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6. Echocardiographic principles > Echo parameters > Flashcards

Echo parameters Flashcards

1
Q

Optimal planes for PVs

A

R parasternal transverse images at level of LA And Ao, LAX, L parasternal transverse images with LA and LAA, modified apical 4 chamber view

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2
Q

Pattern of PV flow

A
  • Flow is pulsatile and continuous.
    o LA filling: mostly during ventricular systole → + S deflection
     Can be biphasic
     Directly related to mean LAP
     ↑ HR and age
    o LA emptying: early diastole → drop in LA pressure while blood flow into LV
     Blood is passively pulled into LA as blood moves through MV into LV → + D deflection
     Simultaneous to E wave
    o Atrial contraction: backward mvt of flow into PVs because of ↑ LA pressure → - A deflection
     Simultaneous to A wave
     Affected by: end diastolic LAP, LA fct, LV compliance, HR/rhythm
     Velocity ↑ w age, duration ↓ with age
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3
Q

Optimal plane for transmitral flow

A

o L parasternal 4 and 5 chamber view
o Sample gate at tip of leaflets wide open
o PW Doppler

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4
Q

Flow profile affected by

A
  • Best flow profiles with highest velocity, ↓ spectral broadening and good definition of A and E waves
    o Rapid HR:
     >125bpm may cause overlap of E and A waves
     >200bpm = no separation
    o Affected by preload, myocardial relaxation
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5
Q

Pattern/phases of transmitral flow

A

o Early phase of ventricular filling (E wave): from MV opening → peak ventricular filling
o Late phase (A wave): atrial contraction
o E usually > A wave → E:A ratio >1
 ↑HR can bring ratio closer to 1
* ↓ E wave → ↓ ventricular volume due to ↓ filling time
* ↑ A wave → ↑ flow due to atrial contraction

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6
Q

Peak E wave affected by

A

IVRT, LA/LV gradient, ventricular compliance

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7
Q

E wave incr with

A
  • ↑LAP
  • ↓LVP (↑ relaxation rate)
  • ↓ compliance
  • Small MV area
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8
Q

E wave decr by

A
  • ↓LAP
  • Impaired relaxation
  • ↑ compliance
  • Large MV area
    *Usually result in ↑A wave because of higher contribution to LV filling
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9
Q

A wave incr with

A

 ↑ with ↑HR

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10
Q

What other thing can be seen on transmitral flow

A
  • MV opening click present, closing click barely present
    o Lack of opening click suggest gate to far in LV
    o Loud opening gate suggest gate to close to MV annulus
     ↓ E velocity and deceleration time
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11
Q

RV inflow patterns

A

= similar to LV inflow
o Velocities are lower (↓ pressure drop RA → RV)
o Inspiration ↑ peak flow velocity
 Especially E wave → E + E:A ↑ w inspiration

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12
Q

When does ventricular outflow starts

A

Flow starts toward end of QRS → ends after T wave

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13
Q

Optimal plane for Ao flow velocity

A

o Should show LV length about 2x width
 Apical 5 chamber view
 Subcostal 5 cham ber view
o Doppler gate just distal to AoV

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14
Q

Pattern of Ao flow

A

o Rapid acceleration, peak reach in 1/3 of systole
 Little spectral broadening until peak is reached
 Most healthy dogs <2m/s
* >2.5m/s = abnormal
* 2-2.5m/s = grey zone
 Mean Ao flow acceleration = 32cm/m2
o Slower deceleration → asymmetric profile
o Shorter ejection time vs PA flow

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15
Q

LVOT flow optimal plane

A
  • Apical 5 chamber place
    o Gate proximal to AoV → btwn IVS and anterior MV leaflet
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16
Q

Pattern of LVOT flow

A

similar to Ao flow w lower velocity

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17
Q

Pulmonic flow optimal plane

A
  • Gate placed distal to valve w/I PA
  • Good angle of interrogation but depth may be an issue for adequate recording
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18
Q

Pattern of PA flow

A

symmetrical and rounded
o Acceleration time slower vs Ao → peak reached mid systole
 Mean AT:ET in dogs = 0.43
o Peak flow velocity usually <1.3m/s
o Slightly longer ET and ↓ PEP compared to Ao flow (↓afterload)

