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126 Cards in this Set
- Front
- Back
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what is cardiac performance
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the effenceicy of the heart to pump out blood and keep BP high enough to perfuse all of the peripheral tissues
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LVSW=
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SV X LVPP
**LVPP is measured on a P/V Loop. its the difference btwn the P at the beginning of iosovolumetric contract, and the peak P (mid systole) |
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How can CO be Altered
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By changing SV or HR
CO = SV X HR |
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List the ways SV is altered?
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Contractility
Afterload Preload |
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List the ways HR is altered?
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ANS
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what does the area of the P/V loop represent?
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work done by vent
LVSW= SV X LVPP **LVPP is found by: peak Systolic P - Diastolic P |
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if given a series of P/V curves what a good way to quickly compare the amt of work done by each loop?
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look at the area. larger area is larger work that was done
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How does preload change the shape of a P/V loop?
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????/
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How does afterload change the shape of a P/V loop?
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????
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How does HR change the shape of a P/V loop?
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????
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How does Contractility change the shape of a P/V loop?
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????
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what is preload and what does it determine?
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its the amt of blood in the vent at the end of diastole (EDV)
**determines resting fiber length, recall increasing fiber length will increase the force of contraction (the other way to increase force of contraction in contractility by Ca) |
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what is the frank sterling law of the heart?
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increased force of contraction when there is an increased preload, due to increased fiber length. Increased fiber length mean increased force of contraction
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ability to eject blood from the heart is proportional to...
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the amt of blood in the heart
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does cardiac mm operate at maximal L/T relationship?
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nope, there is LOTS of room to increase fiber length in order to get a greater force of contraction
**fiber length is increased by increasing preload |
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why does increasing cardiac mm fiber length increase the force of contraction
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fiber isnt at optimal length, room for growth
longer fibers will have more cross bridges that can form ***as EDV increases the sarcromers get longer, the tension peaks, and a larger SV is ejected |
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what changes preload
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increased venous return
increased EDV |
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when preload in increased how is the P/V loop changed?
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the SV increases
**the area in the curve increases: LVSW increases **Frank Sterling: when EDV increases, SV increases **preload is increased EDV (increased venous returN) |
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What determines Preload? (5)
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1. Time for vent to fill, when HR increases time to fill decreases and EDV decreases, SV decreases
2. Ventricular Compliance: when compliance decreases preload decreases 3. Filling Pressure: negative intrathoracic pressure (breath in) will increase venous return (affect on S2?!) 4. Contribution of Atrial Systole to filling: when vent fill time is reduced this is important 5. Pericardial constraint: increased fluid around heart will decrease compliance nad decrease compliance |
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How does Ventrical Filling time affect Preload?
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when fill time is decreased, EDV decreases, AV decreases
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How does Ventricular Compliance affect preload?
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Decreased compliance (V/P) will decrease EDV, and decrease Sv
**with low compliance there is a larger pressure change that is required to get the same amt of volume in |
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How does Filling Pressure alter preload?
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when you breath in the intrathoracic pressure decreases and venous return increases, this will increase venous return and increase EDV and increase SV.
**recall when this happens the ejection time of the R side of the heart and the pulm valve will close even later than normal. This widens the S2 heart sound |
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How/When is the contribution of atrial systole important to vent filling
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when fill time is reduced
this can keep EDV high under normal conditions doesnt add a whole lot of extra volume |
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how does the pericardium affect preload?
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it can constrain the heart so compliance is reduced and EDV decreases
Pathological |
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how fast does the heart need to beat to affect the CO
*NO sympathetic stimulation |
>150
increase in HR will decrease the amt of time for reduced filling, this will decrease SV. BUT.... No change in CO because HR is increased CO = SV X HR |
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how fast does the heart need to beat to affect the CO
***WITH sympathetic stimulation |
(exercise)
SV will increase due to increased contractility, CO can increase dramatically |
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what the difference btwn increased HR with and without sympathetic stimulation
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WITH: increase CO because contractility (ca) increases, AV and HR increase
WITHOUT: CO is constant (as long as HR is less than 150) Sv is decreased but HR increases to keep CO constant |
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a compliant vessel will undergo a large change in ________ at a constant _______
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volume
pressure |
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what reduces compliance
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hyperstrphy
ischemia |
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low compliance vessels develop ________ pressure during ___________ which slows filling
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High
diastole |
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is compliance infinate?
