELETON & WITH APPLIED
ASPECTS

CARDIAC SKELETON
• The four major cardiac valves are anchored to
fibrous rings called valve annuli at the heart's
base.
• These valve annuli join to form the fibrous
skeleton of the heart, which includes the
aortic valve as its cornerstone and extensions
connecting to the other three valves.
• The cardiac skeleton also contains the
membranous septum and fibrous trigones,
providing the anatomic substrate for mitral-
aortic continuity.
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine.Libby, P.Bonow, R.O.,Mann, D.L.,Tomaselli, G.F.,Bhatt, D.L.,Braunwald, Solomon, S.D.; 9780323722193; R - https://books.google.co.in/books?id=U1VrzgEACAAJ; 2021 Elsevier

BASE OF HEART
A. Section through the base of the
heart, looking from base toward apex,
with the atria and great arteries
removed, shows all four cardiac valves
B. A comparable schematic diagram of the fibrous cardiac
skeleton. The centrally located aortic valve forms the cornerstone
of the cardiac skeleton. Its fibrous extensions anchor and support
the other three valves

CARDIAC SKELETON
• The right fibrous trigone, the largest and strongest component, connects the
aortic, mitral, and tricuspid valves and allows passage of the atrioventricular
(AV) bundle (his bundle).
• The fibrous cardiac skeleton isolates the atria from the ventricles, except for the
av bundle's passage through the right fibrous trigone.
• Diseases or surgical alterations of one valve can impact adjacent valves' shape
or angulation and may affect nearby coronary arteries or conduction tissue.

INTERVALVULAR FIBROSA ALSO FORMS PART
OF THE FLOOR OF THE TRANSVERSE SINUS
Long-axis section of the left
ventricle. The intervalvular fibrosa
(dashed triangle) lies between the
anterior mitral leaflet and the
posterior cusp of the aortic valve
and abuts the floor of the
transverse pericardial sinus (*).
Ao, ascending aorta; IW, inferior
wall; LA, left atrium; LV, left
ventricle; RVO, right ventricular
outflow; VS, ventricular septum

FIBROUS SKELETON OF THE HEART
A. COMPOSED OF DENSE CONNECTIVE
TISSUE.
B. LIES IN THE PLANE BETWEEN THE ATRIA
AND THE VENTRICLES.
C. THIS PLANE CORRESPONDS TO
ATRIOVENTRICULAR GROOVE /
ORIFICES OF HEART.
RV RV
LV LV

D. IS PRESENT IN THE FORM OF
CIRCULAR FIBROUS RING, →
INTERCONNECTED BY INTERVENING
FIBROUS TISSUE.
E. SURROUNDS THE FOUR VALVES

F. There are four such rings-- ,, for four orifice
of heart
i & ii- - Atrioventricular rings– for tricuspid
opening & for bicuspid opening. It is 8-
shaped.
iii- aortic ring -------- at
root of aorta
iv-pulmonary ring---- at
root of pulmonary trunk
(Front)
superior view of AV-
plane
posterior

G. Rings are interconnected
1 AV-ring is connected to AORTIC
ring by a large mass of fibrous
tissue called trigonum fibrosum
dextrum.
2. Mitral ring is connected to aortic
ring by small mass of fibrous
tissue called trigonum fibrosum
sinistrum
3. Pulmonary ring & aortic ring are
connected by tendon of
infundibulum.

trigonum fibrosum
dextrum.
trigonum fibrosum
sinistrum
Aortic valves
pulmonary
valves

1. It forms the central support of the heart.
2. Provides attachment to
i. Bicuspid & tricuspid valves directly.
ii. Cardiac muscle fibres of atria & ventricles.
iii. Membranous part of interventricular septum.
3. Keeps the cardiac valves competent.
H. FUNCTION OF FIBROUS SKELETON

4. Acts as an electrical insulator
• It blocks the direct spread of electrical impulses from the atria to
the ventricles. Impulses go only through bundle of His.
5. Prevents overdilation of the valve openings.
Applied– weakening of it may lead to cardiac
valves incompetence--- means incomplete
closure leading to mitral regurgitation, aortic
regurgitation, tricuspid regurgitation, ..

NOTE
• Tricuspid valves & mitral valves are directly attached to
ring.
• Semilunar valves are directly attached to wall of vessel,
not to ring.

CONDUCTIVE SYSTEM OF THE HEART
Conductive system of the heart is:
• made up of specialised cardiac muscle fibres.
• responsible for initiation and conduction of cardiac
impulse/A.P, by its own.
• these impulses cause cardiac muscle contraction.