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19
Q

What affects AT of PA flow

A

 ↓ vascular resistance → ↓ acceleration time in PA

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20
Q

What incr PA flow peak

A

 ↑ with inspiration

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21
Q

LAA flow

A
  • Fill in ventricular systole
    o Fe: 0.24 to 0.93m/s
  • Empty during A contraction in late diastole
    o Fe emptying velocity: 0.19 to 1m/s
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22
Q

Spectral Doppler flow measurements: peak velocity

A

maximal upward/downward motion
o In cm/s or m/s

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23
Q

Spectral Doppler flow measurements: mean velocity

A

o Tracing of the flow envelop → area under the curve = distance a volume of blood travels
 Velocity time interval, flow velocity integral or time velocity integral
o Proportional to SV
o Cm

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24
Q

STI

A

ET
AT
AT/ET
PEP
Vcf

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25
Q

Ventricular ejection time

A

o At baseline, from onset → end of flow
o Effect of HR can be minimized by normalizing the interval w HR
 Uses the slope of HR vs LVET graph = 0.55

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26
Q

Acceleration time

A
  • Time to peak flow = acceleration time
    o Onset of flow at baseline to maximal peak flow velocity
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27
Q

AT/ET

A

fraction of time spent to reach maximal velocity

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28
Q

Pre ejection period

A

o Similar to IVCT: AoV + MV closed → build up of LV pressure
o From onset of QRS → onset of systolic flow
o Ratio PEP/LVET = more accurate indicator of LV fct

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29
Q

Velocity of fiber shortening

A

o Combines ET to FS%
o Measure how fast the LV shortens
o Can be normalized to HR (/HR x100)

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30
Q

Vcf equation

A

Vcf = (LVIDd-LVIDs)/(LVIDd x ET)

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31
Q

Diastolic time interval

A

IVRT

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32
Q

IVRT: what, optimal plane

A
  • Isovolumic relaxation time (IVRT):
    o Indirectly measure ventricular relaxation: time for LV to equalize LAP
     From apical 4 or 5 chamber view
     Cursor in LVOT close to MV
     From end of Ao flow → start of MV flow
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33
Q

Incr IVRT

A

 Delayed relaxation
 ↓LAP
 ↑AoP

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34
Q

Normal IVRT in dz

A

o ↑LAP normalizes IVRT in dz

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35
Q

External factors affecting doppler flows

A
  • ↑ HR: ↑ peak and mean velocity
  • Inspiration
  • ↓ weight
    No effects: age, sex, breed
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36
Q

Tissue Doppler

A
  • Information about myocardial velocity
    o Color tissue Doppler: mean myocardial velocity
     Lower velocities vs pulsed
     Endocardial velocities < epicardial velocities from radial fibers
    o Pulsed wave tissue Doppler: peak myocardial velocity
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37
Q

Phases of TDI

A

o Positive systolic motion: S’
o Early diastolic motion: E’
o Late diastolic motion: A’
o IVRT: end of S’ → start of E’
o IVCT: end of A’ → start o f S’

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38
Q

Goals of color flow Doppler

A
  • Evaluate for insufficiencies: trivial or mild regurgitation not hemodynamically significant.
    o Usually no murmur
    o Pathologic regurgitation
     Semi quantitative evaluation: size of color flow jet in atria
  • Color M mode: helps separate events diastole vs systole
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39
Q

Factors affecting systolic function

A

o HR
o Contractility
o Preload → amount of blood distending ventricles at end diastole
 Force stretching myocardium → Starling law = ↑ stretch → ↑ contraction force
 Eccentric hypertrophy → ↑LV mass in response to ↑ volume
o Afterload
 Force against which the heart must contract → systemic/pulmonary BP
 Concentric hypertrophy → ↑wall thickness w/o ↑ volume
 Inverse relationship w myocardial fiber shortening
o Distensibility
o Coordinated contraction

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40
Q

Systolic dysfct =

A

impaired pumping ability and ↓EF%

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41
Q

SV reflects

A

PUMP PERFORMANCE

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42
Q

EF reflects

A

VENTRICULAR FUNCTION

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43
Q

Particularity of RV contraction and phases

How is it eval?