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nope, there will come a point when compliance drops off.
a large cahnge in volume accompainied by a small change in pressure: high compiance |
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what enhances venous return
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taking a breath in
inspiration decreases intrathoracic pressure, this increases venous return and inceases preload (EDV) this also will make a longer ejection fraction for the ri side of the heart and the pulm valve will close EVEN later. widen S2 sound |
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what is cardiac tamponade
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fluid in precardium, restricts LV filling (decreases EDV), decreases SV, ineffective cardiac performance
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what does the pericardium protect against?
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L vent volume overload
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what is afterload
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**increased aortic pressure
the resistance that the vent contractes against **aortic/pulm resistance |
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what are the main components of determine afterload for the L side of the heart
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**afterload: the amt of resistance the vent has to overcome
Arterial Pressure PVR (Peripheral vascular resistance) Arterial wall compliance Mass of the column of blood in aorta viscosity of blood |
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what is the estimate of afterload
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Resistance against which the vent contracts is eltimated by MAP (mean arterial pressure)
MAP = DP + (PP/3) **PP= SP-DP |
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how does muscular shortening and velocity of ejection relate to afterload
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a decreased muscular shortening will INCREASE afterload
a decreased velocity of ejection will INCREASE afterload |
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during what phase of the cardiac cycle is afterload overcome
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at the very end of isovolumetric contraction
**the pressure in the aorta has been overcome |
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how does an increase in afterload affect SV
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SV is decreased
ESV increases |
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where is the E of contraction 'spent' when afterload increases
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more E required to move through isovolumetric contraction so there is less E left over to do eject blood
SV decreases and ESV is increased |
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when EDV is constant and afterload increases what happens when...
1. Aortic Vavle 2. ESV 3. SV |
1. opens later, closes sooner (S2 is heard more clearly, S2 widens)
2. increase 3. decrease |
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How is afterload increased
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1. aortic stenosis
2. increased arterial pressure 3. increased PVR 4. Increased blood viscosity 5. decreased arterial compliance |
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How does the body compensate for the increased ESV that is seen with increased afterload
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vent filling remains the same so EDV will increase in order to keep the SV constant
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does an increase in afterload increase the LVSW
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yep, the area of the curve is increased
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when contractility increases what happens to SV and ESV
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SVincreases
ESV decreases |
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contractility is
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the eability of the heart to do work at anyt given fiber length
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what affects contractility
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Ca+2
ANS Hopmones (Epi) |
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Fiber length is proportional to what?
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EDV
**when EDV is constant, fiber length is constant, SO in order to increase the force of contraction you need to increase contractility (rahter than preload) |
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what does NE do to the heart
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SNS
B1 receptors positive inotropic effect increases SV and EF at a given EDV |
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what factors are affected by SNS
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1. Rate of contraction/relatation increases
2. Force of contraction increases |
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when contractility increases:
EF velocity SV ESV |
increases
increases decreases |
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what does isovolumic contraction tell us about contracility
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rate of vent P changes
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contractility is independent of
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preload
afterload |
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does an increase in afterload increase the LVSW
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yep, the area of the curve is increased
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when contractility increases what happens to SV and ESV
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SVincreases
ESV decreases |
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contractility is
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the eability of the heart to do work at anyt given fiber length
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what affects contractility
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Ca+2
ANS Hopmones (Epi) |
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Fiber length is proportional to what?
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EDV
**when EDV is constant, fiber length is constant, SO in order to increase the force of contraction you need to increase contractility (rahter than preload) |
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what does NE do to the heart
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SNS
B1 receptors positive inotropic effect increases SV and EF at a given EDV |
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what factors are affected by SNS
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1. Rate of contraction/relatation increases
2. Force of contraction increases |
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when contractility increases:
EF velocity SV ESV |
increases
increases decreases |
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what does isovolumic contraction tell us about contracility
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rate of vent P changes
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contractility is independent of
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preload
afterload |
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can contractility be measured directly?
