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58 Cards in this Set

  • Front
  • Back

RV DIMENSIONS:




1)What basal and mid RV diameter measurements classify the RV as dilated?




2) What longitudinal dimension classifies the RV as enlarged?



1) basal > 42mm


mid > 35mm




2) longitudinal > 86mm



RA DIMENSIONS:




What 1) area 2) length 3) diameter classify the RA as enlarged?

1) > 18 cm^2




2) > 53 mm




3) >44 mm

RVOT DIMENSIONS:




1) What are the upper cut-offs for RVOT measured from PSAX (distal RVOT) and PLAX (prox RVOT)?




2) What is the most accurate sight to use and why?

1) PSAX - distal >2.7cm


PLAX - prox >3.3 cm




2) Distal - just before the PV - more reproducible

RV WALL THICKNESS:




1) What is the upper cut off for RV wall thickness?




2) What can cause RVH or wall thickening?




3) Sight of measurement and why?

1) > 0.5 cm




2) PHTN - RVH


thickening - infiltrative disorders like amalyoid




3) subcostal


- better beam alignment - ax res > lat res

RV SYSTOLIC FUNCTION:




1) Name 5 ways to assess RV systolic function and there cut off values.





1) TAPSE - m-mode - <1.6 cm


2) DTI lat annulus - < 10 cm/s


3) PW MPI - > 0.4


4) DTI MPI - >0.55


5) FAC - < 35 %



RV DIASTOLIC FUNCTION:




1) How is this performed?




2) What 3 values are used as indicators of RV diastolic dysfunction.

1) PW at TV leaflet tips for tricuspid inflow




2) a; E/A <0.8 or >2.1


b; E/E' >6


c: DT <120 ms

1) Name 5 views that the RV can be assessed from.




2) Why is it important to use so many views?

1) PLAX, RV PLAX (inflow), PSAX, Ap 4C, RV focused 4C, subcostal




2) Complex morphology, cant see all structures from one view

R. HEART CORONARY SUPPLY:




1) What is the main coronary artery that supplies the RV?




2) what branch is this via?




3) What branch supplies the posterior 1/3 of the ventricular septal wall? Via what?





1) RCA




2) acute marginal branch




3) Posterior descending artery via posterior septal perforators.





R. HEART CORONARY SUPPLY:




4) What branch supplies the moderator band?




5) In 30% of patients the ______ _______ arises for a separate coronary ostium and supplies the ______.

4) first septal perforating branch o f the LAD CA




5) conus artery, infundibulum

6) 10% of hearts, the____________ branch of the _______ ____________ supplies a portion of the RV free wall.




7) What may supply the RV apex?

6) posterolateral, circumflex artery




7) LAD

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RA




1) what are 3 ways the RA assists in RV filling?

1) a- acting as a reservoir for systemic venous re turn when TV closed


b- acting as a passive conduit in early diastole when TV ope


c- acting as a passive conduit in late diastole during atrial contraction

2) What are the 3 linear measurements used to assess the RA? What are there cut offs?

2) area (18cm^2),


length/major axis (53mm),


width/minor axis (44mm)

PSP/ RVSP




1) a TR velocity > ___ to ___ corresponds to an SPAP of ~ ____mmHg, assuming and RAP of 3-5mmHg.




2) What does this indicate?

1) 2.8 - 2.9 m/s, 36




2) elevated RVSP and PAP

R. HEART CORONARY SUPPLY:




7) What CA supplies which part of the RV/ RVOT... Anterior, inferior, RVOT, lateral, moderator band and septum.

7) Anterior RV - RCA acute marginal branch


*Inferior - RCA posterior decending artery


*RVOT - RCA conus branch


*Lateral - RCA acute marginal branch


*Mod band - LDA


*Septum - LAD (apex end) RCA post desc artery (crux end)

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RAP




1) RAP is most commonly estimated by what 2 things?




2) As RAP increases where is the pressure transmitted to and what does this result in?

1) IVC diameter and insp collapse




2) transmitted to the IVC = reduced collapse with insp and dilation

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RAP




3) where do you measure the IVC?