A

o Starts at apex → upper region of RV chamber = slow + continuous mvt of blood into lungs
o 3 phases
 Contraction of papillary muscles
 Mvt of RVFW → IVS
 Wringing of RV 2nd to LV contraction
o Mostly qualitative evaluation
 Estimates of volume and EF inaccurate
 Hu: fractional area % change (FAC):
* Apical 4 chamber view
 Other parameters: CaVC, PAP from TR

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44
Q

M-mode eval of systolic fct

A

FS%
LVIDd
LVIDs

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45
Q

FS% affected by

A

preload, afterload, contractility

not a measure of contractility but fct

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46
Q

Factors causing decr FS%

A

↓ preload, ↑ afterload, ↓contractility

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47
Q

Factors causing incr FS%

A

↑ preload, ↓ afterload, ↑ contractility

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48
Q

FS% equation

A

FS% = (LVIDd-LVIDs)/(LVIDd ) x 100

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49
Q

Ventricular volume calculation

A
  • Teicholz method
  • Modified Simpson’s rule
  • Bullet or area-length method
  • Systolic/ diastolic indices
    EF%
  • Ventricular geometry and mass
50
Q

Teicholz method

A

to calculate EF and SV
o Assume LV is an ellipse
 LV volume overload: change LV geometry → ↑ sphericity = not accurate

51
Q

Which volumetric eval has best correlation w/ actual volume in dz state

A
  • Modified Simpson’s rule
    o Best correlation w actual LV volume in dz states → unaffected by changes in geometry
52
Q

Modified Simpson’s rule

A

o End diastolic (after MV closure) and systolic frames (before MV open) → tracing endocardial borders
 Computerized calculation: volumetric sum of stack of discs
 Ideally 2 LAX planes, maximize length and width (length =2xwidth)

Volume = 0.85 A2/L

53
Q

Bullet or area-length method

A

assume bullet shaped ventricles
o Use transverse dimensions of LV length and width

54
Q

Normal volume index in dogs

A

systolic <30ml/m2, diastolic <70ml/m2

55
Q

Equations to find volume from systolic and diastolic 2D/M-mode measures

A

LV diastolic volume (LVVd) = (7 x 〖LVd〗^3)/(2.4+ LVd)

LV systolic volume (LVVs) = (7 x 〖LVs〗^3)/(2.4+ LVs)

LV SV = LVVd-LVVs

LV EF = (LVVd-LVVs)/(LVVd ) x 100

56
Q

EF%

A

measure of volume leaving the ventricle, not = Ao forward SV

EF = (EDV-ESV)/EDV x 100

57
Q

LV mass equation

A

Total weight of myocardium

LV mass = 1.05 (total volume – chamber volume)
= 0.8 x (STd + PWTd + LVIDd)3 – LVIDd3) +0.6

58
Q

Relative wall thickness equation

A

RWT = (2 x PWTd)/LVIDd

59
Q

Use of STI in systolic fct eval

A
  • May be better indicators of systolic fct vs FS%
    o As accurate as invasive methods to assess LV performance in Hu
    o Not indicator of contractility but fct
60
Q

STI affected by

A

Afterload
Preload
COntractility

61
Q

Incr afterload

A

 ↑ = time to generate pressure is longer
* ↑PEP, ↑LVET

62
Q

Decr afterload

A

 ↓ = easier function, sooner reach pressure
* ↓PEP, ↑LVET, ↑ Vcf

63
Q

Incr preload

A

 ↑ = activate Frank Starling
* ↓PEP, ↑LVET

64
Q

Decr preload

A

 ↓ = no Frank Starling
* ↑PEP, ↓LVET

65
Q

MV annulus motion

A

o Correlated w EF% in Hu and dogs
 Strong relationship w BW. Normalized by:
* /BSA
* Use FS as follows
o Normal in dogs: 0.46-1.74cm

66
Q

TV annulus motion

A
  • Tricuspid annular motion (or plane systolic excursion → TAPSE)
    o Normal range in Hu: 1.5-2cm
     <1.5cm associated with poorer px for L CHF from DCM or PH
67
Q

Volumetric flow

A
  • Based on conservation of mass principle: mass in = mass out
    o Mass = density (D) x volume (V) x area (A) → density is constant
    o Q = flow
     Flow volume: is determined by flow velocity integral (VTI)
  • Can also be determined by: VTI = (peak velocity x ET)/2
  • ↑ VTI → can indicate volume (ie shunt) vs ↓VTI can indicate poor flow
     Area: any of 4 valves
  • CSA = pir2 → where r is the radius of the valve
  • Left sided measurement correlate well with invasive methods, but R sided measures have higher variability (variable diameter of PA because of poor lateral resolution)
68
Q

What is myocardial performance index

A
  • Index of global function: include diastolic + systolic time intervals
    o Also called Tei index
69
Q

