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92 Cards in this Set
- Front
- Back
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the degree of LV systolic dysfunction is a good predictor of what?
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-clinical outcome for cardiovascular diseases such as:
-ishemic disease -valvular disease -cardiomyopathis -congenital heart disease |
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what segment of the cardiac cycle is sytole?
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from mitral valve closure to aortiv valve closure
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where on the ECG is sytole?
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ventricular depolarization(onset of QRS complex), and end systole is after repolorization(after t-wave)
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explain the cardiac cycle throughout systole
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-systole begins when the LV pressure exceeds the LA pressure resulting in closure of the MV
-this is followed by IVRT-cardiac muscles depolarize and vent. pressures increase -ventricular pressure exceeds aortic pressure and AoV opens -ejection-AV oening to closing THEREFOR: systole includes IVRT and ventricular ejection |
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what is normal fractional shortening?
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btw 20-40%
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what are the factors that effect contractility?
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-preload
-afterload -intrinsic contractile function -heart rate |
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Explain preload
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(VOLUME)
-affects the ventricle during distole -increased preload=increased force of contraction |
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explain afterload
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(PRESSURE)
-aortic resistance/impedance/wall stress -increase afterload=redced ventricular foce and volocity of contraction(reduced myocardial fiber shortening) -affects the ventricle during systole |
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what will increase myocardial intrinsic contractility?
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-drugs and hormones and sympatheic nervous sytem
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what happens with increase heart rate?
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-increased cardiac output, therefore, increased force of contraction
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the degree of LV systolic dysfunction is a good predictor of what?
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-clinical outcome for cardiovascular diseases such as:
-ishemic disease -valvular disease -cardiomyopathis -congenital heart disease |
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what segment of the cardiac cycle is sytole?
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from mitral valve closure to aortiv valve closure
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where on the ECG is sytole?
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ventricular depolarization(onset of QRS complex), and end systole is after repolorization(after t-wave)
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explain the cardiac cycle throughout systole
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-systole begins when the LV pressure exceeds the LA pressure resulting in closure of the MV
-this is followed by IVRT-cardiac muscles depolarize and vent. pressures increase -ventricular pressure exceeds aortic pressure and AoV opens -ejection-AV oening to closing THEREFOR: systole includes IVRT and ventricular ejection |
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what is normal fractional shortening?
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btw 20-40%
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what are the factors that effect contractility?
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-preload
-afterload -intrinsic contractile function -heart rate |
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Explain preload
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(VOLUME)
-affects the ventricle during distole -increased preload=increased force of contraction |
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explain afterload
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(PRESSURE)
-aortic resistance/impedance/wall stress -increase afterload=redced ventricular foce and volocity of contraction(reduced myocardial fiber shortening) -affects the ventricle during systole |
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what will increase myocardial intrinsic contractility?
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-drugs and hormones and sympatheic nervous sytem
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what happens with increase heart rate?
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-increased cardiac output, therefore, increased force of contraction
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what are ejection phase indexes?
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-ejection fraction
fractional shorteing Lv mass venocity and circuferential fiber shortening CO and SV |
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explain ejection fraction and FS
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EF=volume=m-mode, 2D, or simpsons
FS=diameter=m-mode/2D |
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what are some non-ejection indexes?
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-systolic time intervals
-LV dP/dT -accel time -pressure-volume analysis-preload |
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what is the qualitative method for systolic function?
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-EPSS
-Ao root motion -sphericity of LV -velocity integrals of LV and RVOT by PW |
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what are the problems with quantification of systolic function?
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-endocardial dropout
-forshortening LV(will overestimate) -reginonal wall abnormalities -disco orination of contration |
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what helps to better view the endocardium?
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haronic imging and contrast agents
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how is wall motion scored? how then is the WMSI obtained?
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1. normal
2. hypokinesis 3. akinesis 4. dyskineses 5. aneurysmal WMSI=average score normal=1; abnormal=1.7 |
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what is eccentric hypertrophy?
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the whole heart is big
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what is the formula for SV?
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SV=(v2(.785)(VTI))
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where is diastole on an ECG?
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and of T TO END OF p
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what are the 4 phases of diastole?
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IVRT
Rapid filling Diastasis Atrial systole |
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Explain IVRT
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begins w/ AoV closed and goes till MV opens
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rapid filling phase
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-begins as MV opens
-rate of filling is related to PG |
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Diastais
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-passive filling
-allows flow from PV directly into LV |
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Atrial systole
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10-15 percent filling
-ends w/ MV closure -affected by: -myocardial stiffness -pericardial costraint on LV -atrial resitance to contraction |
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auxotonic relaxation
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-the last 3 phases of diastole where the MV is open
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What is LV filling determined by?
