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126 Cards in this Set

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what is cardiac performance
the effenceicy of the heart to pump out blood and keep BP high enough to perfuse all of the peripheral tissues
LVSW=
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)
How can CO be Altered
By changing SV or HR

CO = SV X HR
List the ways SV is altered?
Contractility
Afterload
Preload
List the ways HR is altered?
ANS
what does the area of the P/V loop represent?
work done by vent

LVSW= SV X LVPP

**LVPP is found by: peak Systolic P - Diastolic P
if given a series of P/V curves what a good way to quickly compare the amt of work done by each loop?
look at the area. larger area is larger work that was done
How does preload change the shape of a P/V loop?
????/
How does afterload change the shape of a P/V loop?
????
How does HR change the shape of a P/V loop?
????
How does Contractility change the shape of a P/V loop?
????
what is preload and what does it determine?
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)
what is the frank sterling law of the heart?
increased force of contraction when there is an increased preload, due to increased fiber length. Increased fiber length mean increased force of contraction
ability to eject blood from the heart is proportional to...
the amt of blood in the heart
does cardiac mm operate at maximal L/T relationship?
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
why does increasing cardiac mm fiber length increase the force of contraction
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
what changes preload
increased venous return
increased EDV
when preload in increased how is the P/V loop changed?
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)
What determines Preload? (5)
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
How does Ventrical Filling time affect Preload?
when fill time is decreased, EDV decreases, AV decreases
How does Ventricular Compliance affect preload?
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
How does Filling Pressure alter preload?
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
How/When is the contribution of atrial systole important to vent filling
when fill time is reduced

this can keep EDV high
under normal conditions doesnt add a whole lot of extra volume
how does the pericardium affect preload?
it can constrain the heart so compliance is reduced and EDV decreases

Pathological
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
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
what the difference btwn increased HR with and without sympathetic stimulation
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
a compliant vessel will undergo a large change in ________ at a constant _______
volume
pressure
what reduces compliance
hyperstrphy
ischemia
low compliance vessels develop ________ pressure during ___________ which slows filling
High
diastole
is compliance infinate?
nope, there will come a point when compliance drops off.

a large cahnge in volume accompainied by a small change in pressure: high compiance
what enhances venous return
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
what is cardiac tamponade
fluid in precardium, restricts LV filling (decreases EDV), decreases SV, ineffective cardiac performance
what does the pericardium protect against?
L vent volume overload
what is afterload
**increased aortic pressure

the resistance that the vent contractes against

**aortic/pulm resistance
what are the main components of determine afterload for the L side of the heart
**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
what is the estimate of afterload
Resistance against which the vent contracts is eltimated by MAP (mean arterial pressure)

MAP = DP + (PP/3)

**PP= SP-DP
how does muscular shortening and velocity of ejection relate to afterload
a decreased muscular shortening will INCREASE afterload

a decreased velocity of ejection will INCREASE afterload
during what phase of the cardiac cycle is afterload overcome
at the very end of isovolumetric contraction

**the pressure in the aorta has been overcome
how does an increase in afterload affect SV
SV is decreased

ESV increases
where is the E of contraction 'spent' when afterload increases
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
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
How is afterload increased
1. aortic stenosis
2. increased arterial pressure
3. increased PVR
4. Increased blood viscosity
5. decreased arterial compliance
How does the body compensate for the increased ESV that is seen with increased afterload
vent filling remains the same so EDV will increase in order to keep the SV constant
does an increase in afterload increase the LVSW
yep, the area of the curve is increased
when contractility increases what happens to SV and ESV
SVincreases
ESV decreases
contractility is
the eability of the heart to do work at anyt given fiber length
what affects contractility
Ca+2

ANS
Hopmones (Epi)
Fiber length is proportional to what?
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)
what does NE do to the heart
SNS
B1 receptors
positive inotropic effect
increases SV and EF at a given EDV
what factors are affected by SNS
1. Rate of contraction/relatation increases
2. Force of contraction increases
when contractility increases:
EF velocity
SV
ESV
increases
increases
decreases
what does isovolumic contraction tell us about contracility
rate of vent P changes
contractility is independent of
preload
afterload
does an increase in afterload increase the LVSW
yep, the area of the curve is increased
when contractility increases what happens to SV and ESV
SVincreases
ESV decreases
contractility is
the eability of the heart to do work at anyt given fiber length
what affects contractility
Ca+2

ANS
Hopmones (Epi)
Fiber length is proportional to what?
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)
what does NE do to the heart
SNS
B1 receptors
positive inotropic effect
increases SV and EF at a given EDV
what factors are affected by SNS
1. Rate of contraction/relatation increases
2. Force of contraction increases
when contractility increases:
EF velocity
SV
ESV
increases
increases
decreases
what does isovolumic contraction tell us about contracility
rate of vent P changes
contractility is independent of
preload
afterload
can contractility be measured directly?
nope

we can measure EF- 50-70% is normal
what are two ways HR influences cardiac performance
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)
What must be the reasons for increased HR if CO is increased
SNS
explain Treppe (bowditch staircase)
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
what is the relatioship btwn CO and HR when SV is constant
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
what is the compensatory mech to ensure CO is maintained at an increased HR
increase contractility
if HR increases and SV also increases due to compensation what happens to CO?
increases
on a PV loop how do you visualize increased preload?
increased EDV

(increased to the right)
on a PV loop how do you visualize in increased afterload?
decreased SV

(increased to the top)
on a PV loop how do you visualize increased contractility
increased EF
decreased ESV

(increased to the top/left)
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
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
MAP
mean arterial pressure
mean aortic pressure

MAP = DP + PP/3
LVSW
LVWI
LVMW
LVSW= MAP X SV (LVPP X SV)