COMPONENTS OF CONDUCTING SYSTEM
1. Sinoatrial node/SAnode.
2. Atrioventricular node/AV
node.
3. Atrioventricular bundle
[bundle of His].
4. Right and left branches of
A
V bundle (of His).
5. Purkinje fibers.

SA NODE
• Also k/a node of Keith & Flack.
• Situated in the wall of Rt. Atrium, in the
upper part of sulcus terminalis just
below the opening of SVC.
• It is called PACEMAKER of the heart bcz it
generates impulse & initiates the
contraction of cardiac muscle producing
heart beat.

• Impulse travels through atrial wall to reach the AVnode.
• Impulse or heart beat or heart rate=70-100 beat/min.
[average approx.70/min.]

ATRIOVENTRICULAR NODE/A
VNODE
• Also k/a node of Tawara.
• Smaller than SAnode.
• Located in the traingle of Koch /or / in the
lower & dorsal part of the atrial septum
just above the opening of coronary sinus.
• It generates impulse at the rate of 40-60
beat / min.

ATRIOVENTRICULAR BUNDLE [BUNDLE OF HIS]
• It begins from A V node & crosses the A V
ring & travel along the interventricular
septum. [membranous part].
• Divides at the upper part of muscular part
of IV-septum.
• Divides into two branches – Rt. & Lt.
Bundle branch.

BUNDLE BRANCH
Right branch of AV bundle —
• Passes down on right side of
interventricular septum.
• Large part of it enters the moderator
band to reach anterior wall of Rt.
ventricle.
• where it divides into Purkinje fibres.
• Likewise, Left branch of AV
bundle — goes on left side in
left ventricle.

PURKINJE FIBRES
• These are terminal branches of Rt. & Lt. Branches of Bundle of His.
• Form sub- endocardial plexus.
• They generates impulse at the rate of 20-35 beat / min.
Applied – arrhythmia – it is loss of
normal rhythm of contraction / heart beat.
-- due to damage of conductive
system.
blood supply – nearly whole conductive
system except left branch AV bundle – is
supplied by RCA.
Left br. Of AV bundle by LCA.

HEART IS MYOGENIC
1. Means A.P. is generated by
muscle itself, not by nerve.
2. Conductive system of heart is
made up of cardiac muscles.
3. Nerves supplying the heart,
can only influence / modify
the rate of impulse production
or A.P
.
4. If all nerves are cut even then
heart will continue to beat.[d/t
impulse from SA node].
5. Sympathetic nerve stimulation
increase the rate of impulse
generation.
6. Para-Sympathetic [vagus] nerve
stimulation decrease the rate of
impulse generation.

• Conductive system of the heart is made up of specialized cardiac
muscle fibres, which is responsible for initiation and conduction
of cardiac impulse/A.P, by its own.
• [process of impulse generation / A.P. independent of nerve
supply.] MEANS
- if all nerve connections to the heart are cut, even then the heart
continues to produce A.P. & beat/CONTRACT rhythmically. Hence our
heart is myogenic.

• BUT sympathetic & parasympathetic nerves can modify the
heart rate & force of contraction.
• Sympathetic stimulation increase heart rates & force of
contraction.
• Para-Sympathetic stimulation decrease heart rates & force of
contraction.

INNERVATION
• Although the heart’s inherent
rate of contraction is set by the
SA node, this rate can be altered
by extrinsic neural controls.

INNERVATION
• The nerves to the heart consist of
visceral sensory fibers.
• Parasympathetic fibers that slow
heart rate.
• Sympathetic fibers that increase
the rate and force of heart
contractions.

4
19-2
CARDIAC CONDUCTION SYSTEM
1
2
3
4
5

1. Sinoatrial
(SA) node
Right
atrium
2. Internodal
pathway
Right
ventricle
6. Purkinje
fibers
Left
ventricle
5b. Left branch
of bundle of His
4. Bundle of His or
AV bundle
3. ATRIOVENTRICULAR
(AV) NODE
Interatrial pathway
5a. Right
branch of
bundle of25His

INTERATRIAL PATHWAY
Right atrium Left atrium
SA node
Internodal
pathway
AV node
Purkinje
fibers
Right ventricle Left ventricle
1st
beat
Bundle
of His
2nd
beat
19-26

19-27
Our focus

• The fibrous skeleton of the heart lies in the plane
between the atria and the ventricles.
• Muscles of atria is not in continuity with muscles
of ventricle [d/t fibrous skeleton].
4. ACTS AS AN ELECTRICAL INSULATOR:

• This fibrous skeleton is bad conductor of electrical
impulse. So it prevents direct entry of electrical
impulse from atria to ventricle.
• Electrical impulse from atria to ventricle goes
through bundle of His only.

