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Systems Phys 2022 > Excitation Contraction Coupling Cardia Cycle > Flashcards

Excitation Contraction Coupling Cardia Cycle Flashcards

1
Q

What happens when you add increasing doses of Diltiazem (a Ca channel blocker) to a cell?

A

Ca channels that open during phase 2 are blocked → plateau phase of AP gets shorter → contraction of muscle gets increasingly shorter

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2
Q

What is Ca that comes in during the plateau phase important to?

A

Contraction of cardiac muscle

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3
Q

What happens to the twitch force of a cell when you add increasing doses of Diltiazem?

A

It decreases

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4
Q

Define: sarcolemma

A

outer-cell membrane

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5
Q

Define: T-tubule

A

invagination of cell membrane that goes deep in muscle and communicates with EC space.

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6
Q

How does the AP open Ca channels along the membrane?

A

AP travels along the cardiac muscle and down the T-tubule when the cardiac muscle depolarizes → Ca channels open along the membrane

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7
Q

Where is Ca stored inside the cell?

A

Sarcoplasmic reticulum

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8
Q

When do Ca Channels open?

A

when there is a voltage change between -10 mV and +10 mV

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9
Q

What is the main mechanism for getting Ca from the cytosol back into the SR?

A

ATPase pump

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10
Q

How does extracellular Ca aid in muscle contraction?

A

Ca channel opens → Ca flows in → Ca binds to rhyinadine channels → allows Ca to flow from SR into cytoplasm → intracellular Ca concentration increases → contraction

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11
Q

How does the membrane voltage increase from -10 mV to 10 mV?

A

Fast sodium channels open

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12
Q

How do Catecholamines function in muscle contraction?

A

E or NE bind β1 receptor → causes activation of adenylyl cyclase → increases cyclic AMP → stimulates cAMP-PK → Phosphorylates Phospholamban and Troponin → enhance relaxation of muscle

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13
Q

What happens when phospholamban is phosphorylated?

A

it decreases inhibition → enhances activity of Ca pump → pumps Ca back into SR faster

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14
Q

What is phospholamban?

A

Regulatory protein that inhibits Ca pump

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15
Q

What happens when Troponin I is phosphorylated?

A

it has reduced affinity for Trp C for Ca → Ca still binds but not as tightly → Ca is releases from Troponin more quickly

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16
Q

How do catecholamines affect the cardiac muscle?

A

It makes them more efficient in handling Ca → more efficient in contracting, creating pressure, and pumping out greater SV

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17
Q

What happens when a Ca channel is phosphorylated?

A

It stays open longer and conducts more Ca → more efficient contraction b/c more Ca in cell

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18
Q

What does the Ca pump do to the cardiac muscle cell?

A

it uses ATP to remove Ca from the cytosol and put it in the EC

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19
Q

What does the Na-Ca exchanger pump do to the cardiac cell?

A

It removes Ca from the cell by exchanging 3 Na for 1 Ca

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20
Q

What do Cardiac Glycosides do to cardiac muscle cells?

A

they inhibit Na-K pump which results in intracellular Na+ accumulation

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21
Q

What is the resulting effect of a Cardiac glycoside?

A

Na concentration outside cell decreases

less sodium gradient to exchange Na for Ca

more calcium in cell

Increased calcium in cell promotes a better contraction in the ventricle

dont enhance relaxation

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22
Q

Define: Systole

A

Contraction and shortening

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23
Q

Define: Diastole

A

Relaxation and refilling

move calcium back into storage

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24
Q

What is the equation for Cardiac Output?

A

CO = HR X SV

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25
Q

How can you increase HR using the autonomic nervous system?

A

by stimulating sympathetic nervous system

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26
Q

How does Ca cycling influence SV?

A

it increases it

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27
Q

What governs the systolic phase of Ca cycling?

A

AP (depolarization in the heart) → Ca channels open, firing of SA node causes depolarization

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28
Q

In general, how does Ca effect muscle contraction?

A

Ca binds to Troponin C → troponin moves and uncovers myosin binding site → myosin binds to actin → shortening occurs → contraction

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29
Q

What effect does ACh have on the contractile force of the heart?

A

Decrease HR

Decrease force of contraction

Decrease SV by reducing Contraction

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30
Q

What effect does NE have on the contractile force of the heart?

A

Increases contractile force

increases SV

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31
Q

What is the mechanism behind Calcium induced Calcium release?

A

Ca ions bind to a channel protein on SR, opening a channel and allows Ca out of storage into cytoplasm

32
Q

What increases SV?

A

Contractility

Preload

33
Q

How does afterload effect SV?

A

it reduces it

34
Q

How do contractility and Preload effect CO?

A

they increase ut

35
Q

What does afterload do to CO?

A

limits CO

36
Q

What happens to SV as you increase afterload?

