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Applied Clinical Procedures > MUGA > Flashcards

MUGA Flashcards

1
Q

what quantitative data do we get from a MUGA?

A
  • global and regional EF
  • phase and amplitude (Fourier Analysis)
  • stroke volume and paradox image
  • peak filling/emptying rates
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2
Q

word to describe “less or diminished contraction” of wall motion

A

hypokinesis

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3
Q

word to describe “late contraction” of wall motion

A

tardokinesis

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4
Q

word to describe “out of phase with the rest” wall motion

A

dyskinesis

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5
Q

word to describe no wall motion

A

akinesis

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6
Q

how is stroke volume calculated?

A

SV = (ED volume - bkg) - (ES volume - bkg)

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7
Q

normal SV

A

~80-100 ml/beat

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8
Q

how is ejection fraction calculated?

A

((EDvol - bkg) - (ESvol - bkg)/(EDvol - bkg)) * 100

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9
Q

how is cardiac output calculated?

A

SV * HR

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10
Q

normal cardiac output

A

5-6L/min

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11
Q

normal EF

A

~50-80%

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12
Q

peak filling/emptying rates

A

reflection of early rapid filling phase of DIASTOLE and measures LV compliance (elasticity)

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13
Q

normal emptying/peak filling rate

A

> 2.5 EDV/sec

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14
Q

of frames needed to obtain reliable peak filling rate

A

> 32 frames

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15
Q

what is seen in an acquired MUGA image

A

liver/spleen
lungs
aorta and pulmonary arteries

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16
Q

what does pericardial effusions look like?

A

thicker lines between heart and liver (cold line)

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17
Q

best view for right atrium

A

ANT
LAO during vent systole

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18
Q

normal variant for right atrium

A

enlargement

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19
Q

best view for left atrium

A

LAO or LLAT

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20
Q

best view for right ventricle

A

LAO or ANT

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21
Q

if a patient has LBBB, what occurs in the ventricles?

A

out of sync contractions between R and L ventricles

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22
Q

enlargement of the right ventricle could mean…

A

pulmonary hypertension or cardiomyopathy

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23
Q

best view for L ventricle

A

LAO

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24
Q

normal LVEF

A

50-80% (at rest)

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25
Q

normal RVEF

A

40-60%

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26
Q

stress LVEF

A

+ 5-10%

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27
Q

SV = ?

A

EDV - ESV

28
Q

phase

A

ex. LV and RV contracting at the same time, and oppo of artia contraction

29
Q

amplitude

A

amount of contraction

30
Q

stroke volume image

A

subtracting ES frame from the ED frame giving result to ring that represents stroke volume
ED-ES = SV

31
Q

paradox image

A

subtracting ED from ES, being left with nothing unless paradoxical motion occurring
ES-ED

32
Q

what are possible pathologies for an abnormal MUGA

A
  • cardiotoxicity
  • CAD/MI
  • CHF (congestive heart failure)
  • cardiomyopathy
33
Q

what chemotherapy agents are linked to cardiotoxicity?

A
  • anthracyclines (doxurubicin/adriamycin)
  • trastuzumab (herceptin)
34
Q

what baseline EF indicates high risk for cardiotoxicity?

A

<30%

35
Q

mild cardiotoxicity

A

drop in EF <10%, EF >45%

36
Q

moderate toxicity

A

drop in EF = 15%, EF <45%

37
Q

severe toxicity

A

drop in EF = 20%, EF <30%

38
Q

how will wall motion be effected by CAD?

A

area of ischemia or infarct in the area of wall motion abnormality with hypokinesis or akinesis on STRESS study

REST = no wall motion abnormality (unles infarct or very sig. ischemia)

39
Q

CAD:
rest images

A

amp and phase normal unless severe CAD (>75%)

40
Q

CAD:
stress images

A

phase - areas of hypokinesis or akinesis
amplitude - loss of contractility from ischemia
SV - void in ring in areas of hypo or akinesis

41
Q

LV dysfunction (low EF or abnormal wall motion) + normal RV = ?

A

ischemia

42
Q

bilateral ventricular enlargement and dysfunction = ?

A

inflammation

43
Q

what can be an early sensitive indicator of CHF?

A

decrease in PFR

44
Q

dilated cardiomyopathy

A

chambers of heart are enlarged

45
Q

hypertrophic cardiomyopathy

A

myocardium thicken, so chambers are smaller

46
Q

restrictive cardiomyopathy

A

change in compliance, resistance to filling, less stretchy

47
Q

what can cause dilated cardiomyopathy?

A

CAD, viral/bacterial infection, chronic hormone disorders, alcohol, drugs, chemo, pregnancy, RA

48
Q

what are the effects of dilated cardiomyopathy?

A
  • valvular regurgitation
  • decreased LVEF
  • increased risk of clot formation (stagnation)
49
Q

causes of hypertrophic cardiomyopathy

A
  • unknown… possibly genetic
50
Q

what are the effects of hypertrophic cardiomyopathy?

A
  • fibrosed tissue
  • LV dysfunction, decreased perf.
  • eventual decrease SV, EF
  • A Fib, mitral valve reguritation
51
Q

appearance of dilated cardiomyopathy

A

dilation in all 4 chambers
decrease LVEF. RVEF. LV wall thickness

52
Q

appearance of hypertrophic cardiomyopathy

A

normal or small LV cavity, normal or slightly elevated LVEF

53
Q

appearance of restrictive cardiomyopathy

A

normal LV cavity, normal or decreased LVEF, normal or enlarged RV cavity and normal or decreased RVEF

54
Q

true aneurysm

A

3 layers of heart wall
ant or anteroapical wall usually

55
Q

aneurysm

A

weakening of wall

56
Q

false/pseudo aneurysm

A

doesn’t involve endocardium

57
Q

mitral or aortic regugitation

A

no increase in EF on stress MUGA

58
Q

aortic stenosis

A

normal or elevated LVEF at rest, decline in EF during stress
(due to increased afterload pressures of stenosed valve)

59
Q

tricuspid regurgitation

A

dilated RV and decreased RVEF

60
Q

choice for assessment of valvular heart disease

A

doppler echocardiography

61
Q

false positives

A

underestimates LVEF

62
Q

including LA or aorta in ROI
increase/decrease LVEF?

A

decreases LVEF

63
Q

subtracting too little background
increase/decrease LVEF?

A

decreases LVEF

64
Q

subtracting too much background
increase/decrease LVEF?

A

increases LVEF

65
Q

excluding part of LV in ROI
increase/decrease LVEF?

A

increases LVEF

66
Q
A

Applied Clinical Procedures (6 decks)

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