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40 Cards in this Set
- Front
- Back
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1. Why is force (tension) developed?
What happens as EDV increases? |
Develop a force as a result of cross bridge cycle
1. Stretch muscle so sarcomere length increases 2. The force of contraction increases 3. Stroke volume increases |
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2. What is plotted in a pressure-volume (PV) loop?
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Instantaneous pressures and volumes w/ volume plotted on the X axis and pressure plotted on the Y axis
Take pressure and volume from Wigger's curve and plot **time is not involved |
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3. When do the four corner's of the loop occur?
What are the four corners? |
Occur at the time the valves change positions
AO = aortic valve opening MO = mitral valve opening AC = aortic valve closure MC = mitral valve closure |
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4. What does each side of the loop represent?
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A phase of the cardiac cycle
1. Right side = IVC 2. Top = ventricular ejection 3. Left side = IVR 4. Bottom = ventricular filling |
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5. What does the width of the loop represent?
What does the area within the loop represent? |
Stroke volume
Represents the stroke work - the work performed by the left ventricle during one heart cycle **do more work, area goes up so does energy used by heart |
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6. What is AC represent?
What does AO represent? What does MO represent? What does MC represent? |
AC = end of systole
-volume decreases, pressure increases AO = end of IVC -no volume change, pressure increases MC = end of diastole -biggest volume, low pressure MO = end of IVR -no volume change, pressure decrease |
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7. What is the upper boundary of the loop?
What is preload? |
Afterload
**pressure that has to be overcome to eject stroke load **this ventricular pressure should be close to aortic pressure EDV |
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8. What defines the lower boundary of the loop?
What is PVR? What determines the diastolic pressure-volume relationship? |
Defined by the diastolic pressure-volume relationship (PVR)
The relationship between ventricular pressure and volume measured when the myocardium is relaxed during filling Determined by diastolic ventricular compliance |
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9. How is compliance calculated?
How is a decrease in compliance related to PVR? How does this affect pressure? |
C = ΔV / ΔP
Decrease in compliance is represented by an upward shift in PVR Higher (filling) pressure at any volum |
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10. Relate volume, pressure and compliance.
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If volume increases then pressure increases
As volume in ventricle increases then compliance decreases **heart becomes more stiff |
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11. How does scar tissue or a calcified pericardium affect compliance?
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Decreases diastolic ventricular compliance
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12. How does a stiff heart affect the EDV?
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Stiff heart has less EDV (can't fill as much)
Small EDV = shorter sarcomeres so decrease force Decrease in force means the SV decreases If SV falls then CO falls and MBP falls |
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13. What determines the upper left corner of the PV loop?
What does the ESPVR represent? |
Determined by the end-systolic pressure-volume relationship (ESPVR)
Represents the maximum pressure that the ventricle can develop at any volume assuming contractility is constant |
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14. What does the EPSVR show about volume and pressure?
When must ventricular ejection end? Why? |
As the volume of the ventricle decreases, its maximum capability to develop pressure decreases
Must end when the upper left corner of the PV loop intersects the ESPVR B/c if the ventricular volume was to decrease further the ventricle would not be able to produce enough pressure to overcome aortic pressure |
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15. When the heart has low compliance (stiff) how is the right ventricular diastolic pressure?
How are other pressures? How is the pressure in the systemic capillaries? |
It is high so right atrial pressure is also high
All pressures going backward from heart are high (including central venous pressure) Systemic capillaries have high pressure, forcing water out causing swelling **mean BP is low though |
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16. What does the ESPVR slope represent?
What does the upper boundary of the PV loop represent? What is this closely related to? |
Represents contractility
Represents afterload Closely related to mean blood pressure (MBP) |
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17. How can afterload be assessed?
(three ways) |
Measure:
1. Diastolic pressure (pressure ventricle must overcome to begin ejection) 2. Peak systolic left ventricular pressure 3. Mean pressure during ejection |
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18. How is preload best represented?
Where can this be measured on the PV loop? |
Best represented by the EDV
(end diastolic volume) Measured at right lower corner of the PV loop |
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19. What will an increase in preload (EDV) result in in a normal person?
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Increase in SV
**sarcomeres are stretched more w/ increase in EDV so have more force thus increase SV **CO increases w/ increase in SV (HR remains the same) **MBP is higher since SV is higher |
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20. What does an increase in EDV do the PV loop?
What does an increase in width of PV loop signify? What mechanism does an increase in EDV activate? How does this affect the Starling curve? |
Displaces the right side of the PV loop to the right
This in turn increases the width of the PV loop Signifies an increase in SV Activates the Frank-Starling mechanism Moves the ventricle higher on the curve |
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21. What is the Frank-Starling mechanism?
