Embedded Files
Diastolic Ventricular Function (Lai8)
Diastolic Ventricular Function (Lai8)
Diastole =
-Isovolumetric relaxation- semilunar vlv closes --> AV vlv flow onset
-Rapid filling- start when Pventric < Patrial, so Q thru AV vlv
-Early Diastolic Flow = E wave- pks in early diastole as Pventric is at minimum, then decels as
ventric pressure starts to increase as it is filled
-Diastasis- mid-diastole when Patrial =Pventric after early filling, so little Q thru AV vlv
-Atrial Contraction- late diastole incr in Patrial, to be >Pventric--> 2nd wave of Q across AV vlv
-late diastolic velocity profile = A wave
-filling d/o ventric syst fx, AV vlv fx, rate of ventric relaxation, passibe compliance/stiffness of atria and ventricles, atrial systolic fx, loading/volume conditions of atria and ventricles, intraathoracic P changes w resp, HR, rhythm
Mitral Inflow
-PW at MV leaflet tips on AP4C, as parallel to mitral inflow as possible
-the peak E and A will be much decreased if you're in the LA!!
Measurements:
-Diastolic time interval
-Peak velocity at Early filling & w Atrial contraction
-Area filling fractions
-Velocity and area ratios
-Peak filling rat
-IVRT is shortened
-Isovolumetric Relaxation Time (IVRT)- time fr Ao vlv closure to initiation of diastolic flow at MV
-measure fr the A2 (Ao closure) sound on the phonocardiogram thru initiation of diastolic Q at MV
-or arrange transducer so you can get LVOT Q also w a 5 chamber view (time fr end of Ao Q...)
-IVRT is indexed to HR
-Poor LV relaxation--> long IVRT (takes longer for ventric P to be lower than atrial...)
-IVRT is shorter if incr LA P and poor LV compliance
-Deceleration Time (DT) during early filling fr E pk to end of Q is also used to describe relaxation
-longer time bn E pk and end of filling--> worse LV relaxation
-this time shortens as HR increases... so not good if pt tachycardic
-E:A ratio describes pattern of LV diastolic filling
-Velocity Time Integral (VTI) = area under the curve during E and A together,
-Area of filling in first 1/3 and 1/2 of diastole also used to describe inflow
-Doppler pk filling rate = pk E velocity * mitral annulus cross sectional area ( which is Î d/4)
-Peak filling rate (stroke vol/s) = pk E (cm/s) / MV VTI (cm)
PVn Inflow
-PW in R or L upper pulm vn fr AP4C, as parallel as possible, w sample as far into the vn as possible
Measurements:
-pk systolic velocity
-pk diastolic velocity
-Velocity Time Integral (VTI) during syst and diast phases compared w total area under curve
-syst/diastolic velocity and VTI ratios
-systolic pulm vn flow is often biphasic in infants and young kids- bc dissociation bn atrial relaxation and MV annular displacement
-high systolic velocity measured
-Velocity and duration of atrial reversal - differentiate diastolic doppler pattern if there's incr LA and LV EDP.
--Caveat- pulm vn compliance plays a role in the Doppler pattern in kids, so in healthy infants, pt may have continuous phasic fwd Q thru the pulm vn w reversal of Q w atrial contraction.
-Atrial flow reversal in a neonate should be concerning for AbNl incr LAP, bc of limited Q thru pulm vasc bed as a fetus.
-In healthy kids, flow reversal is common in atrial systole, bc the prox PVns are more compliant, so don't need to c/s LV dysfx...
-Duration of flow reversal in PVns w atrial contraction IS a more Snindicator of diastolic dysfx, espec if it is > than A-wave duration on MV inflow (!)
Tricuspid & Systemic Venous Inflow
-can use same MV indices for TV to assess RV diastology
-it's harder on the R side bc of inspiratory variation... (see pic)
-inspiration--> incr fwd Q thru TV
-E incr by 25% and A by 20% w insp in Nl kids
-SVC inflow- biphasic, w dominant systolic RA filling
-No flow reversal in SVC during atrial systole- bc RA compiance is incr compared to LA
-unlike LA, there's no age related variability in pattern
-pattern affected by RA htn, TV dysfx, pericardial dz, arrhythmias
-Marked syst vn Q reversal w atrial contraction = signif RA htn or TS
-Decreased/Reversed systolic Q = signif TR, loss of AV synchrony, or restrictive dz
-Large pericardial effusion--> limit diastolic filling w absent/reversed diastolic syst vn Q @ exhale
-assoc w marked decr in TV E wave velocity w onset or exhalation and reciprocal changes in MV E wv
Inflow Doppler Analysis AbNlies:
AV Valve Stenosis
-atrial htn fr restricted Q across AV vlv
-Prolonged P gradient decay fr atrium to ventricle
-Incr pk E w marked prolongation of E wave decel
-Variable A wave velocities
-Inflow pattern is influenced by the stenosis and HR, so can't assess ventricle diastole
-venous doppler pattern shows high diastolic atrial P and delayed diastolic emptying so that venous diastolic inflow is reduced w mild-mod stenosis, absent w sev stenosis
-atrial P can be markedly incr w atrial systole, --> prolonged and high velocity flow reversal at end diast.
AV Valve Insufficiency
-the regurg jet Q increases systolic atrial P
--> systolic reversal of flow in vns, (seen only w severe regurg)
-Mod regurg--> decr fwd systolic flow; and Nl biphasic flow pattern if mild regurg
-Caveat: direction of the regurg jet relative to the vn checked may change the matters a lot. (if to jet twd wall then less effect on inflow pattern)
Pulm/Syst Vn Obstruction
-see continuous high velocity turbulent Q w loss of the biphasic pattern seen Nly
-loss of end systolic and end diastolic deceleration to baseline (which is a hallmark of Nl inflow)
-Newborns, espec if signif L to R shunt lesions, can have more continuous pattern of pulm vn Q, but the biphasic syst and diast pks are maintained w doppler velocities that appproach baseline at end syst and end diast.
Arrhythmias
-...
Doppler Tissue Imaging
-disadvantage of PW/CW Doppler is that they are much affected by the myocardial loading conditions (at of preload...)
-DTI checks myocardial motion by tracking the wall velocities thru the cardiac cycle
-check w PW at mitral, septal, and tricuspid annular motion
-TV annular motion is NOT affected much by respiration, so independent unlike TV inflow PW
-MV annular motion is NOT affected much by intravasc volume, unlike MV inflow
-ventric expansion/contraction occurs on the base-apex and ant-post axes, and annuli move along the former axis
-Systole- annulus moves twd apex; Early diastole- recoil of the ventricle fr contracted state; Late diastole- annular motion affected by both syst and diast
-check fr AP4C view, w wall as parallel to transducer as possible
-the DTI filter looks for low velocity, high amp signals of myocardium--> avoids blood Q
-best gate is 3-5mm in kids; Nyquist 15-30cm/s; sweep of 100-150mm/s
-septum can be made the most parallel but is affected by RV so doesn't completely reflect LV
-Measurements:
-E (aka E') is early diastole
-A is late diastole (atrial systole wave)
-S is systole
-can also look at diastolic time interval, and isovolumetric relaxation (time fr end of systole to start of early diastole)
-early diastolic deceleration time- fr pk early diastole to return of the diast velocity to baseline prior to annular motion fr atrial contraction.
