Cardiac Ultrasound Imaging Protocol

Cardiac
SECTION I: Anatomy and Physiology of the Heart
Rationale: Accurate assessment and performance of echocardiograms requires sonographers

to assemble a comprehensive knowledge of the anatomy, embryology, physiology,
pathophysiology, and echocardiographic appearances of the heart and surrounding structures.
An understanding of these is essential for the performance of high quality examinations and
is requisite to quality patient care.
1. Describe the heart anatomy

2. Explain the blood flow through the coronary arteries
3. List the events that lead to myocardial contraction
4. Compare and contrast the anatomy of aorta and vena cava
5. Describe the location and function of each portion of the cardiac conduction system
6. Describe the anatomy of the pericardium, the myocardium, and endocardium
7. Explain the relational anatomy of the heart in the thoracic cavity
8. Describe the location of the apex in relationship to other structures in the heart
9. Explain how body habitus influences the position of the heart in the thoracic cavity
I. Anatomy and Physiology of the Heart
A. Chambers and Related Septa

1. Morphologic and anatomic features
a. Right atrium (RA)
1) Eustachian valve
2) Chiari network
b. Right ventricle (RV)
c. Left atrium (LA)
d. Left ventricle (LV)
e. Interatrial septum (IAS)
1) Septum primum
2) Septum secundum
3) Fossa ovalis
f. Interventricular septum (IVS)
1) Inlet
2) Trabecular
3) Infundibular (outlet)
4) Membranous
g. Coronary sulcus
h. Atrioventricular groove
i. Crux of the heart
B. Valves and Related Apparatus

1. Cardiac valves
a. Atrioventricular valves (AV)
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1) Mitral valve (MV)

a) Anterior leaflet
i. Scallops (A1, A2, A3)
b) Posterior leaflet
i. Scallops (P1, P2, P3)
c) Papillary muscles
d) Chordae tendinae
e) Annulus
2) Tricuspid valve (TV)
a) Septal leaflet
b) Posterior leaflet
c) Anterior leaflet
d) Papillary muscles
e) Chordae tendinae
f) Annulus
b. Semilunar valves
1) Aortic valve (AV)
a) Right coronary cusp (RCC)
b) Left coronary cusp (LCC)
c) Non-coronary cusp (NCC)
d) Sinus of Valsalva
e) Annulus
f) Commissures
g) Subvalve, supravalve
2) Pulmonic valve (PV)
a) Leaflets
b) Subvalve
c) Supravalve
C. Arterial-Venous System
1. Aorta (Ao)
a. Origination and termination
b. Anatomic location
c. Segments
1) Aortic Annulus
2) Sinus of Valvalva
3) Sinotubular junction
4) Ascending Ao
5) Ao Arch
6) Descending Ao
7) Abdominal Ao
d. Major branches
1) Brachiocephalic (innominate)
2) Left common carotid
3) Left subclavian
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2. Pulmonary artery
a. Branches
1) Main pulmonary artery (MPA)
2) Pulmonary artery bifurcation
3) Right pulmonary artery (RPA)
4) Left pulmonary artery (LPA)
3. Coronary arteries
a. Left coronary artery
1) Left anterior decending (LAD)
2) Circumflex
b. Right coronary artery (RCA)
c. Congenital variations
d. Flow patterns
e. Flow reserve
4. Superior vena cava (SVC) and inferior vena cava (IVC)
5. Pulmonary veins
6. Coronary venous system
a. Coronary sinus
1) Differentiation from descending Ao
b. Atrioventricular groove
7. Vessel wall layers
a. Tunica intima
b. Tunica media
c. Tunica adventitia
D. Layers of the Heart

1. Pericardium
a. Visceral
b. Parietal
2. Myocardium
a. Layers
1) Subepicardium
2) Midwall
3) Subendocardium
3. Endocardium
E. Relational Anatomy
1. Mediastinum anatomy
2. Heart position
a. Levocardia
b. Mesocardia
c. Dextrocardia
d. Levoposition
e. Dextroposition
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3. Thoracoabdominal situs
a. Solitus
b. Inversus
c. Ambiguous
4. Atrial situs
a. Solitus
b. Inversus
c. Ambiguous
5. Atrioventricular connection
6. Ventriculoarterial connection
7. Great vessel relationship
F. Pulmonary Versus Systemic Circulation

1. Components of the pulmonary circulation
a. Right atrium (RA)
b. Right ventricle (RV)
c. Main pulmonary artery (MPA) and branches
d. Pulmonary capillaries
e. Pulmonary veins
2. Components of the systemic circulation
a. Left atrium (LA)
b. Left ventricle (LV)
c. Aorta (Ao)
d. Systemic capillary network
e. Cerebral, peripheral, and abdominal veins
f. SVC
g. IVC
h. Hepatic veins
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SECTION II: Basic Embryology
1. Sequence the formation of the heart beginning with the primitive heart tube through
the development of the six aortic arches
2. Describe cardiac septation including atrial and ventricular
3. Describe the formation of the atrioventricular valves and the semilunar valves
4. Compare fetal and neonatal circulation
II. Basic Embryology of the Heart
A. Primitive Heart Tube

3. Development sequence of heart tube
4. Primitive vascular tube
a. Sinus venosus
b. Cardiac loop
c. Bulbus cordis/truncus arteriosus
5. Bulboventricular loop
a. Dextrolooping (D-loop)
b. Levolooping (L-loop)
6. Regions of heart tube
a. Sinus venosus
b. Primitive atria
c. Atrioventricular canal
d. Primitive ventricle
e. Bulbus cordis
f. Truncus arteriosus
g. Aortic sac and arches
7. Septation
a. Endocardial cushion
b. Atrioventricular canal
c. Truncoconal region
d. Atrial septum formation
1) Septum primum
2) Septum secundum
e. Interventricular septum (IVS) formation
8. Six aortic arches
a. Maxillary arteries branches external carotid artery (ECA) - 1st pair
b. Stapedial arteries - 2nd pair
c. Proximal common carotid artery (CCA) and distal internal carotid artery
(ICA) - 3rd pair
d. Ao Arch (L) - left 4th pair
e. Proximal right subclavian (R) - right 4th pair
f. Rudimentary - 5th pair
g. (L) Left pulmonary artery and ductus - left 6th pair
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h. (R) Right pulmonary artery - right 6th pair

9. Cardiac valve formation
a. The atrioventricular valves
b. The semilunar valves
B. Comparison of Fetal and Postnatal Circulation

1. Prenatal circulation
h. Umbilical vein
i. Ductus venosus
j. Eustachian valve
k. Foramen ovale
l. Ductus arteriosus
2. Neonatal circulation
a. Ligamentum arteriosum
b. Fossa ovalis
c. Ligamentum venosum
d. Ligamentum teres
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SECTION III: The Echocardiographic Examination
1. Describe a 2-D echocardiographic examination using proper nomenclature

2. List equipment controls commonly used for each mode
3. Identify common M-mode patterns associated with cardiac disease
4. Associate the best Doppler approach based on location of various cardiac diseases
5. Apply pertinent Doppler formulas to the cardiac setting
6. Explain provocative, positional, and breathing maneuvers that affect venous inflow
and cardiac output
7. Explain the appearance of echocardiographic artifacts on an image
8. Describe myocardial segmentation
9. Differentiate between all normal anatomy visualized on an echocardiogram
10. Describe the coronary arterial system
III. The Echocardiographic Examination
A. Basic Imaging Principles

1. Tomographic planes
2. Nomenclature
3. Image orientation
4. Technical quality
B. Scanning Views
1. Parasternal
a. Long-axis
1) Ascending aorta
2) Aortic root
3) Aortic valve (AV)
4) Left ventricular outflow tract (LVOT)
5) Left atrium (LA)
6) Inlet portion of left ventricle
7) Mitral valve (MV)
b. Long-axis right ventricular inflow tract (RVIT)
1) Inlet portion of the right ventricle
2) Tricuspid valve (TV)
c. Long-axis right ventricular outflow tract (RVOT)
1) Outlet portion of RV
2) PV
d. Short-axis
1) High parasternal
2) Level of aortic valve, great vessels, and atria
a) TV
b) RVOT
c) PV
d) MPA bifurcation
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e) Left atrial appendage (LAA)

3) Left ventricle
a) Mitral valve cusps (basal-level)
b) Papillary muscles (mid-level)
c) Apex
d) IVS
e) Origin of coronary arteries
2. Apical views
a. 4-chamber
1) Ventricles and atria
2) MV
3) TV
4) Pulmonary veins
5) Coronary sinus (posterior tilt)
b. Apical 4-chamber with aortic valve (apical 5-chamber)
1) LV
2) LA
3) LVOT (anterior tilt)
4) AV (anterior tilt)
5) Proximal aortic root (anterior tilt)
c. 2-chamber
1) LV
2) LA
3) Left atrial appendage (LAA)
d. Long-axis 3-chamber
1) LV
2) LA
3) LVOT
4) MV
5) AV
3. Subcostal views
a. 4-chamber view
1) Chambers and atria
2) MV
3) TV
4) IAS
5) IVS
b. 4-chamber with aortic valve
1) LVOT
2) AV
c. Short-axis views
1) Left ventricle
2) Mitral valve cusps (basal-level)
3) Papillary muscles (mid-level)
4) Apex
5) IAS
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6) Origin of coronary arteries

d. Inferior vena cava (IVC)/RA
1) Hepatic veins
e. Bicaval view
1) SVC
2) IVC
3) IAS
4. Suprasternal views
a. Long-axis of aortic arch
1) Ascending
2) Transverse
3) Descending
4) Branch vessels
b. Short-axis of aortic arch
c. SVC
d. Pulmonary veins
5. Other acoustic windows
a. Mid clavicular
b. Right parasternal
c. Posterior
C. Echocardiography Anatomy and Physiology

1. Orientation of images
a. Terminology
b. Display
2. Coronary artery distribution
3. Left Ventricle (LV)
a. Dimensions, area, volumes
b. LV mass, wall thickness
c. Function
1) Global systolic
2) Regional systolic
a) 16 segments - regional wall motion
b) 17 segments - perfusion
3) Diastolic
d. Interdependence of LV and RV
e. LV wall segments
1) Subdivisions of heart
a) Base
b) Mid
c) Apical
2) Normal anatomic location of walls in planes
a) Parasternal long-axis
b) Parasternal short-axis sweep
c) Apical 4-chamber
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d) Apical 2-chamber
e) Apical long-axis
f. Subdivision of LV
1) Left ventricular inflow tract (LVIT)
a) Anatomic location
b) Imaging views
2) Left ventricular outflow tract (LVOT)
b) Functional location
c) Imaging views
4. Right Ventricle (RV)
b. Global systolic function
c. Echo findings with RV volume overload
d. Echo findings with RV pressure overload
e. Moderator band
f. Subdivision of RV
1) Right ventricular inflow tract (RVIT)
b) Imaging views
2) Right ventricular outflow tract (RVOT)
b) Imaging views
5. Left atrium (LA)
b. LA function
c. Left atrial appendange
d. Pulmonary veins
6. Valves
a. Atrioventricular valves
1) Composition
2) Function
3) Mitral valve
b) Leaflet names and characteristics
4) Tricuspid valve
b. Semilunar valves
1) Composition
2) Function
3) Aortic valve
4) Pulmonic valve
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7. Great vessels
a. Aorta
1) Anatomic segments and location
2) Imaging views
b. Pulmonary artery
1) Anatomic location
2) Imaging views
8. Coronary sinus
a. Anatomic location
b. Characteristics
c. Imaging views
1) PLAX
2) Apical 4-chamber (posterior tilt)
d. Differentiation of coronary sinus from surrounding structures
1) Location
2) Sonographic appearance
a. Anatomic locations
b. Branching patterns
c. Perfusion patterns
d. Factors that influence coronary flow
1) Heart rate (HR)
2) Diastolic aortic pressure
3) Left ventricular diastolic pressure
4) Degree of coronary stenosis
e. Imaging views
D. Echocardiography Modalities
1. Two-Dimensional (2-D) echocardiographic examination
a. Equipment controls
1) Depth
2) Dynamic range
3) Edge enhancement
4) Focal zones
5) Gain
6) Harmonics
7) Line density
8) Processing curves
9) Sector size
10) Transducer frequency
11) Transmit power
12) Zoom
b. Transducer manipulations
1) Rotation
2) Angulation
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3) Tilting (heel-toe)
4) Probe pressure
5) Sliding
2. M-mode Instrumentation
1) Depth
2) Gain
3) Sweep speed
b. M-mode technique
1) 2-D guided cursor placement
2) Advantages/disadvantages
3) Clinical application
a) Chamber and wall measurements
b) Fractional shortening
c) Findings with pathology
4) Color M-mode
a) Timing of events
b) Clinical application
c. Imaging planes
3. Color Doppler
1) Gain
2) Color maps
3) Invert
4) Scale/PRF
5) Sector size
6) Sector position
b. Color characteristics
1) Flow directionality
2) Flow disturbances
3) Flow profiles
4) Pulse wave mechanism
5) Advantages/disadvantages
c. Imaging planes
d. Clinical application
1) Valvular regurgitation
2) Localization of stenotic valves and shunts
4. Spectral Doppler
1) Gate position
2) Gate size
3) Angle correction
4) Angle steering
5) Invert
6) Transmit power
7) Gain
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8) Reject/wall filter
9) Velocity/range scale
10) Baseline shift
11) Sweep speed
b. Doppler characteristics
1) Pulsed wave versus continuous wave
2) Doppler equation
3) Flow directionality
4) Display
a) Timing (systolic, diastolic)
b) Direction (positive, negative)
c) Quality (normal, disturbed)
5) Doppler tissue imaging (DTI)
a) Low wall filter setting (high pass velocity setting)
b) Low gain settings
c) Color flow assignment
d) Frame rate
e) Scale adjustment
f) Sample size or placement
g) Respiratory variation
h) Clinical use and formulas
i) Wave forms
i. Em - early diastolic annular motion
ii. Am - annular motion during atrial contraction
iii. Sm - systolic annular motion
c. Stand alone dedicated CW transducer
1) Clinical application
d. Imaging planes
e. Clinical application
1) Valvular stenosis or regurgitation
2) Assessment of intracardiac pressures
3) Shunts
4) Systolic function
5) Diastolic function
E. Provocative Maneuvers
1. Physical maneuver
a. Valsalva maneuver
b. Mueller
c. Isometric handgrip
d. Straight leg raising
e. Squatting
f. Inspiration
g. Expiration
h. Tilt table
2. Pharmacologic
3. Clinical application of each
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F. Recognition of Technical Errors

1. Artifacts
a. Reverberation
b. Side lobes
c. Near field clutter
d. Echo drop out or shadowing
e. Mirror image
f. Translational motion
g. Aliasing
2. Instrumentation errors
a. Overgain or undergain
b. Improper focal location
c. Improper processing curves
d. Improper set-up or software package
e. Inappropriate PRF/scale (Doppler)
f. Inappropriate PW gate size or position
g. Inappropriate sweep speed (M-mode/spectral Doppler)
h. Improper ECG lead placement
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SECTION IV: Principles of Cardiac Hemodynamics and Cardiac Cycle
1. List the factors that affect blood flow

2. Describe the relationship between pressure and velocity as it relates to the Bernoulli
equation
3. Describe clinical applications and pitfalls of common cardiac Doppler hemodynamics
4. List normal pressures of cardiac chambers and great vessels
5. Relate phases of the cardiac cycle to electrocardiographic events
6. Describe spectral Doppler physiology as it relates to valvular and pulmonary vein
flow
IV. Principles of Cardiac Hemodynamics
A. Fluid Dynamics
1. General description
a. Flow and related terms
b. Power, work, and energy
c. Potential and kinetic energy
d. Hydrostatic pressure
e. Volumetric flow
f. Velocity
g. Capacitance
h. Compliance
i. Fluid viscosity
B. Deriviations of Equations
1. General description
a. Resistance equation
1) R = 8 L r4
b. Volumetric flow equation (continuity equation)
1) Conservation of mass - flow proximal to valve must equal flow across
the valve
2) (Area1) x (VTI1) = (Area2) x (VTI2)
c. Pressure flow relationships
1) Poiseuilles law
a) Q = (P1 - P2) r4
8 L
b) Bernoulli principle
a) Conservation of energy
b) Bernoulli equation
i. P1 - P2 = ½p(V22 - V12) + pµ, 2 dv ds + r(V)
dt
ii. Assumption
i) Flow acceleration + viscous friction are negligible
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ii) (½p) mass density is 4 for normal blood

iii) No energy transfer
iii. Modified Bernoulli equation
i) P1 - P2 = 4(V22 - V12)
iv. Simplified Bernoulli equation
i) P1 - P2 = 4V2
ii) V1 negligible is the assumption
v. Clinical use
i) Valvular stenosis (aortic, pulmonic)
ii) Pulmonary artery pressure
3) Reynolds number
a) Point at which turbulence occurs
b) Re - Vq2r
C. Physiology and Hemodynamic Information Derived from Doppler

1. Pressure and flow resistance
a. Stroke volume (SV)
1) Doppler SV = CSA x VTI
2) Normal SV = 75 - 100 ml
2. Cardiac output (CO)
a. CO = SV x heart rate (HR)
1) Normal CO = 5 - 7.5 liters/minute
3. Cardiac index (CI)
a. CO/patients body surface area (BSA)
1) CI = CO/BSA
a) CI measured in liters/minute/meter2
4. Delta pressure (dp) over deltatime (dt) mmHg/msec
a. Time in milliseconds (msec) it takes the LV to generate 32 mmHg; first
derivative of LV pressure rise
1) dp/dt
2) <27msec = normal for LV
3) 27msec - 32ms = borderline
4) >32msec = abnormal
5. Continuity equation - based on conservation of mass
a. Aortic valve area (AVA)
1) AVA = .785 (LVOT diameter2) TVILVOT
TVIAV
2) Aortic valve area
a) 2.5 - 4.5 cm2 = normal
b) 1.2 - 2.4 cm2 = mild aortic stenosis (AS)
c) 0.8 - 1.1 cm2 = moderate AS
d) <0.80 cm2 = severe AS
3) Pitfalls
b. Mitral valve area (MVA)
1) MVA = LVOT diameter2 x 0.785 x TVI LVOT
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TVI MV
6. PISA
a. Mitral regurgitation
1) Regurgitant flow rate
a) 2 r2V1 = flow rate cc/sec
2) Effective regurgitant orifice area (EROA)
a) Flow rate cc/sec/MR peak velocity cm/sec
3) Regurgitant volume (RV)
a) RVcc - EROA cm2 x VTI MRcm
4) Pitfalls
b. Mitral stenosis
1) Mitral valve flow rate cc
a) Flowrate in cc/sec = 6.28 x r2 x %(angle/180°) x V1
2) Mitral valve area (MVA cm2) = flowrate cc/sec/V2
a) V2 = peak E velocity cm/s
3) Pitfalls
7. Pressure half time
a. Time it takes for mitral valve gradient to fall by half its initial value
b. Mitral valve area (MVA)
1) MVA cm2 - 220/halftime (msec)
2) Halftime = deceleration time x 0.29
a) 4.0 - 6.0 cm2 = normal
b) 1.5 - 2.5 cm2 = mild stenosis
c) 1.0 - 1.5 cm2 = moderate stenosis
d) <1.0 cm2 = severe stenosis
c. Aortic insufficiency (AI)
1) Halftime = deceleration time x 0.29
a) Pressure halftime >550 msec = mild
b) Pressure halftime 550 - 300 msec = moderate
c) Pressure halftime <300 msec = severe
d. Pitfalls
8. Regurgitant fraction (RF)
a. RF aortic valve (AV)
1) RFAV = SVAV - SVMV
SVAV
b. RF mitral valve
1) RFMV = SVMV - SVAV
SVMV
c. Pitfalls
9. Qp:Qs - ratio
a. Used to evaluate shunt flow
b. Shunt flow = Right ventricular outflow tract (RVOT)
Left ventricular outflow tract (LVOT)
c. Ratio of 1.0 = normal
d. Ratio of >1.0 = left to right shunt
e. Ratio of <1.0 = right to left shunt
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f. Pitfalls
D. Normal Pressures
1. Chamber and great vessel pressure
a. LA ~ 10 mmHg
b. RA = 0-5 mmHg
c. RV = 25 mmHg peak systolic pressure, 5 diastolic pressure
d. LV = 120 mmHg peak systolic pressure, 80 mmHg diastolic pressure
e. PA = 25 mmHg peak systolic pressure, 10 mmHg diastolic pressure
f. Aorta = 120 mmHg peak systolic pressure, 80 mmHg diastolic pressure
g. Arterioles - 40 mmHg
h. Capillaries - 10 mmHg
E. Cardiac Cycle
1. Electrical characteristics
a. Conduction system
1) Sinoatrial (SA) node
2) Intra-atrial tracts
3) Atrioventricular (AV) node
4) Bundle of His
5) Right and left bundle branches
b. Electrocardiogram
1) P wave
2) QRS complex
3) ST segment
4) T wave
2. Mechanical characteristics
a. Systole
1) Pressure changes within chambers
2) Valve opening and closing
b. Diastole
1) Pressure changes within chambers
2) Valve opening and closing
3. Ventricular diastole
a. Isovolumic relaxation time (IVRT)
1) LV pressure falls rapidly
2) Follows aortic valve closure
3) IVRT ends when LV pressure falls below LA pressure and MV opens
b. Passive filling/early filling
1) Rapid filling
2) Pressure equalization
3) Factors that increase passive filling
a) Mitral/tricuspid regurgitation
b) Atrial/ventricular septal defect
4) Factors that decrease passive filling
a) Increased heart rate
b) Mitral stenosis
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c) Increased ventricular end-diastolic pressure

c. Diastasis
d. Atrial systole (atrial contraction)
1) Atrial pressure exceeds ventricular pressure
2) MV opens and late LV filling occurs
4. Ventricular systole
a. Isovolumic relaxation time (IVRT)
b. Isovolumic contraction time (IVCT)
c. Rapid ejection
d. Reduced ejection
e. Factors that influence ventricular systole
1) Ventricular function
2) Afterload
3) Preload
4) Frank-Starlings law
F. Pulmonary Veins
1. Vein characteristics
2. Anatomic location
3. Doppler interrogation
4. Wave form charateristics
a. Systole
b. Diastole
G. Cardiac Catheterization
1. Clinical utility
a. Intracardiac pressure
b. Oxygen saturation
c. Coronary artery assessment
d. Other
2. Normal pressure tracings
a. Right heart
b. Left heart
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SECTION V: Ventricular Function
1. Define ventricular function terminology

2. Identify the etiologies, signs and symptoms, and risk factors of ischemic heart disease
3. Classify the types of wall motion abnormalities
4. Describe 2-D, M-mode, and Doppler features associated with ischemic heart disease
5. Identify formulas associated with assessment of ventricular function
6. Differentiate ways to assess global LV function and regional LV quantification
V. Ventricular Function
A. Determinants of Left Ventricular Performance

1. Contractility
d. Inotropic state of myocardium
e. Best determinants
f. Limitations
2. Heart Rate
3. Preload
a. Define
b. Frank-Starling relation
1) Left ventricular end diastolic volume (LVEDV) versus left ventricular
end diastolic pressure (LVEDP)
2) SV increases as end-diastolic volume increases
4. Afterload
a. Define
b. Determinants
1) Ventricular volume and pressure
2) Atrial resistance
3) Aortic impedance
4) Mass of blood in aorta
5) Viscosity of blood
c. LaPlace relation
1) Pressure * radius/wall thickness
2) Inverse relation to LV systolic function
5. Coordinated LV contraction
B. Wall Motion Abnormalities

1. Hypokinesis
2. Akinesis
3. Dyskinesis
4. Hyperkinesis
5. Wall motion scoring index
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C. Global LV Systolic Performance