3) 0.5-3cm proximal to the ostium of the RA

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RAP




4) What con provide a complimentary insight into RAP and what flow patterns are seen?

4) Hepatic venous flow




low or normal RAP = systolic dominance - S wave greater then the d wave




high RAP = systolic dominance is lost - S wave significantly decreases S/D wave ratio <1

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RAP




5) What are 2 other qualitative signs for assessing RAP?

5) dilated RA, IAS that bludges into LA though out cardiac cycle

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RAP




6) What IVC diameters and collapsibility % make us assume and RAP of 3mmHg(0-5mmHg), 8mmHg (5-10mmHg) and 15mmHg (10-20mmHg).




7) What are to indices to use if the IVC parameters are not definite?

6)


* = 21mm, > 50%


* intermediate values


* > 21mm , < 50%




7) R diastolic filling pattern E/E' >6 and D wave dominance in hepatic vein


- present - upgrade to 15mmHg


- absent - downgrade to 3 mmHg

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RV




1) What 3 things can cause the RV to dilate?




2) What is one quick visual way you can tell if the RV is dilated?

1) Pressure, volume, RVF




2) It must be no bigger then 2/3 the size of the LV ( in Ap 4C view) and the cardiac apex should be make of the LV (PSAX view)

3) What makes the RV hard to assess and what is the consequence of this?

3) Complex geometry, no fixed reference points, view from many different windows to assess, hard to really classify size and function - use RV focused view

4) where should RV linear measurements for basal, mid and longitudinal measure be taken from?

4) all in RV focused view




Basal - TV leaflet insertions (lateral and septal)


Mid - at the leave of the LV pap muscles


Long - plane of the tricuspid annulus to RV apex

CONVENTIONAL 2D ASSESMENT OF R. HEART:




RVOT




1) What does the regional delay in contraction of the RVOT contribute to?




2) What are the best views to view it from?




3) At what point in the ECG should it be measured?

1) peristalsis like contraction of the RV




2) PLAX and subcostal




3) QRS complex

VOLUMETRIC ASSESSMENT OF RV




1) What is % RV FAC?




2) How is it obtained?




3) what is the lower reference value for normal RV sys func?

1) [(E Dia area - E sys area)/ (E Dia area)] x 100


a measure of RV systolic function




2) By tracing the endocardium of the RV at end systole and end diastole




3) 35%

4) What view is the area length method of RV sys func (RVEF) assessment done in? What is the limitation?




5) What is the lower reference limit for RVEF?

4) Ap 4C


Limitation is that this view does not include RVOT and imaging of free wall is difficult




5) 44% (same for 3D but not enough data yet)

RV + IVS MORPHOLOGY




1) What causes D shaped flattening of the IVS in SAX view? What is this generally due to?

1) Caused by the change in ralitive pressure gradients between the LV and RV at each stage int he cardiac cycle. Generally secondary to increased LVFP or caused by TR (which leads to RV/ RA dilation)

2) When does D flattening occur for RV volume overload?




3) When does D flattening occur for pressure overload?

2) End of diastole only (marked shift)




3) Though out the cycle (increased at end systole)




Note - assess though out study - not diagnostic but good hint

HAEMODYN ASSESSMENT OF RV + PULM CIRC




1) How can you estimate mPAP?

1) mPAP = 1/3 (SPAP) + 2/3 (PDAP)


or


mPAP = 79- (0.45 x PA accel time (AT))


if AT <120ms mPAP = 90 - (0.62 xAT)




Note: shorter the AT = higher the PVR and therefore PAP

2) In the absence of a gradient across the PV or RVOT (no shunting...) the RVSP = ____?




3) Who doe you calculate the RVSP?

2) SPAP




3) RVSP or SPAP = 4V^2 + RAP




Note - if SPAP . 35-40mmHg - investigate for PHTN

4) how do you estimate PADP? and Why would you?


4) From the mean gradient of the TR jet or from the end diastolic velocity of the PR jet.