-Limits: depend strongly on the angle of interrogation, might be affected by translational shifts in heart position during the cardiac cycle, and segmental wall motion might not reflect global fx
Color M-Mode Flow Propagation
-assess ventric filling by M-Mode of early diastolic flow velocity fr the AV vlv to the apex
-check fr AP4C w cursor parallel w diastolic inflow
-adjust the color Doppler interrogation area to get longest column of flow fr the AV annulus to the apex
-it estimates ventric filling and correlates well w the time constant of LV relaxation
-NOT affected by preload
-mainly affected by LV relaxation
-abNl relaxation--> slower rate of early diastolic flow propagation
-Vp = Propagation Velocity = the slope of the line drawn fr apex to base on the color tracing
-= measures the rate of flow propagation (how long it takes to get bn 2 pts)
-lower Nyquist to display the 1st color aliasing (usually about 75% of pk E velocity)
-higher slope = faster flow propagation and more rapid ventric relaxation
Myocardial Deformation Imaging
-Strain Rate/Strain Imaging
-Quantify LV and RV fx - assess regional myocardial fx, while negating the effects of cardiac translational motion and of local tethering effects (a problem w PW assessment of annular motion in TDI)
-corresponds to the rate of deformation of a specific segment of myocardium
-curves are calculated fr tissue velocity data:
-Strain Rate = (difference of 2 velocities in the segment of interest)/distance bn the 2 velocity points
-It is integrated over time; expressed as a %
-Limits: angle dependence, signal noise (thus not used much...)
-Ultrasonic Speckle Tracking- doppler independent way to get directionally unconstrained imagin of the myocardial motion
-speckles = US reflectors within tissue
-helps get diastolic velocities, diastolic strain rate, times to pk for each parameter
-track the endocardial contour...
LA Volume
-good marker of the duration and severity of LV diastolic dz
-reflect chronic, cumulative filling P over time
-well correlated with the severity of diastolic dysfunction as estimated by Doppler (in old ppl)
-LA > 32cm3/m2 is a R/F for 1st CV event (a-fib, stroke, HF) in old ppl, and correlates w their survival
-LA vol varies w cardiac cycle, so only max volume is measured
-best to check at MV opening
-Can measure by checking area of LA in 2 views (like Simpson's biplane) or by area-length method - both have been validated but both underestimate volume compared to CT/MRI
-LA = 8/[(3pi)(A1)(A2)/L] with L the shorter of either view
-Limits: can foreshorten LA (the length in the 2 views shouldn't differ by more than 5mm), the max LA volume should be measured- just before MV opening; LA border should be measured consistently- w inf border is the mid pt of the MV annulus, NOT the leaflet tips, and the tracing of the border should exclude the LAA and PV confluence
DIASTOLIC DISEASE
Notes]Transthoracic and Transesophageal Echocardiography Echo MeasurementsEsEcho Measurements
Fractional Shortening
FS% - ((LVEDD - LVESD)*100)/LVEDD
-in PSSA, at level of paps
-not accurate w flat IVS
-not a measure of global ventric fx
Ejection Fraction
=Diast vol - syst volume
-depends on good endocardial border definition (enhanced w contrast, but we don't in peds...)
-higher incidence of intra-observer and inter-observer variability.
Ejection Fraction
-Diastolic Volume - Systolic Volume
-Simpson's Biplane method- divide LV into 20 disks, check area, calc volume, then calculate diff in sys and diast...
Intracardiac Pressures
RV or PA P
-Normal = 15-30mmHg
RVP= 4(TR pk velocity)2 + RA
Systolic BP = 4(VSD pk velocity)2
-if no LVOTO
Systolic BP = 4(PDA pk velocity)2
LV Systolic BP = 4(VSD pk velocity)2 = (systolic BP + 4*LVOT2) - (4*VSD2)
-Must obtain TR, VSD, and PDA velocities from various views with CW Doppler. Use the highest velocity; ensure complete envelope.
PA Diastolic P
-Normal = 10-12mmHg
-PA End Diastolic P = 4(PR end diastolic velocity)2 +RA P (because RAP =RVEDP)
-PA mean P = 4(PR early diastolic velocity)2
LV Systolic P
-Normal = Newborn: ~70mmHg, Child 90mmHg, Teen 100-110mmHg
-LVP = 4MR2 + LAP
-LVP = Systolic BP if there's no LVOTO
-LVP = Systolic BP +4LVOT2 (measure LVOT with CW at Aortic Valve)
LV Diastolic P
=Diastolic BP at arm - 4(end diastolic Ao regurg)
LAP
-Normal 4-12mmHg
LAP = Systolic BP -4MR2
Mutliple Levels of Obstruction
Pressure gradient = 4(V22 -V12)
-Must obtain V1 by PW
-where V1 is the velocity at 1 point (e.g. subAo) and V2 is at 2nd pt (e.g. Ao vlv)
Mean Pressure Gradients
-use CW beam
-must check from multiple views to ensure good alignment; CW beam should be parallel to flow
-Excessive gain may overestimate pk and mean gradient
-trace the gradients over several beats and average them
AS Severity:
-Mild <25; Mod 25-50; Sev >50mmHg
MS Severity:
-Mild 3.5-5; Mod 6-12; Sev >12mmHg
Pulm Vn:
-Nl mean gradient is <0.8mmHg
dP/dt
-Measures pressure changes over time to assess ventricular systolic function
-use MR for LV; TR for RV
-use CW jet in AP4C view
-Use sweep speak of 150-200mm/s (higher sweep speed allows better resolution of the slope...)
-Measure time bn 1m/s and 3m/s velocity
- dP/dt (mmHg/s) = 4*1000*(V22 -V12)/ (delta t msec)
-because you use 1 and 3m/s for each V, then:
dP/dt = 32000/(delta t msec)
-LV Normal >1200, Borderline 1000-1200, AbNl <1000 mmHg/s
-RV Normal >400 mmHg/s
-low number indicates that you need a longer amount of time to gain a higher pressure
-advantages- not affected by ventric geometry
-disadvantages- normalized by incr AL (htn, AS)
-relies on MR being presentRVSTI
RV Systolic Time Interval
-the time between the signal to contract and the actual start of contraction, relative to overal contraction time...