6. Ejection phase indexes
a. Ejection fraction (EF)
b. Fractional shortening (FS)
c. Velocity of circumferential fiber shortening (Vcf)
d. CO and SV
7. Non-ejection phase indexes
a. Systolic time intervals
1) Pre-ejection time
2) Pre-ejection time/LV ejection time
b. LV dP/dt
c. Acceleration time of aortic flow
d. Pressure/volume analysis
8. Indirect methods
a. Mitral E-point septal separation
b. Aortic root motion
c. Descent of cardiac base
d. Sphericity of LV
e. Velocity integrals of outflow
1) LV
2) RV
4. Potential limitations
a. Endocardial dropout
b. Influence of load conditions
c. Regional wall motion abnormalities
d. Some methods require no major shape distortion
e. Oblique measurements/angles
f. Limited frame rate of 2-D imaging
g. LV forshortening
h. Translation artifact
i. Discoordination of contraction
5. Improve endocardial delineation
a. Harmonic imaging
b. Contrast agents
6. Indirect methods
a. Mitral E-point septal separation
b. Aortic root motion
c. Descent of cardiac base
d. Sphericity of LV
e. Velocity integrals of outflow
1) LV
2) RV
D. Assessment of Ventricular Systolic Function

1. Fractional shortening
a. Technique
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1) M-mode
2) 2-D
b. Calculations
1) EDD - ESD
EDD
c. Normal values
1) NL = >29% at mid LV cavity
2) NL = >22% at LV base
d. Limitations
1) Less accurate in the presence of wall motion abnormalities
2) Load dependent
2. Stroke volume
3. Cardiac output and index
4. Ejection fraction
a. Characteristics
1) Ratio of SV to SDV
2) Most commonly used clinical index of LV function
3) Influenced by preload, afterload, and heart rate
4) Visual estimated valid with interobserver variablitiy
b. Calculations
1) End diastolic dimension (EDD)
2) End systolic dimension (ESD)
3) Windows
a) Parasternal
b) Apical
4) Assumes LV is prolate ellipsoid
5) Limitations
a) Less accurate in the presence of wall motion abnormalities
b) Abnormal LV shape
c) Does not measure changes in long-axis length
d) Load dependent
c. Normal values
1) 61% (+/- 10%)
2) Interobserver reproducibility (+/- 10%)
d. Limitations
1) Due to altered loading conditions
a) MR: %EF normal with intrinsic myocardial dysfunction
b) AS: %EF decreased with nomal myocardial function
c) Severe anemia
d) Hemodialysis patients
5. Left ventricular mass
a. M-mode method
1) Penn formula
a) LVM = 1.04 x [(Dd + S + PW) 3] (Dd)3
2) ASE formula
a) LVM = 0.80 X 1.04X (Dd + S + PW)3 (Dd)3 + 0.6
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3) Normal values
a) Men: <130 gm/m2
b) Women: <100 gm/m2
b. 2-D method
1) Area-length
2) Truncated ellipsoid
3) Normal values
a) Men: <90 gm/m2
b) Women: <80 gm/m2
4) Limitations
a) Relatively wide standard deviation
b) Requires change >35 gm to reach 95% confidence intervals
6. Change in pressure by change in time (dP/dt)
a. Characteristics
1) Relatively load-independent
b. Calculations
c. Appropriate measurement placement
d. Normal values
7. LV volumes
a. Simpsons rule and modified Simpsons rule
1) Biplane more accurate
2) Single plane
a) (Area)2/length in which V = 0.85
b) Suitable if LV symmetric
3) Quick method (regression equation)
a) EDV = (3.42 * D * L) n 6.44
b. End systolic volumes (ESV)
1) Most reproducible volume measure
2) Insensitive to cardiac loading
3) Powerful predictor of cardiac events
4) Normal values
a) Men: 34 mL
b) Women: 29 mL
c. End diastolic volumes (EDV)
1) Endocardium more difficult to image at end diastole
2) More variable than ESV
3) Normal values
a) Men: 111 mL
b) Women: 80 mL
d. Technical considerations
1) Image maximization
2) Both atrioventricular valves imaged
3) Avoid aorta and coronary sinus
4) Selection of precise time in cardiac cycle for measurement
5) ED frame in larges LV cavity just after MV closure
6) ES frame in smallest LV cavity just before MV opening
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8. Tissue Doppler imaging

a. Characteristics
b. Appropriate measurement placement
E. LV Quantification
1. Prognosis
a. CAD
b. Acute MI
c. Cardiomyopathy
1) Volume/mass ration
2. Methods for regional function
a. 17 segment wall score
b. Tissue Doppler imaging
1) Strain
3. Considerations
a. Hypertension
1) LV mass predicts morbidity/mortality
2) LV wall thickness/cavity dimension predicts morbidity/mortality
b. Interdependence of LV and RV
c. Global RV systolic function
4. Associated conditions
a. LVH
b. Ischemic heart disease
c. DCM
d. HCM
e. RCM
f. RV pressure and volume overloads
g. Valvular heart disease
h. Pericardial disease
i. Transplant rejection
5. Therapeutic implications
a. Angiotensin-converting enzyme inhibitors
b. Timing of surgery in volume overload states (MR, AI)
c. Timing of surgery in pressure overload states (AS)
F. Assessment of Ventricular Diastolic Function

1. General principles
a. Four phases of diastole
1) Isovolumic relaxation
2) Early rapid diastolic filling
3) Diastasis
4) Late diastolic filling caused by atrial contraction
b. Parameters of diastolic function
1) Relaxation
a) IVRT
b) Maximum rate of pressure decline (dP/dt)
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c) Time constant of relaxation

2) Compliance
a) dP/dV
b) Chamber stiffness constant
3) Ventricular diastolic pressures
4) Ventricular diastolic filling curves
2. Echocardiography evaluation
a. 2-D imaging
1) Chamber dimensions
2) Wall thickness
3) Automated endocardial border tracing
b. Doppler imaging
1) Assessment of MV inflow
a) E-wave/A-wave ratio
b) Deceleration time (DT)
c) IVRT
d) Mitral E-wave velocity (E)
e) Mitral A-wave velocity (A)
f) Mitral A-wave duration
g) Time from mitral valve opening to E-wave velocity
2) Assessment of pulmonary vein flow patterns
a) Systolic wave velocity (S)/velocity time integral (VTI)
b) Diastolic (D) wave velocity/VTI
c) Duration time
d) Systolic to diastolic ratio
e) Atrial reversal wave (AR) velocity
f) AR duration
g) AR duration minus A-wave duration
3) Assessment using tissue Doppler
a) Peak early diastolic myocardial velocity (Em)
b) E to Em ratio
4) Assessment using color M-mode
a) Velocity of propagation of early filling (Vp)
3. LV filling patterns
a. Technical factors
1) Sample volume location
2) Doppler modality (PW versus CW)
3) Intercept angle
b. Physiologic factors
1) Respiration
2) Heart rate
3) PR interval
4) Age
5) Preload
6) Afterload
7) Exercise
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8) Valsalva
9) LV systolic function
10) Atrial contraction function
11) Diastolic function
12) Cardiac function
c. Normal Doppler values
1) AR <35 cm/s
2) AR duration A duration <20msec
3) DT 150- 220msec
4) E/A > 1
5) Em >8cm/s
6) IVRT 60-100msec
7) Vp using color M-Mode
d. Abnormal relaxation
1) Doppler values
a) AR <35 cm/s
b) AR duration A duration <20msec
c) DT >220msec
d) E/A < 1
e) Em <8cm/s
f) IVRT >100msec
g) Vp
2) Significance
a) Initial stage
b) No increase in mean LA pressure
c) Difficult to assess with elevated heart rate
d) Seen in
i. Hypertenstion (HTN)
ii. Coronary artery disease (CAD)
iii. Cardiomyopathies
iv. Elderly
e. Pseudonormalization
1) Doppler Values
a) AR >35 cm/s
b) AR duration A duration >20msec
c) DT 150-220msec
d) E/A >1
e) Em <8cm/s
f) IVRT 60-100msec
g) S/D <1
h) Vp < 45 cm/s
2) Significance
a) Spectral Doppler of mitral inflow appears normal
b) Underlying relaxation abnormality with elevated LA pressure
c) Preload reduction may unmask abnormality
i. Valsalva
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ii. Nitroglycerin
d) Seen in:
i. Dilated cardiomyopathy (DCM)
ii. Restrictive cardiomyopathy (RCM)
iii. Ischemic cardiomyopathy
f. Restrictive/Noncompliance
1) Doppler Values
a) AR >35 cm/s
b) AR duration A duration <20msec
c) DT <150msec
d) E/A >2
e) Em <8cm/s
f) IVRT <60msec
g) S/D <1
h) Vp < cm/s
2) Significance
a) Late stage
b) Severe decrease of LV compliance
c) Elevated mean LA pressure at rest
d) May reverse with preload reduction maneuvers
g. Estimation of LV filling pressures
1) Normal LV filling pressures
a) Abnormal relaxation pattern except with severe LVH
2) High LV filling pressures
a) E/A>1
b) E/A is high and DT is shorter than expected
c) Restrictive pattern
d) AR duration - A duration > 30 msec is consistent with elevated
filling pressures
e) < 8 - normal filling pressures
f) 8-15 indeterminate filling pressures
g) > 15 elevated filling pressures
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SECTION VI: Coronary Artery Disease (CAD)
1. Correlate ventricular wall segments to coronary artery distribution

2. Differentiate complications associated with myocardial infarction
VI. Coronary Artery Disease (CAD)
A. Coronary Artery Anatomy and Function

a. Flow distribution
b. Artery location
c. Relation between coronary arteries and myocardial wall segments
d. Flow measurements and limitations
e. Coronary flow reserve
f. Myocardial perfusion with contrast echo
g. Anatomy
1) Normal imaging in PSAX
a. Left main at left posterior sinus
i. 4 oclock position
b. RCA at right aortic sinus
i. 11 oclock position
B. Coronary Artery Abnormalities

1. Anomalous origins and course
2. Aneurysms
a. Kawasaki disease
b. Atherosclerotic aneurysms
c. Polyarteritis
d. Syphilis
e. Infection
f. Trauma
g. Other
3. Fistulas
a. Incidence in general population
b. Emptying pathway
1) Cardiac chambers
2) PA
3) Coronary sinus
c. Artery affected
4) RCA 50%
5) LCA 45%
6) Both 5%
d. Continuous murmur
e. Echo features
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7) Dilated coronary artery

8) Chamber enlargement
9) Color Doppler may detect shunt flow
C. Myocardial Ischemia
1. Coronary artherosclerosis
2. Sequence of events in ischemia (ischemic cascade)
3. Relation of wall motion and thickness to artery perfusion
4. Echocardiographic findings
1) Regional wall motion abnormalities
1) Confounding factors
e. Conduction or pacing abnormalities
f. Translocation motion
g. Loading conditions
h. Altered imaging planes
2) Diastolic function changes
3) Stress echocardiography
D. Myocardial Infarction (MI)

1. Detection and location of MI
a. Regional wall motion abnormality
1) Wall motion score index
2) Relationship of wall motion abnormalities to coronary artery anatomy
b. Complications and associated findings
1) Myocardial stunning and hibernation
2) Myocardial rupture
3) Acute ventricular septal rupture
4) Papillary muscle dysfunction/rupture
5) Mural thrombi
6) MR
a) Dilated LV
b) Papillary muscle dysfunction
7) Aneurysm
8) Pseudoaneurysm
9) Post MI pericardial effusion (Dresslers syndrome)
10) Ischemic cardiomyopathy
11) RV infarction
E. LV Post Infarction/Follow-up
1. Characteristics
2. Echocardiographic features
a. Recovery of function
b. Effect of revascularization
c. LV thrombus
3. Myocardial remodeling
a. Infarct expansion
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b. Global dilatation
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SECTION VII: Valvular Heart Disease
1. Describe common etiologies of valvular heart disease

2. Discuss signs and symptoms associated with valvular heart disease
3. Describe key echocardiographic findings associated with valvular heart disease
4. Explain the methods for estimation of right atrial and right ventricular systolic
pressure
5. Describe typical echocardiography views utilized in assessing valvular stenosis and
regurgitation
6. List the parameters used in qualitative and quantitative assessment of valvular heart
disease
7. Discuss the challenges of stenotic valve assessment in the presence of reduced LV
function or significant regurgitation
8. Describe common locations of vegetation formation
9. Identify the signs and symptoms of infective endocarditis
10. List examples of mechanical and bioprosthetic valves
11. List common complications of prosthetic valves
12. Differentiate between advantages of using mechanical versus bioprosthetic valves
13. Describe Doppler calculations used to assess prosthetic valves
VII. Valvular Heart Disease
A. Mitral Stenosis (MS)

1. Etiology
a. Rheumatic
b. Mitral annular calcification (MAC) and calcific MS
c. Congenital
d. Drug-induced valvulopathy
e. Other
2. Pathophysiology
a. Narrowing of MV orifice with obstruction to diastolic forward flow
b. MV gradient and LA pressure increase to maintain cardiac output
c. Increased LA pressure eventually leads to LA enlargement, backwards
failure, and pulmonary hypertension
3. Clinical presentation
a. Signs and symptoms
1) Dyspnea
2) Fatigue
3) Chest pain
4) Hemoptysis
5) Palpitations
6) Ortners syndrome (hoarseness)
b. Physical findings
1) Atrial fibrillation
2) Edema
3) Hepatic congestion
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4) Pulmonary edema
5) RV lift
6) Apical diastolic thrill
c. Auscultatory findings
1) Loud S1
2) Opening snap
3) Low-pitched diastolic rumble
4) Holosystolic murmur (with MR)
5) Accentuated P2 (pulmonary hypertension)
a. Thickened and calcified mitral leaflets and subvalvular apparatus
b. Doming of anterior mitral leaflet during diastole (hockey-stick
appearance)
c. Immobility of posterior leaflet
d. Fish-mouth orifice in short-axis view
e. Commissural fusion
f. Decreased mitral opening
g. LA enlargement
h. LV small with normal function (pure MS)
i. PHTN
1) Secondary RA and RV enlargement
2) Elevated TR velocity
j. Candle-flame appearance (Color flow)
k. Coexisting valvular lesions
l. Spontaneous contrast or thrombus in LA, LAA
5. Quantitation
a. Pressure gradients (CW Doppler)
1) Peak (initial gradient)
2) Mean
b. MV area
1) 2-D planimetry (short-axis view)
2) PHT method
a) MVA = 220/PHT
3) Continuity method
a) MVA = LVOT diam2 x 0.785 x TVI LVOT
TVI MV
4) PISA
a) MVA = 6.28 x r2 x aliasing velocity x
Peak mitral stenosis velocity 180p
c. Values
Grade MVA (cm2) Mean (mm Hg) PHT (msec)
Normal 4.0 - 6.0
Mild 1.6 - 2.0
Moderate 1.1 - 1.5
Severe 1.0 10 > 220
d. Degree of pulmonary hypertension (TR velocity)
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e. Technical considerations and pitfalls

1) Should not use PHT method immediately after balloon valvuloplasty,
with severe AR, or with decreased LV compliance
2) Should not use continuity method if significant AR or MR
3) Angle correction may be required with PISA method
4) Mean gradient dependent on heart rate and cardiac output
6. Role of hemodynamic stress testing
a. Useful in patients with symptoms out of proportion to resting
hemodynamics or those with sedentary lifestyle
b. Substantial rise in mean gradient and PA pressure with exercise indicates
hemodynamically significant MS
7. Role of TEE
a. Assessment for spontaneous contrast, LA, LAA thrombus
b. Evaluation of morphology and hemodynamics with suboptimal surface
study
8. Role of echocardiography in percutaneous balloon mitral valvuloplasty
a. Patient selection
1) MV score index
2) Severity of MR
3) Absence of LA, LAA thrombus
4) Minimal or no commissural calcium
b. Echo guidance
1) Transseptal puncture
2) Balloon positioning
3) Assessment of results
4) Detection of complications
c. Complications
1) MR
2) Cardiac perforation and tamponade
3) ASD
9. Related testing
a. EKG
2) LA enlargement
3) RVH and right axis deviation (with pulmonary hypertension)
b. Chest x-ray
1) LA enlargement with normal LV size
2) Pulmonary venous hypertension
3) Right heart enlargement
4) Pulmonary edema
c. Cardiac catheterization
1) Angiography to identify underlying CAD
2) Increased pressure gradient across MV
3) Balloon valvuloplasty may be performed
10. Common treatment
a. Medical
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1) Antibiotic prophylaxis
2) Treatment for heart failure
3) Anticoagulation if clinically indicated
b. Surgical
1) Balloon valvuloplasty
2) Open or closed commissurotomy
3) MV replacement
B. Mitral Regurgitation (MR)

1. Etiology
a. MV prolapse (MVP)
b. Flail mitral leaflet
c. Ruptured chordae
d. Mitral annular dilatation or calcification
e. Papillary muscle dysfunction or rupture
f. Rheumatic or myxomatous valve
g. Drug-induced valvulopathy
h. Congenital malformation
i. Endocarditis or perforation
j. Regional or global LV remodeling
2. Pathophysiology
a. Backward flow of blood through an incompetent mitral valve during
ventricular systole
b. Chronic mitral regurgitation
1) Progressive increase in degree of MR leading to LV volume overload
2) Impaired forward cardiac output due to volume of regurgitant flow
3) Heart compensates for volume overload with LV dilatation and
hypertrophy
4) Increased LA pressure causes LA dilatation
5) Increased LVEDP and LA pressure eventually lead to backwards
failure and pulmonary hypertension
c. Acute mitral regurgitation
1) Rapid development of significant MR
2) LV unable to compensate for increased volume
3) Marked increase in LA pressure in non-compliant left atrium
4) Increased LA pressure leads to increased pulmonary capillary pressure
and pulmonary edema
3. Clinical presentation (chronic and acute MR)
1) Progressive dyspnea
2) Fatigue and exhaustion
3) Palpitations
4) Atypical chest pain
1) Atrial fibrillation (chronic)
2) Elevated JVP
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3) Hepatomegaly
4) Peripheral edema
5) Displaced, active LV impulse
6) Pulmonary edema (acute)
1) Holosystolic murmur (chronic)
2) Early systolic murmur (acute)
3) S3, S4 with heart failure
4) Accentuated P2 with pulmonary hypertension
a. Functional anatomy
1) Mitral annulus (dilated, calcified)
2) Mitral leaflets (thickened, flail, prolapse)
3) Chordae tendineae (elongated, ruptured)
4) Papillary muscle (displaced, ruptured)
5) Ventricular myocardium (remodeled)
b. LV dilatation
c. LA enlargement
d. Color flow jet of MR
e. Evidence of pulmonary hypertension
2) Dilated IVC/hepatic veins
5. Qualitative and semi-quantitative assessment
a. Color flow imaging
1) Jet size and configuration
a) Jet area to LA area ratio
b) May be deceptive with acute MR: maximal jet area is limited by
small receiving chambers and rapid equalization of pressures
c) Central jets may appear larger because blood cells are entrained on
all sides of the jet
d) Interpret in context of jet geometry and surrounding solid
boundaries
2) Direction and eccentricity of jet
3) Color M-mode (to establish timing)
4) Vena contracta
a) Narrowest portion of jet that occurs at or just downstream from the
orifice
b) Obtain in high resolution view
c) Image in multiple planes perpendicular to the commissural line
(usually parasternal long-axis view)
d) Measure width of the neck of the jet at the time of its largest
diameter
e) Width < 0.3 cm usually denotes mild MR
f) Width > 0.7 cm usually denotes severe MR
g) Not valid in the presence of multiple jets
b. Pulsed-wave Doppler
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1) Mitral inflow E wave velocity

a) Predominant early filling with severe MR
b) E velocity > 1.2 -1.5 m/sec consistent with severe MR (in the
absence of severe diastolic dysfunction)
c) Must rule out co-existing stenosis
2) Pulmonary vein flow abnormalities
d) Usually see predominant systolic forward flow
e) Blunting of systolic forward flow occurs with increasing severity
of MR
f) High LA pressure and atrial fibrillation may also cause diminished
systolic forward flow
g) Severe MR may cause systolic flow reversal
h) Eccentric jet may selectively enter one pulmonary vein
c. Continuous-wave Doppler
1) Density of CW Doppler signal proportional to regurgitant volume
2) Peak MR velocity dependent on pressure gradient between LV and LA
a) Normal velocity = 5 to 6 m/sec
b) Decreased velocity indicates elevated LA pressure, but does not in
itself indicate severity of MR
3) Duration of MR signal is typically holosystolic
4) Shape of MR Doppler signal
a) Symmetrical shape: reflects mild MR
b) Asymmetrical shape: reflects severe MR (due to rapid increase in
LA pressure)
5) Assess RVSP: indirect clue to severity of MR and compensation to
volume overload
6. Quantitative parameters
a. Methods
1) Continuity
2) PISA
b. Parameters
1) Regurgitant volume
2) Regurgitant fraction
3) Regurgitant orifice area
c. Values
Grade RV (cc) RF (%) ERO (cm2)
Mild <30 <30 <0.20
Mild-moderate 30-44 30-39 0.20 0.29
Moderately-severe 45-59 40-49 0.30 0.39
Severe >60 > 50 >0.40
d. Pitfalls
1) Learning curve of operator
2) Data acquisition errors
3) Continuity method invalid if multivalvular regurgitant lesions or
significant shunts present
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4) Difficult to calculate accurate regurgitant volumeby continuity method

in the presence of valvular stenosis, dense annular calcification, or
prosthetic valve
7. Related testing
a. EKG
1) LA enlargement
2) LV enlargement
3) Left axis deviation
5) RVH with pulmonary hypertension
b. Chest x-ray
1) Cardiomegaly (chronic)
2) Pulmonary congestion
3) PA and right heart enlargement (late)
4) Pulmonary edema
2) Increased right heart pressures
d. Role of TEE
1) Evaluation of morphology, assessment of hemodynamics, and
quantitation with suboptimal surface study
2) Intra-operative evaluation
8. Common treatment
a. Medical
b. Surgical
1) Role of echo in timing of surgery
2) MV repair
a) Resection
b) Chordal transfer, reattachment
c) Artificial chordae
3) MV replacement (MVR)
2. Mitral valve prolapse (MVP)

1. Etiology
a. Myomatous disease
b. Marfan syndrome
c. Flail leaflet
a. Signs and symptoms as for MR
b. Physical presentation
1) Most patients asymptomatic
2) Palpitations
3) Chest pain
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4) Dyspnea
5) Fatigue
1) Mid-systolic click
2) Mid-to-late systolic murmur if MR present
3) Click and murmur occur earlier in systole with preload reduction
(Valsalva, standing)
4) Click and murmur occur later in systole with increased ventricular
volume (squatting)
a. Diagnosis based on parasternal long-axis view
b. Systolic displacement (>2 mm) of one or both mitral leaflets into the LA,
below the plane of the mitral annulus
c. Leaflets may be thickened (> 5mm) or myxomatous
d. Elongated chordae
e. LA and/or LV enlargement with significant MR
f. Mitral regurgitation, typically eccentric and late-systolic
g. Progression of MR severity over time
4. Related testing
a. EKG
1) Normal in asymptomatic patients
b. Chest x-ray
1) Normal in asymptomatic patients
1) Rarely performed for diagnostic purposes
5. Common treatment
a. None unless significant MR is present
b. Endocarditis prophylaxis
c. Serial echo as indicated
3. Aortic stenosis (AS)

