12/5/2014 Medical Physiology Cardiac Muscle Mechanics Eric Olson Flashcards Preview

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Flashcards in 12/5/2014 Medical Physiology Cardiac Muscle Mechanics Eric Olson Deck (45):
1

T/F: Cardiac muscle is similar to striated skeletal muscle and shows A and I bands.

True

2

What structure separated adjacent cardiac myocytes?

Intercalated disc

3

What cell linkages are found at intercalated discs?

Gap junctions (and desmosomes)

4

Do T-tubules exist in cardiac muscle?

Yes, and they invaginate along the Z line.

5

Why is cardiac muscle called a functional syncytium?

Because even though cardiac muscle cells are uninucleate or binucleate, the presence of gap junctions allows all cardiac muscle cells to act as a unit. The syncytium can be split into two syncytia: atrial and ventricular

6

Cardiac muscle has abundant reserves of ___ to store oxygen to aid in aerobic metabolism.

Myoglobin

7

Does cardiac muscle maintain energy reserves?

Yes, in the form of glycogen and lipid inclusions.

8

How are ryanodine receptors opened in cardiac muscle (different from skeletal muscle)?

Calcium-induced calcium release (CICR)

9

What is Calcium-induced calcium release (CICR)?

In a cardiomyocyte AP, a small amount of calcium influx through the L-type calcium channel binds to the ryanodine receptors in the SR, and the SR opens releasing a ton of calcium.

10

What are the differences between skeletal and cardiac (ie ventricular) AP?

1. Timing: Cardiac AP is ~250ms, whereas skeletal AP is ~5ms
2. Length: No summation in cardiac muscle (twitch only)
3. Cardiac AP is calcium-dependent, skeletal AP is sodium-dependent.

11

What are the Phases (0 to 4) of the cardiac (ie ventricular in this case) AP?

1. Phase 0 - Na+ depolarization, cell potential goes from -85mV to +30mV.
2. Phase 1 - Initial phase of repolarization
3. Phase 2 - Plateau stage
4. Phase 3 - Repolarization completes
5. Phase 4 - After repolarization is complete

12

What is Phase 1 of the cardiac AP stimulated by?

Closing of the Na channels
Brief activation of transient inward current (I-to)

13

What happens during Phase 2 of the cardiac AP?

Rate of repolarization of slowed by influx of Ca ions.
Ca current in
K current out

14

What happens during Phase 3 of the cardiac AP?

K ions out

15

What cells do not have Phase 4 as part of their cardiac AP?

Any cells that have endogenous pacemaker activity, ie SA node.

16

Calcium coming in through L-type calcium channels contributes how much to the twitch?

It is 20% of the calcium needed for twitch.

17

T/F: In cardiac muscle, ryanodine receptors on the SR are physically coupled to L-type calcium channels.

False. This is how it is in skeletal muscle only. Cardiomyocytes use CICR.

18

T/F: In the depolarized (ie Phase 2) stage of the cardiac AP< the sodium-calcium ATPase exchanges (NTX) can "work in reverse" letting into the cell 1 calcium for 3 sodiums out.

True, but this is not the main source of calcium.

19

What is SERCA?

Sarcoplasmic and endoplasmic reticulum ATPase that pumps Ca back into the SR during repolarization. This is the main way the Ca is cleared.

20

Because of the trans-sarcolemmal influx of calcium, cardiac muscle is much more sensitive to _____ than is skeletal muscle, and therefore cardiac muscle is also more sensitive to L-type calcium channel blockers.

Extracellular calcium

21

How does CICR work w/r/t ryanodine receptors?

Calcium binds the ryanodine receptor, it opens, more calcium comes in, binds neighboring ryanodine receptors etc. etc., like a domino effect

22

Cardiac muscle contraction works like skeletal muscle contraction in that calcium binds to ____ which leads to the movement of tropomyosin off the myosin binding sites on the thin filament.

Troponin C

23

T/F: Myosin heavy chains in cardiac and skeletal muscle are of the same type.

False. Myosin heavy chains in cardiac muscle are different than in skeletal muscle.

24

What process is used in skeletal muscle but not cardiac muscle to increase the force of contraction?

Recruitment. *NOT used in cardiac muscle.

25

Without parasympathetic innervation, the SA node HR is about how many BPM?

100. The vagus nerve (ACh release) adjusts it to about 60 BPM.

26

What is the basis for the Frank-Starling Law of the Heart?

The force of contraction increases at increased end-diastolic length.

27

The Frank-Starling Law of the Heart states:

The more the ventricle is filled with blood during diastole, the greater the volume of ejected blood will be during the resulting systolic contraction. This is NOT based on thick nd thin filament overlap, only on the LOAD of the blood on the muscle fiber.

28

Increased load stretched the myocardium and increases the affinity of troponin C for __1__, leading to an increase in contractile force for a given level of sarcoplasmic calcium.. This is called an increase in __2__.

1. Calcium
2. Sensitivity

29

What is the muscle-definition of preload?

The initial sarcomere length

30

The force that any single muscle fiber generates is proportional to the initial sarcomere length (aka preload) OR, equivilantly:

the end-diastolic volume of the ventricle

31

In the human heart, maximal force is generated with an initial sarcomere length of?

2.2 micrometers

32

Troponin C's affinity for calcium has the effect of more formation of what?

Crossbridges per AP (lead to greater force of systolic contraction)

33

Give an example of an inotropic agent.

Norepinephrine

34

Norepinephrine has what effect on cardiac muscle?

More calcium released from SR --> Increased contractility

35

After administration, how many beats does it take for the amplitude of the AP to increase?

None, It happens immediately.

36

After administration, how many beats does it take for the tension (in grams) of the heart to increase?

About 8 beats. AP increases immediately, but the rise in intracellular calcium needs to catch up.

37

Positive inotropic agents such as norepinephrine have 2 specific effects on cardiac muscle activity. What are they?

1. Increase contractility
2. Curve of tension vx time becomes both higher AND steeper, meaning the twitch length is shorter (systole is shorter) --> higher HR while diastolic filling is maintained.

38

In beta-adrenergic stimulation, is norepinephrine, the increase in cAMP leads to increased intracellular calcium *and* what?

Activation of a protein kinase which phosphorylated a protein called Phospholamban.

39

What is the effect of activated phospholamban?

Increased sensitivity of SR Ca pump, meaning faster repolarization (AP duration shorter). (Positive inotropic and chronotropic effects)

40

Tension is absent at what concentration of sarcoplasmic calcium in both smooth and cardiac muscle?

100 nM

41

Tension is at a maximum value at 10 uM concentration of sarcoplasmic calcium in what muscle?

BOTH smooth and cardiac muscle

42

Changes in contractility shift the _____-tension curve upward.

Length (increase in contractility due to increased entry of Ca)

43

Can administration of norepinephrine change the tension/load of cardiac muscle without changing the length of the muscle?

Yes, the length-tension curve stays the same shape, but shifts upward to reflect the additional tension produced (see page 364-365 of notes). This is isometric tension.

44

Does norepinephrine administration change the work performed by cardiac muscle?

Yes, the length can change at a given load + NE admin.

45

What is the maximal length-tension curve?

Just a way of saying that on a curve of tension vs length, at some point the muscle cannot shorten anymore despite the load being put on it. It is capped at 12 mm control and 11 mm with NE admin, for example.

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