-measure with PW through pulmonary valve
-RVSTI = PEP - EP
-PEP = Pre-Ejection Period = time fr Q wave on EKG to start of ejection
-EP = Ejection Period = measured ejection time
-Nl RVSTI <0.34
-Not accurrate if there is atrial/ventricular shunting
Myocardial Performance Index (MPI)
-Measures LV systolic + diastolic function
-On AP4C w PW at MV tip leaflets for LV, and TV tip leaflets for RV for inflow
-& on AP5C with PW at Ao vlv for LV, and PSSA with PQ at Pulm vlv annulus
-Measure A - time bn MV or TV closure to the next MV or TR opening. Or if pt has MR or TR, measure the duration of the MR or TR.
-Measure B - Ejection time (time obtained fr the Ao PW tracing...)
-MPI = (A-B)/B
-Nl in adult LV = 0.39 +/- 0.05 ...
-not based on ventric geom, independent of HR, BP, age, but not good w arrhythmia, or if AV vlv xx, or poor envelope...Pressure Half-Time (assess AR severity)
-Time it takes for the peak pressure to drop to half its original pressure
-Position CW in line with Ao Regurg jet
-set Doppler scale to at least 5m/s
-measure 3-5 beats if HR regular, 8-10 if HR irregular
-use package on the machine...
-AR Severity by PHT (msec)
-Mild >500, Mod 250-500, Mod-Sev 200-350, Sev <200
-thus with more severe AR the Ao and LV will more quickly reach the same pressure bc of the regurg, so the time to get to half the initial pressure difference will be low.
-Pitfalls- doesn't always reflect AR severity well
-determined by LV diastolic compliance and P, so incr LV diastolic P will decr the PHT
-systemic vasodilation (e.g. vasodilators) will lower the Ao P and thus decr the PHT
-ch LV adaption to severe AR will increase the PHT
Pressure Half-Time (assess MS severity)
-Time it takes for the peak pressure to drop to half its original pressure
-Position CW on AP4C parallel to MV inflow
-Use machine's package to place caliper on a deceleration slope [Luke: take the line all the way to the baseline (through the a wave...)]
-The more severe the MS, the less steep the slope.
-Normal PHT 30-60msec; borderline 60-90msec; mild 90-150msec, moderate 150-219, sev >220.
-Pitfalls: elevated LVEDP because of signif Ao regurg --> incr PHT (bc increased LV P)
-if impaired LV diastolic relaxation--> inaccurate PHT
-if poor CW alignment--> inaccurate PHTVena Contracta (for AR)
=The narrowest portion of a jet that occurs at or just downstrem from the regurg orifice
-Zoom into the Ao Vlv
-Make color box as narrow as possible with the least depth
-set Nyquist to 50-60cm/sec
-Measure narrowest portion of the regurg jet (A) and the Ao vlv Annulus (B)
-VC = A/B(100%)
-AR Severity by BC (%): Mild <25%, Mod 25-40%, Sev >40%
-Limits: not good for multiple AR jets, or for an eccentric/irregularly shaped jet
Pericardial Effusion & Tamponade
-In AP4C with PW inflow at MV and TV tips
-Decrease sweep speed to 35mm/sec
-Measure highest E1 and smaller E2
-Respiratory variation (%) = (E1-E2)/E1
-AbNl respiratory variation or Doppler Evidence of Tamponade physiology:
-TV >40% incr in Insp Flow; MV >25% decrease in insp flow
-"Clinical" tamponade (Pt likely has Sx):
-TV >70% incr in insp flow; MV >30% decr in inspy flow
LA Volume
-Trace LA in end atrial-diastole on AP4C and AP2C view (just before leaflet starts to open) for Area
-& Measure Length from top of LA to the level of the annulus (not the leaflet tips necessarily)
-LA volume is indexed to BSA, so:
-LA vol/BS (mL/m2) = [(Area 1 * Area 2 * 0.85)/(shorter of the two lengths)]/BSA
-Nl is 22 +/-6mL/m2
-Mild Dilation 28-34, Mod 34-40, Sev >40 mL/m2
Diastology
Pulmonary Vein - Nl 5-10mmHg
-Measure A wave from Pulm vn and from MV inflow
-NL Apulm vn/AMV <1.3
-if >1.3--> LVEDP is likely >18mmHg (Nl LVEDP <6mmHg)
MV Inflow PW at tips of leaflets- measure E and A waves
-Measure E wave on PW as above, and Measure E' wave on DTI (LV lateral wall)
-Mitral E/E' Ratio - Nl <10, if >10 then LVEDP is likely >15mmHg
{Notes] Lecture Notes on TEE by Dr. W. Miller-Hance, 5/2014TEE Lecture NotesTEE Lecture - W Miller-Hance May-2014
Hx
-First started in adults in 1970s
-1980s used in adults w CHD
-1990- first pediatric TEE probe, w biplane made thereafter --> can interrogate outflow tracts bc can see heart in vertical/longitudinal axis too in addition to horizontal axis
-mid 1990s- multiplane ped probe available
Indications in CHD pts
-Ayres JASE 2005 paper
-mainly periop check, and also dx thrombi, etc....
-closure of ASD, VSD, etc
Pre-op exam
-baseline, confirm the dx, ID new/diff pathology, exclude additional defects, help plan surgery/anesthesia
-Post-op exam
-assess repair, ID problems w wean fr CPB, help influence postop mgt...
Pedi TEE Practices
-used in most cases at TCH, other settings only in some patients or only if a specific problem is present...
-Probe/scan
-some place probe before, and some after CPB started
-some leave probe in until the very end of the case (at risk of xx related to prolonged probe insertion...)
-some do a focused exam, some do a complete exam
-usually a peds cardiologist doing it in US, but in Eu it is usually anesthesia
-Probe selection - recs for wt:
-Pedi Micro (2.5kg or greater pt wt)
-Pedi Mini (3.5 kg or greater, some used at 3kg))
-Adult 2D (25kg or greater; some ppl use 20kg)
-Adult 3D (note square at tip, not circle... help ID which is 3D) (30kg or greater)
-c/s premie, 22q11del, abNl craniofacial anatomy as risk for TEE entry, so use smaller probe...
-Down's has harder anatomy to insert TEE, ?why...
Contraindications
-Ayres JASE 2005 guidelines
-Absolute: TEF, esoph obstruction/stricture, perferated hollow viscus, poor airway ctrl, severe resp dp, uncooperative unsedated pt
-Relative: h/o esoph surg, esoph varices/divertic (? if really count), vasc rings, arch anomaly, gastric/esoph bleeding, oropharyngeal pathology, severe coagulopathy, cervicap spin injury/xx
-?how long G tube/fund is it ok to do TEE
-?TAPVR is c/i xx bc probe compresses on confluence
-?anticoag pt - ?pt on mech circ support
-?Downs etc - they have high vagal tone, so not uncommon to get brady, even sinus arrest, espec if pt had sx w the laryngoscopy
Complications
-...
-at time of incision, don't have it in stomach, espec flexed, bc surgeon has mistaken it for xyphoid--> cut thru the stomach!
