Echo parameters Flashcards
(121 cards)
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
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
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
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
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
6
Q
Peak E wave affected by
A
IVRT, LA/LV gradient, ventricular compliance
7
Q
E wave incr with
A
- ↑LAP
- ↓LVP (↑ relaxation rate)
- ↓ compliance
- Small MV area
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
9
Q
A wave incr with
A
↑ with ↑HR
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
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
12
Q
When does ventricular outflow starts
A
Flow starts toward end of QRS → ends after T wave
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
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
15
Q
LVOT flow optimal plane
A
- Apical 5 chamber place
o Gate proximal to AoV → btwn IVS and anterior MV leaflet
16
Q
Pattern of LVOT flow
A
similar to Ao flow w lower velocity
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
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)
19
Q
What affects AT of PA flow
A
↓ vascular resistance → ↓ acceleration time in PA
20
Q
What incr PA flow peak
A
↑ with inspiration
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
22
Q
Spectral Doppler flow measurements: peak velocity
A
maximal upward/downward motion
o In cm/s or m/s
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
24
Q
STI
A
ET
AT
AT/ET
PEP
Vcf
25
Ventricular ejection time
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
26
Acceleration time
* Time to peak flow = acceleration time
o Onset of flow at baseline to maximal peak flow velocity
27
AT/ET
fraction of time spent to reach maximal velocity
28
Pre ejection period
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
29
Velocity of fiber shortening
o Combines ET to FS%
o Measure how fast the LV shortens
o Can be normalized to HR (/HR x100)
30
Vcf equation
Vcf = (LVIDd-LVIDs)/(LVIDd x ET)
31
Diastolic time interval
IVRT
32
IVRT: what, optimal plane
* 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
33
Incr IVRT
Delayed relaxation
↓LAP
↑AoP
34
Normal IVRT in dz
o ↑LAP normalizes IVRT in dz
35
External factors affecting doppler flows
* ↑ HR: ↑ peak and mean velocity
* Inspiration
* ↓ weight
No effects: age, sex, breed
36
Tissue Doppler
* 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
37
Phases of TDI
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’
38
Goals of color flow Doppler
* 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
39
Factors affecting systolic function
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
40
Systolic dysfct =
impaired pumping ability and ↓EF%
41
SV reflects
PUMP PERFORMANCE
42
EF reflects
VENTRICULAR FUNCTION
43
Particularity of RV contraction and phases
How is it eval?
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
44
M-mode eval of systolic fct
FS%
LVIDd
LVIDs
45
FS% affected by
preload, afterload, contractility
not a measure of contractility but fct
46
Factors causing decr FS%
↓ preload, ↑ afterload, ↓contractility
47
Factors causing incr FS%
↑ preload, ↓ afterload, ↑ contractility
48
FS% equation
FS% = (LVIDd-LVIDs)/(LVIDd ) x 100
49
Ventricular volume calculation
* Teicholz method
* Modified Simpson’s rule
* Bullet or area-length method
* Systolic/ diastolic indices
EF%
* Ventricular geometry and mass
50
Teicholz method
to calculate EF and SV
o Assume LV is an ellipse
LV volume overload: change LV geometry → ↑ sphericity = not accurate
51
Which volumetric eval has best correlation w/ actual volume in dz state
* Modified Simpson’s rule
o Best correlation w actual LV volume in dz states → unaffected by changes in geometry
52
Modified Simpson’s rule
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
Bullet or area-length method
assume bullet shaped ventricles
o Use transverse dimensions of LV length and width
54
Normal volume index in dogs
systolic <30ml/m2, diastolic <70ml/m2
55
Equations to find volume from systolic and diastolic 2D/M-mode measures
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
EF%
measure of volume leaving the ventricle, not = Ao forward SV
EF = (EDV-ESV)/EDV x 100
57
LV mass equation
Total weight of myocardium
LV mass = 1.05 (total volume – chamber volume)
= 0.8 x (STd + PWTd + LVIDd)3 – LVIDd3) +0.6
58
Relative wall thickness equation
RWT = (2 x PWTd)/LVIDd
59
Use of STI in systolic fct eval
* 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
STI affected by
Afterload
Preload
COntractility
61
Incr afterload
↑ = time to generate pressure is longer
* ↑PEP, ↑LVET
62
Decr afterload
↓ = easier function, sooner reach pressure
* ↓PEP, ↑LVET, ↑ Vcf
63
Incr preload
↑ = activate Frank Starling
* ↓PEP, ↑LVET
64
Decr preload
↓ = no Frank Starling
* ↑PEP, ↓LVET
65
MV annulus motion
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
TV annulus motion
* 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
Volumetric flow
* 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
What is myocardial performance index
* Index of global function: include diastolic + systolic time intervals
o Also called Tei index
69
What myocardial performance index means
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
What affects myocardial perf index