• Although each cardiac muscle has capacity to generate &
conduct (carry) electrical impulse.
• Thus fibrous skeleton helps in coordinated conduction
of A.P. or electrical impulse to ventricle.--------
coordinated ventricular contraction.

CARDIAC SKELETON
VALVE OF HEART

TRICUSPID VALVE
The tricuspid valve consists of five components: annulus, leaflets, commissures, chordae tendineae,
and papillary muscles.
The anterior tricuspid leaflet is the largest and most mobile, creating an intracavitary curtain that
partially separates the inflow and outflow tracts of the right ventricle.
The posterior leaflet is usually the smallest of the tricuspid valve leaflets.
The septal leaflet has limited mobility due to its numerous chordal attachments to the ventricular
septum.

TRICUSPID VALVE
The tricuspid valve annulus is relatively distensible, which is unique compared to the other cardiac
valves, resulting from the discontinuity of collagenous tissue on the right atrioventricular (AV) free wall.
Dilatation of the right ventricle can lead to circumferential tricuspid annular dilatation, causing variable
degrees of tricuspid valve regurgitation.

MITRAL VALVE
Competent mitral valve function relies on proper interaction of these
components and adequate left atrial and ventricular function.
Abnormalities in the mitral valve apparatus can impact the
feasibility of mitral valve repair (surgical or percutaneous).
The mitral valve annulus is a complete fibrous ring anchored by
the tough fibrous skeleton of the heart, leading to asymmetrical
annular dilatation.
The anterior leaflet is large, semicircular, and partially separates
the ventricular inflow and outflow tracts.
The posterior leaflet is more shallow and divided into three scallops.
The mitral apparatus comprises five components: annulus, leaflets, commissures, chordae
tendineae, and papillary muscles.

MITRAL VALVE
Commissures are splits in the leaflet tissue, with papillary
muscles beneath them giving rise to commissural chords.
Mitral valve prolapse is characterized by thickened and
redundant leaflets, annular dilatation, and elongated
chordae tendineae.
Rheumatic involvement causes chordal shortening and
thickening without annular dilatation, leading to mitral
stenosis or insufficiency.
Postinfarction mitral regurgitation is associated with left
ventricular dilatation, papillary muscle scarring, and
leaflet tethering.
Important structures during mitral valve repair or
replacement include the left circumflex coronary artery and
the coronary sinus, located near the mitral valve annulus.
Gross anatomy of the mitral valve and
papillary muscles–chordal apparatus, as
demonstrated in an excised and unfolded
valve. Each commissure overlies a papillary
muscle. Arrows point to minor
commissures. A, anterior leaflet; ALPM,
anterolateral papillary muscle; P, posterior
leaflet; PMPM, posteromedial papillary
muscle.

AORTIC VALVE
Aortic valve has three components: annulus, cusps, and commissures.
Unlike the mitral and tricuspid valves, the aortic valve lacks a tensor
apparatus.
Commissures form tall, peaked spaces between the cusps at the level
of the aortic sinotubular junction.
The three half-moon-shaped aortic cusps are avascular, and their size
may not be equal in all hearts.
Lunular fenestrations near commissures are common but rarely cause valve
issues.

AORTIC VALVE
Accurate measurements of the basal ring and sinotubular
junction are crucial for aortic valve replacement.
Aortic stenosis can result from commissural fusion or
decreased cusp mobility, while aortic regurgitation can be
caused by decreased cusp size or aortic root dilatation.
The aortic valve's location allows for unique opportunities
in electrophysiology procedures.
During aortic valve replacement, care must be taken to avoid
injury to nearby structures, and infective endocarditis can lead
to complications involving adjacent areas.

PULMONARY VALVE
The pulmonary valve is similar in design to the aortic valve.
Pulmonary artery sinuses are embedded within the muscle
bundles of the right ventricular infundibulum.
In cases of pulmonary valve atresia with an intact
ventricular septum, hypertrophy of muscle bundles and a
narrow right ventricular outflow tract accentuate this
relationship.
The pulmonary and tricuspid valves are separated by
infundibular muscle.