-esoph perf..
-bleeding, mucosal erosions - can be very high per one study...
-if flex and pull back probe w/o unflexing it, --> buckle the esophagus, --> hard to get probe out, need to advance it to stomach, straighten it out, and then ok to pull back...
Wanda's approach to Probe Selection
-Indication? --> ok
-Contraindication? --> if yes, c/s epicardial or no imaging
-Wt >15-20kg--> adult multi, unless 15-20 then pedi mini
- >3kg then pedi mini, other c/s micro if really needed, or just a pedi biplane, otherwise c/s epicardial or ICE probe (limited)
Location of TEE WIndows
-UE - upper Esoph
-ME- middle Esoph
-LE- lower Esoph
-Transgastric - at level of diaphragm
- Deep Transgastric- in stomach, looking straight up...
-always ensure probe is UNLOCKED when moving probe up and down...
-See JASE 2013 comprehensive PTE standard views...
...
[Doc] TEE Cheat Sheet Diagrams - otes on how to obtain every imagehttps://drive.google.com/file/d/1PJTNTbqwxXYJvB5KWx3rYy5sMwPkQM8Z/view?usp=sharing[Website] Toronto TEE training site - excellent resources to learn TEEhttp://pie.med.utoronto.ca/tee/TEE_content/TEE_standardViews_intro.html[Notes] Lai EchoLai - DiastologyDiastolic Ventricular Function (Lai8)
Diastole =
-Isovolumetric relaxation- semilunar vlv closes --> AV vlv flow onset
-Rapid filling- start when Pventric < Patrial, so Q thru AV vlv
-Early Diastolic Flow = E wave- pks in early diastole as Pventric is at minimum, then decels as
ventric pressure starts to increase as it is filled
-Diastasis- mid-diastole when Patrial =Pventric after early filling, so little Q thru AV vlv
-Atrial Contraction- late diastole incr in Patrial, to be >Pventric--> 2nd wave of Q across AV vlv
-late diastolic velocity profile = A wave
-filling d/o ventric syst fx, AV vlv fx, rate of ventric relaxation, passibe compliance/stiffness of atria and ventricles, atrial systolic fx, loading/volume conditions of atria and ventricles, intraathoracic P changes w resp, HR, rhythm
Mitral Inflow
-PW at MV leaflet tips on AP4C, as parallel to mitral inflow as possible
-the peak E and A will be much decreased if you're in the LA!!
Measurements:
-Diastolic time interval
-Peak velocity at Early filling & w Atrial contraction
-Area filling fractions
-Velocity and area ratios
-Peak filling rat
-IVRT is shortened
-Isovolumetric Relaxation Time (IVRT)- time fr Ao vlv closure to initiation of diastolic flow at MV
-measure fr the A2 (Ao closure) sound on the phonocardiogram thru initiation of diastolic Q at MV
-or arrange transducer so you can get LVOT Q also w a 5 chamber view (time fr end of Ao Q...)
-IVRT is indexed to HR
-Poor LV relaxation--> long IVRT (takes longer for ventric P to be lower than atrial...)
-IVRT is shorter if incr LA P and poor LV compliance
-Deceleration Time (DT) during early filling fr E pk to end of Q is also used to describe relaxation
-longer time bn E pk and end of filling--> worse LV relaxation
-this time shortens as HR increases... so not good if pt tachycardic
-E:A ratio describes pattern of LV diastolic filling
-Velocity Time Integral (VTI) = area under the curve during E and A together,
-Area of filling in first 1/3 and 1/2 of diastole also used to describe inflow
-Doppler pk filling rate = pk E velocity * mitral annulus cross sectional area ( which is Î d/4)
-Peak filling rate (stroke vol/s) = pk E (cm/s) / MV VTI (cm)
PVn Inflow
-PW in R or L upper pulm vn fr AP4C, as parallel as possible, w sample as far into the vn as possible
Measurements:
-pk systolic velocity
-pk diastolic velocity
-Velocity Time Integral (VTI) during syst and diast phases compared w total area under curve
-syst/diastolic velocity and VTI ratios
-systolic pulm vn flow is often biphasic in infants and young kids- bc dissociation bn atrial relaxation and MV annular displacement
-high systolic velocity measured
-Velocity and duration of atrial reversal - differentiate diastolic doppler pattern if there's incr LA and LV EDP.
--Caveat- pulm vn compliance plays a role in the Doppler pattern in kids, so in healthy infants, pt may have continuous phasic fwd Q thru the pulm vn w reversal of Q w atrial contraction.
-Atrial flow reversal in a neonate should be concerning for AbNl incr LAP, bc of limited Q thru pulm vasc bed as a fetus.
-In healthy kids, flow reversal is common in atrial systole, bc the prox PVns are more compliant, so don't need to c/s LV dysfx...
-Duration of flow reversal in PVns w atrial contraction IS a more Snindicator of diastolic dysfx, espec if it is > than A-wave duration on MV inflow (!)
Tricuspid & Systemic Venous Inflow
-can use same MV indices for TV to assess RV diastology
-it's harder on the R side bc of inspiratory variation... (see pic)
-inspiration--> incr fwd Q thru TV
-E incr by 25% and A by 20% w insp in Nl kids
-SVC inflow- biphasic, w dominant systolic RA filling
-No flow reversal in SVC during atrial systole- bc RA compiance is incr compared to LA
-unlike LA, there's no age related variability in pattern
-pattern affected by RA htn, TV dysfx, pericardial dz, arrhythmias
-Marked syst vn Q reversal w atrial contraction = signif RA htn or TS
-Decreased/Reversed systolic Q = signif TR, loss of AV synchrony, or restrictive dz
-Large pericardial effusion--> limit diastolic filling w absent/reversed diastolic syst vn Q @ exhale
-assoc w marked decr in TV E wave velocity w onset or exhalation and reciprocal changes in MV E wvInflow Doppler Analysis AbNlies:
AV Valve Stenosis
-atrial htn fr restricted Q across AV vlv
-Prolonged P gradient decay fr atrium to ventricle
-Incr pk E w marked prolongation of E wave decel
-Variable A wave velocities
-Inflow pattern is influenced by the stenosis and HR, so can't assess ventricle diastole
-venous doppler pattern shows high diastolic atrial P and delayed diastolic emptying so that venous diastolic inflow is reduced w mild-mod stenosis, absent w sev stenosis
-atrial P can be markedly incr w atrial systole, --> prolonged and high velocity flow reversal at end diast.
AV Valve Insufficiency
-the regurg jet Q increases systolic atrial P
--> systolic reversal of flow in vns, (seen only w severe regurg)
-Mod regurg--> decr fwd systolic flow; and Nl biphasic flow pattern if mild regurg
-Caveat: direction of the regurg jet relative to the vn checked may change the matters a lot. (if to jet twd wall then less effect on inflow pattern)
Pulm/Syst Vn Obstruction
-see continuous high velocity turbulent Q w loss of the biphasic pattern seen Nly
-loss of end systolic and end diastolic deceleration to baseline (which is a hallmark of Nl inflow)
-Newborns, espec if signif L to R shunt lesions, can have more continuous pattern of pulm vn Q, but the biphasic syst and diast pks are maintained w doppler velocities that appproach baseline at end syst and end diast.