acute changes in loading conditions but not abnormal geometry of HR
71
Define diastolic function
* Allows the heart to fill appropriately at normal pressures
o Diastolic failure: CHF w normal systolic fct
o From AoV closure → MV closure
72
Interactive components of diastolic fct
Myocardial relaxation
Atrial contraction
Rapid and slow filling phases
Loading conditions
Pericardial sac
Elastic properties of the heart
73
Parameters assessing diastolic fct
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
Delayed relaxation definition, causes
* LVP remains ↑ in diastole
o Delayed LV filling
o ↑ contribution of atrial contraction to filling
o From: hypertrophy, ischemia
75
Compliance definition
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
Causes of decr compliance
fibrosis, infiltrative process, hypertrophy, structural abnormalities
77
Delayed relaxation parameters changes
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
Pseudonormalization: def and parameters changes
* 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
how to differentiate pseudonormal pattern vs normal
* Differentiation from normal
o PV flow: high velocity Ar flow
80
What can affect pattern de diastolic dysfct
* 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
What is the Bernoulli equation and what do we use it for
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
Limitations of Bernoulli
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
Types of PG
* 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
Systolic LV pressure estimation from echo
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
Systolic RV pressure estimation from echo
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
Diastolic systemic pressure estimation from echo
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
Diastolic pulmonic pressure estimation from echo
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
Regurgitant fraction equation
* 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
Shunt ratio: what used for
* 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
What is pressure 1/2 time
* Time for peak flow velocity to reach ½ of its initial value
o Rate of ↓ in MR velocity = rate of ↓ in LVP
91
MR Pressure 1/2 time influenced by
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
AI pressure 1/2 time assess
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
Ventricular inflow pressure 1/2 time
* 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
DDX incr EPSS
A. Dilated cardiomyopathy
B. Aortic insufficiency
C. Mitral valve stenosis
D. PDA
E. Canine X linked muscular dystrophy
95
EPSS def, normal value
End-point septal separation
* Max anterior motion of anterior leaflet of MV
* Abnormal >6mm
96
EPSS indicates
o Systolic dysfct → reduced posterior motion of IVS
o LV dilation
o Reduced MV motion
97
Define strain
% change in length during myocardial contraction and relaxation
98
How to calculate strain
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
What is strain rate
temporal derivation of strain → information about the speed at which deformation occur
o Rate of change in length during myocardial contraction
100
How to calculate strain rate
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
What can influence myocardial deformation (ie strain)
is load dependent
o Interpret along with wall thickness, shape and pre/afterload
102
Strain imaging
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
Normal aspect of imaging curves: strain
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
Normal aspect of imaging curves: strain rate
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
Advantages of strain
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
Limitations of strain
o Artifacts: reverberation → segments can appear akinetic
o Doppler: need good alignment with interest region
107
TDI and strain rate
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
Speckle tracking
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
What can we calc w/ speckle tracking
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
Clinical applications of strain
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
Tissue Doppler imaging: spectral doppler
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
3 modes of TDI
PW
Color TM
Color 2D
113
PW TDI mode
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
PW TDI mode limitations
* Maximal measurable velocity
* Allow assessment of only single sample
* Sample volume cannot be changed to track a region of interest
115
Color TM TDI mode
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
Color TM TDI mode advantage
calculate velocities of an entire section of myocardium
117
Color TM TDI mode limitations
aliasing artifacts, velocities only on selected TM US line
118
Color 2D TDI mode
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
Normal velocity profiles: TDI Radial + longitudinal velocity profiles of LVFW
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
Normal velocity profiles: TDI L radial myocardial motion
heterogenous
Subendocardial fibers move > quickly vs subepicardial
Systolic and diastolic radial intramyocardial gradient
121
Normal velocity profiles: TDI Longitudinal motion of LVFW
Myocardial velocities ↓ from base → apex
Systolic and diastolic longitudinal intramyocardial gradient
