Systolic function and Aortic valve Flashcards
measures of systolic function
fractional shortening nml >30
fractional area change nml >50
ejection fraction >55
SV and CO
Dp/dt
V of circumferential shortening
End systolic elastance
preload recruitable stroke work
strain rate
tissue doppler peak systolic velocity
Fraction indices
all are (Diastolic - systolic) / diastolic
Qp/Qs
SVpa/SVlvot, helps to determine shunt
Inward radial motion of normal , hypokinetic, akinetic, dyskenitic function
normal - greater than 30%
hypokinetic - 10-30 %
Akinetic less than 10%
dyskinetic - paradoxical systolic motion
Dp/Dt
slope of LV pressure rise from 4-36 mmHg, need MR jet, measured at 1 and 3 m/s
Normal is 1610 +/- 290 mmHg/sec (around 1300 min)
velocity of circumferential shortening
FS with ET in denominator
end systolic elastance
Load Independent. Slope of PV loop at end systole points. Steeper slope is better systolic function
preload recruitable stroke work
Stroke work is the area under curve of PV loop. If this is plotted as function of end diastolic volume
Steeper slope is better systolic function
preload adjusted max power
Stroke work/EDV^2 or
stroke work/ EDA^(3/2)
load independent
tissue doppler peak systolic velocity
faster sā is better systolic function, no normal values to be tested on
influenced by tethering and translation
strain rate
Strain is dimensionless, and change in length produced by application of stress
strain rate is strain/time
Translation and angle independent but limited by noise
load independent
Aortic root size
normally less than 4 cm in adult
Basic views of Aortic valve
ME AV SAX, LAX
Deep TG LAX
TG LAX
ME 5 chamber
AI acute vs chronic
acute- stroke work preserved, elevated end diastolic pressure
chronic - compensates by dilating and lower end diastolic pressure, larger stroke volumes. Eventually sarcomeres stretch too far and causes decompensation
Intervene before it becomes too dilated and decreased SV
Severity of AI
Jet height : LVOT diameter
mod 25-64%
Jet area : LVOT area
mod 5-59%
Jet depth
mod tip of AL
VC
greater than 6mm severe
Slope of jet decay
greater than 3 m/s severe
PHT
mod 200-500 ms, affected by diastolic function
Flow reversal in Aorta
3 things determine prognosis in AI.
LV dysfunction
LV dilation
Asc Ao dilation- sinus best predictor (normal 25-31mm)
High risk AI patients
symptomatic
Reduced EF
end systolic diameter indexed >25mm/m2 (81 vs 34% survival at 10 years)
Low risk group Marfan syndrome for AI
Indexed sinus / predicted sinus diameter that is less than 1.3 or less than 5% change annually
When to replace valve
symptomatic or
asymptomatic with severe chronic AR, or chronic AR with root dilation
Types of AI classes
type 1 a- 1 d is normal cusp motion
type 2 - cusp prolapse, common
type 3 - cusp restriction
Aortic stenosis assessment
peak velocity - mod 3-3.9 m/s
mean grad - 30-49 mmHg
max grad - 40-69 mmHg
DVI mod 0.25-0.5 independent of patient size, stroke volume (TVI LVOT/TVI AV) or ( A valve/ A LVOT)
AVA mod 1-1.5 cm2
Indexed AVA mod 0.6-0.85 cm2/m2
If mean gradient is high then you are done
If low, need to see if there is low flow and use cont eq or DVI
Modified gorlin equation
Shows how you can have low gradient but still have aortic stenosis
AVA = CO/ Peak grad
continuity equation
flow in equals flow out
can use Vpeak or VTI
psuedoaortic stenosis
not enough stroke volume to pop valve open.
peak instantaneous vs peak to peak gradient
peak instantaneous > p 2 p gradient
Echo is instantaneous, p2p is cardiac cath
In 3d en face view of mitral valve where is LAA and interatrial septum
LAA screen left, IAS screen right
Right heart views
4 C - FAC , Septal and post/ant leaflet
RV I/O
TG SAX
TG RV inflow
Deep TG RV outflow
Asc AO SAX
Ao Arch SAX
ME bicaval and modified bicaval
Innominate vein
can be recognized on right hand side of aortic arch in upper esophageal aortic arch short axis view
RVSP calculation
4Vtr^2 + RAP
Estimate pulmonic pressure assuming no pulmonic valve stenosis
RV function assessment
more qualitative than LV
highly compliant, low resistance, sensitive to loading conditions
20% of post CPB failure due to RV
RV failure
can occur just by opening pericardium
2-3% of patients after heart transplant and 20-30% after LVAD
retrograde cardioplegia doesnt protect because of thebesian veins draining into RV and not sinus.