1. Etiology
a. Degenerative calcification
b. Congenital aortic valve disease
1) Bicuspid aortic valve (BAV)
2) Unicuspid aortic valve
c. Post inflammatory disease
1) Rheumatic
2) Non-rheumatic
a) Irradiation
b) Drug-induced valvulopathy
c) Endocarditis
2. Pathophysiology
a. Narrowing of AV orifice with obstruction to systolic forward flow
b. Decreased AV orifice causes increased gradient
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c. Heart responds to increased afterload with increased contractile function

and LVH
d. Elevated LVEDP eventually leads to LA enlargement, backwards
failure, and pulmonary hypertension
1) Angina
2) Dyspnea, exertional dyspnea
3) Paroxysmal nocturnal dyspnea
4) Congestive heart failure
5) Syncope, presyncope
1) Narrow pulse pressure
2) Slow rising, late peaking carotid pulse (parvus et tardus)
1) Harsh systolic ejection murmur (crescendo-decrescendo) that may
radiate to carotids
2) Diastolic murmur if AR present
a. Aortic valve 2-D appearance
1) Cusp number
2) Presence/location of raphe
3) Systolic doming of AV if bicuspid
4) Eccentric closure
5) Thickened/calcified leaflets
6) Restricted mobility
b. Aorta
1) Post-stenotic dilatation
2) Aortoseptal angle
3) Possible coarctation with BAV
c. LV
1) LVH
2) LVOT obstruction
3) Normal or small LV size
4) Hyperdynamic LV function (until late)
d. LA enlargement
e. Color Flow
1) Turbulent forward flow
2) Associated aortic regurgitation
5. Quantitation
1) Peak instantaneous
2) Mean
3) Utilize multiple imaging windows to obtain Doppler signal most
parallel to flow
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a) Apical
b) Subcostal
c) Right parasternal
d) Right supraclavicular
e) Suprasternal
f) Left parasternal
4) Use nonimaging CW Doppler probe
a) Smaller footprint allows optimal positioning and angulation
b) Non-imaging transducer has higher signal-to-noise ratio than
duplex transducer
5) Assessment unreliable in the presence of subaortic obstruction
a) Bernoulli invalid with stenosis in series
b) Cannot measure LVOT velocity
6) Alternative method for peak gradient:
a) MR velocity (4V2) + LA Pr ( 15) = LVSP
b) LVSP LVOT gradient Systolic BP = AV gradient
b. AV area
1) 2-D planimetry
a) AVA = (LVOT diameter)2 x 0.785 x TVI LVOT
TVI AV
c. Values
Grade AVA (cm2) Mean (mm Hg) Peak velocity (m/sec)
Normal 2.5 - 4.5
Mild 1.2 2.4 < 30 < 3.0
Moderate 0.8 1.1 30-50 3.0 4.0
Severe 0.80 > 50 > 4.0
d. Dimensionless index
1) LVOT and AV velocity or TVI ratio
2) May be used if unable to measure LVOT diameter
3) < 0.2 indicates severe AS
6. Low output-low gradient AS
a. Small calculated valve area with limited excursion of leaflets, but mean
gradient is low in the setting of LV systolic dysfunction
b. Two possible explanations
1) True anatomically severe aortic stenosis
2) Functionally severe aortic stenosis
c. Low-dose pharmacologic stress echo
1) Stroke volume increases with increase in contractility
2) Doppler data obtained at each infusion stage
3) True stenosis: No change or minimal increase in AVA
4) Functional stenosis: Valve area increases
7. Related testing
a. EKG
1) LVH
2) LA enlargement
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b. Chest x-ray
1) LVH
2) LA enlargement
3) Post-stenostic dilatation of ascending aorta
4) AV calcification
1) Determines peak-to-peak gradient (different from echo peak
instantaneous)
2) Determines mean gradient
d. Role of TEE
1) Evaluation of morphology with suboptimal surface study
2) Preferred method for planimetry of AV area
3) Difficult to obtain accurate Doppler data
8. Common treatment
a. Medical
b. Surgical
1) Balloon valvuloplasty (in children)
2) AVR
E. Aortic regurgitation (AR)

1. Etiology
a. Aortic root abnormalities
1) Aortic root dilatation
2) Aortic dissection
b. Aortic leaflet abnormalities
1) Congenital (bicuspid)
2) Degenerative valve disease
3) Rheumatic valve disease
4) Endocarditis
5) Drug-induced valvulopathy
6) Miscellaneous other
2. Pathophysiology
a. Backward flow of blood through an incompetent AV during ventricular
diastole
b. Chronic
1) Progressive increase in AR leading to LV volume overload
2) Heart compensates for volume overload with LV dilatation and
hypertrophy
3) Forward stroke volume increased by Frank-Starling mechanism
4) Effective forward cardiac output maintained with normal function
5) LVEDP begins to rise as ejection fraction and cardiac output decrease
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Cardiac
6) Increased LVEDP and LA pressure eventually leads to backwards

failure and pulmonary hypertension
c. Acute
1) Rapid onset of AR leads to volume overload
2) LV unable to compensate for increased regurgitant volume
3) Leads to elevated left ventricular end-diastolic pressure (LVEDP) and
acute pulmonary edema
1) Patients often asymptomatic until AR becomes significant
2) Exertional dyspnea
3) Angina
4) Fatigue
5) Palpitations, tachycardia
6) Lightheadedness, syncope
1) Apical impulse displaced due to LV enlargement (chronic)
2) Wide pulse pressure (low diastolic BP)
3) Tachycardia (acute)
4) Pulmonary edema (acute)
1) Early, blowing, diastolic decrescendo murmur
2) Austin-Flint murmur
3) Secondary systolic ejection murmur
a. Functional anatomy
1) Aortic root abnormalities
a) Aortic root dilatation
b) Anulo-aortic ectasia
c) Sinus of valsalva aneurysm (ruptured or unruptured)
d) Aortic dissection
2) Aortic leaflet abnormalities
a) Bicuspid aortic valve
b) Endocarditis
c) Post-inflammatory disease
d) Calcific disease
e) Post valve surgery
b. LV dilatation (chronic)
c. Reduced LV systolic function (late)
d. Normal LV size with hyperdynamic systolic function (acute)
e. LA dilatation (chronic)
f. Associated findings
1) Diastolic flutter of anterior mitral valve leaflet
2) Jet lesion on septum, anterior mitral valve leaflet
3) Premature closure of mitral valve with diastolic MR (acute)
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4) Premature opening of aortic valve (acute)

g. Color flow jet of AR
h. Evidence of pulmonary hypertension
2) Dilated IVC/hepatic veins
1) Direction of flow (central jet, eccentric jet)
2) Color and color M-mode helpful in demonstrating timing and
thickness of jet and diastolic reversal in descending thoracic aorta
3) Regurgitant jet width to LVOT width ratio
a) Parasternal long-axis view
b) Severe AR: > 65% ratio
4) Regurgitant jet area to LVOT area ratio
a) Parasternal short axis view immediately below the aortic valve
(within 1 cm of the valve)
b) Severe AR: > 60% ratio
5) Vena contracta
orifice, measured at the time of its largest diameter
b) Image in multiple planes perpendicular to the commissural line
(usually parasternal long-axis view)
c) Not valid in presence of multiple jets
d) Severe AR: > 0.6 cm
1) Mitral inflow
a) Premature cessation of flow across mitral valve
b) Fluttering motion due to turbulence of posteriorly-directed jet
c) Restrictive mitral inflow pattern caused by high LVEDP
2) LVOT velocity
a) Increased velocity and TVI due to increased flow volume
3) Descending thoracic aorta
a) Mild AR: mild early diastolic flow reversal
b) Duration and velocity of reversal increase with increasing severity
of AR
c) Severe AR: holodiastolic flow reversal
4) Abdominal aorta diastolic flow reversal
c. Continuous-wave Doppler
2) Duration of AR signal is holodiastolic
3) Pressure half-time of AR signal
a) Mild AR: PHT > 500 msec
b) Severe AR: PHT < 200 msec
c) Pitfall: PHT also influenced by LV diastolic compliance and
pressure
4) Assess RVSP
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Cardiac
6. Quantitative parameters
a. Methods
1) Continuity
2) PISA
b. Parameters
1) Regurgitant volume
2) Regurgitant fraction
3) Regurgitant orifice area
c. Values
Grade RV (cc) RF (%) ERO (cm2)
Mild < 30 <30 < 0.10
Mild-moderate 30-44 30-39 0.10 0.19
Moderately-severe 45-59 40-49 0.20 0.29
Severe > 60 >50 > 0.3
d. Pitfalls
2) Difficult to calculate accurate regurgitant volume with continuity
method in the presence of valvular stenosis, dense annular
calcification, or prosthetic valve
7. Role of TEE
a. Evaluation of morphology and hemodynamics with suboptimal surface
study
b. Intra-operative evaluation
8. Related testing
a. EKG
1) LVH (chronic)
2) Left axis deviation (chronic)
3) AV block may be seen in the presence of infective endocarditis
4) Sinus tachycardia (acute)
b. Chest x-ray
1) Cardiomegaly (chronic AR)
2) Widened mediastinum with aortic dissection
9. Common treatment
a. Medical
b. Surgical
1) Echo predictors of surgical outcome
2) AV repair or replacement
F. Tricuspid Stenosis (TS)
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Cardiac
1. Etiology
a. Rheumatic
b. Congenital
c. Carcinoid
d. Drug-induced valvulopathy
e. Eosinophilic endomyocardial disease
f. Miscellaneous other
2. Pathophysiology
a. Rarely occurs as an isolated lesion
b. Narrowing of tricuspid valve orifice with obstruction to diastolic forward
flow
c. Increased RA pressure eventually leads to RA enlargement and signs of
right heart failure
1) Dyspnea
2) Fatigue
3) Right upper quadrant abdominal pain
1) Jugular venous distention with cannon a waves
2) Hepatomegaly
3) Ascites
4) Peripheral edema without pulmonary congestion
1) Tricuspid opening snap
2) Diastolic rumble (may be accentuated with inspiration)
3) Absence of normal respiratory splitting of S2
4) Murmur of TR
a. Valve thickened and/or calcified
b. Restricted leaflet motion
c. Diastolic doming of the tricuspid valve
d. RV size may be increased if concomitant TR
e. RA dilatation
f. Inferior vena cava (IVC) enlargement
g. Increased antegrade velocities with turbulent flow
h. TR often present
i. Co-existing valve lesions
j. Best to obtain Doppler data during apnea (end-expiration)
5. Quantitation
1) Peak (initial gradient)
2) Mean
a) Severe stenosis 7 mmHg
b. TV area (rarely used clinically)
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Cardiac
a) TVA = LVOT diam2 x 0.785 x TVI LVOT

TVI TV
2) PISA
a) TVA = 6.28 x r2 x aliasing velocity x
Peak tricuspid stenosis velocity 180p
3) Severe stenosis < 2.0 cm2
c. Degree of pulmonary hypertension (TR velocity)
d. Technical considerations and pitfalls
2) Angle correction may be required with PISA method
3) Mean gradient dependent on heart rate, cardiac output, and respiratory
cycle
6. Related testing
a. EKG
1) RA enlargement
3) RVH
b. Chest x-ray
1) RA enlargement
2) Dilated SVC
1) Elevated right heart pressures
2) Gradient between RA and RV
7. Common treatment
a. Medical
b. Surgical
1) Commissurotomy
2) TV replacement
G. Tricuspid Regurgitation (TR)

1. Etiology
a. Functional
1) Pulmonary hypertension due to left heart failure
2) Cor pulmonale
3) Primary pulmonary hypertension
4) DCM
5) RV infarction
b. Anatomic
1) Rheumatic
2) Congenital
3) Carcinoid
4) Drug-induced valvulopathy
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Cardiac
5) Endocarditis
6) Injury
7) Miscellaneous other
2. Pathophysiology
a. Backward flow of blood through incompetent tricuspid valve during
ventricular systole
b. Progressive increase in degree of TR leading to RV volume overload
c. Impaired forward cardiac output due to volume of regurgitant flow
d. Heart compensates for volume overload with RV dilatation and
hypertrophy
e. Increased RA pressure causes RA dilatation
f. Process eventually leads to right heart failure
1) Usually asymptomatic for a long period
2) Weakness
3) Fatigue
4) Findings of heart failure
1) Jugular venous distention with prominent v wave
2) Hepatomegaly
3) Pulsatile liver
4) Hepatojugular reflux
5) Peripheral edema
6) Ascites
8) Hyperdynamic RV impulse
1) Holosystolic, blowing mumur; may be accentuated with inspiration
2) Diastolic flow rumble
3) Right-sided S3
4) Paradoxic splitting of S2
5) Loud P2
a. Functional versus anatomic cause
b. RV volume overload (RVVO)
c. Increased RV and RA size
d. Paradoxic septal motion
e. Dilated IVC and hepatic veins
1) Jet size and configuration
a) Jet area to RA area comparison
b) May be deceptive in acute regurgitation: maximal jet area is
limited by small receiving chambers and rapid equalization of
pressures
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Cardiac
2) Direction and eccentricity of jet

3) Color M-mode (to establish timing)
4) Vena contracta
orifice, measured at the time of its largest diameter
b) Not valid in presence of multiple jets
c) Width > 0.7 cm usually denotes severe TR
5) PISA
a) Validated only in small studies
b) Rarely needed clinically
1) Tricuspid inflow E wave velocity
a) Predominant early filling with severe TR
b) E velocity > 1.0 m/sec consistent with severe TR in the absence
of severe diastolic dysfunction
c) Must rule out co-existing stenosis
2) Hepatic vein flow abnormalities
a) Diminution of systolic forward flow occurs with increasing
severity of TR
b) High RA pressure and atrial fibrillation may also cause diminished
systolic forward flow
c) Severe TR may cause systolic flow reversal
c. CW Doppler
2) Velocity of TR is not related to severity of TR
3) Duration of TR signal typically holosystolic
4) Shape of TR Doppler signal
a) Symmetrical shape: reflects mild TR
b) Asymmetrical shape: reflects severe TR (due to rapid increase in
RA pressure
5) Use of the Bernoulli equation to assess RVSP may be unreliable if the
regurgitant orifice is not restrictive
6. Related testing
a. EKG
1) RA enlargement
2) RBBB
b. Chest x-ray
1) RA and RV enlargement
2) Prominent SVC
1) Right heart hemodynamics
7. Common treatment
a. Medical
1) Often none (may be well tolerated for years)
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Cardiac
3) Treatment for right heart failure

b. Surgical
1) Annuloplasty
2) TVR
H. Pulmonary Stenosis (PS) - See Section Congenital Heart Disease
I. Pulmonary regurgitation (PR)

1. Etiology
a. Pulmonary hypertension
b. Endocarditis
c. Congenital abnormalities
d. Carcinoid
e. Rheumatic
2. Pathophysiology
a. Backward flow of blood through an incompetent pulmonary valve during
ventricular diastole
b. Pathologic regurgitation is infrequent and is typically seen in the presence
of significant right heart structural abnormalities
c. Severe hemodynamic compromise due to isolated severe PR is rare
1) May be well tolerated for years
2) Dyspnea
3) Fatigue
1) Palpable RV impulse (right sternal border)
2) Jugular venous distention
3) Hepatomegaly
4) Peripheral edema
5) Ascites
1) Low pitched diastolic murmur
2) Loud P2 with PHN
3) Systolic ejection murmur with severe PR due to increased flow
a. Anatomic cause: abnormalities
1) Cusp number
2) Cusp motion
3) Valve structure
b. Dilated RV, RA, and PA
c. RVVO (paradoxical ventricular septal motion)
d. Diastolic flutter of PV
e. Evidence of PHTN
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Cardiac

a. Color flow Imaging
1) Jet size and spatial orientation
2) Few parameters have been validated
b. PW Doppler
1) RVOT velocity
a) Increased velocity due to increased flow volume
2) Evidence of flow reversal in PA
c. CW Doppler
2) Duration of PR signal is holodiastolic
3) Steep deceleration slope
a) Also influenced by RV diastolic compliance and pressure
4) Assess PAEDP
6. Related testing
a. EKG
1) RVH
2) Right axis deviation
3) RBBB
b. Chest x-ray
1) RV enlargement
2) Enlarged PA
1) Right heart hemodynamics
2) Pulmonary angiography shows diastolic flow reversal into RV
7. Common treatment
a. Medical
1) Often none (may be well tolerated for years)
3) Treatment for right heart failure
b. Surgical
1) Annuloplasty
2) PV replacement
J. Infective Endocarditis
1. Etiology
a. Microbial infection of the endothelial lining of the heart
b. Most common bacterial organisms
1) Streptococcus viridans
2) Staphylococcus aureus
2. Pathophysiology/natural history
a. Occurs primarily on cardiac valves, but may occur on other endocardial
surfaces or intracardiac devices
b. High mortality/complication rate
c. Higher-risk patients
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Cardiac
1) Prosthetic heart valves

2) Native valve disease
3) Congenital heart disease
4) IV drug users
1) Fever
2) Fatigue/weakness
3) Flu-like symptoms
4) Weight loss
1) Vascular phenomena
a) Petechiae
b) Splinter hemorrhages
c) Oslers nodes
d) Janeways lesions
2) Embolic events (systemic or pulmonary)
3) Clubbing
4) Splenomegaly
5) Findings consistent with valve obstruction/regurgitation
1) New or changing murmur
d. Diagnostic criteria
1) Duke major and minor
4. 2-D/M-mode features
a. Echo hallmark: vegetation
b. Common locations
1) Atrial side of MV and TV
2) Ventricular side of AV and PV
3) Secondary jet lesions
c. Less common locations
1) Chordae
2) Mural endocardium
3) Eustachian valve
4) Pacemaker wire
d. Echogenic intracardiac mass
1) Typically irregular shape
2) Pedunculated or sessile
3) Rarely impair valve motion
4) Often flutter or vibrate
e. New valvular regurgitation
f. Secondary effects of valvular regurgitation
g. Abscess
h. New partial dehiscence of prosthetic valve
5. Complications
a. Cusp or leaflet rupture/flail
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Cardiac
b.
Perforation
c.
Abscess
d.
Aneurysm
e.
Fistulae
f.
Dehiscence of prosthetic valve
g.
Pericardial effusion
h.
Hemodynamic compromise
1) Regurgitation (acute or chronic)
2) Valvular stenosis
3) Shunt
4) CHF
i. Embolization
1) Cerebral
2) Systemic
3) Pulmonary
6. Differential diagnosis
a. Nonbacterial thrombotic endocarditis
b. Active versus healed vegetations
c. Lambls excrescences and valve strands
d. Tumors, thrombi
e. Sutures, strands on prosthetic sewing rings
f. Focal, nonspecific thickening or calcium deposits
7. Related testing
a. EKG
1) New conduction abnormalities
2) New arrhythmia
3) Evidence of ischemia or MI (coronary artery embolism)
b. Laboratory testing
1) Anemia
2) Positive blood cultures
c. Chest x-ray
1) Evidence of CHF
d. Role of TEE
1) Greater sensitivity than TTE
2) Intraoperative imaging
8. Common treatment
a. Medical
1) Prevention endocarditis prophylaxis
2) Antimicrobial therapy
b. Surgical
1) Valve repair or replacement
2) Role of echo in timing of surgery
K. Valvular Heart Disease Associated with Systemic Conditions
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Cardiac
1. Systemic lupus erythematosus

a. General
1) Chronic inflammatory disease
2) Valvular involvement often clinically silent
b. Echo findings
1) Mild, nonspecific valve thickening
2) Libman-Sacks endocarditis (nonbacterial thrombotic)
a) Typically only mitral or aortic valves involved
b) Usually small with little independent motion
c) Irregular borders
3) Valve regurgitation
4) Valve stenosis (rare)
5) Sensitivity of TTE low; TEE useful
2. Antiphospholipid syndrome
a. General
1) Hypercoagulability syndrome
2) Valve lesions further increase risk for thromboembolic complications
3) Superadded bacterial endocarditis may occur
b. Echo findings
1) Nonspecific valve thickening
2) Libman-Sacks endocarditis (nonbacterial thrombotic)
3. Rheumatoid Arthritis
a. General
1) Autoimmune disorder
2) Immune system attacks the joints, specifically the synovium (thin layer
of cells that line and lubricate the joints)
b. Echo findings
1) Valvular lesions similar to rheumatoid nodules
2) Leaflet fibrosis, thickening, retraction
4. Ankylosing spondylitis
a. General
1) Chronic systemic inflammatory disorder
2) Primarily affects the axial skeleton (hips and shoulders)
b. Echo findings
1) Nonspecific thickening of aortic and mitral leaflets
2) Thickening of base of anterior mitral leaflet (subaortic bump)
3) Increased echogenicity of posterior aortic wall
L. Prosthetic Valves
1. Classification and characteristics
a. Autograft (Ross procedure)
1) Native pulmonary valve sewn into aortic position
2) Central flow
3) Valve retains ability to grow
4) Trivial or no regurgitation
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Cardiac
5) Very low mean gradient

b. Homograft
1) Human donors
2) Stentless
3) Typically harvested as a block of tissue (aortic valve, root, and
ascending aorta) and trimmed as needed
4) Central flow
5) Trivial or no regurgitation
6) Very low mean gradient
c. Bioprosthetic (tissue)
1) Stented
a) Common examples (porcine)
b) Common examples (bovine pericardium)
c) Central flow
d) Trivial or no regurgitation
2) Stentless
a) Intended for aortic or pulmonary position
b) Common examples (porcine)
c) Very low mean gradient
d. Mechanical
1) Bileaflet
a) Two semicircular disks attached to a rigid valve ring by small
hinges
b) Flaps pivot open 75-90°
c) Common examples
d) Two large lateral and one small central orifice create central flow
e) Least obstructive mechanical prosthesis; allows more laminar
blood flow
f) Normal leakage volume at margin of central discs and at the
periphery between disc and sewing ring
2) Tilting (single) disk
a) Single circular disk rotates within a rigid annulus, with the disk
secured by lateral or central metal struts
b) Common examples
c) Disc tilts from 60-80° to open a major and a minor orifice
d) Low velocity, normal leakage volume; predominantly central with
smaller peripheral jets
3) Ball cage
a) Circular sewing ring with several metal struts that cage a small
hollow ball
b) Blood flows around the spherical occluder
c) Changes in chamber pressure causes ball to move back and forth
d) Least optimal hemodynamics
e) Normal closing volume regurgitation
f) High profile limits use in patients with small ventricles
e. Valve conduits
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Cardiac
1) Mechanical or tissue prosthesis attached to a vessel graft or conduit

2. Tissue versus mechanical prostheses
a. Tissue prostheses
1) Advantages
a) Less obstructive; better hemodynamics
b) Fewer complications due to thromboembolism
c) May not require anticoagulation
2) Disadvantages
a) Less durable than mechanical valves
b) Leaflets may become regurgitant or stenotic due to tissue
degeneration and calcification
c) Limited availability of homografts
b. Mechanical prostheses
1) Advantages
a) Extremely durable
2) Disadvantages
a) Inherently more obstructive
b) Vulnerable to thromboembolism
c) Require anticoagulation
d) May experience catastrophic failure
3. Prosthetic valve dysfunction
a. Prosthetic stenosis/obstruction
1) Prostheses are inherently somewhat obstructive
2) Gradient varies with
a) Valve type
b) Valve size
c) Anatomic position
d) Cardiac output
3) Etiology of obstruction
a) Leaflet changes: thickening or calcification
b) Thrombus or pannus
c) Patient-prosthesis mismatch
b. Prosthetic regurgitation
1) Etiology
a) Leaflet degeneration
b) Prolapse or flail segment
c) Thrombus or pannus
d) Endocarditis
e) Abnormalities in disk or poppet seating or motion
f) Dehiscence
2) Normal prosthetic regurgitation
a) Leakage volume
i. Built-in transvalvular regurgitation of short duration
ii. Decreases incidence of thrombosis
iii. Volume increases with valve size and decreasing heart rate
iv. Low velocity color profile
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Cardiac
v. Multiple color jets related to multiple orifices

b) Closure volume
i. Volume displaced by occluder during closure
ii. Ball cage prosthesis has largest closing volume
3) Abnormal prosthetic regurgitation
a) Transvalvular (prosthetic) regurgitation
i. Abnormal leakage through the valve
ii. Tissue valves tend to leak with age and calcification
iii. May see trivial leakage with a normal tissue prosthesis
iv. Thrombus on mechanical valves may cause regurgitation
b) Perivalvular (periprosthetic) regurgitation
i. Usually eccentric, high velocity and turbulent
ii. Leakage from outside the sewing ring
iii. Usually due to valve bed abnormalities or endocarditis
c. Thromboembolism
1) Higher risk with
a) Mechanical valves
b) Atrial fibrillation
c) Large LA
d) LV dysfunction
d. Hemolysis/anemia
1) Mechanical trauma to red blood cells
2) Some degree present with all mechanical prostheses
3) Periprosthetic leaks, eccentric regurgitant jets, and obstruction are
common culprits
e. Endocarditis
1) Higher risk of SBE in patients with prosthetic valves
2) Prophylaxis recommended
f. Pannus
1) Fibrous ingrowth of tissue
2) Rarely affects tissue prostheses
3) May cause obstruction or regurgitation
4) Disc and bileaflet valves are particularly prone
g. Prosthetic structural failure
1) Poppet/cage variance
2) Strut fracture
3) Valve degeneration or calcification of tissue valves
h. Valve bed abnormality often a complication of endocarditis
1) Pseudoaneurysm
2) Ring abscess
3) Fistula
4) Dehiscence
4. Echocardiographic assessment
a. Should include assessment of all cardiac chambers and other valves for
incidental evidence of normal or abnormal prosthetic valve function
b. Imaging challenges
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Cardiac
1) Acoustic shadowing or artifacts from mechanical prosthesis or struts