A

it inhibits SV

37
Q

Define: Preload

A

the force present in a relaxed muscle (measure of how close you are to optimal length)

38
Q

Define: Optimal Length (Lo)

A

length at which you get max contraction in skeletal muscle

get max shortening

39
Q

is preload fixed in the heart?

A

no

40
Q

What determines Preload in vitro?

A

it varies with resting length of muscle

41
Q

What determines Preload in vivo?

A

venous pressure and end diastolic volume

42
Q

Define: End Diastolic Volume (EDV)

A

amount of blood in ventricle at end of filling phase

43
Q

What determines preload?

A

amount of blood that fills ventricles prior to being stimulated to contract

44
Q

What does the preload force set?

A

the length of the resting muscle

45
Q

Why does cardiac muscle operate at less than its optimal legth?

A

the more it is filled the better it contracts until it gets to a certain length

if you over stretch it, function starts to drop off

46
Q

Define: Frank-Starling Relationship

A

The sequential increase in output by putting more blood in the ventricle

47
Q

What happens as more preload is added to the ventricle?

A

The ventricle will contract more efficiently

48
Q

Define: Afterload

A

The force exerted by a shortening muscle (force that opposes shortening of muscle)

(i.e. the weight you hold)

49
Q

What is the afterload of the right ventricle?

A

pulmonary artery

50
Q

What is the afterload of the Left Ventricle?

A

aorta

51
Q

How is afterload determined in vitro?

A

by the applied load

52
Q

How is afterload determined in vivo?

A

by arterial pressure

(systemic arterial pressure for the left ventricle (aorta) and pulmonary arterial pressure for the right ventricle

53
Q

What does the RV empty its blood contents?

A

When it overcomes the pressure of pulmonary artery to open the pulmonic valve

54
Q

What does the LV empty its blood contents?

A

when it overcomes the pressure of the aorta to open the aortic valve

55
Q

Define: Contractility (Inotropy)

A

The variable state of muscle performance at a given muscle length

The ability to increase cardiac function not dependent on length

56
Q

What do most pathways that regulate contractility involve?

A

Ca++

57
Q

what is the relationship between contractility, length, and preload?

A

Contractility is independent of length and preload

58
Q

What is the result of contractility being independent of length and preload?

A

no matter what the preload of a muscle is at, the max velocity of shortening comes back to the same point

no matter what the length of your muscle is stretched to, if you increase contractility, you can make muscle contract more efficiently

59
Q

what is contractility distinguished from in muscle performance?

A

length-dependent changes

60
Q

How do you increase contractility?

A

increase Ca content

61
Q

What happens to SV if you increase contractility?

A

it increases

62
Q

What is contractility determined by?

A

dP/dt

(rate at which pressure increases)

63
Q

Define: Chronotrope

A

anything that effects heart rate

64
Q

Define: Positive Chronotrope

A

increases heart rate

(sympathetic nervous system stimulation [release of NE or E])

65
Q

Define: Negative Chronotrope

A

decreases heart rate

(ACh → binds muscarinic receptor)

66
Q

Define: Inotrope

A

influences contractility

67
Q

Define: Positive inotrope

A

increases contractility

(NE, E bind β1 receptors and enhance Ca cycling

68
Q

Define: Negative Inotrope

A

Decreases contractility → ACh

69
Q

What is parasympathetic (chronotrope/inotrope)?

A

Negative Chronotrope

Negative Inotrope

70
Q

What is sympathetic (chronotrope/inotrope)?

A

positive chronotrope

positive inotrope

71
Q

Equation: Ejection Fraction

A

EF = EDV - (ESV/EDV) → EF = SV/EDV

72
Q

Define: Ejection Fraction

A

% of blood in ventricle that gets ejected each time heart beats

(ratio of the volume of blood ejected from LV per beat (SV) to the volume of blood in the LV at the end of diastole (EDV)

73
Q

Define: End diastolic volume (EDV)

A

max volume in ventricle prior to contraction

74
Q

Which one of the following would most likely occur as a direct result of applying a Ca++ channel blocker to a ventricular myocyte?

A. no effect

B. An increase in contractility

C. an increase in HR

D. a reduction in the duration of phase 2 of the action potential

E. Loss in phase 1 of the action potential

A

D. a reduction in the duration of phase 2 of the action potential

75
Q

In contracting calcium muscle, calcium…

A. is present in an amount that usually saturates all intracellular calcium binding sites

B. comes from both the extracellular space and from the SR

C. enters the cell during the rapid upstroke (phase 0) of the AP

D. all of the above

E. none of the above

A

comes from both the extracellular space and from the SR

76
Q

The Frank-Starling Relationship…

A. Explains the effect of ACh on ventricular performance

B. Explains the relationship between afterload (wall stress) and maximum +dP/dt

C. Is determined during isovolumic contraction

D. Explains the influence of positive inotropic agents on cardiac function

E. None of the above

A

E. None of the above

Systems Phys 2022 (25 decks)

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