Ventricular arrhythmias can originate from the pulmonary
valve or supravalvular portion of the pulmonary arteries.
The pulmonic valve is typically positioned cephalad to
the aortic valve, with the supravalvular portion of the
aortic valve nearby.
This relationship is relevant for electrophysiologists.
PULMONARY VALVE

MEDICAL ASPECT

NORMAL MITRAL VALVE ANATOMY.
Bulwer BE, Rivero JM, eds. Echocardiography Pocket Guide: The Transthoracic Examination. Burlington, MA: Jones & Bartlett
Learning; 2011, 2013:132.

MITRAL STENOSIS

MITRAL STENOSIS
ECHOCARDIOGRAPHIC FEATURES
Rheumatic mitral stenosis (MS) results in narrowing of
the mitral orifice.
Pathognomonic echocardiographic features include a
fish-mouth configuration of the mitral orifice.
Commissural fusion, chordal thickening, and fusion,
as well as leaflet thickening and calcification,
contribute to the narrowing.
Parasternal long- and short-axis views and apical views
are used to assess these features.
Rheumatic mitral stenosis (MS) results in narrowing of the
mitral orifice. Pathognomonic echocardiographic features
include a fish-mouth configuration of the mitral orifice.
Commissural fusion, chordal thickening, and fusion, as
well as leaflet thickening and calcification, contribute to
the narrowing. Parasternal long- and short-axis views and
apical views are used to assess these features.

MITRAL STENOSIS
ECHOCARDIOGRAPHIC FEATURES
Commissural fusion leads to restricted diastolic excursion of the leaflet tips, with relatively
preserved mobility of the leaflet belly, resulting in a pattern called "doming."
Anterior leaflet doming is more easily observed due to the posterior leaflet's early
immobilization in the rheumatic process.
Leaflet and chordal thickening with or without calcification can be observed.
Degenerative mitral annular calcification is common with aging and renal disease but rarely
causes significant MS unless severe.

QUANTIFICATION OF SEVERITY
Normal mitral valve area (MVA) is 4 to 5 cm2,
severe MS correlates with MVA ≤ 1.0 to 1.5
cm2.
Direct planimetry of the orifice area from
a parasternal short-axis view is one
method for quantification.
Proper positioning of the imaging plane
at the flow-limiting orifice level is
crucial to avoid misleading results.
Using the lowest possible gain setting is
essential to obtain an accurate orifice
measurement.
3D echocardiography is a valuable tool for
precisely identifying the valve orifice.
Approaches to planimetry of the mitral valve area (MVA) in rheumatic mitral stenosis. Top,
Planimetry of 2D parasternal short-axis images. Middle, 3D TEE view of the stenotic orifice
from the perspective of the left ventricle, which can be directly planimetered. Bottom,
Multiplanar reconstruction of 3D TEE volumes can ensure that a short-axis view precisely at
the level of the limiting orifice is selected for planimetry

QUANTIFICATION OF SEVERITY
Mean gradient determination is a simple Doppler
method to assess MS severity, but heart rate and
concomitant MR should be considered.
Pressure half-time (PHT) method calculates MVA as
220 divided by PHT, but it has limitations in certain
situations.
Proximal isovelocity surface area (PISA) approach
and 2D/Doppler-based methods are alternative
ways to calculate MVA.
Integrated imaging and Doppler findings optimize the
assessment of mitral stenotic severity.
Tracing the CW mitral stenotic spectrum

PROXIMAL ISOVELOCITY SURFACE AREA (PISA)
METHOD FOR CALCULATION OF MVA. IN PATIENTS
WITH MITRAL STENOSIS (MS)
• Flow acceleration proximal to the stenotic
orifice will result in a flow convergence zone
that is characterized by color aliasing and a
PISA shell (upper left).
• The definition of the PISA shell and thus
accuracy of the PISA radius measurement can
be improved by shifting the baseline Nyquist
limit in the direction of flow (upper middle).
• In the lower left and middle panels, the
aliasing velocity is 40 cm/sec.
• Application of the continuity equation allows
MVA to be calculated as MVA = [2(πr 2
)(Valiasing)/(Peak Vmitral)] × α/180.
• The angle correction is used to correct for
deviation of the shell from hemisphericity.
A4C, Apical four-chamber view

PATIENT SELECTION FOR BALLOON
VALVULOPLASTY
The Wilkins echocardiographic scoring system is useful in predicting procedural success in severe
MS patients undergoing transcatheter intervention (Wilkins score >8 = poorer outcomes).
The less common Padial scoring system can predict freedom from severe MR (Padial score ≥10).
Assess the amount of associated MR on echocardiography before considering percutaneous
balloon mitral valvotomy (avoid if moderate or greater MR is present).
Percutaneous intervention is contraindicated if LA appendage thrombus is detected on TEE (due to
risk of embolization from guide wires and catheters).