2) May require multiple, unconventional imaging planes and extensive
image adjustment
3) Consider use of TEE, especially for mitral prostheses
c. Patient should have baseline echo within 30 days of valve replacement to
fingerprint the prosthesis
d. Serial studies
1) Compare to fingerprint echo
2) Assess for obstruction, regurgitation, or complications
e. Clues to prosthetic dysfunction
1) High or increasing gradient
2) Decreased valve area
3) Increased intensity of CW Doppler signal
4) Progressive chamber dilatation
5) Recurrent or unexplained pulmonary hypertension
6) Flow convergence on LV side of MV
7) Intermittent flow variations
5. 2-D assessment
a. Cardiac chamber size and function
b. Stability of sewing ring
1) Stable versus excessive or rocking motion
c. Evidence of obstruction or regurgitation
1) Reduced occluder, cusp or leaflet motion
2) Abnormal thickening or calcification of leaflets
3) Flail leaflet
d. Extraneous echoes
1) Pannus
2) Thrombus
3) Suture material
4) Vegetation
5) Remnants of native valve apparatus
e. Valve bed abnormalities
1) Abscess
2) Pseudoaneurysm
3) Fistula
6. Color flow Doppler
a. Identify presence and severity of valvular or perivalvular regurgitation
7. Doppler assessment (general comments)
a. Assess prosthesis as if a stenotic native valve
b. Use multiple transducer positions (parallel to flow)
c. Indicate window from which the optimal Doppler signals were obtained
d. Average 3-5 beats in sinus rhythm, 8-10 in atrial fibrillation
8. Doppler assessment of aortic valve prosthesis
a. Measure peak prosthetic velocity
b. Measure mean gradient (more useful than maximal gradient)
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Cardiac
1) If LVOT velocity is elevated (high-output state), LVOT mean gradient

should be subtracted from prosthetic mean gradient
2) Average gradients (patient-to-patient variability)
a) Stented heterograft, tilting disk and bileaflet 13-15 mmHg
b) Starr-Edwards 23 mmHg
c) Homograft 8 mmHg
c. Calculate prosthetic effective orifice area (EOA)
1) Use continuity equation as if calculating AV area
2) Measure LVOT diameter in parasternal long-axis view
a) Measure LVOT diameter (insertion of sewing ring to ventricular
septum and anterior mitral leaflet) during systole
b) May use sewing ring diameter of prosthesis, but less accurate
c) Note use of measured LVOT diameter or sewing ring
approximation in report
3) Measure LVOT velocity and TVI with PW Doppler
a) Place PW sample volume below region of flow convergence
(usually about 1 cm below prosthesis)
b) Trace signal to obtain velocity and TVI
4) Measure peak prosthetic velocity and TVI with CW Doppler from
multiple windows
5) Calculate LV stroke volume and EOA
Aortic prosthetic EOA = LVOT diameter2 x 0.785 x LVOT TVI
Aortic prosthetic TVI
d. Dimensionless obstructive index (DOI)
1) May use if unable to measure LVOT diameter
DOI = LVOT TVI
Aortic prosthetic TVI
2) DOI < 0.20 is consistent with obstruction if the sewing ring diameter is
< 23 mm
e. Intraventricular gradients
1) May occur after surgery for AVR
2) Due to hemodynamic change - reduction of afterload in a small,
hypertrophied ventricle
f. Interpretation of Doppler data
1) Need initial post-operative or pre-dismissal echo, then serial echo
2) Consider valve type and size
3) Consider EOA
9. Doppler assessment of MV prosthesis
a. Measure E and A velocities of mitral inflow by CW Doppler
b. Measure mean gradient by CW Doppler
1) Related to heart rate and flow
2) Mean gradient for mitral prosthesis averages 4-5 mmHg at normal
heart rate
c. Calculate prosthetic effective orifice area (EOA) using continuity equation
(if no significant MR or AR)
Mitral Prosthetic EOA = LVOT diameter2 x 0.785 x LVOT TVI
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Cardiac
Mitral prosthetic TVI

d. Measure pressure half-time
1) This method may overestimate EOA of normal prosthesis
2) Useful value for comparison in subsequent echoes
a) Mitral Prosthetic EOA = 220/PHT
e. Calculate pulmonary artery pressure
f. Interpretation of Doppler data
1) Compare to baseline post-operative echo
2) Consider valve type and size
3) Consider mean gradient in relation to heart rate
4) Excessive increase in mean gradient or PAP with exercise
5) Consider EOA
10. Doppler assessment of tricuspid valve prosthesis
a. CW Doppler (average 5-10 signals due to respiratory variation)
1) E and A velocities
2) Mean gradient (averages 2-3 mmHg)
3) Pressure half-time
4) Pulmonary artery pressure
11. Assessment of prosthetic/periprosthetic valve regurgitation
a. Surface echo can usually adequately assess aortic prosthetic regurgitation,
but not mitral prosthetic regurgitation
b. Two-dimensional echo
1) Assess chamber sizes and function
2) Determine etiology of regurgitation
c. Color Flow Doppler
1) Determine whether regurgitation is valvular or perivalvular
2) Note presence of eccentric jet
3) Look for flow convergence on the ventricular side of MV prosthesis
4) Use multiple imaging planes and non-standard views
d. PW Doppler
1) Mitral deceleration time (AR)
2) Assess diastolic flow reversal TVI in descending or abdominal aorta
(AR)
3) Note presence of systolic flow reversals in pulmonary veins (MR)
e. CW Doppler
1) Note velocity, intensity, and duration of regurgitant signal
2) Note change in velocity, gradient, or pressure half-time from prior
echo
3) Calculate PA pressure
f. Quantitate regurgitation if possible
12. Role of transesophageal echocardiography (TEE)
a. May be useful if surface study suboptimal
b. Difficult to assess mitral prosthetic regurgitation by surface echo due to
shadowing
c. TEE probe is on atrial side of MV prosthesis, so mitral prosthetic
regurgitation can be more clearly defined
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Cardiac
d. Intraoperative assessment
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Cardiac
SECTION VIII: Cardiomyopathies
1. Discuss the echocardiographic features associated with hypertrophic cardiomyopathy

(HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), and
arrhythmogenic RV dysplasia
2. Differentiate between the echocardiographic features of cardiomyopathies
3. Differentiate between primary and secondary etiology in DCM
4. List common infiltrative systemic myocardial diseases
VIII. Cardiomyopathies
A. Hypertrophic Cardiomyopathy
1. Epidemiology
a. Prevalence
b. Associated risk factors for sudden death
c. Genetics
2. Etiologies
3. Clinical presentations
c. Auscultatory finding
4. Types/varied patterns
a. Classic - asymmetric septal hypertrophy (ASH)
b. Midventricular
1) With apical aneurysm
2) Without apical aneurysm
c. Apical
d. Concentric
e. Other
5. Provocative maneuvers
a. Standing
b. Valsalva
c. Amyl nitrate
6. 2-D features
a. Small or normal LV cavity
b. Normal or hyperdynamic LV function
c. Extent of hypertrophy
d. Mitral apparatus
1) Systolic MV anterior motion (SAM)
a) One or both leaflets
b) Degree
c) Mechanism
i. Venturi effect
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Cardiac
ii. Anterior papillary muscle displacement and elongation

d) Other situations
i. MV repair
ii. AV replacement
iii. Hypovolemia
iv. Endogenous and exogenous catecholamines
2) Elongated anterior mitral leaflet (AML)
3) Increased area of AML
4) Calcified mitral annulus
e. LA enlargement
f. Narrowed LVOT diameter
g. Altered texture of myocardium
h. Basal septal endocardial thickening (contact lesion)
7. M-mode features
a. Normal or small LV size
b. Extent of hypertrophy
c. Normal or increased shortening fraction
d. LA enlargement
e. Abnormal MV motion
1) Reduction of E-F slope
2) SAM of leaflet
3) Mitral annular calcification
f. B-bump
g. AV mid-systolic closure
h. Color M-Mode of MV and LVOT obstruction
8. Doppler features
a. Diastolic dysfunction assessment
1) Characteristics
a) Impaired relaxation
b) Decreased compliance
c) Increased LVEDP
d) Decreased EA ratio
e) Normal filling pattern
i. Normalization by MR
ii. Normalization by increased LA pressure
2) Poor correlation between DT and LA pressure
3) Presumed cause of symptoms in patients with no obstruction
b. MR with or without SAM present
1) MR likely seen with obstructive SAM
2) Eccentric
a) Posterolateral
b) Late systolic
3) Primary MR versus secondary MR
c. Level of obstruction (LVOT versus midcavity
1) Doppler wave patterns
a) Late peaking
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Cardiac
b) Reliably assessed by Bernoulli equation

2) Provocative maneuvers
9. Limitations and pitfalls
a. Differential diagnosis
1) Chronic hypertension
2) Cardiac amyloid
3) Pheochromocytoma
4) Freidreichs ataxia
5) Inferior MI with previous LVH
b. Dynamic LVOT obstruction not specific
1) Hyperdynamic LV systolic function
a) Anemia
b) Volume depletion
c) Catecholamines
2) Hypertensive HCM in elderly
3) Postoperative period
4) Sub aortic obstruction post AVR
5) Acute anteroapical MI with pre-existing basal septal hypertrophy
10. Related testing
a. EKG
c. Correlative imaging
11. Common treatments
a. Role of echo
1) Evaluation of therapy
2) Pacemaker implementation and therapy
3) Septal ablation
4) Myotomy/myectomy
B. Dilated Cardiomyopathy
1. Epidemiology
a. Prevalence
b. Genetics
2. Etiologies
4. 2-D features
a. Chamber enlargement
b. Hypokinesis of LV
c. Regional wall motion abnormality
d. Mural thrombi in apex or aneurysm
e. Spontaneous echo contrast
5. M-mode features
a. Chamber dilation
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Cardiac
b. Hypokinesis of LV
c. Decreased LV wall thickening
d. Decreased fractional shortening
e. Increased EPSS
f. Reduced aortic root motion
g. Reduced ejection fraction
6. Doppler features
a. MR and TR assessment
b. Diastolic dysfunction assessment
c. RV systolic pressure assessment
d. LVEDP assessment
7. Prognostic role of echo
a. EF
b. DT
c. RV function
8. Related testing
a. EKG
9. Common treatments
C. Restrictive/Infiltrative Cardiomyopathy
1. Etiologies of restrictive cardiomyopathy
a. Primary
1) Idiopathic
b. Secondary
1) Amyloid heart disease
2) Hemochromatosis
3) Heart muscle disease
a) Post-irradiation heart disease
b) Carcinoid heart disease
c) Doxorubicin/daunorubicin toxicity
d) Progressive systemic schlerosis
4) Eosinophilic endomyocardial disease
2. Classifications of infiltrative CM
a. Infiltrative
1) Insterstitial
a) Amyloid
b) Hemochromatosis
c) Sarcoid
d) Malignancy
2) Storage
a) Glycogen
b) Lipid
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4. 2-D features
a. Diffuse speckling or granular appearance of myocardium (amyloid)
b. Pericardial or pleural effusion
c. Bi-atrial enlargement
d. Small to normal LV cavity
e. Possible LVH
f. Normal systolic function
5. M-mode features
a. Normal LV size
b. Concentric LVH
c. Decreased LV shortening fraction
d. Pericardial or pleural effusion
6. Doppler features
a. MR and TR assessment
b. Diastolic dysfunction assessment including DTI
c. Minimal or absent respiratory variation in Doppler flows
a. Constrictive pericarditis
8. Related testing
a. EKG
9. Common treatment
D. Arrhythmogenic RV Dysplasia
1. Etiology
2. Characteristics
a. Loss of RV myocardium with fatty or fibro-fatty replacement of tissue
b. Associated with ventricular arrhythmia
c. Associated with sudden death in young
4. 2-D features
a. Dilated RV
b. Aneurysm, outpouching of the RV
c. Focal RV wall thinning
d. RV wall motion abnormality
e. Abnormal RV muscle composition
5. Other arrhythmogenic RV cardiomyopathies
a. RVOT tachycardia
b. Benign extrasystoles
c. Uhls anomaly
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d. Biventricular dysplasia
6. Related testing
a. EKG
7. Common treatment
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SECTION IX: Systemic and Pulmonary Hypertensive Heart Disease
1. Explain the pathophysiology of systemic hypertensive disease

2. Explain the pathophysiology of pulmonary hypertensive disease
3. List classifications of pulmonary hypertension
4. Describe the echocardiographic features associated with systemic and pulmonary
hypertensive disease
5. Define Eisenmengers Syndrome
IX. Systemic and Pulmonary Hypertensive Heart Disease
A. Systemic Hypertension
1. Etiology and risk factors
2. Pathophysiology
a. Increased afterload leads to left ventricular hypertrophy (LVH) and
increased mass
b. Ventricular hypertrophy leads to diastolic dysfunction
3. 2-D and color flow features
a. Increased LV mass and mass index
b. Concentric LVH
c. Normal or hyperdynamic ejection fraction (early)
d. Dynamic LVOT or mid-cavitary obstruction
e. LA enlargement due to increased left ventricular end-diastolic pressure
(LVEDP)
f. Aortic root dilatation
g. MAC with associated mitral regurgitation
h. AV sclerosis with associated AR
4. Diastolic abnormalities
a. Abnormal relaxation
1) Early
2) Minimal or no symptoms at rest
b. Pseudonormalization
1) Later
2) Minimal or no symptoms at rest
3) Symptoms with mild/moderate exertion
c. Restrictive filling
1) Significantly elevated LV pressure
2) Symptoms at rest or with minimal exertion
5. Prognostic value of echocardiography
6. Complications of hypertension
7. Treatment
B. Pulmonary Hypertension (PHTN)

1. Definition
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a. Pulmonary artery systolic pressure (PASP) > 25 mm Hg at rest or > 30

mmHg with exercise
2. Etiology
a. Primary
b. Secondary
3. Pathophysiology
a. Response of RV to chronic pressure overload is right ventricular
hypertrophy (RVH) and dilatation
4. Classification
a. Pulmonary arterial hypertension
b. Pulmonary venous hypertension
c. PHTN associated with hypoxemia
d. PHTN due to chronic thorombotic and/or embolic disease
e. Miscellaneaous
5. Echocardioraphic features
a. RV enlargement and hypertrophy
b. Dilated PA and branches
c. RA enlargement
d. Decreased RV systolic function (late)
e. D-shaped LV in short axis view
f. Paradoxical septal motion
g. Mid-systolic closure of PV
h. Dilated IVC and hepatic veins
i. TR and PR secondary to annular dilatation
j. Elevated PASP and PAEDP
6. Eisenmengers Syndrome
a. Reversal of intracardiac shunt from left-to-right to right-to-left secondary
to severe pulmonary hypertension
7. Cor pulmonale
a. Acute (pulmonary embolism)
b. Chronic
8. Prognostic value of echocardiography
9. Treatment
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SECTION X: Pericardial Diseases
1. List key etiologies of pericardial disease

2. Explain the pathophysiology and hemodynamics of cardiac tamponade and
constrictive percarditis
3. Describe key echocardiographic features of cardiac tamponade and constrictive
pericarditis
4. Explain Doppler criteria associated with cardiac tamponade and constrictive
pericarditis
5. Describe key echocardiographic features of congenital absence of the pericardium
X. Pericardial Diseases
A. Normal Pericardium
1. Structure
2. Function
B. Pericarditis/Pericardial Effusion
1. Etiologies
3. Echocardiographic Features
a. Echo-free space
b. Variable size and location
4. Differentiation from pleural effusion, epicardial adipose, and other posterior
echo-free spaces
5. Treatment
C. Cardiac Tamponade
1. Etiologies
1) Chest pain
2) Dyspnea
1) Tachycardia
2) Narrow pulse pressure
3) Pulsus paradoxus
4) Elevated jugular venous pressure (JVP)
5) Becks triad
d. ECG findings
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e. Correlative imaging
3. Hemodynamics
a. Accumulation of pericardial fluid causes pericardial pressure to rise and
compromise systemic venous return in right atrium
b. Ventricular filling is impaired and cardiac output is decreased
c. Intrapericardial pressure is influenced by both volume of fluid and rate at
which it accumulates
d. Dissociation of intrathoracic and intracardiac pressures due to insulating
effect of effusion
e. Relatively fixed combined cardiac volume (ventricular interdependence)
4. Echocardiograpic features
a. Pericardial effusion
b. RV or RA chamber collapse
c. IVC plethora
d. Reciprocal changes in ventricular volumes (septal shift)
e. Swinging heart if large effusion
5. Doppler features
a. Respiratory variation in velocities
b. Inspiration
1) Decreased mitral E velocity
2) Decreased pulmonary venous diastolic forward flow
3) Increased tricuspid E velocity
c. Expiration (reciprocal changes)
1) Increased mitral E velocity
2) Increased pulmonary venous diastolic forward flow
3) Decreased tricuspid E velocity
4) Decrease or loss of hepatic vein diastolic filling with marked
expiratory reversal
d. Technical caveats
1) Use of respirometer preferred
2) Typical respiratory patterns are reversed in a mechanically ventilated
patient
3) Changes may not be seen in patients with high filling pressures, ASD
or RVH
6. Echo-guided pericardiocentesis
a. Treatment of choice
1) Locate optimal site of puncture
2) Determne depth of pericardial effusion and distance from pucture site
to effusion
3) Confirm position of needle by use of agitated saline
b. Pigtail catheter introduced and left in for several days with intermittent
drainage
c. Low complication rate
D. Constrictive Pericarditis
1. Etiology
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a. May develop in the aftermath of virtually any pericardial injury or

inflammation
1) Dyspnea
2) Chest pain
1) Jugular venous distention
2) Edema
3) Ascites
4) Kussmaul sign
5) Pulsus paradoxus
6) Hepatosplenomegaly
1) Pericardial knock
d. ECG findings
e. Correlative imaging
3. Pathophysiology and hemodynamics
a. Thickened and/or fibrotic pericardium externally constrains diastolic
filling of the heart
b. Elevated diastolic pressures
c. Rapid early diastolic filling that stops abruptly as limit of ventricular
expansion is achieved
d. Fibrotic pericardium prevents full transmission of intrathoracic pressure
changes (dissociation of intrathoracic and intracardiac pressures)
e. Exaggerated ventricular interdependence
4. 2-D/M-mode features
a. Thickened pericardium
b. Normal LV size and EF
c. Respiratory variation in ventricular size
d. Enlarged atria
e. Flattening of LV posterior wall in diastole
f. Abrupt posterior motion of ventricular septum in early diastole (septal
bounce)
g. Dilated IVC and hepatic veins
h. Ascites
5. Doppler features
a. Respiratory variation in velocities
b. Mitral inflow pattern typically restrictive
c. Inspiration
1) Decreased mitral E velocity
2) Decreased pulmonary venus diastolic forward flow
3) Increased tricuspid E velocity
d. Expiration (reciprocal changes)
1) Increased mitral E velocity
2) Increased pulmonary venous diastolic forward flow
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3) Decreased tricuspid E velocity

4) Decreased or loss of diastolic filling with marked expiratory reversal
e. Tissue Doppler
1) Em velocity relatively normal or accentuated in constriction (> 12
cm/sec)
f. Technical caveats
1) Use of respirometer preferred
2) Typical respiratory patterns are reversed in a mechanically ventilated
patient
3) Changes may not be seen in patients with high fillng pressures, ASD,
or RVH
6. Diffenentiating constriction from other disorders
a. Restriction
1) Lack of respiratory variation
2) Tissue Doppler Em velocity is reduced
3) E/Em ratio is increased
4) Color M-mode shows prolonged slope
b. COPD or obesity
1) Prominent increase in SVC forward flow during inspiration
2) Mitral inflow not typically restrictive
3) Hepatic vein flow not characteristic of constriction
7. Pitfalls
a. High filling pressure
b. Sample volume placement (translational motion)
c. Atrial fibrillation
d. Localized constriction
8. Treatment
a. Pericardiectomy
E. Other Pericardial Disease

1. Tumors
a. Types
1) Primary
2) Metastatic
b. Characteristics
c. Echocardiographic features
1) Variable
2) Most often multiple
d. Associated findings
1) Pericardial effusion
2. Pericardial cyst
a. Characteristics
b. Echocardiographic features
1) Echolucent space
2) Frequently adjacent to RA
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F. Congenital Absence of Pericardium

1. General
a. Uncommon
b. More frequent in males
2. Types
a. Total absence
b. Partial absence
a. Unusual echo windows
b. Cardiac hypermobility
c. Marked shift of cardiac chambers to the right
d. Abnormal ventricular septal motion
4. Complications
a. Herniation or strangulation of left atrial appendage with partial absence
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SECTION XI: Cardiac Tumors/Masses
1. List benign and malignant cardiac tumors

2. Describe echocardiographic criteria used for evaluating tumors
3. Differentiate cardiac tumors from cardiac structures
4. List potential sources of artifactual echoes within the chambers
XI. Cardiac Tumors/Masses
A. Thrombus
1. Echocardiographic characterization
a. Location and site of attachment
b. Size
c. Degree of mobility
d. Shape
e. Coexisting cardiac abnormalities
2. Potential for embolization
a. Size
b. Protrusion into cavity
c. Mobility
3. Technical suggestions
a. Use high-frequency, short-focus transducers
b. Decrease depth of field
c. Move focal zone nearer apex
d. Use nonstandard views
e. Use contrast
4. Pitfalls
a. Artifact
b. Must differentiate from prominent trabeculations, papillary muscles,
anomalous chords
c. Laminated (nonprotruding) thrombi more difficult to appreciate
5. LV thrombus
a. Predisposing conditions
1) Underlying regional wall motion abnormalities
2) LV aneurysm
3) Diffuse LV systolic dysfunction
1) Contour distinct from endocardial border
2) Often more echogenic than underlying myocardium
3) Located in region of abnormal wall motion
6. LA and LAA thrombus
a. Predisposing factors
2) MS
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3) Prosthetic MV
4) LA enlargement
b. Association with spontaneous echo contrast
c. TEE more sensitive than TTE
d. Clinical significance
1) Increased risk of thromboembolism
2) Relative contraindication to balloon mitral valvotomy
3) Relative contraindication to cardioversion
7. RA thrombus and thrombus-in-transit
a. Predisposing factors
2) RA enlargement
3) Catheters, pacemakers
b. Clinical significance
1) Embolization (pulmonary or paradoxical)
2) Thrombi on catheters, pacemakers have potential for infection
c. Often a popcorn appearance
d. Need to distinguish from
1) Congenital remnants (Eustachian valve, Chiari network)
2) Reverberation artifacts
3) Lipomatous hypertrophy of atrial septum
8. RV thrombus
a. Relatively uncommon
9. Treatment
a. Anti-coagulation
b. Thrombolytics
c. Thrombectomy
B. Primary
1. Benign
a. Myxoma
b. Papillary fibroelastoma
c. Fibroma
d. Rhabdomyoma
e. Lipoma
f. Hemangioma
g. Miscellanoues others
2. Malignant
a. Sarcomas
b. Mesothelioma
c. Malignant lymphoma
d. Miscellaneous others
3. Characteristics
a. Etiology
b. Clinical presentation
1) Signs and symptoms
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2) Physical findings
3) Auscultatory finding
c. Common locations
a. Occur more frequently in right heart
b. Sessile, with intracavitary extension
C. Secondary (metastatic)
1. Most often metastasize to pericardium with associated effusion
2. Myocardial invasion, intracavitary extension
3. Occur more frequently in right heart
4. Tumors invading right heart from IVC
a. Renal cell carcinoma
b. Hepatoma
c. Uterine tumors
5. Characteristics
a. Etiology
b. Clinical presentations
2) Physical findings
3) Auscultatory findings
D. Role of Echocardiography
1. Location
2. Tumor characteristics
a. Morphology
b. Single or multiple
c. Size
d. Degree of mobility
e. Point of attachment
3. Effect on cardiac and valvular function
4. Limitations
a. Inability to determine histology
b. Limited acoustic access in some patients
c. Limited field of view (mediastinum, adjacent structure)
d. Differential diagnosis
E. Differentiation from Other Masses