What myocardial performance index means

A

o Correlates well with diastolic and systolic fct of RV and LV in dogs
 Use ventricular ET + IVRT/IVCT to derive overall assessment of global fct
 Can be derived from PW or TDI
 Normal <0.4
o Can identify suclinical DCM in Newfoundland + dysfct in dogs w TR, MR, PH
o Also correlate w LV filling pressures

70
Q

What affects myocardial perf index

A

acute changes in loading conditions but not abnormal geometry of HR

71
Q

Define diastolic function

A
  • Allows the heart to fill appropriately at normal pressures
    o Diastolic failure: CHF w normal systolic fct
    o From AoV closure → MV closure
72
Q

Interactive components of diastolic fct

A

 Myocardial relaxation
 Atrial contraction
 Rapid and slow filling phases
 Loading conditions
 Pericardial sac
 Elastic properties of the heart

73
Q

Parameters assessing diastolic fct

A

o IVRT
 From AoV closure → before MV opening
 No change in volume, all valves closed
 ↓ pressure as myocardium relaxes
o PV flow:
 PVa >0.35m/s
 a-dur >20ms vs transmitral atrial flow
 Venous systolic flow < diastolic flow (S < D)
o Transmitral valve flow: 3 phases
 Rapid ventricular filling → E wave (E/A >2)
 Slow ventricular filling → E deceleration = equilibration of LA and LV pressures (<140ms)
 Atrial contraction → A wave
o TDI-E’ and A’
 E/E’ >15

74
Q

Delayed relaxation definition, causes

A
  • LVP remains ↑ in diastole
    o Delayed LV filling
    o ↑ contribution of atrial contraction to filling
    o From: hypertrophy, ischemia
75
Q

Compliance definition

A

reflection of heart distensibility
o Compliant chamber = proper filling at normal P
o Noncompliant chamber = rapid ↑ pressure as filling occurs
 Larger role in late diastole when ventricle is partially filled

76
Q

Causes of decr compliance

A

fibrosis, infiltrative process, hypertrophy, structural abnormalities

77
Q

Delayed relaxation parameters changes

A

o Transmitral valve flows: ↓ peak E, ↑ A, ↓E:A, ↑ deceleration time (>200ms)
o ↑ IVRT (>100ms) → if severe = ↓IVRT
o TDI: ↑LAP → ↓E’ (<8cm/s) = ↑E:E’ >15

78
Q

Pseudonormalization: def and parameters changes

A
  • Normal transmitral flow profile despite diastolic dysfct
    o As LAP ↑ → ↑E wave → changes E:A ratio back to normal
     E:A can still > 1
     Short IVRT (60-110ms)
     Short, early deceleration (150-200ms)
     Normal or ↓ A
     Low E’ velocity (<8), ratio E:E’ = 9-14
79
Q

how to differentiate pseudonormal pattern vs normal

A
  • Differentiation from normal
    o PV flow: high velocity Ar flow
80
Q

What can affect pattern de diastolic dysfct

A
  • Valvular regurgitation: can alter pattern
    o AI: ↑LV diastolic pressures rapidly in diastole
     Rapid E deceleration as pressure gradient ↓ rapidly
    o MR: large pressure gradient LA → LV
     ↑E wave
81
Q

What is the Bernoulli equation and what do we use it for

A

based on principle of conservation of energy
o Constant volume of blood moved through orifice/vessel
o P ↑ proximal to obstruction → proportional ↑ velocity
o Modified equation: small overestimatimation of gradient

Used to calculate PG

Change in P = 4(V22 – V21)
Modified: (PG) = 4V2

82
Q

Limitations of Bernoulli

A

 Dependent on blood volume = inaccurate with high flow states
* Insufficiency through valve or stenotic area (AI, AS, shunt, anemia, sepsis)
 Tunnel lesion: effect of friction no longer insignificant (overestimate gradient)
 Blood viscosity: overestimation if ↓
 Large intercept angle
 V1 is not negligeable

83
Q

Types of PG

A
  • Peak to peak PG: difference from max ventricular pressure → vessel pressure
  • Doppler derived PG: max instantaneous pressure difference btwn ventricular and vessel pressure
    o Can be as much as 30-40% > vs peak to peak
84
Q

Systolic LV pressure estimation from echo

A

fairly = systemic BP in absence of LVOTO
o Driving pressure of MR = LVP = systemic BP
o LVP around 100-120mmHg, LAP <10mmHg → PG around 100mmHg expected for MR