MITRAL REGURGITATION
•Type I: Normal leaflet motion; common abnormalities include leaflet
perforation, altered coaptation due to bulky vegetation, or annular dilation
from chronic AF.
•Type II: At least one leaflet extends above the annulus plane; causes include
mitral prolapse or flail due to valvular abnormality, chordae rupture, or
papillary muscle dysfunction.
•Type IIIA: Restricted leaflet motion during both systole and diastole, typically
from rheumatic disease.
•Type IIIB: Limited leaflet motion in systole due to pathologic tethering caused
by LV systolic dysfunction and remodeling; most common in secondary or
functional MR.
Carpenter proposed a classification system for MR based on
pathophysiology, suitable for echocardiographic evaluation.
• Minor mitral valve leakage is normal physiologically.
• Pathologic regurgitation has various causes; echocardiography helps diagnose, quantify,
and identify underlying functional disturbances and related diseases.

PRIMARY (DEGENERATIVE) MITRAL
REGURGITATION:
• Mitral prolapse or flail due to primary leaflet and/or chordal pathology is termed
degenerative MR.
• Echocardiography is the gold standard for diagnosis:
• Mitral flail: free edge of the mitral leaflet falls back into the left atrium due to loss of
chordal support.
• Mitral prolapse: free edge remains tethered by chordae, and the leaflet billows
pathologically into the left atrium.
• Parasternal long-axis view used for prolapse diagnosis (leaflets extending 2mm above
the annular line).
• Apical four- and two-chamber views show normal extension above annular boundaries
(not used for prolapse diagnosis).

PRIMARY (DEGENERATIVE) MITRAL
REGURGITATION:
• Anatomic substrate for degenerative MR ranges from diffuse myxomatous change
(barlow) to localized fibroelastic deficiency.
• Mitral prolapse more prevalent in patients with connective tissue disorders.
• 3d echocardiography useful for characterizing pathology and determining which
scallop(s) are prolapsing or flail.
• Repair likelihood highest for isolated P2 pathology, followed by A2, medial, and lateral
scallops.
• 3d tee helpful in identifying involvement of multiple scallops and associated anomalies.

SECONDARY (FUNCTIONAL) MITRAL
REGURGITATION:
• Secondary or functional MR occurs when leaflets, chords, and papillary muscles are
structurally normal.
• Most common cause is lv systolic dysfunction and remodeling (CARPENTIER TYPE IIIB).
• Ischemic MR term used when dysfunction is due to cad.
• Atrial functional MR occurs with preserved ventricular function due to annular dilation
from AF (CARPENTIER TYPE I).
• 3d echocardiography shows functional MR results from an imbalance between closing
and tethering forces on Mitral leaflets.

SECONDARY (FUNCTIONAL) MITRAL
REGURGITATION:
• Pathologic tethering causes apical displacement of leaflet coaptation, the hallmark of
functional MR.
• Reduced closing forces due to impaired LV systolic function.
• Pathologic tethering forces can occur due to annular dilation and/or reduced annular
contraction, or from chordal connection to papillary muscles.
• Papillary muscle contractile dysfunction per se does not cause Functional/Ischemic MR.

QUANTITATION OF MITRAL REGURGITATION
• ASE recommends an integrated approach for quantifying
mitral regurgitation (MR).
• Semiquantitative measures: Jet area (Jet area to LA area
ratio), Peak Mitral E Wave size, Vena Contracta Diameter,
and Pulmonary Venous Flow Patterns.
• Peak E velocity reflects diastolic gradient between LA and
LV, elevated with MR and increased LA pressure.
• Vena contracta assessed in zoom mode on parasternal
long-axis view, narrowest region of the jet.
• PISA approach for quantitation of regurgitant volume and
effective regurgitant orifice area (eroa).
• Quantitative doppler method compares antegrade flow
across mitral valve with a non-regurgitant reference valve
(usually aortic valve) for mr volume and fraction calculation.
PISA approach to quantitating the effective regurgitant orifice area (EROA)
for MR. To optimize the PISA shell, the baseline is shifted in the direction
of the jet. EROA is computed as EROA = 2(πr2 )(Valiasing)/(VMaxMR).
Regurgitant volume can be calculated as EROA × VTIMR, where VTIMR is
the velocity-time integral of the MR spectrum.