1. Extracardiac
a. Cysts
1) Mediastinal
2) Pancreatic
3) Pericardial
4) Bronchogenic
b. Hematoma
c. Thymoma
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d. Teratoma
e. Diaphragmatic or hiatal hernia
f. Aorta
2. Intracardiac
a. Crista terminalis
b. Congenital remnants
c. Trabeculations
d. Moderator band
e. Papillary muscles
f. Redundant chordae
g. Myxomatous tissue
h. Vegetations
i. Tuberculomas
j. Lipomatous hypertrophy of the atrial septum
k. Mitral annular calcification
l. Chiari network
m. Eustachian valves
n. Catheter or pacemaker wire
o. Others
3. Artifacts
a. Side lobes
b. Reverberation
c. Improper gain settings
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SECTION XII: Diseases of the Aorta
1. Describe echocardiographic features associated with Marfan syndrome

2. List the etiologies of aortic aneurysm and dissection
3. Describe three classifications of dissection
4. Explain the echocardiographic features of aortic aneurysm and sinus of Valsalva
aneurysms
XII. Diseases of the Aorta
A. Marfan Syndrome
1. Etiology
1) Cardiac manifestations
2) Non-cardiac manifestations
3. 2-D features
a. Aortic root dilatation
1) Dilated aortic annulus
2) Dilated Sinuses of Valsalva
b. Dilated ascending aorta
c. Annuloaortic ectasia
d. Aortic dissection
e. Myxomatous mitral valve and mitral valve prolapse
4. Doppler features
a. AR
b. MR
5. Related testing
a. EKG
6. Management
B. Aortic Aneurysm
1. Definition: dilatation of aorta with intact vessel layers (intima, media,
adventitia)
2. Etiology
a. Atherosclerosis
b. Medial degeneration
1) Annuloaortic ectasia
2) Marfan syndrome
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3) Associated with bicuspid aortic valve

4) Other heritable disorders
c. Trauma
d. Syphilis
e. Mycotic
f. Noninfectious aortitis
g. Aortic dissection with dilatation of persisting false lumen
a. Signs and symptoms (often asymptomatic)
4. Classification
a. Morphology
1) Fusiform
2) Saccular
b. Location
1) Ascending
2) Arch
3) Descending
4) Thoracoabdominal
5. Goal of imaging
a. Confirm or exclude diagnosis
b. Measurement of diameter and length
c. Determine involvement of aortic valve or arch vessels
d. Differentiate from aortic dissection
e. Detect mural thrombus
a. Aortic dilatation
b. Aortic regurgitation
c. Diastolic flutter of mitral valve with significant AR
d. Flow in false lumen if dissected
7. Role of TEE
8. Complications
a. Aortic regurgitation
b. Aortic rupture
1) Pericardium
2) Left pleural space
c. Aortic dissection
d. Thromboembolism
e. Compression of adjacent structures
9. Related testing
a. EKG
10. Management
a. Medical
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b. Surgical
1) Time of operation controversial
2) Depends on many factors: cause, size, rate of change
c. Endovascular stenting
d. Serial imaging
C. Aortic Dissection
1. Definition: A tear in the intima through which a column of blood enters the
aortic wall, destroying the media and stripping the intima from the adventitia
in a longitudinal fashion
2. Etiology: same as for aneurysm
1) Chest pain, typically radiating to the back, sudden onset, unremitting
2) Shock/hypotension
4. Classifications
a. Stanford Types A and B
b. DeBakey Types I, II, III
a. Intimal flap
b. True lumen versus false lumen (2D and color flow)
c. Possible LV enlargement
d. Thrombus in the false lumen
e. Effusion
f. Increased aortic wall thickness (Intramural hematoma)
g. Aortic regurgitation due to
2) Asymmetric dissection causes incomplete coaptation
3) Dissection into commissure causes incomplete coaptation
4) Intimal flap prolapses through AV
h. Pericardial and/or pleural effusion
i. Compression of LA
j. RWMA with coronary ostia involvement
6. Goal of imaging
a. Confirm or exclude diagnosis
b. Determination of location, characteristics, and extent of dissection
c. Presence, severity, and mechanism of AR
d. Presence of pericardial or pleural effusion
e. Involvement of coronary arteries or branch vessels
f. Detection of rupture
7. Role of TEE
a. Diagnostic procedure of choice
b. Advantages
c. Limitations
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Cardiac
a. Reverberations, catheters
b. Mirror-image artifacts
c. Hemiazygous sheath
d. Thoracic aortic aneurysm with thrombus
9. Related testing
a. EKG
10. Management
a. Medical
b. Surgical
c. Endovascular stenting
D. Sinus of Valsalva Aneurysm

1. Types and location
a. Right coronary sinus (most common)
b. Noncoronary sinus
c. Left coronary sinus
d. Many variations
e. May present as ruptured or unruptured
2. Etiology
a. Congenital
b. Trauma
c. Infective endocarditis
d. Syphilis
e. Marfan syndrome
a. Signs and symptoms (ruptured)
1) Dyspnea
2) Chest pain
3) Gradual onset and progression of symptoms
1) Wide pulse pressure
1) Almost continuous murmur
4. Associated congenital anomalies
a. Round or fingerlike (windsock) outpouchings
b. Dilatation of one or more sinuses
c. Abnormal dilatation of one or more of the sinuses; most often the right
d. TV systolic flutter
e. High velocity systolic/diastolic flow pattern with color and CW Doppler
f. Compression of adjacent structures
6. Complications
a. Rupture into cardiac chamber
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b.
RVOT obstruction
c.
Endocarditis
d.
AR
e.
TR
f.
Erosion into ventricular septum
g.
Obstruction of adjacent structures
1) Coronary artery compression
2) SVC obstruction
3) TS
7. Serial evaluation of unruptured aneurysm
8. Related testing
a. EKG
9. Management
a. Medical
b. Surgical
E. Other Aortic Pathology

1. Aortic atherosclerosis
2. Aortic pseudoaneurysm
3. Penetrating aortic ulcer
4. Aortic hematoma
5. Traumatic injury of the aorta
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SECTION XIII: Normal and Altered Electrical Activation
1. Describe normal electrical pathways

2. Define normal electrical wave forms seen on EKG
3. Describe echocardiographic findings associated with altered electrical activation
4. Identify abnormal EKG tracings
5. Recognize abnormal ECG tracing
XIII. Normal and Altered Electrical Activation
A. Normal Electrical Activation

1. Electrical pathways
a. Sino atrial (SA) node
b. Atrio ventricular (AV) node
c. Bundle of His
d. Left and right bundle branches
e. Purkinje fibers
2. Electrical waves, intervals, and segments
a. P wave
b. QRS
c. T wave
d. U wave
e. P-R interval
f. Q-T interval
g. QT segment
h. ST segment
B. Altered Electrical Activation

1. Electrocardiographic features
a. Left bundle branch block (LBBB)
b. Right bundle branch block (RBBB)
c. Wolff-Parkinson White (WPW)
d. Ischemic changes
1) ST segment depression
2) ST segment elevation
3) Q waves
e. Arrhythmias
1) Premature ventricular contraction
2) Premature atrial contraction (PAC)
3) Sinus arrhythmia
4) Supraventricular tachycardia
5) Quadgeminy, trigeminy, bigeminy
6) Atrial flutter
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8) Ventricular tachycardia
9) Ventricular fibrillation
10) Junctional
f. Heart block
1) First degree AV block
2) Second degree AV block
3) Wenckebach, mobits I, II
4) Complete heart block
g. Pacemaker
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SECTION XIV: Congenital Heart Disease
1. Describe echocardiographic findings associated with various types of congenital heart

disease
2. Discuss clinical signs and symptoms associated with congenital heart disease
3. Explain how the segmental approach is utilized to identify and characterize
congenital heart disease see embryology section
4. Describe how the echocardiography exam is tailored for each type of congenital heart
disease listed in this outline
5. List the parameters used in qualitative and quantitative assessment of congenital heart
disease for each type described in this outline
6. Describe common surgical repairs seen in the adult patient
XIV. Congenital Heart Disease
A. Segmental Approach (see Embryology Section)
B. Anomalies of Position
1. Dextroposition
a. Heart displace to the right due to a mass (space occupying lesion) in the
left chest
2. Dextroversion
a. Most common form of dextrocardia
b. Usually associated with atrial-ventricular discordance and ventricular
arterial discordance
3. Mirror image dextrocardia
a. Type 1
1) Situs inversus totalis
2) Normal heart
b. Type 2
1) Atrial - ventricular concordance
2) Ventricular arterial discordance
3) Rare
c. Type 3
1) Atrial - ventricular discordance
2) Ventricular arterial discordance
d. Type 4
1) Atrial - ventricular discordance
2) Ventricular arterial concordance
3) Inverted normally related great vessels
4) Rare
4. Assessment of dextrocardia
a. Determine the site of the apex
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b. Determine direction apex is pointing with reference to long-axis of the

heart
5. Imaging technique
a. Parasternal long axis
1) Transducer orientation known by identifying long axis of heart and
orienting the orientation mark superiorly
2) Superior direction should be demonstrated towards the right side of the
monitor
3) Inferior direction should be demonstrated on the left side of the
monitor
b. Parasternal short axis
1) Rotate transducer 90 degrees clockwise from parasternal long axis
view
2) Right sided monitor should always display left sided structures
3) Left sided monitor should always display right sided structures
4) Orientation marker directed to the left
5) Determine systemic atrium
6) Determine pulmonic atrium
7) determine morphologic RA
8) Determine morphologic LA
9) Determine PA
10) Determine Aorta
11) Determine right/left and anterior/posterior relationship of morphologic
RV to morphologic LV
c. Apical
1) Orientation directed towards the left
2) Verify morphological RA, RV, LA, LV
3) Verify great vessel relationship
4) Verify left/right and anterior/posterior relationships of RA,RV,LA,LV
d. Subcostal cardiac views
1) Orientation marker for coronal views directed to the left
2) Orientation marker for sagittal views directed 90 degrees clockwise to
coronal views
3) Verify morphological RA, RV, LA, LV
4) Verify great vessel relationship
5) Verify left/right and anterior/posterior relationships of RA,RV,LA,LV
e. Subcostal abdominal views
1) Orientation marker to the left for transverse views
2) Orientation marker superior for sagittal views
3) Identify IVC and follow course of IVC
4) Evaluate for dilated veins posterior to the aorta which may indicate
interruption of the IVC and dilated azygous and hemiazygous veins
f. Suprasternal notch views
1) Orientation marker same as levocardia
2) Orientation marker to left clavicle for left arch
3) Orientation marker to right clavicle for right arch
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Cardiac
4) Orientation marker for suprasternal short axis arch same as levocardia

a) Evaluate pulmonary venous return
b) Evaluate systemic venous return from superior body
c) Evaluate arch side
C. Anomalies of Venous Return

1. Anomalies of systemic venous return - SVC
a. Left SVC draining into RA via coronary sinus
b. Left SVC draining into LA
c. Levoatrial cardinal vein
d. Right SVC to LA
e. SVC aneurysm
2. Anomalies of systemic venous return IVC
a. Interruption of the IVC
1) Absence of hepatic segment with azygous vein continuation
2) Absence of the abdominal segment with hemiazygous continuation
3) IVC draining into LA
3. Total anomalous systemic venous return
a. Absence of right SVC
b. Absence of hepatic segment of IVC
1) Blood flows from IVC to azygous vein to left SVC to LA
2) Hepatic veins drain into LA
3) Common atrium
4. Anomalies of pulmonary venous return
a. Supracardiac
1) Pulmonary veins drain into an anomalous vertical vein and into the
SVC
2) Echocardiogram findings may demonstrate an enlarged SVC, RA, RV,
and main pulmonary artery
b. Intracardiac
1) Pulmonary venous drainage into the coronary sinus
2) Echocardiogram findings demonstrate the whale tail sign
a) Demonstrated in subcostal coronal and sagittal images
c. Infracardiac
1) Evaluate for vertical vein obstruction as it connects to the systemic
vein in the abdomen or as it crosses the diaphragm
d. Echocardiographic assessment for anomalous pulmonary venous return
1) Look for a confluence of all four pulmonary veins superior
(supracardiac), posterior (intracardiac) or inferior (infracardiac) to the
LA
2) Venous flow going away from the heart in a vertical vein
e. Echocardiographic assessment postoperative repair
1) Evaluate for flow obstruction at anastomosis of pulmonary veins to
LA, pulmonary vein orifices and pulmonary veins
5. Anomalies of innominate vein
a. Courses posterior to the aorta (retroarota)
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Cardiac
b. Echocardiogram suprasternal notch long and short axis views

c. demonstrate this finidng
6. Anomalies of the coronary sinus
a. Varying degrees of unroofing of coronary sinus with out a left SVC
b. Varying degrees of hypoplasia
D. Anomalies of the Atria

1. Atrial septal defect (ASD)
a. Etiologies
1) Patent foramen ovale
a) Found in 25% of population
b) Overlapping of a large foramen secundum and/or foramen ovale
c) Located in the fossa ovalis region
2) Secundum
a) Most common adult congenital heart defect
b) Perforations in interatral septum
c) Excessive resorption of septum primum
d) Located in the midportion of the atrial septum
3) Primum
a) Primum and secundum type ASDs make up 67% of all ASDs
b) Failure of septum primum to fuse with endocardial cushions
c) Located in the inferior atrial septum
4) Sinus venosus
a) Approximately 8% of all ASDs
b) Also known as superior vena caval (SVC) septal defects
c) Sinus venosus not properly incorporated into the RA
d) Located in superior and posterior portion of atrial septum
5) Inferior vena caval
a) 21% of all ASDs
b) Counterpart of SVC ASD
c) Result of complex development malformation in sinus venosus
d) Faulty development of inferior limbic septum
e) Located in inferodorsal portionof inferior limbic septum
6) Atrial Septal defect in septum intermedium
a) Rare
b) Defect occurs as a true persistence of embryonic foramen primum
c) Located between limbic septum, pars atrioventricularis of
membranous septum and coronary sinus
7) Coronary sinus
a) Rare
b) Results from a lack of formation of atriosinus venosus fold
c) Original large communication between atria and sinus venosus
preserved
d) Located between the inferior limbic septum, pars atrioventricularis
of membranous septum and IVC orifice
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Cardiac
b. Pathophysiology
1) Hole between the two atria
2) Defect in atrial septum
3) Initially left to right shunting (due to right ventricular compliance
being less than left ventricular compliance), prolonged shunting can
result in right to left shunting with elevated right sided pressures and
Eisenmengers physiology (rare with ASDs)
4) Conditions that increase left to right shunting through ASD
a) Left ventricular hypertrophy
b) Ischemic cardiomyopathy
c) MS
d) MR
5) Volume overload
6) Pressure overload
c. Clinical presentation
a) Symptom free for many years
b) Shortness of breath (SOB) on exertion
c) Recurrent respiratory infections
d) Atrial arrhythmia (especially atrial fibrillation)
e) Systolic murmur through PV
f) Large shunts may have diastolic murmur through tricuspid valve
(TV)
a) Systolic murmur through PV
b) Diastolic murmur through TV
c) Wide fixed splitting S2
3) Echocardiographic features
a) ASD
b) Type of defect
c) Size of defect
d) Note RV function
e) Enlarged right atrium (RA)
f) Enlarged right ventricle (RV)
g) Evaluate for volume overload
i. Evaluate for D-shaped LV
h) Evaluate for pressure overload
i) Dilated TV annulus over time
j) Enlarged pulmonary artery (PA)
k) Enlarged pulmonic annulus overtime
l) Paradoxical septal motion
m) Color flow Doppler (directional information)
n) Spectral Doppler (PW) assist with directional information
o) M-mode
i. Enlarged RV
ii. Paradoxical septal motion
p) Contrast echocardiography
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Cardiac
d. Quantitation
1) Qp:Qs ratio
a) Stroke volume Right ventricular outflow tract (RVOT) / Stroke
volume left ventricular outflow tract (LVOT)
b) Normal ratio should be 1:1
c) Ratio > 1.0 indicates a left to right shunt
d) Ratio of < 1.0 indicates a right to left shunt
2) Values
a) PA Pressure
b) Estimate from tricuspid regurgitant Doppler signal
c) Values for pulmonary pressure
Grade mmHg Mean (mm Hg)
Normal <30
Mild 30-40
Moderate 40-70
Severe >70 40
e. Technical considerations and additional views
1) Secundum defects best seen in the subcostal 4-chamber view
a) Color Doppler parallel to flow
b) No septal drop out, imaging perpendicular to atrial septum
2) Subcostal long-axis view also helpful to see ASDs (both secundum
and sinus venosus)
3) Apical 4-chamber view
a) Septum primum defects
b) Septum primum defect associated with complete AV canal defect,
assess atrial defect, inflow ventricular septal defect (VSD) AV
valve morphology
4) Subcostal 4-chamber view
a) Secundum defects
b) Primum defects
c) Sinus venosus defect - sweep posterior
5) Subcostal short-axis view
a) Enface view of AV valve
6) Subcostal sagittal view of IVC/SVC
a) Sinus venosus -slightly rightward on atrial septum
b) Coronary sinus defects seen very posterior and inferior
7) Color Flow Doppler
a) Useful to detect shunt direction and assist with size evaluation
b) Evaluate for valvular insufficiency
c) Assist with evaluation to differentiate partial AV canal from
complete canal
8) PW Doppler
a) Interatrial pressure gradient
i. Useful for estimating LA pressure
f. Assessment of ASD
1) Location
2) Size and tissue rim (important to know for closure device)
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Cardiac
3) Direction of shunt (i.e. left to right or right to left)

4) RV function
5) Estimated PA pressure
g. Role of saline contrast imaging
1) Useful to detect transient right to left shunt through PFO or ASD
2) Useful to evaluate for negative contrast in the RA with left to right
shunt
h. Role of TEE
1) Assessment for size
2) Assess shunt flow
3) Evaluate type of defect (i.e. especially sinus venosus type)
i. Related testing
1) EKG
a) RBBB
b) Left axis deviation with primum ASDs associated with AV canal
defect
c) Atrial fibrillation
2) Chest x-ray
a) Enlarged heart
b) Enlarged PV
c) Pulmonary plethora
3) Cardiac catheterization
a) Step up in oxygen saturation
j. Common treatment
1) Catheterization
a) Secundum or PFO
b) Closure device
2) Surgical
a) Sinus venosus and AV canal defect
k. Post operative/repair evaluation
1) Evaluate for residual shunt
2) Evaluate for PHTN
l. Associated lesions
1) Secundum and PFO
a) Mitral valve prolapse
2) Primum
a) AV canal defect
b) Cleft atrioventricular valves
c) AV valve regurgitation
3) Sinus venosus
a) Anomalous pulmonary venous return
b) Right upper and lower pulmonary veins to SVC/RA/LA junction
2. Cor triatriatum
a. Etiology
1) Abnormal membrane in the left atrium that subdivides the atrium into
two chambers resulting in a supravalvular mitral stenosis
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Cardiac
b. Patholphysiology
1) Supravalvular stenosis results in enlargement of the atria and possible
dilation of pulmonary veins
2) If an ASD is present, the chamber may not be dilated, as the ASD
assists with decompressing chamber pressure
3) Obstruction results in pulmonary venous and pulmonary arterial
hypertension
1) Membrane seen in LA
2) May have dilated chamber above membrane
3) May have dilated pulmonary veins
d. Technical considerations and additional views
1) Parasternal long - axis
a) Membrane stretch obliquely across LA
a) Membrane seen coursing across LA
b) Use spectral Doppler to obtain peak and mean pressure gradients
across the lesion
c) Utilize color flow Doppler to align the spectral Doppler and
capture highest velocity
3) Associated lesions
a) Persistent left SVC
b) AVSD
c) Coarctation of aorta
d) ASD
e) Anomalous pulmonary venous return (APVR)
3. Supravalvular mitral stenosing ring
a. Etiology
1) Membrane located between the LA and the MV either just above the
MV or in the funnel of the MV leaflets
b. Patholphysiology
1) Membrane causing flow disturbances can result in damage to MV
leaflets
2) Obstruction can result in elevated LA pressure especially if no ASD
1) Membrane seen in diastole when MV is open
a) Attached at level of leaflets
b) Attached at body of leaflets and stretched across MV funnel when
valve is open
2) MV leaflets appear thickened and/or myxomatous
1) Multiple planes through MV evaluating for membrane when valve is
open
2) Spectral Doppler
a) Elevated peak velocity
b) Persistent gradient through diastole
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Cardiac
c) Normal (especially if ASD present)

3) Associated lesions
a) Persistent left SVC
b) VSD
c) Coarctation of aorta
d) ASD
e) Multiple left heart lesions (Shone complex)
Atrial-Ventricular Valve Anomalies

1. Atrial-ventricular (AV) canal
a. Etiologies
1) Abnormal development of endocardial cushions
a) 0.19:1000 live births
b) 4.0-5.0% of all congenital heart defects (CHD)
c) 40% of children with trisomy 21 and a CHD will have an AV canal
defect
d) Located in the fossa ovalis region
e) Failure of septum primum to fuse with endocardial cushions
f) Located in the inferior atrial septum
i. Categorized as incomplete (partial), complete or intermediate
ii. Incomplete type consists of primum ASD, common atrium,
cleft mitral vlave
iii. Complete AV canal absence of the inferrior portion of the atrial
septum and posterior ventricular septum
iv. Intermediate type AV canal consist of two complete AV vlave
rings, primum ASD, restrictive posterior VSD
b. Pathophysiology
1) Hole between the two atria and/or ventricles based on type of AV
canal
2) Incomplete type same as ASD, complete type same as VSD
3) Volume overload
4) Pressure overload
a) Incomplete type same as ASD
b) Complete type same as VSD
a) ASD
b) Type of defect (complete, intermediate, incomplete)
c) Size of ventricles (balanced or unbalanced)
d) Note function
e) Estimate RV and PA pressures
f) Color flow Doppler (directional information)
g) PW may assist with directional information
d. Quantitation
1) Values
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Cardiac
a) PA Pressure
b) Values for pulmonary pressure
Normal <30
Mild 30-40
Moderate 40-70
Severe >70 40
e. Technical considerations and additional views
a) Septum primum defects
b) Septum primum defect associated with complete AV canal defect,
assess Atrial defect, inflow ventricular septal defect (VSD) AV
valve morphology
2) Subcostal 4 chamber view
a) Primum defects
3) Subcostal short axis view
a) Enface view of AV valve
a) Useful to detect shunt direction and assist with size evaluation
b) Evaluated for valvular insufficiency
c) Assist with evaluation to differentiate partial AV canal from
complete canal
f. Assessment of VSD
1) Shunting lesion location
2) Size of defect
3) Shunt direction (left to right or right to left)
4) RV function
6) Morphology of AV valve(s)
7) Degree of AV insufficiency
g. Related testing
1) EKG
a) Counterclockwise frontalplane
b) Left axis deviation
c) Ventricular hypertrophy
i. Dependent upon volume of left-right shunt
ii. Degree of PHTN
iii. Degree of AV insufficiency
2) Chest x-ray
a) Small ASD-normal
b) Large shunt enlarged heart, increased pulmonary markings
a) Estimate right heart pressures in patients with pulmonary vascular
obstructive disease
h. Common treatment
1) Surgical
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Cardiac
2) Prophylaxis for prevention of endocarditis

