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TEE > 3. LV Systolic Performance and Pathology > Flashcards

3. LV Systolic Performance and Pathology Flashcards

1
Q

What is a normal LV Ejection Fraction?

A

55% for both men and women

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2
Q

What are the pros and cons of linear measurements of LV function?

A

Pro:
Lowest interobserver variability
Accurate

Con:
Least accurate representation of LV function where there are regional abnormalities

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3
Q

Linear measurements of LV function - Types?

A
  1. Endocardial fractional shortening
  2. LV wall thickness
  3. Relative wall thickness
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4
Q

Endocardial fraction shortening

A
  • Type of linear measurement to assess LV function
  • Using M-mode of transgastric short-axis of LV just above papillary muscles

= (LVIDd-LVIDs)/LVIDd x 100

Normal men: 25-43%
Normal women: 27-45%

LVIDd=LV internal diameter, diastole
LVIDs=LV internal diameter, systole

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5
Q

Left ventricular wall thickness

A
  • Type of linear measurement to assess LV function
  • Using transgastric short-axis of LV
  • Measure both septal wall and inferior wall at END DIASTOLE

Septal Wall: right septal surface to left septal surface
Inferior Wall: Epicardial surface to endocardial surface

Normal men: 0.6-1.0cm
Normal women: 0.6-0.9cm

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6
Q

Relative Wall Thickness

A
  • Type of linear measurement to assess LV function
  • Using M-mode of transgastric short-axis of LV just above papillary muscles at END DIASTOLE
  • Apply to patients with LV hypertrophy

= (2 x PWTd)/LVIDd or (PWTd+SWTd)/LVIDd

Normal men: 0.24-0.42cm
Normal women: 0.22-0.42cm

> 0.42cm = concentric hypertrophy
(wall thickness increased, normal internal diameter)
<0.42cm = eccentric hypertrophy
(dilated internal ventricle)

LVIDd = LV internal diameter diastolic
PWTd = posterior wall thickness, end diastole
IWTd = inferior wall thickness, end diastole
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7
Q

Planimetric Evaluation of LV - Types?

A
  1. Fractional area change
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8
Q

Fractional Area of Change

A
  • Only planimetric eval of LV function
  • Uses transgastric short-axis at level of papillary muscles, or long-axis

= (LVAd-LVAs)/LVAd x 100

Normal men: 56-62%
Normal women: 59-65%

LVAd = LV area, end diastole
LVAs = LV area, end systole
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9
Q

Volume Evaluation fo LV - Types?

A
  1. Volumetric equations from linear measurements

2. Volumetric equations using planimetric measurements

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10
Q

What LV volume increased risk of morbidity and mortality?

A

> 70mL

Normal men: 22-58mL
Normal women: 19-49mL

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11
Q

Cubed Formula

A
  • Used to assess LV function with volumes from linear measurements
  • Relies on assumption of LV being symmetrical and elliptical
  • Overestimates size of dilated ventricles since they tend to dilate primarily along the short axis (which is then cubed)

LV Volume (ml) = LVIDminor ^3

LVIDminor = septal to lateral wall (4 chamber or TG) or anterior to posterior (2 chamber)
- Measured at level of mitral chord

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12
Q

Volumetric Equations using planimetric equations, Types?

A
  1. Single plane ellipsoid
  2. Biplane ellipsoid
  3. Hemisphere-cylinder or bullet
  4. Modified Simpson’s (disks)
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13
Q

Single plane ellipsoid for LV volume

A
  • Relies on assumption of LV being symmetrical
  • Measurements obtained in 4 chamber or 2 chamber

LV Volume (mL)= 8 x [(LVAlax)^2/3piLVIDmj]

LVAlax = LV area from 2 or 4 chamber
LVIDmj = LV internal diameter major, end diastole
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14
Q

Biplane ellipsoid for LV volume

A
  • Relies on assumption of LV being symmetrical
  • Incorporates LVIDmj and LVAlax (both aquired from 2 or 4 chamber) and LVIDmin and LVAsax (obtained from TG short-axis above papillary muscles)

= (piLVIDmj/6) x (4LVAsax/piLVIDmin) x (4LVAlax/pi* LVIDmj)

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15
Q

Bullet Formula for LV volume

A
  • Preferred method to use if difficulty seeing the endocardial border of the apex

