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Flashcards in Cardiac Pressure Volume Loop Deck (27)
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1
Q

equivalents for ventricle-specific values from isolated muscle values:

  • force/tension
  • length change
  • work = force * length change
  • power
  • isometric and isotonic contractions
A

for ventricle:

  • pressure (afterload)
  • volume change (preload)
  • work = pressure * volume change = preload * afterload
  • power is the same; dW/dt
  • isovolumic and isotonic contractions
2
Q

steps of cardiac cycle in terms of valves opening and closing

A
  1. mitral valve open to mitral valve close (diastole to preload; isotonic relaxation)
  2. mitral valve close to aortic valve open (isovolumic contraction)
  3. aortic valve open to aortic valve close (systole to afterload; isotonic contraction)
  4. aortic valve close to mitral valve open (isovolumic relaxation)
3
Q

mitral valve open to mitral valve close

A

ventricular filling (isotonic relaxation)

  • increase in pressure due to increase in passive tension as ventricle muscle stretches
  • -increase in passive tension = preload
  • ventricle fills until it reaches end diastolic volume (EDV) and mitral valve closes in preparation for contraction
4
Q

mitral valve close to aortic valve open

A

isovolumic contraction of ventricle, isometric contraction of muscle fibers
-since both MV and AV are closed, there’s no way for blood to get out, so the pressure increases

5
Q

aortic valve open to aortic valve close

A

ventricular emptying (isotonic contraction)

  • intraventricular pressure is sufficient to open AV, and ejection begins as ventricle muscle fibers shorten
  • ventricular pressure increases during ejection, then decreases until AV closes
  • AV closes at intersection point with volume pressure curve, as the end systolic volume
6
Q

aortic valve close to mitral valve open

A

isovolumic relaxation of ventricle

-cardiac twitch ends and tension (and pressure) decrease w/o any change in ventricular volume

7
Q

ESPVR

-what is it and what does it imply in regards to the pressure-volume loop?

A

end systolic pressure volume relationship

  • curve that describes maximal pressure that can be developed by the ventricle at any given LV volume
  • implies that the PV loop cannot cross the line defining ESPVR for any given contractile state
8
Q

what is compliance and its relationship to elastance?

A

compliance = dV/dP
-a highly compliant ventricle is “easy” to fill (healthy ventricles during diastole)

elastance = dP/dV (they are inverse)
-a low elastance ventricle is “easy” to fill

9
Q

what does the slope of ESPVR represent? what does this provide?

A

the end-systolic elastance (dV/dP), which provides index of myocardial contractility

10
Q
how does ESPVR change with changes in:
-preload
-afterload
-HR
-increased inotropy (contractility)
-decreased inotropy
what does this mean?
A
  • relatively insensitive to changes in preload, afterload, and HR
  • -makes it improved index of systolic function over other parameters like EF, CO, and SV
  • becomes steeper and shifts to left if inotropy increases
  • becomes flatter and shifts to the right as inotropy decreases
11
Q

EDPVR

  • what is it and what does it describe?
  • what is its slope mean?
A

end-diastolic pressure volume relationship

  • describes passive filling curve for the ventricle, thus the passive properties of the myocardium
  • the slope at any point along curve is reciprocal of ventricular compliance (or stiffness)
12
Q

what happens if ventricle compliance is decreased? when does this happen?

A

the ventricle is stiffer (elastance is higher)

  • this may happen in ventricular hypertrophy
  • higher ventricular end-diastolic pressures at a given end-diastolic volume, or smaller EDV at a given EDP
13
Q

what happens if ventricle compliance decreases? when does this happen?

A

ventricle is easier to fill (elastance is lower)

  • this may happen in dilated cardiomyopathy where ventricle is highly dilated w/o appreciable thickening of wall
  • EDV may be very high, but the EDP may not be greatly elevated
14
Q

what happens at EDV (end-diastolic volume?)

A
  • the ventricle is done passively filling with blood from diastole
  • the ventricle has been stretched, which increases tension (preload)
  • this stretching increases sensitivity of cardiomyocetes via Frank-Starling law
15
Q

what happens to the ventricular afterload if aortic blood pressure is high?

A

the ventricular afterload (pressure) rises

16
Q

is stroke volume affected by changes in preload, afterload, and inotropy?

A

yes, but SV is not strongly influenced by afterload in normal hearts; highly sensitive in failing hearts

17
Q

how is stroke volume related to EDV and ESV?

A

SV = EDV - ESV

18
Q

ejection fraction and normal EF

-what is the equation for EF?

A

fraction of end-diastolic volume ejected out of the ventricle during each contraction

  • healthy ventricles have 55-60%
  • EF = SV/EDV
19
Q

what are reasons that ejection fraction would decrease?q

A

myocardial infarction or cardiomyopathy (damage to myocardium), systolic dysfunction and severe heart failure
-can lead to EF lower than 20%

20
Q

what can EF be used as a clinical indicator of?

A
the inotropy (contractility) of the heart
-increasing inotropy causes increase of EF, while decreasing inotropy decreases EF
21
Q

preload in terms of ventricles

A

end diastolic volume at the beginning of systole

22
Q

afterload in terms of ventricles

A

ventricular pressure at the end of systole, meaning at the time of aortic valve closure

23
Q

when does ventricular pressure equal aortic pressure?

A

at the end of systole (when ventricle is done emptying)

24
Q

what happens to SV with increasing EDV (preload)?

A

SV increases, and there may be sensitization and Starling law in action

25
Q

what happens to SV with increasing afterload?

A

SV decreases, b/c the ventricle has to raise its pressure to meet the aortic pressure (main problem with HTN)

26
Q

what is CO an indicator of, and how is it regulated?

A

indicates how well the heart is performing its function

-regulated by demand for O2 by cells of body

27
Q

what effects do cardiomyopathy, HTN, heart failure, or sepsis have on CO?

A

heart diseases cause decreased CO, but sepsis increases CO

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