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nope
we can measure EF- 50-70% is normal |
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what are two ways HR influences cardiac performance
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1. treppe (bowditch staricase): increased contraction leaves more Ca around to increase contractility
2. CO=HR X SV (When HR is 150-180 CO is reduced bc SV decreases) |
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What must be the reasons for increased HR if CO is increased
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SNS
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explain Treppe (bowditch staircase)
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increased HR lets more Ca into the cell
This Ca is then stored in the SR and used in the next contraction This increases the force of contraction and maintain CO at increased HR |
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what is the relatioship btwn CO and HR when SV is constant
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linear, ar HR increases CO increases when SV is constant
**if SV declines as a result of a HR so fast it impedes vent filling the CO decreases |
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what is the compensatory mech to ensure CO is maintained at an increased HR
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increase contractility
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if HR increases and SV also increases due to compensation what happens to CO?
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increases
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on a PV loop how do you visualize increased preload?
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increased EDV
(increased to the right) |
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on a PV loop how do you visualize in increased afterload?
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decreased SV
(increased to the top) |
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on a PV loop how do you visualize increased contractility
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increased EF
decreased ESV (increased to the top/left) |
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LVSW = actual
LVSW = approximation |
SV X LVPP
*BUT LVPP is hard to measure(its the peak systolic pressure-EDP) SO... LVSW = SV X MAP where MAP = DP + PP/3 **these measure work of ONE BEAT |
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LVMW
Units? |
Left Ventricular minute work. takes the amt of work done by the LV in 1 beat and determines how much work is done by the L vent in 1 minute
LVMW= LVSW X HR LVMW= SV X MAP X HR mL mmHg/min |
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MAP
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mean arterial pressure
mean aortic pressure MAP = DP + PP/3 |
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LVSW
LVWI LVMW |
LVSW= MAP X SV (LVPP X SV)
LVWI= LVSW/SA LVMW= LVSW X HR |
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How can you measure CO?
Fick method |
CO= O2 consumption/ (arterial O2-Venous O2)
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what does CO= O2 consumption/ (O2 atery-O2 venous) mean?
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calculation of cardiac output
Ficks method |
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how much more work does the LV do than the RV?
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6-7X more
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what is the RMR for the heart?
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4.8-6 mL/gm/h
About 25% is for basal, the rest is for contraction |
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How does the ANS affect HR?
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by altering influx of Na at the SA node
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about how much of the E requirement for the heart comes from carbs? what picks up the slack
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35-40%
FA oxidation |
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is the heart aerobic or anaerobic
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aerobic
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What is cardiac efficiency?
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work/energy
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does cardiac efficiency imporve or get worse with exercise
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improves
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what work is harder for the heart? volume or pressure
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volume (preload)
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what are the O2 dependent processes in the heart (why does the heart requireATP)
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1. contractile proteins
2. eletrical activity 3. ion pumps/ion gradients 4. metabolic activity |
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where does the heart get its fuel? endogenous, exogenous
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Exogenous:
blood: glocose, lactate, FA, ketone bodies Endogenous: Glycogen, tryglycerides |
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How does the cell uptake fuel?
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1. Energy demand is dependent on workload. ie more fuel used/taken up during exercise
2. Metabolic State: fast/fed, associated with changes in arterial concentrations of fuel |
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what are the 3 main fuel sources (metabolic pathways) used in the heart
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1. glucose
2. lactate (not as much) 3. FA |
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under normal resting conditions what percent of the total ATP production comes from carbs
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30-40%
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when is the carnitine shuttle used in the heart?
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to get FA into the mito for oxidation
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for glucose metabolism in the heart name the ways glucose enters the heart
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1. glycolysis
2. glucose oxidation 3. lactate oxidation 4. glycogen stores |
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what provides 60-70% of the hearts source of ATP
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FA metabolism
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how are FA taken in and metabolized in the heart?