i. Post operative/repair evaluation
3) Evaluate for AR
4) Evaluate for AS
2. Ebstein anomaly
a. Etiologies
1) Malformation of the tricuspid valve with inferior displacement of the
posterior and septal leaflets, the anterior leaflet is usually large with
abnormal attachments to the RV wall
a) 0.012:1000 live births
b) Often associated with ASD
i. Shunt across ASD may be right to left and therefore patient
presents cyanotic
b. Pathophysiology
1) Incompetent valve
2) 30-78% may also have an ASD
a) May have a right to left shunt across ASD and present cyanotic
a) Split first and second heart sound
b) Approximately 30% will have Wolff-Parkinson-White syndrome
2) Echocardiographic Features
a) Abnormal TV leaflet attachments, may be associated with ASD,
PFO, VSD, and PS
b) TV insufficiency
c) RA size
d) Note function
e) Estimate RV and PA pressures
f) Color flow Doppler (evaluate TV valve for insufficiency and/or
stenosis)
g) Evaluate for PS if prior history
h) Spectral Doppler (evaluate tricuspid insufficiency and pulmonary
flow)
i) Evaluate for associated ASD/PFO
j) M-mode
i. TV closure delay
ii. Increased excursion of anterior TV leaflet
1) Parasternal long axis view
a) RV inflow view
b) Evaluate RA size
c) Evaluate tricuspid insufficiency
d) Evaluate RV outflow view
2) Parasternal short axis view
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Cardiac
a) Evaluate TV
b) Evaluate TV insufficiency
c) Evlaute RVOT and PA
d) Evalute flow across pulmonic valve
3) Apical view
a) Evaluate chamber size
b) Evaluate placement of TV septal leaflet
c) Evaluate TV for insufficiency and stenosis
4) Color flow Doppler
a) Useful to evaluate TV insufficiency
5) Spectral Doppler
a) Evaluate TV insufficiency and pulmonic flow
b) Evaluate TV for stenosis
e. Assessment for Ebstein
1) Degree of TV insufficiency
2) RA size
3) ASD/PFO presence
4) RV function
6) History of RV outflow tract or pulmonary valve obstruction
f. Related testing
1) EKG
a) Tall P waves in limb lead II
b) Right bundle branch block
c) 30% will have Wolf-Parkinson-White syndrome
2) Chest x-ray
a) Cardiomegaly with prominent right sided border
b) Decreased pulmonary blood flow
g. Common treatment
1) Mild cases - nothing
2) Surgical repair
h. Post operative/repair evaluation
1) Evaluate for TV insufficiency
2) Evaluate for residual shunt of ASD if history of ASD repair
3) Evaluate RV inflow post repair (stenosis)
a) Evaluate RV outflow and pulmonic flow obstruction
b) Evaluate for systemic-pulmonary artery shunt if history of
procedure
3. Tricuspid atresia
a. Etiology
1) Failure of right sided venous valves to regress resulting in no
communication between the right atrium and right ventricle
a) 0.039-0.085:1000 live births
b) 2.7% of all CHDs
c) Initial survival is dependent upon interatrial communication
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Cardiac
d) May occur with normal related great vessels or transposition of

great vessels
e) May occur with normal PA and VSD or pulmonary stenosis and/or
atresia
f) By adulthood will have gone through surgical repair
g) Fontan procedure
b. Pathophysiology
1) Atresia of the TV
2) May occur with
a) Normally related great arteries
b) Transposed great arteries
c) Pulmonary atresia
3) Definitive treatment
a) Modified Fontan procedure
i. Direct systemic venous blood flow to PA without going
through a ventricle
ii. Bicaval connects SVC to right pulmonary artery, IVC
connected to underside of heart or RA, separates systemic and
pulmonary venous return, and is designed to prevent
ventricular volume overload
iii. Performed to reduce the problem of ventricular volume
overload and degree of cyanosis
4) Ventricular volume overloading due to both inlets are committed to
one ventricle
a) Ventricular volume overload is dependent upon amount of
pulmonary flood flow
i. Dependent upon presence of pulmonic stenosis or surgical
shunts
ii. When ventricle enlarges, ventricular wall stress increases,
compensatory hypertrophy ensues
iii. Hypertrophy impaired diastolic function
i) Subendocardial ischemia
a) Cyanotic at birth
b) Dependent upon relationship of great arteries, and /or presence of
pulmonary artery atresia/stenosis and how lesions were repaired
c) Dependent upon repair and function of anastomoses/conduits
a) Absence of normal TV
b) Morphology of ventricle
c) Note presence or absence of interventricular communication
d) Note ventricular arterial connections
e) Know what initial findings were at birth and what type of surgical
correction was performed
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Cardiac

a) Examine ventricular septum for presence of VSD
b) Confirm relationship of great vessels
c) Position of outlet septum
d) Evaluate coronary size and presence of left SVC
a) Sweep the interventricular septum for evidence of VSDs
b) Evaluate systolic function of LV
c) Evaluate RVOT and pulmonary artery and branches
3) Apical 4 chamber view
a) Evaluate right ventricular inlet region
b) Evaluate right outlet septum with anterior angle
c) Evaluate LVOT and arterial connection
d) Evaluate mitral inflow and for any insufficiency
e) Evaluate pulmonary vein inflow
4) Subcostal view
a) Evaluate atrial septum
5) Off axis views
a) Conduits or anastomoses from the RA to the PA are usually seen
anteromecially and superior to the atrium
i. Glenn shunt seen in suprasternal short-axis view
i) Evaluate for an obstruction
ii) Evaluate with color and spectral Doppler
ii. Fontan anastomosis imaged in high parasternal and subcostal
views
i) Intra-atrial conduits can be imaged in parasternal and apical
views
ii) Evaluate for an obstruction
iii) Evaluate with color and spectral Doppler
iv) Variations of Fontan (classic Fontan, extracardiac Fontan,
fenestrated Fontan, lateral tunnel, RA-RV Fontan, and total
cavo-pulmonary connection (TCPC)
(http://philachd.org/glossary/f.html)
b) Evaluate patency of conduit/anastomosis
e. Assessment
1) Evaluate surgical anastomoses/conduits for patency and any evidence
of obstruction?
2) Evaluate ventricular function
3) Evaluate pulmonary artery for any evidence of obstruction
4) Evaluate systemic inflow and outflow for obstruction
f. Role of TEE
1) Used to evaluate the entire Fontan conduit
g. Common treatment
1) Surgical repair modified Fontan
1) Evaluate patency of shunts/conduits
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Cardiac
2) Evaluate pulmonary artery flow

3) Evaluate for systemic outflow obstruction
4) Evaluate for systemic inflow obstruction
5) Tailor exam to evaluate the surgical repair
i. Associated lesions
1) Left juxtapositon of RAA
2) Coarctation of aorta
3) Left SVC
4. Hypoplastic left heart
a. Etiology
1) Aortic valve atresia/hypoplasia, mitral valve atresia/hypoplasia and
hypoplasia LV
a) 0.103 -0.267:1000 live births
b) Often associated with coarctation of aorta
c) Small atrial septal defect
b. Pathophysiology
1) Surgical procedure is performed to create a permanent unobstructed
pathway from the RV to the systemic circulation (stage 1 Norwood
procedure)
2) Limit pulmonary pressures through creating a systemic venous
pulmonary artery shunt
3) Limit pulmonary hypertension through creation of an interatrial
communication
4) Final surgery is modified Fontan
a) 3-5 days post birth develop mild cyanosis
b) Untreated lethal malformation
c) Once diagnosed, patients receive prostaglandin E1 to maintain
patency of the ductus arteriosus and then surgical repair
d) Staged surgical repair
i. Norwood
ii. Glenn
iii. Modified Fontan
a) Complications associated with Norwood procedure that can limit
one from having a Fontan procedure
i. Inadequated ASD
i) ASD less than ½ the length of the atrial septum
ii) If restricted ASD, then pulmonary venous hypertension
may ensue
iii) ASD can become progressively smaller usually due to
regrowth or superior limbic atrial septum and can obstruct
the right upper pulmonary vein
ii. Aortic arch obstruction
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Cardiac
i) Arch obstruction can be seen at the proximal suture line,

distal suture line or distal to the reconstructive surgery
iii. PA branch distortion
b) Other problems associated with surgical repair of hypoplastic left
heart syndrome
i. Neoaorta aneurysms
ii. TV insufficiency
iii. Neoaorta insufficiency
iv. Poor RV function
v. Intracardiac thrombi
vi. Poor systemic flow
i) Dilated RA, RV
a) Discrepency in RV and LV size
b) Dilated LA if small ASD
c) Prior to surgical repair small aorta with valve atresia/hypoplasia
and small MV annulus with valve atresia/hypoplasia
d) Post surgical repair
i. Evaluate valve patency and competency of neoaorta
ii. Evaluate Glenn shunt if present
iii. Evaluate Fontan procedure if present
a) Evaluate TV
3) Apical view
a) Evaluate chamber size
c) Evaluate RV function (qualitative assessment)
d) Examine pulmonary venous inflow
4) Suprasternal notch view
a) Aortic arch anatomy
b) Flow throughout arch
a) Useful to evaluate TV insufficiency
b) Useful to evaluate flow through neoaorta
c) Useful to evaluate for obstruction of flow throughout aorta, arch
and descending aorta
d) Useful to evaluate flow through Glenn Shunt and Fontan procedure
6) Spectral Doppler
a) Evaluate TV insufficiency
b) Useful to evaluate flow through neoaorta
c) Useful to evaluate for obstruction of flow throughout aorta, arch
and descending aorta
d) Useful to evaluate flow through Glenn Shunt and Fontan procedure
e. Assessment
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Cardiac
1) Evaluate ASD look for any evidence of restriction

2) Evaluate surgical anastomoses/conduits to ensure patency and free of
obstruction
3) Evlauate ventricular function
4) Evaluate systemic inflow and outflow for obstruction
f. Common treatment
1) Staged surgical repair
a) Norwood
b) Glenn
c) Fontan
g. Post operative/repair evaluation
1) Evaluate patency of shunts/conduits
2) Evaluate neoaorta flow
3) Evaluate for systemic outflow obstruction
4) Evaluate for systemic inflow obstruction
5) Tailor exam to evaluate the surgical repair
F. Ventricular Anomalies
1. Ventricular septal defect (VSD)
a. Etiologies
1) Perimembranous (infracristal, conoventricular)
a) Most common type of VSD
b) Failure of membranous portion of interventricular septum (IVS) to
develop
c) Incomplete closure of interventricular foramen
d) Failure of subendocardial tissue to grow from right side of
endocardial cushion and fuse with aorticopulmonary septum and
muscular part of interventricular septum (IVS)
e) Located in membranous/perimembranous area of IVS , in the
LVOT just below the aortic valve
2) Posterior (canal-type, endocardial cushiontype, AV septumtype,
inlet, juxtatricuspid)
a) Deficiency of inlet portion of ventricular septum
b) Marked discrepancy between the inlet and outlet dimensions of
ventricular mass
c) Seen with AV canal defects
d) Located in the inflow portion of the IVS
3) Trabecular (muscular)
a) Excessive cavitation of myocardial tissue during formation of IVS
and ventricular walls
4) Supracristal (conal septal, infundibular, subpulmonic, subarterial,
subarterial doubly committed, outlet)
a) Located beneath the pulmonic valve and communicate with the RV
outflow tract above the supraventricular crest and are associated
with aortic regurgitation secondary to the prolapse of the right
aortic cusp
5) Malalignment
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Cardiac
a) Occur in several locations

i. Malalignment inflow
i) Atrial and ventricular septa do not align normally
ii) Associated with malalignment inflow VSD and overriding
AV valve
ii. Malalignment outflow
i) Posterior or anterior displacement
ii) Posterior displacement associated with muscular aortic
stenosis and/or aortic arch anomalies
iii) Anterior displacement may or may not be associated with
RVOT obstruction
b. Pathophysiology
1) Hole between the ventricles
2) Left to right shunt occurs when pulmonary vascular resistance is less
than systemic vascular resistance
3) Increased pulmonic flow
4) Decreased systemic CO due to left to right shunt
5) LA enlargement
6) LV volume overload
a) LVH
b) Elevated LVEDP
i. Elevated LA pressure
ii. Elevated pulmonary venous pressure
c) Enlarged LV
a) Small defects (restrictive)
i. May have no hemodynamic disturbance
ii. High velocity jet with loud murmur
b) Large defects (unrestrictive)
i. Cardiac failure
ii. Pansystolic murmur at lower left sternal edge
c) Pulmonary hypertension
i. Eisenmengers syndrome
d. Physical findings
1) Dependent upon size of VSD
2) Dependent upon magnitude of shunt
3) Dependent upon RV and pulmonary hypertension
e. Auscultatory findings
1) Small VSDs and normal to slightly elevated RV and pulmonary
pressures will have normal precordial impulses and normal S1 and S2
heart sounds, murmur holosystolic
2) Muscular VSDs murmur heard over lower sternal border
3) If jet directed toward PA murmur will radiate to upper left sternal
border
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Cardiac
4) Large VSDs prominent RV impulse, S1 normal but as pulmonary

hypertension increases S2 will get louder, holostystolic midfrequency
murmur
5) If Qp:Qs is > 2.0 then mid-diastoloic mitral flow murmur may be
present
f. Echocardiographic features
1) Ventricular septal defect
2) Color flow Doppler demonstrating direction of shunt and to estimate
size
3) Spectral Doppler to calculate gradient across VSD and to demonstrate
flow direction
4) Increased pulmonic flow
5) Evaluate RV size and function
7) Estimate RV pressure
8) 2-D
a) Enlarged LA and LV
g. Quantitation
1) Qp:Qs ratio
a) Stroke volume RVOT/stroke volume LVOT
b) Normal ratio should be 1:1
c) Ratio > 1.0 indicates a left to right shunt
i. Qp:Qs <1.5 small shunt
ii. Qp:Qs 1.5-2.0 moderate shunt
iii. Qp:Qs >2.0 large shunt
d) Ratio of < 1.0 indicates a right to left shunt
2) Values
a) PA Pressure
b) Estimate from tricuspid regurgitant Doppler signal
c) Values for pulmonary pressure
Normal <30
Mild 30-40
Moderate 40-70
Severe >70 40
h. Technical considerations and additional views
1) Off-axis parasternal long axis views to align parallel to flow
b) Sweep ventricular septum with color
2) Parasternal short axis views
b) Sweep the septum to look for defect
c) Doppler PA and evaluate for pulmonary hypertension
d) Supracristal VSDs will be seen at the level of the aortic valve in
the 1 oclock position
e) Perimembranous VSDs will be seen at the level of the aortic valve
in the 9 -12 oclock position
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Cardiac
f) Muscular VSDs will be seen below the level of the aortic valve and
in the muscular septum
a) Useful to detect shunt direction and assist with size and location
evaluation
b) Evaluate for AR
i. VSD assessment
1) Location
2) Size
3) Shunt direction (i.e. left to right or right to left)
4) LV size and function
5) LA size
j. Related testing
1) EKG
a) Small (restrictive) VSDs normal
b) Large (unrestricted) VSDs LVH present due to left ventricular
volume overload
c) Inlet VSD left axis deviation
2) Chest x-ray
a) Small (restrictive) VSDs normal
b) Large (unrestricted) VSDs enlarged heart and increased pulmonary
vascular markings
a) If pulmonary vascular obstructive disease suspected, cardiac
catheterization can accurately measure pulmonary vascular
resistance
k. Common treatment
1) Small (restrictive) VSDs
a) Usually do not require surgical closure unless supracristal
2) Large (unrestricted) VSDs
a) Surgical closure
b) If Eisenmenger syndrome present, VSD should not be closed
c) Prophylaxix for endocarditis
l. Post operative/repair evaluation
2) Evaluate for pulmonary hypertension
m. Associated lesions
1) Conotruncal lesions
2) AV canal defects
2. Ventricular inversion (L-transposition)
a. Etiology
1) Leftward bending of the bulboventricular loop with abnormal
development of the truncal septum
a) Morphologic right ventricle (on left side of heart) connects to the
aorta
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Cardiac
b) Morphologic left ventricle (on right side of heart) connects to the

PA
1) Apical 4 chamber view will demonstrate attachment of left sided AV
valve (tricuspid valve) slightly inferior to right sided AV Valve (mitral
valve)
2) Parasternal short axis view will demonstrate leftward and anterior
displacement of the aorta (L-transposition of the great vessels)
3) Morphologic RV is the systemic ventricle
a) To evaluate RV function dp/dt and Tei index may help
c. Associated findings
1) Ebstein malformation of left-sided AV valve
2) PS
3) VSD
4) Arrhythmias
G. Conotruncal Anomalies
1. D-transposition great arteries (TGA)
a. Etiology
1) Abnormal conotruncal septation
a) 3.8% of all CHDs
b) Aorta is connected to the RV and the PA is connected to the LV
b. Pathophysiology
1) Two parallel circuits exist
a) Systemic venous blood returns to RV and then is recirculated to
systemic circulation through aorta
b) Pulmonic venous blood returns to LV and then is recirculated to
pulmonic circulation through pulmonary artery
c) This condition is incompatible with life unless surgically corrected.
At birth there needs to be mixing of oxygenated and low
oxygenated blood. If there is no ASD or VSD at birth, a balloon
atrial septostomy needs to be performed to allow mixing of blood
between the two circuits
2) Surgical Repairs
a) Mustard or senning (atrial switch)
b) Arterial switch operation (ASO)
b) Single loud second heart sound
c) Surgical repair
i. Mustard or senning
i) Baffles blood from RA to MV to LV
ii) Baffles blood from LA to TV to RV
ii. Arterial Switch
i) Connects PA to RV
ii) Connects Ao to RV
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Cardiac
a) Mustard or senning
i. Evaluate baffles
i) Evaluate for baffle obstruction
ii. Evaluate ventricular function
i) RV is systemic ventricle
ii) LV is pulmonic ventricle
b) Arterial switch (Jatene procedure)
i. Evaluate outflow tracts and great arteries for stenosis or
obstruction
c) Know surgical procedures completed and patient history to know if
ASD and / or VSD were present and repaired
i. If septal defect repaired then evaluate for leak from septal
repair
1) Mustard or senning
a) Off-axis views to evaluate baffles
b) RV focused exam to evaluate RV function
a) Useful to evaluate flow through baffle to evaluate for any
obstruction
b) Useful to evaluate flow through areas of anastomosis
3) Spectral Doppler
a) Evaluate flow through baffels
b) Evaluate flow through great artery anastomosis
e. Questions to answer
1) Mustard or senning
a) Are the baffles patent
b) What is the RV function
2) Arterial switch
a) Is there any obstruction to the great arteries
f. Common treatment
1) Surgical repair
1) Evaluate patency of surgical procedures
3) Evaluate for septal defect repair leaks if performed
2. Tetralogy of Fallot
a. Etiology
1) Unequal conotruncal septation
a) 4-8% of all CHDs
b) Consists of a VSD, pulmonary stenosis, overriding aorta and RVH
i. 25% will have a right sided arch
ii. Variants include a tetralogy of Fallot with absent pulmonary
valve and tetralogy of Fallot with pulmonary atresia
b. Pathophysiology
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1) At birth
a) Cyanotic due to decreased pulmonary flow and right to left shunt
through the VSD
2) Surgical repair
a) Dependent upon size and anatomy of pulmonary arteries
b) Cases in which the pulmonary arteries and/or peripheral pulmonary
arteries are hypoplastic or severely stenosed long-term prognosis
depends on postoperative pulmonary artery pressure
i. postoperatively RV pressure is inversely related to size of
pulmonary arteries and directly related to how severe the PA
stenosis is
ii. High postoperative PA pressure, higher likelihood RV failure
and development of arrhythmias
iii. Postoperative significant pulmonary insufficiency with PS may
develop RV failure and arrhythmias
b) Surgical repair
i. Dependent upon anatomy
2) Echocardiographic Features
a) Evaluate for VSD closure leak
b) Evaluate RV function
c) Evaluate pulmonary artery for stenosis and insufficiency
d) Evaluate for coronary artery anomalies
1) Know anatomy present at birth and how surgically reapaired
2) Parasternal short axis
a) Evaluate RVOT, pulmonary valve and branch Pas
b) Evlauate that Pas are continuous
3) Suprasternal notch view (SSN)
a) RPA SSN short axis
b) LPA SSN long axis
a) Evaluate for PS and PI
b) Evaluate for septal defect repair leak
5) Spectral Doppler
a) Evaluate for PS and PI
b) Calculate gradient if septal defect repair leak
e. Assessment
1) Evaluate for PS
2) Evaluate for PR
3) Evaluate RV function
4) Look for presence of a residual septal defect
f. Common treatment
1) Surgical repair
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1) Evaluate for PS and PI
3) Evaluate for septal defect repair leaks if performed
3. Double outlet right ventricle (DORV)
a. Etiology
1) Abnormal conotruncal development (complex pathophysiology)
resulting in both great arteries arising from the right ventricle
1) Variable group of findings
a) Both great arteries connect to the right ventricular side of septum
or posterior artery partially overrides ventricular septum
b) Mitral aortic discontinuity
a) Assess infundibulum
i. Anterior/posterior with subaortic VSD (most common)
ii. Side/side usually with subpulmonic VSD
iii. Relatonship of great vessels
i) normal
ii) D-TGA
iii) Anterior/Posterior
iv) Side/Side
iv. PS
v. Coronary artery anatomy
4) Subcostal view
a) Relationship of great vessels
b) Relationship of VSD to great vessels
c) Relationship of infundibulum
d) PS
c. Postoperative/repair evaluation
1) RV pressure gradient (TR)
2) Residual VSD
4. Truncus arteriosus
a. Etiology
1) Failure of the truncus to septate resulting in persistence of the truncus
arteriosus
b. Pathophysiology
1) Cyanosis may not be present at birth due to elevated pulmonary
resistance
2) Pulmonic blood flow from combined ventricular output
3) Pulmonary blood flow higher than systemic blood flow
4) CHF
1) Single great vessel arises from the heart and supplies the ascending
aorta and pulmonary arteries
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a) Evaluate for VSD
b) At birth single vessel leaves the heart
c) Surgical repair will involve detaching pulmonary arteries from
common artery and utilizing a homograft to connect the pulmonary
arteries to the RV
i. Post-repair evaluate LVOT for obstruction
ii. Evaluate for regurgitation
d) VSD patch
i. Post-repair evaluate for residual VSD in parasternal long-axis
view
e) Conduit from RV
a) Assess VSD patch
b) Assess truncal valve
c) Conduit from RV
4) Subcostal view
a) Image conduit
5) SSN view
a) Long and short axes views to evaluate arch sidedness
d. Postoperative/repair evaluation
1) VSD closure, evaluate for leak
2) Common arterial trunk committed to LV
3) Reconstruction of RVOT connecting RV to Pas (Rastelli procedure)
a) Conduit (allograft, homograft, xenograft)
b) To image conduit look at chest x-ray
c) Align to valve ring
d) Image in long and short axis views to attempt to show the entire
conduit
e) Utilize PW and CW Doppler to assess patency in conduit
(evaluating for obstruction)
f) Utilize color Doppler to assess for conduit obstruction
g) Stenosis likely to develop at proximal insertion, valve or distal
insertion sites
5. Aortic stenosis
a. Etiology
1) Subvalvular
a) Associated with hypertrophic cardiomyopathy
b) Located in the LVOT
c) Subaortic membrane
2) Bicuspid
a) Incidence 2% of population
b) Congenitally malformed leaflets
i. Thickened leaflets
ii. Fused raphe
3) Congenitally stenotic tricuspid valve
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a) Three cusps
b) Varying degrees of commissural fusion
4) Unicuspid
a) Congenitally malformed leaflets
b) Single slitlike commissure in cross-section
5) Quadricuspid
a) Congenitally malformed leaflets
b) Incidence 0.013%
c) Four diastolic closure lines present in cross-sectional view
6) Supravalvular
a) Narrowing of ascending aorta
b) Can occur sporadically or familial (defect in elastin gene on
chromosome 7)
c) Associated with Williams syndrome
b. Pathophysiology
1) Increased resistance to flow out of the left ventricle
2) Concentric LV hypertrophy (LVH) develops
a) LV mass assists with evaluating the LV work load
3) LA enlargement may also occur in patients with LVH
a) Associated with abnormal LV diastolic function
a) More common in men than women
b) Dependent upon severity
c) Severity is measured on the pressure drop across the valve in
systole
i. Values
Trivial Mild Moderate Severe
0-25 mmHg 26-50 mmHg 51-79 mmHg >80 mmHg

ii. Values above are based on normal cardiac output
d) Syncope (rare)
e) Murmur
i. Systolic crescendo-decrescendo (diamond shape)
ii. Left sternal border radiating to right sternal border
iii. 2/6 suggests severe stenosis
iv. If associated with AI then decrescendo diastolic murmur also
present
f) Critical AS
i. Low cardiac output
ii. Reduced ejection fraction
iii. Shock
iv. Congestive heart failure
a) Normal first and second heart sounds
b) Ejection click heard after first heart sound
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i. High frequency sound heard over mid-left sternal border