Arrhythmias
-...Doppler Tissue Imaging
-disadvantage of PW/CW Doppler is that they are much affected by the myocardial loading conditions (at of preload...)
-DTI checks myocardial motion by tracking the wall velocities thru the cardiac cycle
-check w PW at mitral, septal, and tricuspid annular motion
-TV annular motion is NOT affected much by respiration, so independent unlike TV inflow PW
-MV annular motion is NOT affected much by intravasc volume, unlike MV inflow
-ventric expansion/contraction occurs on the base-apex and ant-post axes, and annuli move along the former axis
-Systole- annulus moves twd apex; Early diastole- recoil of the ventricle fr contracted state; Late diastole- annular motion affected by both syst and diast
-check fr AP4C view, w wall as parallel to transducer as possible
-the DTI filter looks for low velocity, high amp signals of myocardium--> avoids blood Q
-best gate is 3-5mm in kids; Nyquist 15-30cm/s; sweep of 100-150mm/s
-septum can be made the most parallel but is affected by RV so doesn't completely reflect LV
-Measurements:
-E (aka E') is early diastole
-A is late diastole (atrial systole wave)
-S is systole
-can also look at diastolic time interval, and isovolumetric relaxation (time fr end of systole to start of early diastole)
-early diastolic deceleration time- fr pk early diastole to return of the diast velocity to baseline prior to annular motion fr atrial contraction.
-Limits: depend strongly on the angle of interrogation, might be affected by translational shifts in heart position during the cardiac cycle, and segmental wall motion might not reflect global fx
Color M-Mode Flow Propagation
-assess ventric filling by M-Mode of early diastolic flow velocity fr the AV vlv to the apex
-check fr AP4C w cursor parallel w diastolic inflow
-adjust the color Doppler interrogation area to get longest column of flow fr the AV annulus to the apex
-it estimates ventric filling and correlates well w the time constant of LV relaxation
-NOT affected by preload
-mainly affected by LV relaxation
-abNl relaxation--> slower rate of early diastolic flow propagation
-Vp = Propagation Velocity = the slope of the line drawn fr apex to base on the color tracing
-= measures the rate of flow propagation (how long it takes to get bn 2 pts)
-lower Nyquist to display the 1st color aliasing (usually about 75% of pk E velocity)
-higher slope = faster flow propagation and more rapid ventric relaxation
LA Volume
-good marker of the duration and severity of LV diastolic dz
-reflect chronic, cumulative filling P over time
-well correlated with the severity of diastolic dysfunction as estimated by Doppler (in old ppl)
-LA > 32cm3/m2 is a R/F for 1st CV event (a-fib, stroke, HF) in old ppl, and correlates w their survival
-LA vol varies w cardiac cycle, so only max volume is measured
-best to check at MV opening
-Can measure by checking area of LA in 2 views (like Simpson's biplane) or by area-length method - both have been validated but both underestimate volume compared to CT/MRI
-LA = 8/[(3pi)(A1)(A2)/L] with L the shorter of either view
-Limits: can foreshorten LA (the length in the 2 views shouldn't differ by more than 5mm), the max LA volume should be measured- just before MV opening; LA border should be measured consistently- w inf border is the mid pt of the MV annulus, NOT the leaflet tips, and the tracing of the border should exclude the LAA and PV confluenceDIASTOLIC DISEASE
fright/anger/symp discharge
--> b-blockade Rx improves survival
-high risk with swimming, so don't swim alone or w/o floatation device
-some mutations--> abNl K channels, while others --> decr amt of K channels ==> diff phenotypes...
IKr Defects = KCNH2 & KCNE2 genes --> subunits of K Ch for the rapid K current; auto dom
-IKr current--> initiate cardiac repol after excitation-contraction
-incr risk to arrhyth p auditory stimuli -alarm clock, phone...
-IKr ch very Sn to extracel [K+]; the ch's ability to conduct K outward depends directly on [K+]extracell, & as the [K+]extrecell increases, the outward K current increases (??Why)
-thus these pts are very Sn to low K levels
-?if K supp, spironolactone,or K ch openers (nicorandil) will help
SCN5A Defects = defect in Na Ch; make up <10% of LQTS reported; auto dom
-incr risk for arrhyth/sudden death w bradycardia- often die in sleep
-arrhyth is less common than w K ch xx, but more deadly bc unobserved (pt sleeping)
--> Na ch unable to completely inactivate after depolarization--> persistent Na leak into cell, w repeated opening of the ch during sustained depol--> small sustained inward depolarizing current--> "gain of fx" mutation (K ch xx has a loss of fx), --> prolonged plateau of cardiac depol--> delay repol onset--> excess Ca loading of myocyte--> high intracell Ca allows for dvp of early after-depolzarizations --> ventric arrhythmias, especially at lower HR.
-thus ? Tx w pacing atrium to prevent brady + mexiletine- Na ch blocker
-note that other xx to SCN5A that --> loss of fx cause Brugada synd & conduction xx, and not LQTS
Drug-Induced LQTS
-many affected pts actually have a subclinical LQTS mutation that become apparent when the Rx compromises the repoln.
-can be more pronounced if P450 system is needed for metab & is inhibited...
-can be more pronounced w hypOK+ which inhibs Kr current...
Dx
-check QTc
-some pts w LQTS by genetics had QTc within Nl range (!) despite incr risk of death
-EP studies don't help Dx
-Holter, provocative testing w epi, and exercise ECG are more useful to check for repol xx if ECG negative, but they arent consistent either
-There is a scoring sytem baesd on ECG findings, FHx/Hx
-Genetic testing- limited still, but do test for the more common causes (top 5)
-only 50-75% of pts get a dx to date...
Mgt
-not all pts w LQTS have same risk or Tx response
-prevent adrenergic surges
-avoid Rx that are QT prolonging
-limit risk- avoid competitive sports, closely watch when swimming, no bedside alarm clocks or phones
-avoid hypO K- eat high K foods
-beta blockers - 1st line Tx, does improve mortality
-ICD- c/s if signif cardiac arrest, persistent Sx despite b-blocker, or strong FHx of sudden cardiac death
-What if gene +, but pt ASx & Nl ECG?
-1/3 of LQTS + pts have ASx/Nl QT and Nl provocative testing; ?who will remain ASx and pt may present w sudden death, so ? if need Rx or not...
