Cardiac Pressure Volume Loop Flashcards

1
Q

Cardiac Cycle: Isovolumioc Constraction and Relaxation

A
  • ventricle empties for the Pressure of ventricle is greater than pressure of aorta
  • ventricle fills when pressure of atrium is greater than pressure of ventricle
  • the heart cycle circles counter clockwise on the Volume Pressure plot
  • the ventricle fills with blood coming from the atrium during diastole(bottom) and ejects blood in the aorta during systole (top)
  • during the other parts of the cycle the heart contracts without changing volume (isovolumic contraction) or relaxes without changing volume (isovolumic relaxation)
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2
Q

Mitral Valve Open to Mitral Valve Close

A
  • during the phase the ventricle fills with blood
  • the increase in pressure is due to increase passive tension as the ventricle muscle stretches
  • this increase in passive tension is preload
  • the ventricle will fill until it reaches end diastolic volume and the mitral valve closes in preparation for contraction
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3
Q

Mitral valve closed to aortic valve open

A
  • during this phase the ventricular muscle fibers contracts isometrically and the ventricle itself undergoes isovolumetric contraction (pressure increases without a change in volume)
  • both the mitral valve and the aortic valve are closed, so there is no way for the blood to get out
  • thus pressure increases during the isovolumetric contraction
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4
Q

Aortic valve open to aortic valve close

A
  • the intraventricular pressure is sufficient to open the aortic valve and ventricular ejection begins as ventricle muscle fibers shortens
  • ventricular pressure increases during ejection and then decreases until the aortic valve closes
  • the aortic valve closes at the intersection point with the volume pressure curve= end systolic volume
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5
Q

Aortic valve close to mitral valve open

A

-the ventricle undergoes isovolumetric relaxation as the cardiac twitch ends and tension (and pressure) decrease without any change in ventricular volume

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6
Q

Compliance

A
  • a highly compliant ventricle is easy to fill.
  • a healthy ventricle is very compliant during diastole and NOT very compliant during systole
  • elastace- a low elastance ventricle is easy to fill
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7
Q

EDPVR

A
  • end diastolic pressure volume relationship
  • describes the passive filling curve for ventricle and thus the passive properties of the myocardium
  • the slope pf EDPVR at any point along this curve is the along this curve is the reciprocal of ventricular compliance (or ventricular stiffness)
  • if ventricular compliance is decreased the ventricle is stiffer resulting in higher ventricular end diastolic pressure at any given end diastolic volume
  • less compliant ventricle would have a smaller EDV due to impaired filling
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8
Q

ESPVR

A
  • end systolic pressure volume relationship
  • slide of ESPVR represents the end-systolic elastance, which provides an index of myocardial contractility
  • relatively insensitive to changes in preload, afterload, and heart rate
  • the makes it an improved index of systolic function over other hemodynamic parameters like ejection fraction, cardiac output, and stroke volume
  • the ESPVR becomes steeper and shifts to the left as inotropy (contractility) increases, and shifts to the right as inotropy decreases
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9
Q

Cardiac cycle plotted on volume vs pressure curve

A
  • the ventricle passively fills with blood during diastolic filling until it reaches end diastolic volume
  • at EDV the ventricle has been stretched and this increases tension (preload)- this stretching also increases sensitivity of the cardiomyocytes per Frank- Starling Law
  • the mitral valve then closes the ventricular muscle begins to actively contract and pressure increases rapidly (isovolumetrically) until the aortic valve opens
  • the aortic valve opens when blood pressure in the ventricle equals or exceeds the blood pressure in the aorta
  • this point is considered the ventricular afterload and is related to the amount of work that the heart must perform
  • the afterload times volume change is work during contraction
  • if aortic blood pressure is high, the ventricular afterload rises
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10
Q

Stroke Volume

A
  • the volume of blood ejected by the ventricle in a single contraction. It is the difference between the end-diastolic volume (EDV) and the end-systolic volume (ESV)
  • SV= EDV - ESV
  • affected by changes in preload, afterload, and inotrophy (contractility)
  • in normal hearts, the SV is highly sensitive to afterload changes
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11
Q

Ejection Fraction

A
  • the fraction of end-diastolic volume that is ejected out the of ventricle during each contraction
  • EF = SV/EDV
  • healthy is 0.55
  • MI causes damage to myocardium which impairs the ability to eject blood and reduces ejection fraction
  • low EF usually indicates systolic dysfunction and severe heart failure can result in EF lower than 0.2
  • EF is also used as clinical indicator of the inotrophy (contractility) of the heart
  • increase inotropy = increase in EF
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12
Q

Preload

A
  • the end diastolic volume at the beginning of systole

- relates directly the volume of blood that has to be pushed into the aorta against aortic pressure

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13
Q

Afterload

A
  • ventricular pressure at the end of systole, meaning at the time of aortic valve closure
  • the pressure of the aorta that the ventricle must push the object or blood into
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14
Q

Increase in stoke volume

A
  • increase in stroke volume with increasing end diastolic volume (EDV aka Preload)
  • sensitization and the Frank Sterling law
  • increase Po (tension) and stroke volume with increased End Diastolic Volume (preload)
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15
Q

Decrease in stroke volume with increasing afterload

A
  • high aortic pressure raises the ventricular afterload
  • the ventricle had to raise its pressure to meet the aortic pressure
  • unfortunately at this higher pressure the stroke volume is lower, meaning less blood is ejected per heart beat
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16
Q

Increase in stroke volume with sympathetic input

A
  • effect of increasing sympathetic stimulation on cardiac function
  • a sympathomimetic (norepi, or norepi agonist) will shift the ventricular function curve upward
  • Po increases at any given fiber length or end diastolic pressure
  • more work can be performed at any load (aortic pressure)
  • at any given load, end systolic fiber length will be smaller (the ventricle will have less blood at the end of systole)
  • Ejection fraction may increase from 45% to 60%
  • the heart can increase in contractility to compensate and maintain stroke volume when there is higher aortic pressure
17
Q

Mechanisms that can change stroke volume

A
  • Cardiac Parasympathetic (negative chronotropic)- decrease Heart Rate
  • Cardiac Sympathetic (positive chronotropic)- increase heart rate; contractility (positive inotropic) increase stroke volume
  • Arterial Pressure- after load- decrease stroke volume
  • Filling pressure- preload- increase stroke volume
18
Q

Cardiac Output

A
  • the amount of blood pumped by the ventricle in unit time
  • CO = SV x HR
  • an indicator of how well the heart is performing its function. CO is regulated principally by demand for oxygen by the cells of the body
  • hypertension and heart failure associated with changes in CO
  • Cardiomyopathy and heart failure cause a reduction in cardiac output, whereas infection and sepsis are known to increase cardiac output