ii. Absence of this click with other findings suggesting AS may
indicate subvalvular or supravalvular stenosis
a) Thickened leaflets
b) Doming of leaflets
c) LVH
i. LV mass
ii. LV mass/volume ratio
d) LV diastolic function
e) Time to peak velocity (acceleration time)
f) Acceleration time (AT) : LV ejection time (LVET)
i. AT/LVET normal < 0.30
ii. AT/LVET ration > 0.30 pressure gradient > 50 mmHg
iii. AT/LVET ratio > 0.55 obstruction warrant surgery (Haetle et
al)
g) Doppler pressure gradient
h) Aortic valve area
i) Post stenotic dilation
j) Evaluate for subvalvular stenosis
k) Evaluate for supravalvular stenosis
l) M-mode findings
4) Quantitation
a) Values
Grade AVA (cm2) Mean (mm Hg) Peak velocity
(m/sec)
Normal 3.0 - 4.0
Mild 1.0 1.5 < 30 < 3.0
Moderate 0.8 1.0 30-50 3.0 4.0
Severe 0.75 > 50 > 4.0
i. Dimensionless index
i) LVOT and AV velocity or TVI ratio
ii) May be used if unable to measure LVOT diameter
iii) < 0.2 indicates severe AS
ii. Low output-low gradient AS
1) Parasternal long-axis view
a) Evaluate valve excursion
b) Color Doppler evaluate turbulent flow (level) and evaluate for AI
a) Evaluate cusp number
b) Color Doppler
c) LV function
d) LVH
3) Apical 5 chamber view
a) Evaluate Doppler flow
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b) Color Doppler
4) Pedhoff transducer
a) Right parasternal
b) Suprasternal notch
c) Apical
a) Evaluate stenosis
b) Evaluate for valvular insufficiency
6) M-Mode
a) Eccentric AV closure line with bicuspid valve
b) LVH
c) Thickened valve
e. Assessment
1) Level of obstruction
a) Subaortic membrane; valve anatomy does not apper to be stenotic,
Doppler demonstrates high pressure gradient
i. Membrane can be difficult to see on TTE
ii. TEE may be indicated to better depict anatomy
2) Calculate peak gradient
3) Calculate mean gradient
4) Evaluate for LVH
5) Evaluate LV function
f. Related testing
1) EKG
a) Flattening T waves V5 and V6
b) Severe AI may show findings of myocardial ischemia
c) LVH
2) Chest x-ray
a) Normal heart size
b) Prominent aorta with post stenotic dilation
c) Cardiomegaly suggests the presence of AI
a) Pressure gradient
b) Balloon dilation
g. Common treatment
1) Balloon Dilation
2) Surgical valvotomy
3) Surgical valve replacement
1) Evaluate transvalvular pressure gradient
2) Evaluate for AI
1) Coarctation with bicuspid valve
6. Pulmonary artery stenosis
a. Etiology
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1) Pulmonary valve stenosis

a) Cusp fusion
2) Valvular and infundibular stenosis
a) Abnormal hypertrophy of muscular walls of right ventricle and
surrounding conus muscle
3) Hypoplastic pulmonary valve annulus and conus
a) Thickened domed and stenotic valve
b) Narrow or hypoplastic valve annulus
4) Supravalvular
a) Branch pulmonary artery (PA) stenosis
b. Pathophysiology
1) Increased resistance to flow out of the right ventricle
2) Obstruction results in increased RV systolic pressure
3) Afterload increase results in RV hypertrophy and muscle mass
a) Asymptomatic
b) Murmur
i. Crescendo-decrescendo (diamond shape)
ii. Peak intensity occurs later as stenosis increases
iii. Prominent fourth sound if ventricular failure present
iv. If pulmonic insufficiency is present murmur louder when
supine versus upright
c) Critical PS history of cyanosis
a) Thickened leaflets
b) Doming of leaflets
c) RVH
i. RV mass
d) Doppler pressure gradient
e) Evaluate for infundibular stenosis
3) Quantitation
a) Peak instantaneous pressure gradient across pulmonary valve
b) Values for pulmonary pressure
Normal <30
Mild 30-40
Moderate 40-70
Severe >70 40
a) Evaluate RV outflow
b) Color Doppler evaluate turbulent flow (level) and evaluate for PI
a) Evaluate RV outflow, pulmonic valve, pulmonary artery and
branches
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b) Pressure gradient
c) Annular diameter
d) Color Doppler
i. Evaluate for turbulence
ii. Evaluate for PI
e) Spectral Doppler
i. Estimate pressure gradient
3) Subcostal view
a) RVOT
b) Annular diameter
c) Color Doppler RVOT, Pulmonic valve, PA
d) Spectral Doppler RVOT, Pulmonic valve, PA
e. Assessment
1) Level of obstruction
2) PA diameter
3) Peak gradient
4) Evaluate for RV pressure overload
5) Evaluate for RV volume overload
f. Related testing
1) EKG
a) Right axis deviation
b) RVH
2) Chest x-ray
a) Normal heart size and pulmonary vascular markings
b) Prominent main pulmonary artery segment
c) Heart size if PI is present
a) Pressure gradient
b) Balloon dilation
g. Common treatment
1) Balloon dilation
1) Evaluate trans-valvular pressure gradient
2) Evaluate for PI
G. Aortic Arch Anomalies

1. Coarctation of the aorta
a. Etiology
1) Protrusion of tissue into aorta opposite the location of ductus arteriosus
a) 5% of all CHDs
b. Pathophysiology
1) Narrowing of aorta at level of coarctation
2) Increased resistance to flow at coarctation site with drop in pressure
distal to coarctation
3) Usually see a different in blood pressure between arms and legs
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4) Repair
a) Remove obstruction
1) Signs and symptoms at birth
a) Dependent upon severity of lesion
b) May have symptoms of CHF due to ductal closure
c) Ductal closure results in decreased flow to abdominal aorta and
abdominal organs
d) Increased resistance to flow through region of coarctation
i. Increases work of LV
ii. Increased LVEDP
i) Pulmonary edema
2) Signs and symptoms in adolescence
a) Asymptomatic until adolescence
b) Heart murmur
c) Hypertension
a) Narrowing in transverse aortic arch between second and third
branches
i. Coarctation can also be in distal aorta
b) Ascending aorta may be enlarged
c) Post stenotic dilation may be present
d) Increased velocity seen on spectral Doppler in area of coarctation
e) Doppler waveforms in abdominal aorta may show continuous
antegrade flow
f) Color Doppler will reveal turbulent flow in stenotic region
g) Evaluate LV function
h) Evaluate for signs of elevated LVEDP
1) Know anatomy present at birth and how surgically reapaired
a) Evaluate arch for turbulence
b) Evaluate for stenotic area and post stenotic dilation
3) Spectral Doppler
a) Evaluate for increased velocities in the region of coarctation
b) Use PW Doppler to map through the aortic arch to evaluate for any
elevated velocities
e. Assessment
1) Presence of coarctation
a) Performed by PW Doppler mapping through transverse arch and
down descending aorta
b) CW Doppler to obtain highest velocity
f. Related testing
1) EKG
a) Infants RVH
b) Older patients with coarctation normal or LVH
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2) Chest X-ray
a) Variable normal to cardiomegaly and increased pulmonary
vascular markings and prominent ascending aorta
g. Common treatment
1) Surgical repair
2) Balloon dilation with or without stent placement
1) Evaluate for recurrence or residual coarctation
1) Left-sided obstructive lesions
a) Shone complex
b) Bicuspid aortic valve
H. Patent Ductus Arteriosus (PDA)

1. PDA
a. Etiology
1) Failure of the ductus arteriosus to close under hormonal influences
after birth
b. Pathophysiology
1) Left to right shunt from aorta to pulmonary artery
2) Increased blood volume flowing to lungs
3) Increased blood flow returning to the left heart
a) Enlarged LA
b) Enlarged LV
c) Cardiac failure
c. Clinical signs and symptoms
1) Cardiac failure with large shunts
2) Failure to thrive
3) Developmental delay
4) Small lesions may have no symptoms
5) Continuous murmur with accented systolic component
a) Machinery murmur
6) Differential cyanosis
a) Difference in cyanosis/hypoxemia between right and left arms and
lower extremities based on right to left shunt with Eisenmenger
PDA
d. Auscultory findings
1) Continuous murmur with accented systolic component
a) Machinery murmur
e. Echocardiography findings
1) Patent ductus arteriosus communicating from aorta to pulmonary
artery
2) Color flow Doppler demonstrates communication from aorta to
pulmonary artery
3) Enlarged LA
4) LV hypertrophy
5) Enlarged LV
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7) Estimate RV/PA pressure
f. Quantitation
g. Technical considerations and additional views
1) High parasternal short axis view
2) Parasternal short axis view of branch pulmonary arteries
3) long axis aortic arch to ductus view
4) Utilize color flow Doppler to visualize and estimate size of shunt in
each view above
5) Utilize spectral Doppler to demonstrate Doppler waveform and
velocities
h. Related testing
1) EKG
a) Enlarged LA
b) LV hypertrophy
2) Chest Xray
a) Pulmonary plethora
b) Cardiomegaly
c) Severe PHTN (if Eisenmengers syndrome present)
i. Common treatment
1) Newborn period ductal closure promoted by use of prostaglandin
antagonists
2) Patients with PDA have an increased risk of endocarditis, and
therefore closure is recommended
3) Percutaneously closed with device
4) Surgical ligation closure
I. Surgical Repair
1. Blalock Hanlon
a. Atrial septostomy or removal of atrial septum
b. Performed to:
1) Create atrial mixing
2) Conditions used in:
a) TGA
b) Mitral atresia
c) Other entities in which atrial mixing is indicated
2. Blalock Taussig
a. Anastomosis of subclavian artery to PA
b. Performed to:
1) Increase pulmonary blood flow
c. Echocardiographic views to demonstrate shunt
1) Suprasternal or high parasternal window
2) Utilize spectral Doppler to assess gradients
3. Brock Procedure
a. Closed pulmonary valvotomy
b. Performed to:
1) Prior to balloon valvuloplasty
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4. Closures
a. ASD
1) Primary or patch
2) Device
b. VSD
1) Patch
c. PDA
1) Ligation
2) Coil
3) Device
d. AVSD
1) Patch closure ASD VSD
2) AV valve repair
5. Damus-Kaye Stansel
a. Supravalve end-to-side anastomosis of PA to aorta
b. Valved conduit between RV and PA
c. Performed to:
1) Relieve irrepairable subvalvular stenosis
2) Create an aorto-pulmonary window
6. Glenn
a. SVC connected to right PA
b. Performed to:
1) Increase PA flow
a) Tricuspid atresia
b) Pulmonary atresia
7. Norwood procedure
a. PA anastomosis to aorta
b. Conduit from aorta to MPA
c. Performed to:
1) Increase flow to neoaorta
2) Stage procedure leading to Fontan
a) Aortic valve atresia
b) Hypoplastic left heart
8. Rashkind balloon
a. Percutaneous atral septostomy
b. Performed to:
1) Increase atrial mixing of blood
a) TGA
b) Tricuspid atresia
9. Rastelli procedure
a. Valved conduit
1) RV to PA
2) LV to aorta via VSD and patch
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Cardiac
b. Performed to:
1) Increase pulmonary flow or establish flow from ventricles to PA and
Aorta respectively
a) TGA, VSD, subvalvular PS
b) TA
c) DORV
d) PA
10. Potts
a. Anastomosis between descending aorta and left PA
b. Performed to:
1) Increase pulmonary flow
11. Waterston
a. Anastomosis ascending aorta to right PA
b. Performed to:
1) Increase pulmonary flow
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SECTION XV: Stress Echocardiography
1. Describe the purpose of stress echocardiography

2. Differentiate between the indications of exercise versus pharmacologic stress
echocardiography
3. Name common pharmacological agents used in stress echocardiography
4. Identify the equipment necessary for stress echocardiographic examinations
5. Explain the protocol for stress echocardiography
6. Name the pre-echocardiographic and post-echocardiographic views used in stress
testing
7. Identify wall motion abnormalities seen on a stress echocardiogram
8. Identify major coronary arteries associated with 16 and 17 segment perfusion model
XV. Stress Echocardiography
A. Definition
1. Ischemia
a. Oxygen supply demand mismatch
2. Sequence of ischemic response
a. Decrease perfusion
b. Decrease LV compliance
c. Increase LVEDP
d. Decrease LV contractility
e. ECG changes
f. Symptoms
3. Indications
a. CAD screening
b. Assess perfusion pre- and post-revascularization
c. Determine prognosis
d. Evaluate valvular heart disease
4. Contraindications
B. Types of Stress Echocardiography

1. Exercise stress echocardiography
a. Patient preparation and EKG-lead placement
b. Indication
c. Relative contraindication
d. Stress testing system
1) Treadmill
2) Bicycle
3) Other
e. 12-lead EKG system
f. Blood pressure device
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g. Emergency crash cart

h. End points
1) Maximal exertion
2) Clinical ischemia
3) Blood pressure (hyper/hypotension)
4) Sustained tachycardia
5) WMA involving 2 or more segments
6) Predicted heart rate
2. Pharmacologic stress echocardiography
a. Patient preparation
b. Indication
c. Relative contraindication
d. Infusion pump
e. 12-lead EKG system
f. Blood pressure device
g. Emergency crash cart
h. Pharmacological stress agents
1) Affects on heart
i. Atropine to achieve target heart rate
j. End points
1) Clinical ischemia
2) Blood pressure (hyper/hypotension)
3) Sustained tachycardia
4) Wall motion abnormality (WMA) involving 2 or more segments
5) Predicted heart rate
3. Pacing
C. Clinical Applications for Stress Echocardiography

1. Diagnose CAD
2. Determine extent of CAD
3. Evaluate LV function
4. Screen preoperative and postoperative
5. Assess valvular heart disease
6. Evaluate myocardial viability
D. Corresponding Perfusion Zones of the Major Coronary Arteries

1. LAD
2. LCX
3. ACA
E. Procedure
1. Baseline images
a. Parasternal long axis
b. Parasternal short axis
c. Apical 4 chamber
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d. Apical 2 chamber
2. Stress initiated
a. Target heart rate
3. Post-exercise echocardiographic images
a. Time limitations
b. Patient position
c. Time increments
4. Digital image acquisition
5. Tissue harmonic imaging
6. Contrast for LV opacification
F. Ischemic Response
1. Wall motion analysis
a. Absence of hyperkinesis
b. Normal function
c. Hypokenetic
d. Akinetic
e. Dyskenetic
2. False negative
3. False positives
G. Advantages of Stress Echocardiography

1. Shorter imaging time
2. Lack of ionizing radiation
3. Portability
4. Immediate availability of results
5. Lower cost
6. Ancillary information
a. Chamber size and function
b. Valves
c. Pericardial effusion
d. Aortic root disease
e. Wall thicknesses
H. Pitfalls
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SECTION XVI: Transesophageal Echocardiography (TEE)
1. Describe the purpose and protocol of transesophageal echocardiography

2. Identify the equipment necessary for TEE
3. List common clinical indications to perform a TEE
XVI. Transesophogeal Echocardiography (TEE)
A. Transesophageal Echocardiography (TEE)

1. Indications
2. Contraindications
3. Procedure
a. Description
b. Equipment
c. Transducer types
d. Types of sedations
e. Patient preparation
f. Patient sedation
g. Laboratory set up/clean up
h. Transducer care
1) Cleaning
2) Storage
4. Advantages/limitations
5. Complications
6. Probe manipulation
a. Advance/withdraw
b. Rotation (0° - 180°)
c. Turn (right-left/medial-lateral)
d. Anteflex/retroflex
e. Flex right/left
B. Imaging Views
1. High esophageal - depth to include LV
a. 0° four-chamber - retroflex
2) RV size and function
3) LA and RA size, pulmonary veins
4) Withdraw probe for LA appendage
5) MV and TV
6) Anteflex to see aortic valve
b. ~60° two chamber
2) LA and LA appendage
3) MV
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c. ~120° long axis

2) LA size
3) Mitral and aortic valve
4) Withdraw probe for ascending aorta
2. High esophageal - decrease depth to optimize valves
a. ~120° long axis
1) Mitral valve anatomy and function
2) Color Doppler for mitral regurgitation
3) Antegrade mitral flow
4) Aortic valve anatomy and flow
b. ~60° two chamber
3) LA imaging and flow
c. 0° four chamber
2) Anteflex for aortic valve anatomy and function
3) Atrial septum
3. Transgastric
a. 0° short axis
1) LV wall motion, thickness, and dimensions
2) RV size and function
b. ~90° long axis
3) LA imaging and flow
4. Transgastric apical
a. 0° four chamber
1) Anatomy and function
2) Antegrade aortic flow with color Doppler
5. Transgastric to high esophageal
a. 0° short axis descending aorta
1) Image aorta from diaphragm to aortic arch
6. Modify each view according to anatomy and pathology
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SECTION XVII: 3-D/4-D Echocardiography
1. List the clinical indications for 3-D/4-D echocardiography

2. Describe the equipment components necessary to perform 3-D/4-D echocardiographic
examinations
3. Describe advantages and limitations of 3-D/4-D compared to 2-D echocardiography
XVII. 3-D/4-D Echocardiography
A. Imaging Methods and Display

1. Image acquisition
a. 2-D reconstruction
1) Freehand
2) Mechanical rotation
b. Volumetric imaging
1) Real time
2) Volume acquisition
2. Tissue depiction
a. Surface rendering
b. Volume rendering
B. Clinical Indications
1. Ventricular assessment
a. Function
b. Volume/mass
2. Leaflet evaluation
a. MV
b. AV
3. Congenital heart disease
4. Surgical reconstruction
C. Modality Comparison
1. Advantages of 3-D/4-D
2. Limitations of 3-D/4-D
3. Advantages of 2-D
4. Limitations of 2-D
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SECTION XVIII: Contrast Echocardiography
1. Sequence the set-up and imaging procedure for administering contrast

2. List the various contrast agents used in the clinical setting
3. Differentiate between the types of contrast
4. Describe clinical indications and contraindications for the use of contrast
5. Explain appropriate equipment settings necessary to perform an optimal contrast
study
XVIII. Contrast Echocardiography
A. Use of Contrast Agents

2. Agitated saline
a. Indications and contraindication
b. Clinical applications
c. Set up and supplies
3. Contrast media
a. Bubble characteristics
1) Size
2) Stability
3) Composition
4) Acoustic properties
a) Acoustic impedence
b) Resonant frequency
b. Technical criteria
1) Appropriate rate and concentration
a) Bolus
b) Diluted bolus
c) Continuous infusion
d) Set up and supplies
2) Image acquisition
a) Continuous
b) Sequential
c) Gated
3) Appropriate equipment settings
a) Mechanical index (MI)
b) Transducer frequency
c) Harmonics
i. Dynamic range
ii. Receiver filter
iii. Transmit frequency spectrum
d) Focal zone location
e) Compression/dynamic range
f) Gain
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4) Affects of inappropriate settings

5) Indications
a) Suboptimal examination criteria
6) Contradictions
7) Echocardiographic modalities
a) Fundamental
b) Harmonic
c) Color Doppler
d) Power Doppler
c. Applications
1) Endocardial border definitions
2) Myocardial perfusions
3) Doppler signal enhancement
4) Definition of cardiac mass
d. Informed consent
e. Patient monitoring
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SECTION XIX: Advanced Techniques/Procedures
1. Describe advanced techniques/procedures that can be used in echocardiography

2. Describe clinical setting and application of advanced techniques/procedures
3. Develop basic understanding of technical application of each advanced
technique/procedure
XIX. Advanced Techniques/Procedures
A. Intraoperative echocardiography
1. Approaches
a. TEE
b. Epicardial
2. Indications
B. Intravascular ultrasound (IVUS)

1. Description
2. Transducer types/frequencies
a. Mechanical
b. Phased array
3. Clinical uses
4. Limitations
C. Intracardiac Echocardiography (ICE)
D. Echocardiography-Guided Interventional Procedures

1. Pericardiocentesis
2. Biopsy
E. Myocardial Strain Imaging

1. Definition
a. Positive strain
b. Negative strain
c. Color strain tracking
d. Units
2. Clinical application
3. Technical consideration
F. Speckle Imaging
1. Definitions
a. Tissue tracking
2. Clinical application
3. Technical consideration
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G. Evaluation of Ventricular Assist Devices
H. Cardiac Resynchronization Therapy (CRT)

1. Definition
a. Dyssynchrony
1) Interventricular
2) Intraventricular
3) Atrioventricular (AV)
b. Biventricular pacing
c. Cardiac reverse remodeling
d. Responders
e. Nonresponders
2. Patient selection
a. Inclusion criteria
b. Dyssynchrony indexes
c. Echocardiograpic methods/measurements
1) 2D echocardiography
a) LV end-diastolic and end-systolic diameters
b) LV end-diastolic and end-systolic volumes (biplane method of
discs)
c) LV ejection fraction
d) M-mode measurement of time delay between two walls: septal to
posterior wall mechanical delay (SPWMD)
2) Pulsed/continuous wave Doppler echocardiography
a) RV and LV outflow tract velocities
b) dp/dt derived from MR jet acceleration velocity
3) 3D echocardiography
a) LV ejection fraction
b) LV volumes
c) Segmental wall dyssynchrony
4) Tissue Doppler imaging (TDI)
a) Time of peak LV contraction systolic velocity
b) Color TDI
c) Tissue synchronization imaging (TSI)
5) Myocardial strain and strain rate
3. AV optimization
a. Technical aspects of adjusting AV delays
b. Hemodynamic changes seen with changes in AV delays
c. Methods
1) Ritter
2) Iterative
d. Echocardiographic approach
1) Mitral inflow
a) E wave
b) A wave/truncation
c) A wave duration
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Cardiac
d) EA fusion
2) Aortic outflow tract
a) TVI
4. V to V optimization
a. Technical aspects of adjusting ventricular delays
b. Hemodynamic changes seen with changes in V to V delay
c. Methods
1) Iterative
d. Echocardiographic approach
1) Aortic outflow
a) TVI
2) RV, LV outflow ejection time intervals
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Cardiac
SECTION XX: Systemic Disease
1. List common cardiac abnormalities resulting from the following systemic diseases:
amyloidosis, carcinoid, sarcoidosis, hypereosinophilia, hemochromatosis, connective
tissue disorders, endocrine diseases, and vasculitis
2. Discuss the pathophysiology of the aforementioned systemic diseases
3. Describe typical clinical presentations associated with cardiac involvement in
systemic disease
4. Describe key echocardiographic findings associated with cardiac involvement in
systemic disease
XX. Systemic Disease
A. Amyloid
1. General
a. Heterogenous group of diseases
b. Deposition of extracellular proteins in various organs
c. Types of amyloid
1) Primary
2) Secondary
3) Familial
4) Senile
d. Cardiac involvement common
2. Cardiac manifestations
a. Systolic or diastolic heart failure
b. Arrhythmias
c. Conduction disturbances
d. Embolic events
e. Coronary insufficiency (amyloid infiltration of intramyocardial arteries)
a. Symptoms of CHF with cardiac involvement
b. Protein deposition in tongue, heart, kidney, GI tract, blood vessels,
nerves, carpal ligaments
c. Monoclonal immunoglobulin in urine or serum plus any of the following:
1) Unexplained nephrotic syndrome
2) Hepatomegaly
3) Carpal tunnel syndrome
4) Macroglossia
5) Malabsorption/unexplained diarrhea/constipation
6) Peripheral neuropathy
7) Cardiomyopathy
a. Increased LV/RV wall thickness
b. Myocardium may appear granular
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Cardiac
c.
Normal to small LV size with gradual decline in LV function
d.
Thickened cardiac valves with regurgitation (usually mild)
e.
Atrial enlargement
f.
Thickened inter-atrial septum
g.
Thickened papillary muscles
h.
Pericardial/pleural effusion
i.
Spectrum of diastolic dysfunction
j.
Progression of above corresponds to increasing LV wall thickness, systolic
dysfunction and more advanced disease state
5. Related testing
a. ECG
2) Conduction disturbances
3) Low voltage (up to 50% of patients)
4) Pseudoinfarction pattern
b. Bone marrow biopsy
6. Common treatment
a. Medical
1) Supportive treatment of cardiac failure
2) Chemotherapy
b. Surgical
1) Stem cell transplant
2) Cardiac transplantation
B. Carcinoid
1. General
a. Malignant, metastatic endocrine tumor
b. Primary tumors: gastrointestinal (GI) tract (>90%), bronchus, ovaries,
pancreas, biliary tract
c. Carcinoid syndrome
d. Prognosis worse in patients with cardiac involvement
e. Severity of cardiac involvement proportional to
1) Serotonin
2) Kinins
3) Urinary 5-HIAA
a. Hepatic metastases release tumor substances into the right heart
b. Fibrous white plaque deposited that leads to fibrosis and valvular
dysfunction
c. Predominant involvement on right side (TV, PV)
d. Tumor substances inactivated by the lungs
e. Left-sided involvement seen with
1) Intracardiac shunt (right-to-left)
2) Bronchial tumor or lung metastases
f. May be mimicked by drug-induced valvulopathy
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Cardiac
a. Carcinoid syndrome: flushing, hypotension, diarrhea, wheezing,