What does the Frank-Starling mechanism result in? |
Intrinsic capability of a normal heart to change its stroke volume in response to changes in preload
Increase in myocardial force generating capacity **this occurs when the length of the sarcomere is increased |
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22. What does it mean that the heart has "preload" reserve?
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The heart normally operates on the middle of Starling curve and thus the heart has "preload" reserve
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23. Why does the cardiac output decrease when a patient loses blood volume?
Why does the CO increase immediately after an astronaut is exposed to a microgravity environment? |
Preload drops (EDV) so force drops and so does CO (as well as MBP)
Increase in blood volume in heart and head |
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24. Why does the CO decrease immediately after a person changes from a supine to a standing position?
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Blood leaves head and thorax and is redistributed more in lower limbs than heart
As a result EDV lowers as does sarcomere length and force CO and MBP drop so patient can feel faint and even pass out |
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25. What is afterload?
In what two ways can afterload be measured? |
Force or pressure which the ventricle must overcome to eject the SV
1. Ventricular pressure during ejection (upper boundary of PV loop) 2. Systolic wall stress |
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26. How is the ventricular pressure throughout ejection?
What is it closely related to? |
Varies
Closely related to mean arterial blood pressure |
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27. What is systolic ventricular wall stress?
What does it tell us? Where is wall stress the greatest? What does a higher wall stress mean? |
Force per unit area w/in the myocardium during ejection
Tells us the force which must be overcome for a sarcomere to shorten Greatest at thickest area Higher wall stress means harder working sarcomeres to shorten (use more energy) |
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28. What happens to ventricular systolic wall stress during ejection and why?
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Decreases b/c ratio (r/Th) decreases more than the ventricular pressure increases
**during ejection pressure increases but radius decreases **heart wall gets thicker so wall stress drops during ejection **sarocomeres need to generate less force to shorten |
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29. Why could an increase in afterload occur?
What happens if afterload is increased while preload and contractility are held constant? |
1. Patient w/ hypertension b/c of high blood pressure
2. Patients in heart failure b/c ventricle is dilated and thus have large radius and high wall stress SV decreases |
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30. What affect does increased afterload have on the PV loop?
On the Starling curve? |
Width of loop decreases so SV does down
Starling curve is displace down ward on Starling curve |
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31. What is contracility?
How is it affected by sympathetic activation? What ion is contractility closely related to? |
Intrinisic capability of the ventricle to develop pressure which is independent of load
Increase in sympathetic nerve activity increased contractility Close relationship between intracellular [Ca] and contractility (directly proportional) |
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32. What indices are used to estimate changes in contractility?
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1. Ejection fraction
2. Emax (slope of end-systolic pressure volume relationship) 3. Max rate of change of left ventricular pressure during IVC |
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33. What will an increase in contractility w/ no change in preload or afterload result in?
What happens to ventricle ejection volume w/ an increase in contractility? |
Increased in SV
When ventricle ejects it can eject to smaller volume if contractility is increased |
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34. How does increased sympathetic nerve activity affect heart rate?
How does decreased parasympathetic nerve active affect heart rate? |
Increase norepinephrine concentration near SA node and frequency of AP production will increase
Decrease concentration of ACh near SA node and frequency of product of AP will increase |
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35. What is the relationship between heart rate and time for ventricular filling?
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Inverse relationship
**If heart rate is increased, time for ventricular filling reduces so much that SV, CO and BP can be decreased |
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36. What happens in normal people as exercise activity is increased?
What happens to cardiac function in the failing heart? |
Both heart rate and contractility will increase so that CO will increase
CO does not meed needs of body (inadequate CO) |
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37. How is the basal contractility of the failing cardiac myocytes?
As contractility drops what happens to the sarocomere length? |
Is depressed
**force ventricle develops drops Heart begins to dilate so sarcomeres can stretch **done so heart can compensate for drop in contractility |
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38. During heart failure what happens to EDV?
What happens to EDP? What does the result in increased EDP do? |
Increased EDV (dilated ventricles)
Increased EDP Reflects back into the pulmonary and systemic capillaries which increases the rate of filtration and causes pulmonary and systemic edema |
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39. What are some cardiac compensatory mechanisms used in the stressed normal heart and continuously in the failing heart?
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1. Very high level of sympathetic nerve activity in the failing heart
2. Down regulation of the beta adrenergic signaling pathway |
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40. What are treatments?
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1. Diuretics
2. A.C.E. inhibitors -block conversion of agniotension I to angiotension II 3. Decrease contractility by giving beta blockers -reduce effect of sympathetic nerve activity on heart and kidneys |