LV Volume (mL) = 5/6 x LVAsax x LVIDmj

LVAsax obtained in TG short-axis
LVIDmj obtained in 2 or 4 chamber

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16
Q

Modified Simpson’s rule for LV volume

A
  • LV described as a series of 20 disks
  • Underestimates significantly if endocardial border of the apex if difficult to see or with foreshortening
  • Should use x-plane and use both 4 and 2 chamber views
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17
Q

LV Mass from Linear Measurements

A
  • Myocardial volume x density of myocardial tissue
  • Myocardial volume determined by subtracting LV cavity volume from total LV volume
  • LV mass/BSA preferred
  • Increased LV mass stronger predictor of mortality than low EF

= 0.8 x [1.04 x {(LVIDmj + PWT +SWT)^3 - (LVIDmj)^3}] +0.6

LV Mass
Normal men: 88-244g
Normal women: 67-162g

LV mass/BSA
Normal men: 49-115 g/m^2
Normal women: 43-95 g/m^2

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18
Q

LV Mass from Planimetric Measurements

A
  • Either bullet or ellipsoid methods are used with tracing of both endocardial and epicardial surfaces with subtraction of the two
  • Proprietary formula
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19
Q

Rate of Ventricular Pressure Rise - dP/dT

A
  • dP/dT correlates with systolic function

How to:
- MR jet obtained with CWD
- Cursor placed on MR profile at 1 m/s and then at 3 m/s
- Time interval between those two velocities recorded
- Pressure differential over this period of time = 32mmHg by Bernoulli
= 4(3^2)-4(1^2) = 32

dP/dT = 32mmHg/time recorded (s)

Normal > 1000 mmHg/s

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20
Q

What is the gold standard of LV volume?

A

MRI

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21
Q

Tissue Doppler Imaging (TDI) - General

A
  • Low-pass filters are used to screen out high velocity movement (blood) and focus on low velocity of tissues
    • Opposite of usual doppler use
  • Myocardial motion is low velocity, high amplitude (blood is high velocity, low amplitude)
  • Optimize frame rate with narrow image sector
    • Angle of interrogation is critical. Tissue must be parallel to beam or TDI will be underestimated.
22
Q

TDI - Waveform

A

Systole = negative deflection (tissue moving away from probe)

  • BiPhasic during isovolumic contraction
    • Initially downward deflection is early myocardial activation at base of the heart which pulls annulus toward apex (occurs with MV closure)
    • Upward deflection due to displacement of annulus upward due to contraction of apex
  • Monophasic during ejection
    • Annulus moves down as LV completely contracts and ejects
23
Q

TDI - Normal Values

A

Systolic velocity
Normal: > 7.5cm/s
LV Failure: <3cm/s

** Peak velocities

24
Q

Color Tissue Doppler (Curved M Mode)

A

Markers are placed at various points along ventricular wall and provides velocities against time

  • Produces mean velocities (lower than regular TDI numbers)
Red = Movement toward probe
Blue = Movement away from probe

Pros vs TDI

  • Utilizes spatial info and can assess regional and global LV function
  • Can identify post-systolic shortening

Pros vs 2D echo
- Endocardial borders are not needed to be seen, so dropout in walls that lie parallel to beam not a limitation

** Uses TDI technology so angle of interrogation remains critical

25
Q

Strain and Strain Rate

A

Strain = segmental myocardial deformation (shape/length change)

Strain Rate = rate of myocardial deformation change

  • Extrapolation of TDI technology
    • Strain and SR are NOT direct measures of contractility because deformation can be affected by preload, after load, myocardial stiffness.

Blue (positive) = myocardial lengthening
Red (negative) = myocardial shortening
Akinetic = green

In 4 chamber: systole = red, diastole = blue
In TG SAX: systole = blue, diastole = red
b/c in SAX myocardium thickens in systole

Pro v TDI:

  • Is not fooled by tethering, like TDI
  • Better determining infarcted v non-infarcted tissue
26
Q

Speckle Tracking

A

Uses 2D Gray images to calculate strain

  • Unique acoustic marker configurations (speckles) are identified and their movement and direction are tracked to create velocity vectors

Pros v Traditional strain:

  • Speckle tracking doesn’t rely on TDI technology, so angle of interrogation does not introduce error
  • Any wall that can be visualized can be interrogated
27
Q

LV Ventricle Synchrony

A
  • As LV fails, areas of LV begin to contract at slightly different times
    • Either due to conduction system issues, or mechanical (scarring that prohibits proper electrical conduction)
  • Typically inferior or lateral walls will be delayed
  • Can be performed with M-mode or TDI

Abnormal
Septal to posterior wall delay > 130ms
Septal to lateral wall delay >65ms
* These patients benefit from cardiac resynchronization

28
Q

What are the types of cardiomyopathy?

