Left Ventricle Flashcards
Cardinal LV movements?
Longitudinal
Circumferential
Radial thickening
Fractional shortening?
1-dimensional (LVIDd-LVIDs)/(LVIDd) > 25% = normal PSLAX or PSAX Inner edge to inner edge Teicholz method; EF = FSx2 if no WMA
Fractional area change
2-dimensional
(LVEDA - LVESA)/(LVEDA)
FAC > 35% = normal
PSAX. Trace area, include papillary muscles
Ejection Fraction
3-dimensional
(LVEDV-LVESV)/(LVEDV)
A4C & A2C using Biplane method
Tissue doppler S’
Mitral valve annulus excursion velocity
Normal values:
Lateral > 10 cm/s
Septal > 8 cm/s
EPSS
M-mode perpendicular to tip of anterior mitral valve leaflet (A2)
PLAX
Normal < 8 mm
EPSS > 13 mm high PPV for EF < 35%
Caveats with EPSS
Falsely elevated in MS, AI, and dilated cardiomyopathy
Load dependency of dP/dT?
Preload dependent
Afterload independent
Need MR jet
What is dP/dT?
Utility of dP/dT?
Rate of pressure rise in systole
measure of contractility independent of afterload
how to calculate dP/dT?
Limitations?
dP = difference b/t pressures at 100 cm/s and 300 cm/s = 32 mmHg
dT = time it takes for pressure to increase from 4 mmHg to 36 mmHg
Numerator ALWAYS 32.
Need to be very precise and accurate with measurement of will get wildly inaccurate measurement (this is LIMITATION).
Normal typically > 1000 mmHg/s
Velocity of circumferential thickening
Benefit?
FS equation with ejection time (ET) in denominator
VCT = (LVIDd-LVIDs)/(LVIDd)(ET)
Less preload dependent than EF
What are the load INDEPENDENT measurements of LV systolic function?
End-systolic elastance
Recruitable stroke work
Strain rate
LVOT VTI
Measure of how far the RBC travel in LVOT during systole
Used to calculate stroke volume or as independent measure of contractility
Normal 18-22 cm for HR 55-95
Normal values for LVIDd, LVEDA, and LV wall thickness
Where do you measure LV wall thickness?
LVIDd = 4-6 cm
LVEDA = 30-40 cm2
LV septum = < 1.1 cm
Inferior wall = < 1.1
PSLAX, distal to MV leaflet tip, in diastole (inf & septum)
PSAX, septum only, in diastole
Most common non-primary cardiac tumors?
Highest rate of pericardial mets?
Which cancer can extend from IVC into RA?
Metastatic tumor 20x more likely. Lung > lymphoma > breast
Melanoma HIGHEST rate of pericardial mets, but low prevalence, more likely lymphoma
RCC can extend up IVC into RA
Most common primary cardiac tumor?
Most common malignant?
Most common valve tumor?
Atrial myxoma. Left > right.
Angiosarcoma
Fibroelastoma, down-stream side of valve
What three features increase risk for LAA thrombus?
Mitral stenosis
Atrial fibrillation
PWD velocity < 40 cm/s near LAA
Most common cardiomyopathy?
What kind of valve dysfunction does it cause?
What feature associated with increased mortality?
DCM
MR from type IIIb Carpentier leaflet motion (MV restriction in systole ONLY)
EDD index > 4 cm/m2
Echo features of LVOT obstruction?
Late-peaking systolic doppler envelope
“Dagger shape”
MR with contralateral directed jet (posteriorly directed)
M-mode with early systolic closure AV leaflet, fluttering AV cusp
Turbulence or flow acceleration LVOT
How do you distinguish restrictive CM from constrictive pericarditis?
Do both have abnormal mitral inflow patterns?
Both characterized by restricted MV inflow pattern on PWD
RCM has abnormal TDI w/ S’ < 8
Constrictive pericarditis has compensated contraction velocity, normal TDI
Formula for strain?
Formula for strain rate?
What is strain & strain rate?
Strain = (L-L0)/L where L0 = initial length
Strain rate = strain/time = velocity/L
Strain is motion deformation b/t two points that occurs w/ systole.
Measure of contractility.
Uses TDI or speckle tracking.
More negative = better
Benefit of using strain and strain rate?
Distinguishes tethering from true contraction
End-systolic strain can estimate EF
Speckle tracking is angle independent
4 stages of diastole?
IVRT - ventricular pressure decrease, no change in volume Early rapid filling (E) - determined by LAP & ventricular relaxation/pull Diastasis - LAP = LV pressure Late filling (A) - atrial contraction
Stages/progression of diastolic dysfunction
Impaired relaxation → longer DT (> 160 ms) and IVRT, no diastasis, E
What is an “L” wave?
Seen between E and A wave with PWD MV inflow.
Represents increased LAP.
How does valsalva affect diastolic filling?
How is it used to distinguish Grade II diastolic dysfunction from normal function?
Valsalva → inc ITP → dec preload → dec LAP → decreased E wave
In grade II diastolic dysfunction, valsalva can unmask an impaired relaxation MV inflow pattern by decreasing E wave 50% → E < A
Secondary signs of elevated LAP?
TR max velocity > 2.8 m/s LAVI > 34 mL/m2 LA diameter > 5 cm Pulmonary vv flow reversal (S and D wave reversal) Abnormal IAS motion