85
Q

Systolic RV pressure estimation from echo

A

approximate pulmonic BP
o Driving pressure of TR = RVP = pulmonic BP
o LVP around 20-25mmHg, LAP <5mmHg → PG around 20mmHg expected for MR

86
Q

Diastolic systemic pressure estimation from echo

A

derived from AI
o Peak AI velocity = PG btwn LV and Ao
o Normal systemic diastolic P = 60mmHg, LVP in diastole = 10mmHg → PG = 50mmHg

87
Q

Diastolic pulmonic pressure estimation from echo

A

derived from PI
o Peak AI velocity = PG btwn LV and Ao
o Normal PA diastolic P = 10-15mmHg, RVP in diastole = 5mmHg → PG = 50mmHg
 Elevated → confirm PH (normal 2-2.5m/s)

88
Q

Regurgitant fraction equation

A
  • Flow through all valves should be equal
  • With AV regurgitation: flow through AV valve > flow through semilunar valves

Mitral RF = (mitral SV – Ao SV)/mitral SV

89
Q

Shunt ratio: what used for

A
  • Assess severity of shunting (VSD, ASD, PDA) → analyze flow through area before and after shunt (Qp/Qs ratio)
  • ↑ shunting volume → ↑ volume of blood in PA vs Ao
90
Q

What is pressure 1/2 time

A
  • Time for peak flow velocity to reach ½ of its initial value
    o Rate of ↓ in MR velocity = rate of ↓ in LVP
91
Q

MR Pressure 1/2 time influenced by

A

o MR jet velocity affected by LAP
 Normal = low LAP → rapid rise in MR velocity
 Systoic dysfct = ↓ rise in LVP → ↓ rate of ↑ MR velocity

92
Q

AI pressure 1/2 time assess

A

o Assess effect of AI on LV diastolic pressure
o Severe AI = triangular shape profile (vs plateau normally)
 Rapid ↓ in Ao diastolic pressure (runoff in LV) + ↑LVP
 Rapid ↓ in regurgitant jet velocity as driving pressure ↓
o Measurement: diastolic pressure ½ time
 Extend deceleration slope to baseline → measure deceleration time
 Deceleration time x 0.29
 <300m/s suggest hemodynamically significant AI

93
Q

Ventricular inflow pressure 1/2 time

A
  • MV/TV stenosis
    o Delayed normal early diastolic closure because of persistent pressure differential LA to LV → reduced slope
    o Severity correlates directly with pressure ½ time
     ↑ pressure ½ time = ↑ severity
     Normal in dogs = 29 ± 8m/s, cats <30ms
94
Q

DDX incr EPSS

A

A. Dilated cardiomyopathy
B. Aortic insufficiency
C. Mitral valve stenosis
D. PDA
E. Canine X linked muscular dystrophy

95
Q

EPSS def, normal value

A

End-point septal separation
* Max anterior motion of anterior leaflet of MV
* Abnormal >6mm

96
Q

EPSS indicates

A

o Systolic dysfct → reduced posterior motion of IVS
o LV dilation
o Reduced MV motion

97
Q

Define strain

A

% change in length during myocardial contraction and relaxation

98
Q

How to calculate strain

A

o Can be calculated in any of the 3 regional planes: circumferential, longitudinal or radial
o Regional quantification of myocardial function
 Vector: 3 normal + 6 shear strain components for 1 myocardial region
 Longitudinal strain: most commonly used
* Normal = 20% in all LV regions
o Global strain: global LV fct
 Speckle tracking
 Global longitudinal strain = deformation along entire length of LV wall in apical image

99
Q

What is strain rate

A

temporal derivation of strain → information about the speed at which deformation occur
o Rate of change in length during myocardial contraction

100
Q

How to calculate strain rate

A

o Difference btwn 2 velocities → normalized to the distance btwn them (s-1)
 Shortening/thinning = negative values
 Lengthening/thickening = positive values

Strain rate = (Va – Vb)/d

101
Q

What can influence myocardial deformation (ie strain)

A

is load dependent
o Interpret along with wall thickness, shape and pre/afterload

102
Q

Strain imaging

A

similar to measuring myocardial velocity gradient
o Analyze contraction of myocardium // to US beam
o Better spatial resolution & frame rate (up to 200 frame/s) in selected sector
o Color coded
* Evaluation:
o Quantitative: data will form a curve of values over time
o Qualitative: 2D color coding