A
  1. Primary
    - disease confined to the heart (genetic, nongenetic, acquired)
  2. Secondary
    - generalized process involving heart and other organs
29
Q

Types of Primary Cardiomyopathy

A
  1. Genetic
    - Hypertrophic cardiomyopathy (HCM)
    - Noncompaction of the left ventricle
  2. Mixed (Genetic and Nongenetic)
    - Dilated cardiomyopathy (DCM)
    - Primary restrictive cardiomyopathy
  3. Acquired
    - Myocarditis
    - Tako-Tsubo (apical ballooning) cardiomyopathy
    - Peripartum cardiomyopathy
30
Q

Types of genetic cardiomyopathies

A
  1. Hypertrophic cardiomyopathy

2. Noncompaction of the left ventricle

32
Q

Hypertrophic Cardiomyopathy

A
  • Primary genetic cardiomyopathy - autosomal dominant
  • Heterogenous group characterized by hypertrophied, NONDILATED LV that is NOT secondary to HTN or AS
  • Subtypes
    1) Concentric
    2) Septal (diffuse vs asymmetric septal hypertrophy)
    3) Apical
  • Preserved systolic function
  • LV dyssynchrony common
  • Dynamic LVOT obstruction common
33
Q

Dynamic LVOT obstruction and SAM

A
  • Obstruction results from SAM of mitral valve causing coaptation with bulging septum
  • Physiologic theories of SAM
    1) LVOT obstruction produces Venturi effect on mitral valve
    2) Abnormal papillary muscle orientation from LV remodeling
    3) Abnormal elongated anterior mitral leaflet
34
Q

Echo findings of SAM

A
  • AML-septal contact during systole
  • Posterolaterally directed MR jet during mid-systole (poss into diastole)
  • Turbulent LVOT flow
  • Late systolic peaking velocity (dagger) on CW of LVOT
  • Systolic notching on M-mode tracing of aortic valve (early aortic valve closure)
35
Q

Non-compaction of left ventricle

A
  • Congenital cardiomyopathy
  • Characterized by deep sinusoids between enlarged trabeculae
  • Result of arrested embryogenesis of LV
  • Can be isolated or associated with other congenital heart defects
  • Associated problems
    1) Decreased LV systolic function and heart failure
    2) Sudden death
    3) Arrhythmia
    4) Thrombus formation in sinusoids with embolic events
36
Q

Types of Mixed Cardiomyopathies

A

1) Dilated cardiomyopathy

2) Primary restrictive

37
Q

Dilated Cardiomyopathy (DCM)

A
  • LV enlargement with normal wall thickness and increased cardiac mass
  • Mixed genetic cardiomyopathy, causes:
    • Autosomal dominant (1/3)
    • Viral infection
    • Toxins (Etoh, heavy metal)
    • Autoimmune
    • Collagen vascular disease
    • Pheochromocytoma
    • Neuromuscular disease
    • Mitochondrial
    • Metabolic, endocrine
  • Most frequent reason for listing for heart transplantation
  • Dilation occurs mostly along SAX and heart becomes more globular
  • Associated findings:
    • Mitral annulus dilation
    • Function MR 2/2 abnormal papillary muscle orientation and mitral leaflet tethering
    • Biatrial enlargement
    • Apical thrombus
    • Diastolic dysfunction
38
Q

Causes of dilated cardiomyopathy

A

Mixed genetic cardiomyopathy, causes:

  • Autosomal dominant (1/3)
  • Viral infection
  • Toxins (Etoh, heavy metal)
  • Autoimmune
  • Collagen vascular disease
  • Pheochromocytoma
  • Neuromuscular disease
  • Mitochondrial
  • Metabolic, endocrine
39
Q