In patients with PAHTN or HF

5) When will there be an early TR signal cut off? Why and what will this cause?
5) When there is severe "free TR" because the RVP and RAP with rapidly equalise = underestimation of TR severity

6) What is a normal PVR reading and what is an abnormal one suggesting significant PHTN?




7) What can = an increase in PVR?

6) 1.5 woods units (120 dynes/cm/s^2)


3 woods units (240 dynes/cm/s^2)




7) limited capability of the pulmonary vasculature bed to cope with CO due to COPD or congenital heart disease)

8) What happens to SV and PVR in exercise?

8) increase in SV, decrease in PVR

NONVOLUMETRIC ASSESS OF RV FUNC




1) what are the 2 types of myocardial fibers in the RV and what do they do?


1) superficial - squeezes / bellows mmt


longitudinal - apex to base contraction

2) RVEF does not = ____ ________ when there is significant _____?




3) what is the issue with TAPSE when used to assess RV function?

2) RV, contractility, TR




3) Does not look at the whole RV - only a regional measure of function

4) What is RV dP/dT? How is it measured in echo? What is it dependent on?




5) < what RV sP/sT is abnormal?

4) Rate of pressure rise


* From the ascending limb of the TR CW signal between 0.5-2m/s = 15mmHg


* Less accurate for severe TR and load dependent




5) <~ 400mmHg/sec


(dP/dt = mmHg / time in sec = mmHg/sec)

6) What is RMPI (ie: Tei index)?




7) How is RMPI calculated?




8) What are the 2 methods of calculating it and there cut offs?

6) Global estimate of RV syst and diastolic function, based on the relationship between ejection and non ejection work of the heart




7) RMPI = [(IVRT + IVRC) / ET)]




8) PW doppler - 0.4


DTI - 0.55

9) Name are some advantages and disadvantages of RMPI?

9) Advs; avoids geometric assumptions, can be used on most people, DTI measures all variables on one trace, + or - TR jet, good for a range of HR's




disadvs; PW dop need multiple signals = up error, load dependent (unreliable when increased RAP), sensitive to preload

10) What is TAPSE? What is it a measure of? What does it presume?

10) TAPSE = mmt of the RV free wall - measurement of the distance of syst excursion of the lat RV annulus in the longitudinal plane in Ap 4C view.


* Measure of regional RV syst function (longitudinal motion)


* Presumes regional function reflects global function

11) What is the cut off for TAPSE? and what method is used to measure it?

11) < 16mm = abnormal / impaired function


*M-mode of the RV free wall annulus (zoom this)

12) DTI of the lateral RV annulus is another form of what? What does it assume?




13) Where is it measured and how? What is the cut off value? What is measured?

12) Regional assessment of RV syst function. Assumes regional function reflects global function.




13) Using DTI at lat basal TR annulus.


* S' <10 cm/s = abnormal


* The S' wave (not the IVCT peak)

14) How is myocardial acceleration during isovolumetric contraction (MADIVCT) measured? What does it correlate well with?




15) Name 1 advantage and 1 disadvantage of MADIVCT.

14) DTI at lat RV annulus


MADIVCT = (peak isovol myocard velocity/ time to peak velocity)


8 correlates well with severity of illness affecting R. heart function eg MS, obst sleep apnoea




15) adv - load independent.


disadv - no ref values therefore used for screening only

16) What is the difference between strain and strain rate?




17) How is 1D strain measured? name 2 adv's and 2 disadvantages.

16) strain = % change in myocardial deformation


Strain rate = rate of deformation over time (closely correlated with contractility)




17) DTI at basal, mid and apex of RV free wall = longitudinal strain


*adv - less load dep, ? applicable for wide range of pathologies


*disadv - angle dependent, needs high FR, poor signal to noise ratio

18) How is 2D strain measured? Name 2 adv's and 2 disadv's.