QUANTITATION OF MITRAL REGURGITATION
• EROA ≥0.4 cm² and RV volume ≥60 ml indicative of severe MR.
• Color jet size approach easy but influenced by machine
settings, underestimates eccentric jets, and overestimates
non-holosystolic mr.
• PISA method limited in eccentric jets (degenerative and
functional MR) with non-circular regurgitant orifice.
• 3d planimetry may provide a better EROA determination.
• Quantitative doppler technique assumes circular or oval mitral
orifice, LV SV calculated from LV volume versus aortic outflow
suggested as an alternative.
• Clinical decision-making under general anesthesia should be
avoided for MR assessment due to anesthesia-induced
Quantitative Doppler approach to assessing the
severity of MR.

Mitral regurgitation (MR) grading by semiquantitative parameters. Top panels, A time-honored technique of grading simple central mitral regurgitant jets by
freezing the apical window when the color flow jet is greatest (at usual Nyquist limits of 50 to 70 cm/sec), then tracing the area of the jet and expressing it as a
ratio to the area of the left atrium. Ideally this is done in two orthogonal planes and the results averaged. If the jet is very eccentric (i.e., “hugs a wall”), the grade is
generally increased by one grade in this scale. Bottom panels: Left, Vena contracta, or “neck,” of color flow Doppler is measured ideally in the parasternal long-axis
window (or alternatively, apical three-chamber window), and is a linear estimate that correlates with the actual orifice size of the mitral valve during systole. Middle,
MR CW Doppler jet is very dense, consistent with more severe mitral regurgitation. Right, There is systolic flow reversal (the S wave is negative, or below the
baseline) in the right upper pulmonary vein on PW Doppler

AORTIC STENOSIS
The most frequent cause of aortic stenosis (AS) in young patients is congenitally bicuspid or
unicuspid aortic valve.
In elderly adults, a common cause of AS is calcium deposition on a previously structurally
normal tricuspid aortic valve.
Echo cardiographic appearance includes restricted cusp excursion and irregular nodular cusp
thickening.
Systolic TEE images of calcific aortic
stenosis in a patient with a tricuspid valve.
Left, Two-dimensional long axis. There is
minimal opening of the valve. Ao, Aorta.
Middle, Short axis. Right, Three-
dimensional image. The latter two views
better demonstrate the distribution of
calcium

QUANTITATION OF SEVERITY
Normal aortic valve area (AVA) is 3 to 4 cm²; severe aortic stenosis
usually occurs with AVA less than 1.0 cm².
Indexing ava for body surface area (bsa <0.6 cm²/m² for
severe AS) is important in children and small adults.
The bernoulli equation (δp = 4 v²) is used for doppler
interrogation of transvalvular flow to obtain mean and peak
instantaneous gradients in as.
Aortic gradients are best recorded from apical five- or three-
chamber, suprasternal notch, and right parasternal windows;
highest velocities found in the right parasternal view.
Doppler methods provide peak
instantaneous and mean gradients

QUANTITATION OF SEVERITY
Echocardiographically derived peak instantaneous gradient is typically higher than the peak-to-peak gradient
obtained invasively.
Gradients may underestimate severity in low-flow states and overestimate in high-flow states; AVA
determination is crucial.
• AVA can be calculated using the continuity equation:
AVA = (CSALVOT × VTILVOT)/VTIAV or AVA =
(CSALVOT × VLVOT)/VAV (simplified).
• CSA of the LVOT is calculated using the formula CSA =
π(D/2)², where D is the systolic LVOT diameter
measured just proximal to the aortic annulus.
• Optimal sample volume placement for pulse wave
Doppler is in the LVOT, 1 to 2 mm proximal to the
valve on apical five- or three-chamber (TTE) or deep
transgastric (TEE) views.

Cardiac valves and skeleton & With applied aspects -final 1.pptx

Recommended

Recommended

More Related Content

Similar to Cardiac valves and skeleton & With applied aspects -final 1.pptx

Similar to Cardiac valves and skeleton & With applied aspects -final 1.pptx (20)

More from AmeetRathod3

More from AmeetRathod3 (20)

Recently uploaded

Recently uploaded (20)

Cardiac valves and skeleton & With applied aspects -final 1.pptx

Editor's Notes