Dilated cardiomyopathy, associated findings

A
  • Mitral annulus dilation
  • Function MR 2/2 abnormal papillary muscle orientation and mitral leaflet tethering
  • Biatrial enlargement
  • Apical thrombus
  • Diastolic dysfunction
41
Q

Primary restrictive cardiomyopathy

A
  • Characterized by:
    • Normal or decreased volume of BOTH ventricles
    • Biatrial enlargement
    • Normal wall thickness and normal valves
    • Restrictive diastolic physiology
    • Normal systolic function
  • Genetic and non-genetic causes
42
Q

Types of acquired primary cardiomyopathy

A
  1. Myocarditis
  2. Tako-Tsubo (apical ballooning)
  3. Peripartum
43
Q

Myocarditis

A
  • Acquired primary cardiomyopathy
  • Acute and chronic
  • Results in dilated cardiomyopathy and arrhythmias
  • Causes:
    • Infection
    • Drugs, toxins
44
Q

Tako-Tsubo (apical ballooning) cardiomyopathy

A
  • Rapid onset, related to extreme stress and sympathetic stimulation
  • Extensive stunning of mid and apical segments of LV
  • Apical half balloons out during systole, while basal half is hypercontractile
45
Q

Peripartum cardiomyopathy

A
  • Rare cause of severe dilated cardiomyopathy
  • 3rd trimester to 5 months post-partum
  • 50% -> persistent heart failure, 50% -> full recovery
46
Q

Constrictive Pericarditis vs Restrictive Cardiomyopathy

A

Constrictive Pericarditis

  • Thickened pericardium
  • Normal atrial and LV size
  • Normal wall thickness
  • Normal myocardium
  • Normal systolic function
  • Septal movement towards LV during spontaneous inspiration
  • Enlarged IVC and hepatic veins
  • No MR or TR
  • E/A normal or 25% with spontaneous inspiration or mechanical expiration
    • Normal decrease ~5%, COPD 10-15%
  • IVRT increased with inspiration
  • Pulmonary vein flow: S=D during inspiration, D>S with expiration
  • Hepatic vein flow: W shaped waved form (large a wave) with decreased diastolic flow with spontaneous expiration

Restrictive cardiomyopathy:

  • Normal pericardium
  • Enlarged atria
  • Small LV size with increased wall thickness
  • Granular myocardium
  • Reduced systolic function
  • No ventricular independence
  • Enlarged IVC and hepatic veins
  • Usually MR or TR
  • E/A > 2.2
  • No significant decrease in mitral E wave with spontaneous inspiration
  • IVRT does not vary
  • Pulmonary vein flow: S<D, no respiratory variation
  • Hepatic vein flow: Blunted systolic flow, possibly systolic flow reversal if signifacnt TR
47
Q

Left Ventricular Hypertrophy, types

A
  • Types:
    1) Concentric
    2) Eccentric
48
Q

Concentric LVH

A
  • Parallel replication of sarcomeres without significant chamber enlargement
  • Secondary to chronic pressure overload
  • Goal = decrease wall stress
    • wall stress = (pressure x chamber size)/wall thickness
  • Additional LV changes
    • Prolonged IVRT
    • Reduced compliance -> diastolic dysfunction
    • Eventual cardiac function compromise
49
Q

Eccentric Hypertophy

A
  • Serial replication of sarcomeres with LV chamber enlargement
  • Secondary to chronic volume overload
50
Q

Determine types of hypertrophy, LV mass and Relative wall thickness

A

Normal: mass 0.42
Concentric hypertrophy: mass increased; RWT >0.42
Eccentric hypertrophy: mass increased; RWT normal

51
Q

LV True Aneurism

A
  • Frequently 2/2 anterior wall MI
  • Form within 90 days of infarct, <5 days portends worse prognosis

Characteristics

  • Dilated dyskinetic area with myocardial thinning
  • Aneurism neck to maximum aneurism diameter = 0.9-1.0
52
Q

LV Pseudoaneurism

A
  • chronic ventricular rupture contained by the pericardium
  • high incidence of rupture, therefore must be corrected

Characteristics:

  • ratio of orifice to max aneurism diameter <0.5
  • false aneurism expands in systole while LV contracts

TEE (20 decks)

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