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active and passive forces:
-Early diastole-e=active relaxation(cells recoil from elastic energy) and determine LV filling -Late diastole-a-passive properties(myocardial compliance-inverse of stiffness) |
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WHAT ARE the parameters of diastolic function?
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-ventricular relaxation
-myocardial or chamber complience -filling pressures |
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how are stiffness and complience related?
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inversely
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what is the normal E/A ratio?
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>1
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what is the normal IVRT?
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80-100
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ventricular relaxation(early diastole)
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-systolic filling during IVRT
-active process involiving energy from myocardium -factors that affect IVRT=internal loading forces and inactivation of myocardial contraction -abnormal IVRT=prolonged rate &reduction in peak filling rate |
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ventricular compliance
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-change in volume over change in pressure
-influenced by ventricular size, shape and characteristics of the myocardium -elevation is based on diastolic passive pressure |
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filling pressures
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-late diastole
-diastolic filling pressures include: LVEDV-after complete filling LAP-average pressure in LA during diastole |
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how is LAP estimated?
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by pulmonary artery wedge pressure in the cath lab
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what are the factors that affect doppler evaluation of LV distolic funtion? normal, and physiologic factors?
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normal:
-respiration -heart rate -age and PR interval PHYSIOLOGIC: -preload-pressire -volume flow rate -LV systolic function and atrial contraction |
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what are some clinical findings associated w/ isolated diastolic dysfunction?
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--LVH
-restrictive cardiomyopathis -pericardial constriction or temponade |
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what are clinical findings associated with diastolic dysfunction associated w/ systolic dysfunction?
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-acute myocardial infarction
-dialated cardiomyopathy -ishemic cardiomyopathy |
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what echo findings suggest diastolic dysfunction?
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-LVH
-enlarged LA -dialated IVC w/ reduced respiratory collapse |
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how should normal mitral duration compare to PV duration?
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should be greater than PV duration
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what is the IVRT, DT, E/A, mitral duration, and PVs/d comparasin for normal, impared relaxation, pseudonormal pattern, and restrictive diastolic dysfunction?
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IVRT:
N-70-90 I=>90 Ps=<90 R=<70 DT: N-160-240 I=>240 P=160-240 R=<160 E/A: N-1-2 I-<1 Ps-1-2 R->1.5 Pvs:Pvd: I-Pvs>PVd Ps-Pvs<Pvd R-Pvs<Pvd Mitral duration: N=>PV A duration I=either or depending on LVEDP Ps-<PV a duration R-<PV a duration |
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what is significant about tissue doppler in diagosing diastolic dysfunction?
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it is preload independant, so we can distinguish pseudonormalization
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what are the components of pulmonary vein flow?
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-systolic forward flow
-diastolic forward flow -systolic revered flow -diastolic reversed flow |
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what are timing and respiratory changes in forward and reversal velocities of hapativ flow improtant to assess?
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TR, constriction, tamponade, restriction, pulmonay hypertension
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what are the 4 things we use for diastolic dysfunction?
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-IVRT
-MV -PV -Tissue doppler |
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what are the disadvantages of TDI?
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-cannot be used w/ prosthetic or MAC
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what are indices obtained during the ejection phase, and nonejection phase used to assess??
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-ejection phase-used to assess LV systolic phase
-nonejection phase-LV systolic function |
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dP/dT
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measure of the rate of rise of ventricular pressure during IVCT
-using CW -measures time interval btw 2 points -measures the change in pressure over time(time it takes the LV to generage 32 mmHg of pressure during IVCT) |
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what is the formula for dP/dt?
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dP/dt=32/change in time
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how was 32mm derived and why?
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(4x3squared)-(4x1squared)=32
time period btw 1 and 3 ms |
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what is the normal, midl to mod, and sever MR jet-time
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N-<27ms
M-27-40ms S->40ms |
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what comes first; diastolic or systolic dysfunction?
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diastolic (30% of patients w. cogestive heart failure have good systolic function)
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HOw does diastolic dysfunction produce signs of heart failure?
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-elevated LV pressure which causes:
-increase LA pressures -this is reflected back to pulmonary circulation which: -causes SOB and pulmonary congestion |
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what does systolic forward flow of the PV corrispond to on the pressure curve, what happens to systolic filling as LA pressure is elevated?
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-corresponds to the x descent on pressure curve; when LA is elevated, systolic filling from PV is reduced.
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how does diastolic forward flow corrispond to the pressure curve, and the mitral valve?
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diastolic forward flow is the d wave of the PV and it corrisponds to the mitral E-velocity as well as the y descent on the pressure curve.
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what determines the magnitude and duration of flow reversal in the PV?