Brugada Syndrome
= ST elevation in R precordials: V1-V3
-without ischemia, electrolyte xx, structural cardiopulm dz
-incr risk of sudden death fr polymorphic VT--> VF
-auto dom; 5-66/100K ppl have it
-higher in SE Asia; male >>female
-mutation in SCN5A Na ch (loss of fx, ddx LQTS which is gain of fx xx) --> decr Na current bc reduced # or reduced fx of Na ch's.
--> decr inward Na current, so there is a transient outward K in RV epicardium(via Ito ch)--> epicardial to endocardial voltage gradient--> ST elevation seen in R precordials, which may --> re-exciation in ventricle w triggered VT/VF
Dx
-ECG- not very Sn or Sp
-Type I BrS = prominent coved J pt pk w ST elevation of >0.2mV, then negative T wave w no intervening isoelectric phase
-Type II BrS = prominent J pt elevation (>0.2mV), then biphasic T wave w saddleback look
-Type III BrS = less prominent J pt elevation (>0.1mV), w either cove or saddleback look
-ECG may mimic RBBB, espec in Type I
-DDx fr RBBB bc absence of wide S wave in lead I and in L lat precordials
-Can unmask it with Na ch blocker infusion- ajmaline, flecainide, procainamide- ?Sn/Sp
-may ppt a VT/VF
-?benign course if +testing in ASx pt
-Genetics
-limited use bc only one of the genes are ID'd...
-ID's gene in only 15-20% of pts
Mgt
-If Sx--> Tx, but Rx aren't proven to work
-Quinidine at low ds- inhibits the Ito of K that causes the re-excitation
-Mexiletine- Na ch blocker- ? if it works
-ICD only proven way to prevent sudden death
-if Syncope--> clear indication for ICD; otherwise ? if appropriate if ASx pt
-but 30% of ASx ppl will have VF/VT within 3 yrs of evaluation, same as Sx pts ==> currently rec ICD for ASx ppl w +sustained ventric arrhyth on EP study
Anderson Syndrome
=K Sn periodic paralysis, ventric ectopy, dysmorphisms
--> variable phenotype- short, mandib hypoplasia, low set ears, clinodactyly
-w low, Nl or high k can have paralysis, usually responds to K+ admin
-+/- long QT
-may see bidirectional ventric tachy; may --> syncope/sudden death
-KCNJ2 gene xx in at least some- decr strength of ch interaction w phosphatidulinositol 4,5 biphosphate
-Tx w amio & acetazolamide can relieve cardiac and skel muscle Sx
Ion Channelopathies that Enhance Automaticity
Catecholaminergic Polymorphic VT / Familial VT / Arrhythmogenic RV Dysplasia Type 2
-CPVT, FVT, and ARVD2 - due to abNl ca release fr SR, bc of mutations in cardiac ryanodine R type 2, which is the ch for releasing Ca fr SR stores.
-rare, inheritable
-adrenergic induced VT & sudden death
-1/3 of CPVT is fr auto dom mutation in RYR2 (cardiac ryan R' type 2)
-rest are auto rec, bc mutation in calsequestrin, which sequesters Ca in SR
-ARVD2 & FVT are both fr xx of RYR2
-FVT= loose dx, = inherited disposition to VT/VF (can be applied to ARVD, BrS, CPVT)
-QT interval and heart strucutre are usually Nl in CPVT, FVT, and ARVD2, though some pts w ARVD2 have mild thinning/fibrous fatty replacement of RV myocardium (less than other ARVD forms)
-CPVT pts get syncope/sudden death around 8yrs old, earlier if more severe Sx
-Sx usually w stress/exercise; 30-50% incidence of sudden death by 20-30yo if untreated
-isolated PVCs and atrial arrhythmias will occur early after exercise onset, then get runs of monomorphic or bidirectional VT then degen to polymorphic VT, and then VF
-pts have resting bradycardia
-ARVD2 - similar Sx/presentation as CPVT, w stress induced ventric arrhyth
-BUT, ARVD2 pts may have mild path changes to RV ...
Dx
-must see the ventric arrhyth elicited/exercbated by exercise testing ni pt w/o structural hrt dz or LQTS
-Do perform exercise stress testing to check for it if pt has h/o exericse induced syncope w Nl ECG and echo
-& in ASx pt if +FHx, including FHx of exercise nduced syncope or sudden death of ? etiology
-No genetic testing avail
Mgt
-beta-blockers highly effective to reduce M&M
-some pts w persistent stress induce arrhyth despite b-blocker should get ICD too
Familial Ventricular Fibrillation
-several reports of FVF, one bc of SCN5A gene xx without BrS on ECG
Familial Atrial Fibrillation
-rare to have FAF, no definite genetic cause shown
Cardiomyopathies
-due to abNl structural components of myocytes- sarcomeric & cytoskeletal prtns
HCM
-...
-incr risk w Noonan, LEOPARD, Costello syndromes, and w lysosomal storage dz, mito dz
-mutations.. in variety of genes for b-myosin heavy chaine, cardiac troponin T, myosin bindign prtn C, and others...
Dx
-echo...
-...
-arrhythmia risk not shown to correlate well w degree of hypertrophy, so even if mild can still have sudden death
-Genetics....
Mgt
-Tx Sx...
-b-blocekr & CCB to slow progression of hypertrophy by stoping hypercontractile states
-Antiarrhythmic Tx hasnt been shown to improve the outcome of pts w Sx arrhythmias
-ICD indicated if aborted sudden death, unexplaiend syncope espec if child, strong sudden death FHx, VT on Holter or exercise test, absence of a rise in systolic BP w exercise, and severe IVS thickening (>30mm)
-LVOTO related ischemia is a risk for ventric arrhythmia...
HCM w WPW
-PRKAG3 and AMPK gene xx
DCM
-...
-now 30-50% are thought to be genetic in etiology
-Isolated DCM- alpaha tropmysinc, alpha cardaic acting, b-mMHC, troponin T xx
-DCM w skeletal myopathy- seen w xx to dystrophin, sarcoglycan, and desmin which stabilize sarcomere and assist in force transduction...
-Barth Syndrome w DCM- x linked syndrome w CHF as infant and hypotonia, cyclic neutropenia; if survive infancy the ventric fx usually improves, but then may get HF again later
-xx in Tafazzin gene; see elevated 3methylglutaconic acid in urine
-DCM w Systemic Dz- Emery-Dreifuss muscular Dystrophy- early contractures of elbows & Achilles tendons, slow progressive muscle wasting, DCM, & conduction block
-auto dom, auto rec, or x linked; due to lamin A/C gene xx in atutosomal form, and emerin in x linked... all 3 prtns are for nuclear lamina...
Dx
-...echo....
Mgt
-...
-medical Rx for HF...
-ventric arrhythmias--> poor Px (?)
Arrhythmogenic RV Dysplasia
-fatty infiltrate and fibrosis of RV
-#1 cause of sudden death in Italy - 17% of them
-Auto dom
-9 genes involved, ...