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Triglycreide lipolysis and B oxidation of FA
lipoprotein and CM oxidation Ketone body oxidation |
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what allows the heart to switch the 70/30 (fat/carb) oxidation ratio for metabolism?
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Randle Cycle
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randle cycle
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competition of glucose and fatty acids for substrates.
thought to play a role in DM II and insulin resistance |
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what happens in the fasted state
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insulin is low so FFA are more favorable taken into the heart and glucose is inhibited
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when are lipids used for heart fuel more
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fasted state
70% of ATP production from FA |
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what happens in the fed state
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insulin and glucose are high so lipolysis is inhibited and Glucose uptake and metabolism in the heart is increased
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what overcomes the use of FA in the heart?
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increased glucose
FED state |
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as fat oxidation increases, glucose oxidation _______-
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decreases
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what increases as a result of B oxidation? What does this cause?
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B oxidation releases:
citrate: inhibits PFK acetly CoA: inhibits PDH **these inhibit glycolysis |
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what is inhibited by citrate? what is the interplay?
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Citrate is a product of B oxidation of FA so it will inhibit glycolysis
Citrate inhibits PFK |
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what is inhibited by Acetly CoA? what is the interplay
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Acetly CoA is made form B oxidation of Fa so it will inhibit glycolysis
**Acetly CoA inhibits PDH |
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so... B oxidation will increase citrate and Acetly coA which inhibit PFK and PDH respectively. what effect does this have on glucose up take
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when the glycolytic enzymes increase, G6P (glucose 6 Pi) also increases, the G6P inhibits hexokinase which brings glucose into the cell
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how does a lack of B oxidation allow glucose to be matabolized
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Citrate and AcetlyCoA can no longer inhibit PFK and PDH so glycolysis can occur
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FA inhibit what 2 parts of glucose utilization in the heart? what is of greater magnitude/significance
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1. glycolysis
2. glucose oxidation: greater inhibition here, contributes to LV failure |
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what is metabolized more in angina, infarct, DM, post card surgery?
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FA
**randle cycle is manipulated |
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what do high levels of FA metabolism do in the heart
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1. induce arythemias
2. increase O2 consumption 3. promote O2 wasting 4. reduce cardiac performance 5. leads to heart failure |
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why does FA metabolism screw up an ischemic heart
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FA supress glucose oxidation
inhibits Na/KATPase |
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how can you prevent post ischemic dysfunction
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increasing the glucose metabolism of the heart by pharmalogical intervention
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do we want the heart to use glocose or FA
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glucose! FA causes problems
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with DM what happens to glucose metabolism? what happens to FA metabolism
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decreased uptake, decreased oxidation
**heart relies ONLY on FA metabolism...BAD (heart failure, post infarct damage) **restore glucose use to improve cardiac performance |
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what does surgery do to FA levels
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increased!
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release of what hormone will increase FA
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epinepherine
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how can drugs inhibit B oxidation? enzyme? drug name? (metabolism)
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1. inhibit B oxidation enzymes
2. inhibit FA uptake into mito 1. inhibit Ketoacyl CoA thiolase ranozaline trimetazidine |
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what drugs act to inhibit ketoacyl coa thiolase
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ranolazine
trimetazidine |
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how can drugs inhibit B oxidation? enzyme? drug? (uptake)
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1. Metabolism: inhibit B oxidation enzymes
2. inhibition of FA uptake **inhibit carnitine palmitoyl transferase **etomoxir, oxfenicine |
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what is FA uptake blocked
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inhibit carnitine palotimyl transferase
etomoxir, oxfenicine |
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what drugs block FA uptake
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etomoxir, oxfenicine
**inhibit carnitine palmitoyl transferase |
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how can glucose metabolism be stimulated in the heart? drug?
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increase PDH
dichloroacetate |
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do we want acetly CoA levels high or low in the heart? how? drug?
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low: so PDH wont be inhibited and we can do glysolysis
buffer acetly coA into acetylcarnitine Carnitine |
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how does carnitine help the heart?
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it bufferes acetly CoA from B oxidation of the heart. this means PDH can be active and glucose can undergo glycolysis
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