18) New measure of global contractility using frame by frame tracking of the speckles on sequential images - generates strain curve for entire RV


*adv's - angle indep, regional and global assess, better signal to noise ratio


* disadvs - lack of normative data, image quality dep, only assess func from a single plane




(use for research at the moment only)



RV DIASTOLIC FUNCTION




1) Names 5 causes of RV diast. dysfunc

1) * Acute RV damage (eg: MI) = diast. dysfunc with increased filling pressures and increased JVP


* Press and vol overload


* Cardiomyopathies


* Primary lung dieases


* Ageing


+ systemic diseases, LV dysfunc, IHD, CHD

2) How do you measure RV diast. fun? What parameter is included in RV diast. fun assessment?

2) *PW dop at tips of TV = tricusp. inflow vel


* RAP

3) What parameters are used to discribe RV diast. func?




4) What does late diast anterograde flow in the PA indicate?

3) E, A, E/A, DT


+ DTI parameters - E', A', E'/A, IVRT


+ RA area/ vol




4) Restrictive diast filling

5) Name 4 conditions that affect RV diast func assessment.




6) Is there an increase or decrease in the E/A ratio with age?




7) Inspiration increases or decreases E and therefore increases or decreases E/A?

5) age, respiration, heart rate and loading conditions




6) decrease ~ 0.1 per decade




7) increases, increases



8) Tachy increases or decreases E and increases of decreases A, therefore increases of decrease E/A.




9) The RV is small and thin walled therefore is sensitive to preload. What is preload and what does an increase in it mean?

8) increases, increases++, decreases




9) wall stress, decreased preload --> decr E + decr A = decreased E/A (visa versa)

10) What happens to DTI parameters when preload changes?




11) What are the basic changes seen in patients with ischaemia affecting the RV?

10) DTI = less load dependent = a decrease in both E' and A' ----> = no change in E'/A'




11) decreased E


increased ++ A


increased ++ RAP

12) What does RV diastolic dysfunc indicate in people with HF and PHTN?




13) Name 2 advantages of assessing RV diast func.

12) Poor prognosis




13) * Can serial screen to monitor improvement with treatment


* generally present before syst dysfunc, RV dilation and RVH = good easy screening tool

14) What are the reference and cut off values for RV diast parameter values?

14) *E/A = < 0.8 = impaired relaxation




*E/A 0.8-2.1 + E/E' >6 or D dominance in HV = pseudo normal filling




*E/A >2.1, DT < 120 (+ late diast anterograde flow in PA) = restrictive filling

CLINICAL + PROGNOSTIC SIGNIFICANTS OF RV ASSESSMENT




1) What is assessment of RV size and function important for?




2) What is the first marker of increased PVR?

1) Pulmonary and cardiac disease




2) RV dilation -- normal RV used to low PVR = thin compliant walls. If up PVR = increased++ RV size prior to augmentation of pulmonary pressure ---> RVH

3) What does RVH develop due to and why?




4) What does a PE cause?

3) To overcome increased PVR = decreased RV size, increased RV free wall thickness = increased RVSP




4) increased RV vol and diameteres, McConells sign (mid RV wall disconnetic) - reversible with improved haemodynamics

5) What is the progression of right heart changes in people with long standing pulm vasc disease or other forms of secondary PHTN (eg COPD)?




6) The more the LV becomes dysfunctional the better or worse the RV function?


5) RVH with normal values -----> dilation




6) worse = increased risk of RV dilation and dysfunction

7) RV dysfunction is a powerful predictor of outcomes post what?




8) Give an example of diseases that can affect the TV and therefore cause TR which affect size and func of RV.


7) MI




8) Carcinoid, rheumatic TV disease, myxomatous degeneration




Note - vol overload that comes with TR --> RV dilation --> more TR

9) What is the most common congenital defect affecting the right heart? and how does it do this?




10) Name 2 other CHD's that can affect the right heart


9) ASD = increased flow from shunt ---> increased pulmonary pressure + RV dilation




10) *TOF (repaired) = severe PR + severe RV dilation => decreased RV func


*Ebstiens anomaly

11) Name 5 conditions associated with RV diast dysfunction.
PE, PAHTN, TOF repair, COPD, RCA MI, CHF, cardiac transplant, arrhythmogenic RVAM, HCM, essential HTN, AS, AR, MR, LAD MI, Diabeties, amyloidosis, Ageing (+ more)