Dx
-hard to dx at times, even if FHx
-first sx might be sudden death, but usually after teens
-ECG- inverted T wave at R precordial leads
-RV arrhythmia w LBBB pattern
-may have arrhyth after adrenergic stim/exercise, or induced by EP stim
-Can Dx w RV Bx, but bc fibrosis usually starts at RV fee wall, then goes to septum, you can get lots of false negative
-can Dx based on Euro criteria based on MRI/echo, fibrofatty infiltrate by Bx, RV origin VT/VF...
Mgt
-Rx
-EP ablation
-ICD
-genetic counseling bc 50% chance to pass it on...
-limited knowledge overall...
Conduction System Abnormalities
Complete Heart Block
-Nkx2.5 gene may b involved w CHB, seen w ASD TOF, conotruncal xx, Ebsteins, APVR; also --> progressive AV block
Kearns-Sayre Syndrome
-external ophthalmoplegia, retina pigmentary degeneration, premature dementia, DCM, progressive conduction block
-mitochondrial DNA xx
-may also show facial, pharyngeal, trunk/limb weakness, deafness, shortness, incr CSF fluid prtn- d/o size & location of the mito DN A deletion
Progressive Cardiac Conduction Defect
-aka Lenegre or LEv dz
-#1 conduction xx in adults
--> progressive HPS conduction slowing, --> RBBB or LBBB or complete AVB, syncope, sudden death
-some may have SCN5A mutation, but dont show LQTS or BrS Si/Sx
Short QT Syndrome
-w QTc <320msec
-assoc w a-fib
-c/s it strongly in young pt w isolated a-fib
-high incidence of syncope & sudden death due to ventric tachyarrhythmias
-heterogeneous..., fr gain of fx mutations ...HERG, KvLQT1, KCNJ2
Dick - Antiarrhythmic PharmacologyAntiarrhythmic Pharmacology - Dick21
Class I= Na channel blockers
--> prolong Phase 0--> slow conduction velocity
--> make membrane return to a more hyperpolarized state, thus --> prolong refractory pd of fast response fibers bc there's a greater difference between the resting state and the threshold for activation of the Na channels to initiate Phase 0
--> suppress Purkinje/His bundle automaticity, caused by myocardial damage--> SA node resumes its dominance.
Class IA) -->slow rate of rise of Phase 0 to Vmax & prolong refractory pd
Class IB) --> conduction block at diseased myocardium, but no effect on Phase 0 or refractory pd
Class IC) --> signif decr conduction velocity, but ~no effect on refractory pd
IA -
-Quinidine - rarely used bc of xx. like quinine it's antimalerial, antipyretic, ototoxik, skel relaxant
-effect d/o dose: low [ ] --> Anti-cholinergic, at high [ ] --> direct EP effets
-SA nd & Atria: low [ ] --> inr HR; low [ ] slows depol- slows Vmax of ph 0--> slow conduction
-AV nd: low [ ] anti-chol effect--> incr conduction at AV nd, high [ ] --> decr conduction velocity and incr effective refractory pd
-HPS/Ventricle: decr ph 4 slow of depol--> inhibit automaticity, with a
Abnormal Relaxation with Elevated Atrial Pressure
-If there is a moderate incr in LA P fr abNl ventric relaxation, --> intermediate "pseudonormal" inflow
-Worse diastole--> decr ventric compliance & incr atrial diastolic P
-this incr LAP normalizes the early diastolic gradient, so E wave is the same as it usually would be (bc LAP is relatively high, the diff bn LA and LV is the same even though LVP is high), and E/A Nl too
-the inflow pattern looks Nl
-Thus Doppler isn't good to screen for diastolic xx, and pulm inflow is preferred instead
-AR Wave = prolonged reversal of pulm vn flow w atrial contraction = Sn & Sp for incr LV filling P
-This can be Nl in some kids to have some flow reversal, so pay attn to the duration (prolonged relative to the A wave filling on the mitral inflow tracing)
-90% Sn if ratio of pulm vn AR wave:mitral A wave is >1.2 & difference bn both durat'n >29ms
-DTI is good for abNl relaxation as well
-early diastolic mitral DTI (Ea wave) (=early diastolic annular velocity)- lower in pts w abNl relaxation, even if pt is at a stage of pseudonormalization of the MV inflow pattern bc of incr LAP
-Ea correlates (inversely) with prolonged LV pressure decay on cath
-Ea velocity is also preload independent, unlike MV inflow
-E/Ea Ratio- mitral E wave velocity increases as LAP increases, but Ea wave velocity stays low as LAP incr fr diastolic dysfx, so the E/Ea ratio helps predict LAP (it will be higher if higher LAP)
-E/Ea Ratio >10 correlates to PCWP >12mmHg in adults
-Color M-Mode - to assess LV flow - to DDx pt w Nl vs pseudo-Nl filling, & estimate LV filling P
-Decreased Vp (flow propagation) correlate w delayed relaxation
-This continues even as LAP is incr
-E wave:Vp Ratio (MV E/Vp aka E/Vp) of >2 predicted pts w LVEDP >15mmHg w good Sn/ok Sp
-preload independent
-helps DDx pseudo Nl LV filling
Abnormal Ventricular Compliance
-Sev Diastolic dz - poor ventric complaince and much incr LAP
-incr atrial P bc of ventric stiffness
--> incr P gradient accross the AV valve
--> incr pk E wave bc blood is rapidly filling the noncompliant ventricle
-LVP rises quickly as it is filled, so E wave flow is abruptly stopped w a short deceleration time
-Bc LVP is much elevated in diastole, the A wave pk is decreased or absent (remember these are gradients, so thus the diff bn atrial systole P and late ventric diastolic P is small bc of high ventric P...)
-only slightly more P can be generated across the AV vlv fr atrial systole
-AV valve opens early bc of incr LAP, so it is opened while ventricle is still relaxing
-see shortened isovolumetric relaxation time
-PVn inflow--> rapid atrial filling in early diastole w AV vlv opening, but then slows in mid diastole as ventric pressures rapidly rise as they are filled. --> prolonged flow reversal in PVns w atrial contraction bc there is a dramatic incr in both atrial P and ventric P at end diastole
-systemic venous inflow is blunted bc of ch atrial htn and distention
-IVC can also show high velocity reversal of inflow w atrial contraction <-- poor RV compliance
-if flow reversal velocity is > fwd velocity --> correlates to CVP >15mmHg in adults, but likely invalid in kids on positive P ventilation or w airway dz bc of much changes in intraTx P's...
Diastolic Function in Pediatric Patients without Heart Disease
Age-Related Changes in Diastolic Filling
-Major change is as an infant
-Fetus/Neonate: ventric filling is mainly w atrial contraction, so pk E wave is decr, as is the E/A ratio
-Infant mitral pattern- see changes similar to pt w altered ventric relax'n/compliance, and decr early transmitral P gradient
-also see P Vns - incr pk systolic velocity, and decr pk diastolic velocity, w incr S/D and VTI
(compared w older kids)
-due to different diastolic properties of immature myocardium, and bc of changes in HR & PL
-as pt ages, LV filling shifts from late to early diastole--> shift in LA filling fr systole to diastole during the first year of life.
