Cardiac Pressure Volume Loop Flashcards
equivalents for ventricle-specific values from isolated muscle values:
- force/tension
- length change
- work = force * length change
- power
- isometric and isotonic contractions
for ventricle:
- pressure (afterload)
- volume change (preload)
- work = pressure * volume change = preload * afterload
- power is the same; dW/dt
- isovolumic and isotonic contractions
steps of cardiac cycle in terms of valves opening and closing
- mitral valve open to mitral valve close (diastole to preload; isotonic relaxation)
- mitral valve close to aortic valve open (isovolumic contraction)
- aortic valve open to aortic valve close (systole to afterload; isotonic contraction)
- aortic valve close to mitral valve open (isovolumic relaxation)
mitral valve open to mitral valve close
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
mitral valve close to aortic valve open
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
aortic valve open to aortic valve close
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
aortic valve close to mitral valve open
isovolumic relaxation of ventricle
-cardiac twitch ends and tension (and pressure) decrease w/o any change in ventricular volume
ESPVR
-what is it and what does it imply in regards to the pressure-volume loop?
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
what is compliance and its relationship to elastance?
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
what does the slope of ESPVR represent? what does this provide?
the end-systolic elastance (dV/dP), which provides index of myocardial contractility
how does ESPVR change with changes in: -preload -afterload -HR -increased inotropy (contractility) -decreased inotropy what does this mean?
- 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
EDPVR
- what is it and what does it describe?
- what is its slope mean?
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)
what happens if ventricle compliance is decreased? when does this happen?
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
what happens if ventricle compliance decreases? when does this happen?
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
what happens at EDV (end-diastolic volume?)
- 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
what happens to the ventricular afterload if aortic blood pressure is high?
the ventricular afterload (pressure) rises
is stroke volume affected by changes in preload, afterload, and inotropy?
yes, but SV is not strongly influenced by afterload in normal hearts; highly sensitive in failing hearts
how is stroke volume related to EDV and ESV?
SV = EDV - ESV
ejection fraction and normal EF
-what is the equation for EF?
fraction of end-diastolic volume ejected out of the ventricle during each contraction
- healthy ventricles have 55-60%
- EF = SV/EDV
what are reasons that ejection fraction would decrease?q
myocardial infarction or cardiomyopathy (damage to myocardium), systolic dysfunction and severe heart failure
-can lead to EF lower than 20%
what can EF be used as a clinical indicator of?
the inotropy (contractility) of the heart -increasing inotropy causes increase of EF, while decreasing inotropy decreases EF
preload in terms of ventricles
end diastolic volume at the beginning of systole
afterload in terms of ventricles
ventricular pressure at the end of systole, meaning at the time of aortic valve closure
when does ventricular pressure equal aortic pressure?
at the end of systole (when ventricle is done emptying)
what happens to SV with increasing EDV (preload)?
SV increases, and there may be sensitization and Starling law in action
what happens to SV with increasing afterload?
SV decreases, b/c the ventricle has to raise its pressure to meet the aortic pressure (main problem with HTN)
what is CO an indicator of, and how is it regulated?
indicates how well the heart is performing its function
-regulated by demand for O2 by cells of body
what effects do cardiomyopathy, HTN, heart failure, or sepsis have on CO?
heart diseases cause decreased CO, but sepsis increases CO