103
Q

Normal aspect of imaging curves: strain

A

 Peak systolic strain (shortest dimension) = end systole, before AoV closure
 End diastole is 0 → decrease until end systole → IVRT = flattening → rapid increase (E wave) → plateau (diastasis) → A wave increase in late diastole

104
Q

Normal aspect of imaging curves: strain rate

A

mirror image of velocity curve
 Peak systolic strain rate (fastest shortening velocity) = mid systole
* Insensitive to changes in loading
 Negative S curve in systole → positive E curve in early diastole → positive A curve in late diastole

105
Q

Advantages of strain

A

measures only the active/intrinsic motion of the myocardium
o *Myocardial velocity measured by TDI may be over/underestimated by translational motion or tethering of myocardium
o Strain rate will measure actual deformation (= stretching of contraction)

106
Q

Limitations of strain

A

o Artifacts: reverberation → segments can appear akinetic
o Doppler: need good alignment with interest region

107
Q

TDI and strain rate

A

 Regional velocity gradient = temporal derivative of a change in length
o Strain rate can be calculated from 2 velocity samples at known distance apart
o Well validated, but 10-15% interobserver variability

108
Q

Speckle tracking

A

 Specific myocardial patterns (= speckles or features) on B-mode echocardiography
o Follows motion frame by frame
o Track speckles in any direction in 2D image
 Multidirectional tracking
 Angle independency
o Need good image quality + proper image geometry

109
Q

What can we calc w/ speckle tracking

A

 Calculation of myocardial velocity, displacement, strain, strain rate
o Myocardial deformation – cyclical
 Baseline length is arbitrary
 Softwares will use surrogate parameters like R-peak of QRS → not truly related to MV closure as physiologic definition of beginning of systole

110
Q

Clinical applications of strain

A

 Cardiac dysynchrony: temporal differences in max systolic deformation among myocardial segments
o Dilated LV
 Abnormal strain prior to detection of traditional findings
o Systemic dz: systemic hypertension,
o Myocardial disease: DCM, HCM, Adriamycin/doxorubicin toxicity
o Coronary artery dz

111
Q

Tissue Doppler imaging: spectral doppler

A

measure myocardial motion velocities throughout cardiac cycle
o Myocardium moves at slower velocity (<20cm/s) vs blood flow (200cm/s)
o High acoustic reflectivity → high amplitude signals
o Motion of myocardium needs to be // to beam for accuracy

112
Q

3 modes of TDI

A

PW
Color TM
Color 2D

113
Q

PW TDI mode

A

 Analysis of a sample (Doppler gate) = instantaneous myocardial velocities
* Radial myocardial motion: R SAX ventricular view
* Longitudinal myocardila motion: L LAX view
 Velocities + when myocardium moves toward probe, - when moving away from probe

114
Q

PW TDI mode limitations

A
  • Maximal measurable velocity
  • Allow assessment of only single sample
  • Sample volume cannot be changed to track a region of interest
115
Q

Color TM TDI mode

A

 Analyze myocardial velocities along US line on 2D image
 Color coding: identical as conventional color Doppler → clearer color = higher velocity
 Mainly used to analyze radial motion of LVFW and IVS on R ventricular SAX

116
Q

Color TM TDI mode advantage

A

calculate velocities of an entire section of myocardium

117
Q

Color TM TDI mode limitations

A

aliasing artifacts, velocities only on selected TM US line

118
Q

Color 2D TDI mode

A

 Myocardial motion velocity + direction are color coded superimposed on 2D image
 Allow simultaneous analysis of multiple myocardial segments of same ventricular wall
* Permit study of intra/interventricular synchronicity
 Tracking of specific region of interest is possible

119
Q

Normal velocity profiles: TDI Radial + longitudinal velocity profiles of LVFW

A

 Brief IVCT
 Positive systolic wave
 Short IVRT
 2 negative early and late diastolic waves (E and A)
 IVRT, IVCT and E can be biphasic in dogs/cats

120
Q

Normal velocity profiles: TDI L radial myocardial motion

A

heterogenous
 Subendocardial fibers move > quickly vs subepicardial
 Systolic and diastolic radial intramyocardial gradient

121
Q

Normal velocity profiles: TDI Longitudinal motion of LVFW

A

 Myocardial velocities ↓ from base → apex
 Systolic and diastolic longitudinal intramyocardial gradient

6. Echocardiographic principles (10 decks)

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