[think of it- LV filling is w atrial contraction (late diastole), causing LA pressure to drop and as diastole ends and systole starts LA pressure will thus be at it's lowest, allowing LA to fill mainly during systole, thus higher S in newborn. D wave of diastole is lower because by now the LV is filling...]
-In older kids/teens, PVn and MV flows are like adults
Infants
-at birth, ventric relax'n are very impaired, w prolonged isovolumic relaxation time, limited early diastolic inflow, w LV fillingmainly in late diastole w atrial contraction
-by 2months old, the early mitral filling velocity increases by 80% fr newborn values, and then stay stable
-not affected by HR (HR doesn't affect pk filling rate in pts <3mo)
-RV filling also shifts twd late diastole after neonatal period, like the LV...
-As LV filling shifts from late to early diastole with age, the E/A and Ea/Aa velocity ratios change as well reflecting the changes in mitral annular velocities
-MV Annular motion and inflow velocities shift during first week of life, w improved diastolic fx--> more rapid relaxation of LV in early diastole.
-TV Annular motion does not change much in the first week- there is a delay in the RV relaxation
Premie Infants
-also see relaxation abNlies
-see persistent dominant diastolic filling w atrial contraction for first 2 months of life (not just 1st month)
-maybe delayed bc of the signif incr in SV in permies- doubles by 2mo old (term pt incr only 37%)
-Poor diastology affects ability to handle stressors like PDA...
Healthy Kids/Athletes
-MV inflow parameters are very stable fr 3-17yo, w similar E and A and E/A and isovol relax time
-DT does change significantly, related of HR
-DTI correlate signif w age and parameters of cardiac growth; not affected by HR or RR
-Diastolic fx is preserved in athletes despite much change to LV thickness/dimensions
-diast fx has signif impact on pk O2 uptake w exercise
Right Ventricle
-RV fx is diff than LV
-greater longitudinal regional velocities, more displacement of the free TV annulus twd apex, and less circumferential shortening velocities than LV
-makes sense, bc RV has more longitudinal/oblique fibers, and LV more circular fibers at LV lat wall etc
-regional contractility at longitudinal axis "appears to accurately reflect global fx of RV" even w diff inotropic/loading conduction
-RV diastole is also mainly longitudinal as well
=======
Diastology Lecture Notes Jeewa 10-2012
Diastology Lecture Notes Jeewa 10-2012
-No specific individual parameter to check it
-Dopper is good for it...
2D
-LA volume = (0.85*A1*A2)/Length (shortest length in a AP4C or AP2C view)
- a barometer of the degree of diastolic dysfx
Mitral Valve Inflow
-rapid early inflow = E wave
-deceleartion of flow as LV P rises to = LA P, here briefl pd w/o gradient at the valve = diastis
-A wave - w atrial systole
-E/E' - grade I might have Nl, but grade II-IV have a high #, >10 is abNl in general
-blunted waveforms at a higher gradde of diastolic dysfx
-help ddx Constriction- nl myocardium but constricted by fluid/pericadium etc
vs Restrictive- it is a myocardial problem, so the tissue doppplar is abNl....
-E/A- grade I dysfx - A wave larger than E wave
- grade II dysfx- impaired relaxation w pseudonormalization, though E somewhat elevated but A wave is more preserved, see you relying on the atrial kick more
-grade III dysfx- see a narrow, tall E wave form w short decel time, and A wave is blunted and small so less reliance on atrial systole, thus high E/A ratio... = a more restrictive pattern of MV inflow
Conditions asoc w diast dysfx
impaired relaxation-aging, ischemia, CM
reduced compliance- hypertrphy, fibrosis, collagen deposit, restrictive CM
Grade I dysfx- incompelte atrial emptying- incr atrial PL
Grade II dysfx- incr dependence on LA-LV gradient for filling and maint by incr LA P
-incr LAP --> pseudonormalize pattern, w incr early inflow velocity and longer decel time
Grade II- LV compliance sev impaired, so large incr in P for small incr in ventric vol --> high E wave w rapid equilibrate LV and LA P --> very short decel time.., little contributoini of atrial systole...
E/E' ratio >10 is assoc w PCWP >15mmHg w Sn 97$, Sp 78% in adult study (Naegueh JACC 1997)
2D
-LA volume = (0.85*A1*A2)/Length (shortest length in a AP4C or AP2C view)
- a barometer of the degree of diastolic dysfx
Mitral Valve Inflow
-rapid early inflow = E wave
-deceleartion of flow as LV P rises to = LA P, here briefl pd w/o gradient at the valve = diastis
-A wave - w atrial systole
-E/E' - grade I might have Nl, but grade II-IV have a high #, >10 is abNl in general
-blunted waveforms at a higher gradde of diastolic dysfx
-help ddx Constriction- nl myocardium but constricted by fluid/pericadium etc
vs Restrictive- it is a myocardial problem, so the tissue doppplar is abNl....
-E/A- grade I dysfx - A wave larger than E wave
- grade II dysfx- impaired relaxation w pseudonormalization, though E somewhat elevated but A wave is more preserved, see you relying on the atrial kick more
-grade III dysfx- see a narrow, tall E wave form w short decel time, and A wave is blunted and small so less reliance on atrial systole, thus high E/A ratio... = a more restrictive pattern of MV inflow
Conditions asoc w diast dysfx
impaired relaxation-aging, ischemia, CM
reduced compliance- hypertrphy, fibrosis, collagen deposit, restrictive CM
Grade I dysfx- incompelte atrial emptying- incr atrial PL
Grade II dysfx- incr dependence on LA-LV gradient for filling and maint by incr LA P
-incr LAP --> pseudonormalize pattern, w incr early inflow velocity and longer decel time
Grade II- LV compliance sev impaired, so large incr in P for small incr in ventric vol --> high E wave w rapid equilibrate LV and LA P --> very short decel time.., little contributoini of atrial systole...
E/E' ratio >10 is assoc w PCWP >15mmHg w Sn 97$, Sp 78% in adult study (Naegueh JACC 1997)
Pulmonary Vn Inflow
-Nl biphasic flow w S and D and a small retrograde A wave during atrial contraction
-a wave usually <25cm/s and duration shorter than the transmitral A wave
TDI
-see E'>A' in Nl pt, but then reversal w A'>E' in diast dysfx and much blunted waves; may have E'>A' but very blunted waves
Flow Propagation
-Color M mode flow propagation Vp... at inflow MV, see an E/A type relationship...
-E/Vp correlates to filling P - if >1.5, correlates to PCW >15mmHg
-but lack of consensus on technique and small LV or LVH can impact it... small variation can impact number significantly...
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