bronchospasm, endocardial plaque formation
b. Heart failure (late)
a. Tricuspid valve leaflets thickened, retracted, fixed in semi-open position
1) Usually severe TR with mild TS
b. Pulmonary valve leaflets thickened, retracted and rigid
1) Varying degrees of PR and PS (usually more PS than PR)
c. Similar mitral and aortic valve characteristics if left heart is affected (may
occur with PFO or bronchial tumor)
d. Evidence of right heart volume overload
e. Liver metastasis
f. Myocardial metastases
g. Pericardial effusion
5. Related testing
a. Serotonin levels
b. Urinary 5-HIAA
c. Tissue biopsy
6. Common treatment
a. Medical
1) Counter-regulatory hormones
2) Chemotherapy (high-grade malignancies)
b. Surgical
1) Valve replacement/removal
2) Hepatic artery embolization
C. Hypereosinophilic Syndrome
1. General
a. Always associated with hypereosinophilia: an abnormal formation and
accumulation of extremely large number of eosinophils in blood without
identifiable etiology
b. Organ infiltration
c. Multisystem disease: cardiac, skin, neurologic, pulmonary, GI, hepatic,
renal
d. Cardiac involvement most common cause of morbidity and mortality
a. Endomyocardial fibrosis
b. Lofflers cardiomyopathy
a. Pulmonary and/or systemic embolization
b. CHF
c. Sudden death
d. Variable symptoms: dyspnea most common
a. Normal LV and RV size and systolic function
b. Atrial enlargement
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Cardiac
c. Left and/or right ventricular apical thrombus with cavity obliteration

d. Posterior AV valves and subvalvular apparatus (most often PLMV) may
become thickened and tethered with associated MR and/or TR
e. Thick inferobasal LV wall
f. Restrictive physiology due to decreased LV compliance
5. Related testing
a. Labs: Persistent (at least six months) increase in eosinophil count > 1500
cells/mm3
6. Common treatment
a. Medical
1) Treat CHF
2) Anticoagulants
3) Treat underlying hypereosinophilia (steroids)
b. Surgical
1) Thrombectomy
2) Mitral and/or tricuspid valve replacement
3) Endocardial stripping
D. Sarcoidosis
1. General
a. Multisystem granulomatous disease of unknown cause
b. Lungs, skin, heart commonly involved
a. Ranges from a few asymptomatic granulomatous lesions to widespread
infiltration of the myocardium
b. Sudden death
c. Arrhythmias
d. Conduction abnormalities
e. LV dysfunction and CHF
f. Cor pulmonale with pulmonary sarcoid
a. Typically present before age 40
a. Enlarged LV with decreased systolic function
b. RWMA
c. Posterolateral wall thinning with or without aneurysm
d. Diastolic dysfunction (precedes systolic)
e. Valvular dysfunction
f. Pericardial effusion
g. RV and RA enlargement and pulmonary hypertension (cor pulmonale)
5. Related testing
a. ECG: conduction abnormalities, arrhythmias
b. Biopsy
6. Common treatment
a. Medical
1) Pharmacologic therapy to control inflammation
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Cardiac
b. Surgical
1) Pacemaker/AICD
2) Ventricular aneurysm resection
3) Transplant
E. Hemochromatosis
1. General
a. Excess iron storage disease
b. Iron is deposited within cells in organ tissue, interfering with organ
function
c. May be primary (hereditary): inappropriate increased absorption from GI
tract or secondary (acquired): transfusion, iron therapy, etc.
d. Peaks in fifth decade; rare before age 20
a. Dilated cardiomyopathy
b. Cardiac arrhythmias
c. Degree of cardiac dysfunction reflects degree of iron overload
a. Typically male > 40 years old with
1) Diabetes mellitus
2) Skin disease (hyperpigmentation)
3) Liver disease/failure
4) Heart failure
a. Dilated cardiac chambers
b. Global LV systolic dysfunction
c. Normal wall thickness
d. Mild valvular regurgitation
e. Progressive diastolic dysfunction
5. Related testing
a. Endomyocardial biopsy
b. Serum iron levels
6. Common treatment
a. Medical
1) Phlebotomy
2) Manage organ dysfunction
F. HIV Disease/Acquired Immunodeficiency Syndrome (AIDS)

1. General
a. Cellular immune dysfunction
a. Dilated cardiomyopathy/CHF
b. Pericarditis/pericardial effusion
c. RV dysfunction and pulmonary hypertension
d. Endocarditis
e. CAD (may be due to antiretroviral therapy)
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Cardiac
f. Cardiac malignancy
a. Cardiac involvement relatively common but usually clinically silent
b. Significant cardiac abnormalities most common in terminal phase
a. Dilated LV and/or RV with systolic dysfunction
b. Varying degrees of diastolic dysfunction
c. Mitral regurgitation
d. Endocarditis (bacterial and nonbacterial thrombotic)
e. Pericardial effusion with or without tamponade
f. Pleural effusion
g. Constrictive pericarditis
h. Cardiac neoplasm
i. Pulmonary hypertension
5. Related testing
6. Common treatment
a. Medical
1) Treat underlying disease
2) Treat cardiac disease and heart failure
G. Connective Tissue Diseases

1. Rheumatoid arthritis (RA)
a. General
1) Chronic inflammatory disease (primarily involves joints)
2) Age-related
3) More common in women
4) Systemic symptoms: fatigue, myalgias, weight loss, fever, pain
malaise, anorexia
5) May be insidious or sudden onset
6) Limited motion and loss of function
b. Cardiac manifestations
1) Symptomatic cardiac disease not common
2) Pericarditis
3) Myocarditis
4) Endocardial/valvular
5) Conduction system
6) Aortic and pulmonary
1) Pericardial
a) Effusion
b) Constriction
2) Myocardial
a) Global LV dysfunction
b) Regional wall motion abnormalities (rare)
c) Diastolic dysfunction
d) Nodules in myocardium
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Cardiac
3) Valvular
a) Valve thickening and regurgitation
b) Valvular lesions similar to rheumatoid nodules
4) Secondary pulmonary hypertension (rare)
2. Systemic lupus erythematosus (SLE)
a. General
1) Common autoimmune disease characterized by production of
autoantibodies
2) More prevalent and severe in women
3) Cardiac involvement > 40%
1) Valvular (common)
2) Pericardial (common)
3) Myocardial
4) Pulmonary hypertension with pulmonary involvement
5) Conduction abnormalities
6) Vascular thrombosis
1) Valvular
a) Libman-Sacks endocarditis (non-bacterial thrombotic)
b) Valvulitis
c) Diffuse leaflet thickening
d) Regurgitation
e) Valve stenosis (rare)
2) Pericardial
a) Effusion
b) Constriction (rare)
3) Myocardial
a) Global LV dysfunction
b) Regional wall motion abnormalities
3. Antiphospholipid syndrome
a. General
1) Hypercoagulability syndrome
2) High titer of antiphospholipid antibodies
3) Clinical features
a) Recurrent vascular thrombosis
b) Pregnancy loss
c) Thrombocytopenia
d) Positive anticardiolipin test
1) Cardiac dysfunction with coronary thrombosis
2) Pulmonary hypertension with pulmonary thrombosis
3) Valvular (most common)
a) Nonbacterial thrombotic endocarditis
b) Diffuse thickening
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Cardiac
1) Intracardiac, aortic thrombi
2) LV systolic dysfunction
3) Valvular regurgitation
4) Pulmonary hypertension
4. Scleroderma (systemic sclerosis)
a. General
1) Excess connective tissue accumulates in blood vessels, skin, joints,
skeletal muscle, heart
2) More prevalent in women
3) Clinical variants
a) Diffuse
b) Limited cutaneous
1) Clinical evidence uncommon
2) Conduction abnormalities
3) Myocarditis
4) Pericarditis
5) Valvular
1) Myocardial
a) LVH with systolic hypertension
b) LV dysfunction
c) Cardiomyopathy
2) Pericardial
a) Effusion, tamponade
b) Constriction
3) Pulmonary hypertension
H. Ankylosing Spondylitis
1. General
a. Autoimmune disease
b. Chronic systemic inflammatory disorder
c. Primarily affects the axial skeleton (hips and shoulders)
d. Genetic factors
e. Men affected more than women
a. Aortic disease common
b. AV and MV disease
c. Conduction abnormalities
d. Cardiomyopathy
e. Pericarditis
a. Dilatation of aortic annulus and sinus of Valsalva
b. AV thickening and regurgitation
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Cardiac
c. MVP
d. LV systolic dysfunction
e. Pericardial effusion (rare)
I. Marfan Syndrome
1. General
a. Hereditary connective tissue disorder (autosomal dominant)
b. Defect in fibrillin
c. Primarily affects ocular, skeletal, and cardiovascular systems
d. Most common cause of death in adults is aortic dissection
a. MV disease
c. Aortic regurgitation
d. Aortic dissection
a. Aortic root dilatation
c. Annuloaortic ectasia
d. AR
e. Aortic dissection
f. Myxomatous mitral valve with prolapse
g. MR
J. Giant Cell Arteritis

1. General
a. Vasculitis involving large and medium-sized arteries
a. Myocardial inflammation
b. Pericardial inflammation
c. Aortitis
a. Aortic aneurysm and dissection
b. Thickened AV
c. LV systolic dysfunction (myocarditis)
d. Pericardial effusion (pericarditis)
K. Takayasu Arteritis
1. General
a. Granulomatous panarteritis of large vessels
b. Unknown cause
a. Aortitis
a. Aortic dilatation
b. AR
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Cardiac
c. Stenosis and occlusion of large vessels
L. Kawasaki Disease
1. General
a. Acute systemic vasculitis of unknown origin
b. Mucocutaneous, lymph node syndrome
c. Usually seen < 5 years of age
a. Vasculitis of coronary vasa vasorum
b. Leads to coronary artery aneurysms
1) Thrombosis
2) Stenosis
3) Myocardial ischemia, MI
c. Conduction abnormalities
d. Myocarditis
a. Coronary artery aneurysms
b. Pericardial effusion (pericarditis)
c. LV dysfunction (myocarditis)
d. MR
M. Churg-Strauss Syndrome
1. General
a. Systemic vasculitis
b. Characterized by asthma and/or allergic rhinitis, peripheral and tissue
eosinophilia, extravascular granuloma formation, and vasculitis of
multiple organ systems
2. Cardiac/echo findings
a. Pericardial effusion (pericarditis)
b. DCM (myocarditis)
c. Endomyocardial fibrosis
N. Wegeners Granulomatosis
1. General
a. Vasculitis of unknown origin
b. Pathology defined by the triad of small vessel vasculitis, granulomatous
inflammation, and necrosis
c. Multisystem involvement
a. Pericarditis
b. Myocarditis
c. Valvulitis
d. Arteritis
e. Mass lesions (granulomas)
f. Arrhythmias
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Cardiac
a. LV RWMA
b. Global LV hypokinesis
c. Pericardial effusion
d. Valvular regurgitation
O. Endocrine Diseases
1. Hyperthyroidism
a. Sustained overproduction of thyroid hormone, usually due to enlarged
thyroid gland (hypermetabolism)
b. Increased SV, CO, and LV mass
c. DCM (tachycardia-induced)
d. Diastolic dysfunction
e. Atrial fibrillation
f. Pulmonary hypertension (rare)
2. Hypothyroidism
a. Thyroid hormone deficiency
b. Decreased HR and CO
c. Diastolic dysfunction
d. DCM
e. Pericardial effusion
f. Valvular thickening
g. Accelerated atherosclerosis
3. Pheochromocytoma
a. Rare adrenal tumor or tumor along the sympathetic chain (usually intra-
abdominal) that produces excessive catecholamines
b. Increased HR and contractility
c. LV systolic dysfunction with catecholamine crisis
d. LV hypertrophy (occasional)
e. HCM with or without dynamic LVOT obstruction
4. Acromegaly
a. Secretation of excessive growth hormone, nearly always caused by a
pituitary adenoma
b. Cardiac disease occurs in one-third of patients
c. CHF (10-20%)
d. Concentric LVH
e. Diastolic dysfunction
f. Global systolic dysfunction
P. Systemic Infection/Sepsis
1. General
a. Systemic inflammatory response
b. May have infectious or non-infectious etiology
2. Echo features
a. Reversible dilated LV with systolic dysfunction
b. Diastolic dysfunction
c. Endocarditis
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Cardiac
d. Pericardial and pleural effusions
Q. Heriditary Hemorrhagic Telangectasia (Osler-Weber-Rendu)

1. General
a. Autosomal dominant disorder of development of the vasculature
b. Triad: mucocutaneous and visceral telangiectasias, recurrent epistaxis, and
familial history
c. Autosomal dominant
a. High cardiac output
b. Pulmonary arteriovenous malformations (AVM)
c. Coronary arteriovenous malformations (AVM)
a. Presence of pulmonary AVM indicated by late appearance of bubbles in
the left atrium after agitated saline injection
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SECTION XXI: Cardiac Transplantation
1. List primary indications for cardiac transplantation

2. Discuss surgical techniques used in cardiac transplantation
3. Describe complications of cardiac transplantation
4. Describe key echocardiographic findings associated with cardiac transplantation
XXI. Cardiac Transplantation
A. Indications
1. DCM
2. Cardiac amyloid
3. Congenital heart disease
B. Cardiac Transplantation Surgical Techniques

1. Orthotopic
2. Heterotopic
3. Xenotransplantation
4. Artificial heart
C. Role of Echo Assessment

1. LV size and function
a. LV systolic dysfunction may occur early
b. Dysfunction may be secondary to peri-operative donor heart ischemia
2. RV size and function
a. RV systolic function may be reduced secondary to elevated PASP
b. Serial assessment of RVSP
3. Noninvasive clues for rejection
4. Post-transplant CAD
5. Exclusion of pericardial effusion
D. Complications of Cardiac Transplantation

1. Side effects of immunosuppression therapy
2. Coronary artery disease (graft atherosclerosis)
a. Accelerated coronary atherosclerosis
b. Full length of vessel affected (uniform, diffuse involvement)
c. Silent myocardial infarction (no angina due to denervation)
3. Infection
4. Rejection
a. Response of the recipient's immune system to foreign antigens
b. Acute rejection (mononuclear cells infiltrate myocardium and attack
myocardial cells)
c. Confirmed by RV biopsy
5. Post-transplant malignancies
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Cardiac
6. Denervation of the heart

b. Interruption of nerve impulse route due to excision of heart
c. Noncardiac mediators augment heart rate & contractility
d. Delayed response to exercise
e. Chest pain receptors are cut, resulting in inability to feel angina
f. Altered conduction pathways
i. Echocardiographic Features
1. 2-D
a. Normal LV size and function
b. Biatrial enlargement
c. Atrial suture lines visualized
d. Pericardial effusion
e. Paradoxical septal motion
f. Increased left ventricular wall thickness
g. Increased right ventricular dimension
h. Tricuspid regurgitation
2. Doppler findings in transplantation
a. Diastolic function assessment reflects the donor heart
b. Serial assessment of RVSP
c. Assess for increasing TR volume secondary to complications of biopsy
F. Echo Features of Rejection

1. Rejection associated with non-compliance of left ventricle due to extracellular
infiltration and edema
2. Increase in LV wall thickness, LV mass
3. Decrease in LV and/or RV systolic function
4. Increase in RVSP
5. New pericardial effusion
6. Restrictive filling
a. Decreased deceleration time from immediate post-op echo
b. Decreased annular TDI velocity
c. Evidence of elevated filling pressures
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SECTION XXII: Miscellanous Topics
1. List common cardiac abnormalities resulting from cardiac trauma

2. Describe common echocardiographic findings with cardiac trauma
3. Discuss the physiology of athletes heart
4. Describe common echocardiographic findings of atheletes heart
XXII. Miscellaneous Topics
A. Cardiac Trauma
1. Use of echocardiography
a. Early diagnosis
b. Diagnosis may be difficult due to injuries to other organs
c. TEE useful
2. Blunt chest trauma cardiac injury evaluation
a. May be obscured by injury to other organs
b. Right to left cardiac shunt
1) VSD
2) Aneurysm of RVOT
3) Pseudoaneurysm
4) Ruptured septal coronary
5) Disruption of papillary muscle
c. Valve rupture
d. Coronary artery rupture
e. Chamber rupture
3. Blunt chest trauma great vessel injury evaluation
a. Transection of great vessels
b. Aortic rupture
c. Dissection
d. Evaluate
1) Ascending aorta
2) Aortic isthmus
3) Aortic hiatus
4) Aortic arch and branch vessels
a) Innominate
b) Right common carotid
c) Left common carotid
d) Right subclavian
e) Left subclavian
4. Penetrating trauma
a. Foreign objects
1) Bullet
2) Nail
b. Stab wounds
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Cardiac
1) Perforation of annulus
2) Perforation of IVS
3) Prolapse of aortic cusps
5. General echo features
a. Cardiac tamponade
b. Pneumothorax
B. Athletes Heart
1. General
a. History of athletic training and performance
b. Enhanced exercise ability (VO2 max > 40 mL/kg/min)
c. Resting bradycardia
d. Dynamic versus static exercise
a. Increased left ventricular mass (physiologic)
b. Increased LV end-diastolic dimension
c. Increase in LV wall thickness
d. Increased RV cavity dimensions
e. Increased LA size
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ABBREVIATIONS
A
AI Aortic Insufficiency
AMVL Anterior Mitral Valve Leaflet
Ao Aorta
APVR Anomalous Pulmonary Venous Return
AR Atrial Reversal Wave
AR Aortic Regurgitation
AS Aortic Stenosis
ASD Atrial Septal Defect
ASH Asymmetric Septal Hypertrophy
AV Aortic Valve
AVA Aortic Valve Area
C
CAD Coronary Artery Disease
CCA Common Carotid Artery
CHF Congestive Heart Failure
CO Cardiac Output
CRT Cardiac Resynchronization Therapy
CW Continuous Wave
D
DCM Dilated Cardiomyopathy
D-loop Dextrolooping
DT Deceleration Time
DTI Doppler Tissue Imaging
E
ECA External Carotid Artery
ED End-Diastole
EDD End-Diastolic Dimension
EDV End-Diastolic Volume
EF Ejection Fraction
EKG Electrocardiogram
EPSS E-Point Septal Separation
ESV End-Systolic Volume
F
FS Fractional Shortening
H
HCM Hypertrophic Cardiomyopathy
HOCM Hypertrophic Obstructive Cardiomyopathy
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Cardiac
I
IAS Interatrial Septum
ICE Intracardiac Echocardiography
IHSS Idiopathic Hypertrophic Subaortic Stenosis
ICA Internal Carotid Artery
lVC Inferior Vena Cava
IVRT Isovolumic Relaxation Time
IVS Interventricular Septum
IVUS Intravascular Ultrasound
J
JVP Jugular Venous Pressure
L
LA Left Atrium
LBBB Left Bundle Branch Block
LCA Left Coronary Artery
LCC Left Coronary Cusp
L-loop Levolooping
LPA Left Pulmonary Artery
LV Left Ventricle
LVEDD Left Ventricular End-Diastolic Diameter
LVEDP Left Ventricular End-Diastolic Pressure
LVEDV Left Ventricular End-Diastolic Volume
LVH Left Ventricular Hypertrophy
LVIT Left Ventricular Inflow Tract
LVOT Left Ventricular Outflow Tract
LVPW Left Ventricular Posterior Wall
M
MAC Mitral Annular Calcification
MI Myocardial Infarction
MPA Main Pulmonary Artery
MR Mitral Regurgitation
MS Mitral Stenosis
MV Mitral Valve
MVA Mitral Valve Area
MVP Mitral Valve Prolapse
MVR Mitral Valve Replacement
N
NCC Non-Coronary Cusp
P
PA Pulmonary Artery
PAEDP Pulmonary Artery End-Diastolic Pressure
Pas Pulmonary Arteries
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Cardiac
PASP Pulmonary Artery Systolic Pressure

PDA Patent Ductus Arteriosis
PFO Patent Foramen Ovale
PHTN Pulmonary Hypertension
PI Pulmonic Insufficiency
PISA Proximal Isovelocity Surface Area
PLAX Parasternal long axis
PMVL Posterior Mitral Valve Leaflet
PS Pulmonic Stenosis
PSAX Parasteranl Short Axis
PV Pulmonary Valve
PW Pulsed Wave
R
RA Right Atrium
RAP Right Arterial Pressure
RBBB Right Bundle Branch Block
RCC Right Coronary Cusp
RCM Restrictive Cardiomyopathy
RPA Right Pulmonary Artery
RV Right Ventricle
RVEDP Right Ventricular End-Diastolic Pressure
RVH Right Ventricular Hypertrophy
RVIT Right Ventricular Inflow Tract
RVOT Right Ventricular Outflow Tract
RVP Right Ventricular Pressure
RVVO Right Ventricular Volume Overload
S
SAM Systolic Anterior Motion
SPWMD Septal to Posterior Wall Mechanical Delay
SSN Suprasternal Notch
SV Stroke Volume
SVC Superior Vena Cava
T
TDI Tissue Doppler Imaging
TEE Transesophageal Echocardiography
TR Tricuspid Regurgitation
TS Tricuspid Stenosis
TTE Transthoracic Echocardiography
TV Tricuspid Valve
TVA Tricuspid Valve Area
TVP Tricuspid Valve Prolapse
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Cardiac
Vp Velocity propagation
VSD Ventricular Septal Defect
VTI Velocity Time Integral
W
WMA Wall Motion Abnormality
WPW Wolff-Parkinson White
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Cardiac
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Cardiac Ultrasound Imaging Protocol

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Cardiac

SECTION I: Anatomy and Physiology of the Heart

Rationale: Accurate assessment and performance of echocardiograms requires sonographers

1. Describe the heart anatomy

I. Anatomy and Physiology of the Heart

A. Chambers and Related Septa

B. Valves and Related Apparatus

1) Mitral valve (MV)

D. Layers of the Heart

F. Pulmonary Versus Systemic Circulation

SECTION II: Basic Embryology

II. Basic Embryology of the Heart

A. Primitive Heart Tube

h. (R) Right pulmonary artery - right 6th pair

B. Comparison of Fetal and Postnatal Circulation

SECTION III: The Echocardiographic Examination

1. Describe a 2-D echocardiographic examination using proper nomenclature

III. The Echocardiographic Examination

A. Basic Imaging Principles

e) Left atrial appendage (LAA)

6) Origin of coronary arteries

C. Echocardiography Anatomy and Physiology

b) Leaflet names and characteristics

F. Recognition of Technical Errors

SECTION IV: Principles of Cardiac Hemodynamics and Cardiac Cycle

1. List the factors that affect blood flow

IV. Principles of Cardiac Hemodynamics

ii) (½p) mass density is 4 for normal blood

C. Physiology and Hemodynamic Information Derived from Doppler

c) Increased ventricular end-diastolic pressure

SECTION V: Ventricular Function

1. Define ventricular function terminology

A. Determinants of Left Ventricular Performance

B. Wall Motion Abnormalities

C. Global LV Systolic Performance

D. Assessment of Ventricular Systolic Function

8. Tissue Doppler imaging

F. Assessment of Ventricular Diastolic Function

c) Time constant of relaxation

SECTION VI: Coronary Artery Disease (CAD)

1. Correlate ventricular wall segments to coronary artery distribution

VI. Coronary Artery Disease (CAD)

A. Coronary Artery Anatomy and Function

B. Coronary Artery Abnormalities

7) Dilated coronary artery

D. Myocardial Infarction (MI)

SECTION VII: Valvular Heart Disease

1. Describe common etiologies of valvular heart disease

VII. Valvular Heart Disease

A. Mitral Stenosis (MS)

e. Technical considerations and pitfalls

B. Mitral Regurgitation (MR)

1) Mitral inflow E wave velocity

4) Difficult to calculate accurate regurgitant volumeby continuity method

2. Mitral valve prolapse (MVP)

3. Aortic stenosis (AS)

c. Heart responds to increased afterload with increased contractile function

E. Aortic regurgitation (AR)

6) Increased LVEDP and LA pressure eventually leads to backwards

4) Premature opening of aortic valve (acute)

F. Tricuspid Stenosis (TS)

a) TVA = LVOT diam2 x 0.785 x TVI LVOT

G. Tricuspid Regurgitation (TR)

6) Increased LVEDP and LA pressure eventually leads to backwards

E. Differentiation from Other Masses