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transmitral and atriovenous pressure gradients which are influenced by the LA systolic function and LA and LV compliance
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how does the doppler signal amplitude of myocardial wall motion(tissue) compare to blood flow amplitude
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the tissue doppler amplitude is much greater.
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what are the 3 components of tissue doppler?
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Sm-apically directed systolic component
Em-atrially directed myocardial early lengthening velocity Am-atrially directed late distolic myocardial lengthening velocity |
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T/F there is no flow change in early diastolic dysfunction?
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true-flow reversal or A-wave is unchanged
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if e-velocity of MV is reduced, what will happen to the PV?
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d will be reduced
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Abnormal relaxation
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-relaxation occurs at a slower rate(21 yr old w/ baby)
-reduced transmitral pressure gradient which results in longer IVRT and reduced E-velocity -DT prolonged -E/A ratio is reduced -duration of MV same or more than AR duration of PV -same appearance of PV and tissue doppler |
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Pseudonormalized pattern
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-incresed LA pressure masks diastolid dysfunction
-pulmonary vein-reduced s wave and increased d wave, AR higher venocity and longer the mitral A-duration becase of increased LA pressure -tissue doppler-reduced Em; increase Am |
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Restrictive
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-severe reduction in LV compliane, and increased LA pressures
-PV higher than 30cm/s -MV opens earlier=short IVRT increased LA pressure increases transmitral gradient causeing increase E wave -short DT -Increased LVEDP -E/A ratio=>2 -PV-increased d wave, and decrease s wave, increased duration and velocity of atrial contraction(a duration) |
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what will the E/A ration e on a reversable diastolic dysfunction compared to irreversable?
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<1, valsalva does not change EA ration(most serious form of diastolic dysfuction)
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what does the valsalva maneuver do?
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reverses preload-reduced volume
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what is the normal Em velocity of the itral annulus?
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7-8cm/s
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what is one of the most common referals for echo?
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to assess LV function
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what is the formula for mean velocity of circumfrential fiber shortening?
what is the normal? |
mean Vcf=(LVIDd-LVIDs)/(LVIDd)(LVET)
Norm=1-1.9cir/sec |
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what is the formula for FS? what is normal FS?
what is the definition of FS? |
FS=(LVIDd-LVIDs)/LVIDdx100
N=28-41% -defined as the percent shortening of the LV myocardium using the excursion of septal and posterior wall echos |
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what is the definition, formula, and normal EF?
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-percent ratio of the difference btw EDV and ESV
EF=(EDV-ESV)/LDVx100 norm=55-80% |
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how is LV mass determined? what is normal for males and females?
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LV mass= volume of myocardiumxspecific gravity of myocardium(1.04g/ml)
norm M-125-130g/m2 F-105-120g/m2 |
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how is LV mass determined?
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Chamber volume and wall thickness
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with dp/dt, what does the velocity of MR reflect? assuming LA pressure does not increase significantly durin IVRT, what does the rate of rise of the doppler velocity reflect?
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-Velocity of MR reflects the instantaneous pressure gradient btw LA and LV during systole
-rate of rise of Doppler velocity reflefts the rate of rise of LV pressure. |
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what are examples of active and passive forces of LV filling?
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active:
-early diastole -rate of myocardial relaxation and elastic recoil(suction) PASSIVE: -late diastole -chamber compliance -chamber stiffness -LA pressure |
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what are causes of diastolic dysfunction w/ preserved systolic function?
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-LVH due to hypertension
-Hpertrophic cardioyopathy -restrictive cardiomyopathy -ischemic disease w/out prior infarction |
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what are some causes of diastolic dysfunction due to extrinsic compression of the heart?
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-tamponade
-constrictive pericarditis |
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what is a cause of diastolic dysfunction w/ systolic dysfunction?
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-dialated cardiomyopathy
-end stage ischemic disease |
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describe the 4 phases of PV flow?
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PVs1:
-early systole -atrial relaxation -decreased LA pressure PVs2: -mid to late systole -increased PV pressure at a more rapid rate than LA pressure in late systole DIASTOLIC FLOW: -resembles early MV flow FLOW REVERSAL: increases in LA pressure may result in flow reversal into pulmonary veins. |
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what is atrial reversal in the PV associated with in ECG?
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p wave on ECG
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what is the normal PV a-wave reversal? and reversal duration?
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a-wave reversal-<30cm/sec
reveral duration-150msec |
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how can we tell if there is pseudonormalization?
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if the PV a-wave reversal is >35cm/s
-if PV a-wave duration is> MV inflow a-wave |
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what are some complications of diastolic dysfunction?
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-exercise intolerance
-dyspnea(most common) -PH -volume overload=edema ascites -tachycardia=a-fib=clot and CVA |
