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)
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
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
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
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
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
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
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
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
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
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
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
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
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)
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
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