LVWI= LVSW/SA

LVMW= LVSW X HR
How can you measure CO?
Fick method
CO= O2 consumption/ (arterial O2-Venous O2)
what does CO= O2 consumption/ (O2 atery-O2 venous) mean?
calculation of cardiac output

Ficks method
how much more work does the LV do than the RV?
6-7X more
what is the RMR for the heart?
4.8-6 mL/gm/h

About 25% is for basal, the rest is for contraction
How does the ANS affect HR?
by altering influx of Na at the SA node
about how much of the E requirement for the heart comes from carbs? what picks up the slack
35-40%
FA oxidation
is the heart aerobic or anaerobic
aerobic
What is cardiac efficiency?
work/energy
does cardiac efficiency imporve or get worse with exercise
improves
what work is harder for the heart? volume or pressure
volume (preload)
what are the O2 dependent processes in the heart (why does the heart requireATP)
1. contractile proteins
2. eletrical activity
3. ion pumps/ion gradients
4. metabolic activity
where does the heart get its fuel? endogenous, exogenous
Exogenous:
blood: glocose, lactate, FA, ketone bodies

Endogenous:
Glycogen, tryglycerides
How does the cell uptake fuel?
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
what are the 3 main fuel sources (metabolic pathways) used in the heart
1. glucose
2. lactate (not as much)
3. FA
under normal resting conditions what percent of the total ATP production comes from carbs
30-40%
when is the carnitine shuttle used in the heart?
to get FA into the mito for oxidation
for glucose metabolism in the heart name the ways glucose enters the heart
1. glycolysis
2. glucose oxidation
3. lactate oxidation
4. glycogen stores
what provides 60-70% of the hearts source of ATP
FA metabolism
how are FA taken in and metabolized in the heart?
Triglycreide lipolysis and B oxidation of FA

lipoprotein and CM oxidation

Ketone body oxidation
what allows the heart to switch the 70/30 (fat/carb) oxidation ratio for metabolism?
Randle Cycle
randle cycle
competition of glucose and fatty acids for substrates.

thought to play a role in DM II and insulin resistance
what happens in the fasted state
insulin is low so FFA are more favorable taken into the heart and glucose is inhibited
when are lipids used for heart fuel more
fasted state

70% of ATP production from FA
what happens in the fed state
insulin and glucose are high so lipolysis is inhibited and Glucose uptake and metabolism in the heart is increased
what overcomes the use of FA in the heart?
increased glucose

FED state
as fat oxidation increases, glucose oxidation _______-
decreases
what increases as a result of B oxidation? What does this cause?
B oxidation releases:
citrate: inhibits PFK
acetly CoA: inhibits PDH

**these inhibit glycolysis
what is inhibited by citrate? what is the interplay?
Citrate is a product of B oxidation of FA so it will inhibit glycolysis

Citrate inhibits PFK
what is inhibited by Acetly CoA? what is the interplay
/
Acetly CoA is made form B oxidation of Fa so it will inhibit glycolysis

**Acetly CoA inhibits PDH
so... B oxidation will increase citrate and Acetly coA which inhibit PFK and PDH respectively. what effect does this have on glucose up take
when the glycolytic enzymes increase, G6P (glucose 6 Pi) also increases, the G6P inhibits hexokinase which brings glucose into the cell
how does a lack of B oxidation allow glucose to be matabolized
Citrate and AcetlyCoA can no longer inhibit PFK and PDH so glycolysis can occur
FA inhibit what 2 parts of glucose utilization in the heart? what is of greater magnitude/significance
1. glycolysis
2. glucose oxidation: greater inhibition here, contributes to LV failure
what is metabolized more in angina, infarct, DM, post card surgery?
FA

**randle cycle is manipulated
what do high levels of FA metabolism do in the heart
1. induce arythemias
2. increase O2 consumption
3. promote O2 wasting
4. reduce cardiac performance
5. leads to heart failure
why does FA metabolism screw up an ischemic heart
FA supress glucose oxidation
inhibits Na/KATPase
how can you prevent post ischemic dysfunction
increasing the glucose metabolism of the heart by pharmalogical intervention
do we want the heart to use glocose or FA
glucose! FA causes problems
with DM what happens to glucose metabolism? what happens to FA metabolism
decreased uptake, decreased oxidation

**heart relies ONLY on FA metabolism...BAD (heart failure, post infarct damage)

**restore glucose use to improve cardiac performance
what does surgery do to FA levels
increased!
release of what hormone will increase FA
epinepherine
how can drugs inhibit B oxidation? enzyme? drug name? (metabolism)
1. inhibit B oxidation enzymes
2. inhibit FA uptake into mito

1. inhibit Ketoacyl CoA thiolase

ranozaline
trimetazidine
what drugs act to inhibit ketoacyl coa thiolase
ranolazine
trimetazidine
how can drugs inhibit B oxidation? enzyme? drug? (uptake)
1. Metabolism: inhibit B oxidation enzymes
2. inhibition of FA uptake

**inhibit carnitine palmitoyl transferase

**etomoxir, oxfenicine
what is FA uptake blocked
inhibit carnitine palotimyl transferase

etomoxir, oxfenicine
what drugs block FA uptake
etomoxir, oxfenicine

**inhibit carnitine palmitoyl transferase
how can glucose metabolism be stimulated in the heart? drug?
increase PDH

dichloroacetate
do we want acetly CoA levels high or low in the heart? how? drug?
low: so PDH wont be inhibited and we can do glysolysis

buffer acetly coA into acetylcarnitine

Carnitine
how does carnitine help the heart?
it bufferes acetly CoA from B oxidation of the heart. this means PDH can be active and glucose can undergo glycolysis