PVR increases after CPB
parameters of RV function
FAC >35% (mean 49)
EF >45%
TAPSE >15-17 mm (mean 23)
IVA = 1.4 +/- 0.5 m/s (mean 3.7) most load independent for RV
TV Sā <10 abnormal
strain >-20
Isovolumic acceleration
Peak velocity seen before sā on tissue doppler / time it takes to reach peak
Should be somewhere around 2-3 m/s
load independent!
RV volume overload
flattening of septum at end diastole to left hand side
usually from PI, ASD, TR
eccentricity index
vertical dimension / horizontal dimension
Index >1 = RV dysfunction
RV pressure overload
Shifts to left during end systole
RVH thickness >5mm
Mcconell sign
apex moves but base does not indicates PE
RV inflow outlfow leaftlets seen
Posterior on lateral side and a/s on medial side
Tricuspid Regurgitation
Functional TR (normal leaflets) from annular dilation, pap muscle dysfunction, pressure/vol overload, PA cath
structural TR ( abnormal leaflets)
from rheumatic dz, myxomatous dz, ebsteins, carcinoid, endocarditis
Jet area mod 5-10 cm2
vena contracta >7 severe
hepatic flow reversal severe
jet density = more volume
Rheumatic dz
most common cause of TS but less likely than TR , most commonly affects MV alone but can affect MV, AV and TV
Ebsteins anomaly
Large sail like anterior leaflet, TV funnel shaped and apically displaced p/s leaflets
Associated with secundum ASD and SVT (WPW)
carcinoid syndrome
releases serotonin, bradykinin , histamine, prostaglandin
RV valves damaged , thickened, fibrosed. Usually MAO protect LV (PFO can facilitate passage)
can cause both TR and TS but TR more common
CVP and HV waveform timing
x descent which matches s wave on HV
y descent which matches d wave on HV
A and V waves match
Tricuspid stenosis
rare, but most commonly from rhuematic dz. Also from carcinoid or congenital
Normal Peak velocity 30-70 cm/sec
190/PHT
mean gradient >5 mmHg severe but dependent on HR and flow
Pulmonic valve
Hard to visualize
Has anterior , right and left cusps
valve leaflet closest to aortic valve is either left or right, farthest away from AV is anterior cusp
Pulmonic insufficiency
Mild PI is normal
Significant PI usually congenital but can be caused by carcinoid, endocarditis, pHTN, myxomatous dz, radiation
measured with jet area, width and holodiastolic flow reversal in main pa
Early PI velocity used for PA mean pressure
Late pi velocity used for pa diastolic pressure
pulmonic stenosis
usually congenital
measured by peak and mean gradients
seen in TOF ( subpulmonic)
Hemodynamic goal includes maintaining aortic diastolic pressure. RVH and elevated RV pressure leads to coronary perfusion during diastole only. Does not drop o2 demand
Pts frequently arrest
RV differences from LV
TV septal leaflet more apically placed than MV Anterior leaflet
moderator band
presence of TV
presence of trabeculations
absence of two well defined pap muscles
RV MPI
(IVRT + IVCT) / ET , lower is better
Also can use TR signal time - PA signal time / PA signal time
with PWD < 0.43 normal
with TDI < 0.54 normal
RV dp/dt
12/time it takes TR jet to go from 1- 2 m/s.
Affected by loading conditions
<400 mmHg/s is abnormal
Innacurate with severe TR
Things to look for assessing right heart function
CVP+CI
position of IAS
TR?
Geometry
Free wall motion and FAC
RIMP
grading of endocardical thickening
grade 1 normal movement with thickening <30%
grade 2 slightly decreased movement with 10-30% thickening
grade 3 severe hypokinesis with <10% thickening
grade 4 akinesis with no thickening
grade 5 dyskinesis
How to calculate LVEDP using AR CWD
Using modified bernouli equation of the late AI velocity
AoDP-LVEDP=4 Vailate^2
how and when to measure aortic annulus and root
aortic annulus - mid systole inner edge to inner edge
all other measurements end diastole from leading edge to leading edge in perpendicular plane to long axis of aorta.
what is leading edge to leading edge in aorta
includes anterior wall but not posterior wall
