Cardiac muscle Flashcards

1
Q

What are the characteristics of cardiac tissue? <> -Cell length <> -Cell shape <> -Initiation of contraction <> -Conductivity <> -Contractile filaments <> -T-tubules <> -Sarcoplasmic reticulum

A

-Cell length: 100µm <> -Cell shape: branched <> -Initiation of contraction: myogenic (involuntary) <> -Conductivity: electrically coupled <> -Contractile filaments: organised in sarcomeres <> -T-tubules: Yes along the Z-lines <> -Sarcoplasmic reticulum: rudimentary/underdeveloped

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2
Q

What makes the heart myogenic?

A

It doesn’t need an action potential originating from a nerve cell to stimulate a contraction

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3
Q

What does being electrically coupled mean?

A

It means that if there is an action potential generated in one cell, all the other cell contract as well

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4
Q

What part of the contractile filaments is the same in cardiac and skeletal muscle?

A

Sarcomeres are both made of thin and thick filaments overlapping made of primarily actin and myosin

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5
Q

What is the number and location of the nucleus in a cardiac cell?

A

Normally 1 in the centre

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6
Q

Label the diagram. What is another name for this other than a cardiac cell?

A

Myocytes

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7
Q

What is the name of cardiac cells that are in the ventricles?

A

Ventricular muscle cells

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8
Q

What is the length and width of ventricular muscle cells?

A

100 * 30 µm

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9
Q

What is the glue that joins cardiac cells together? Why does it need this?

A

Intercalated discs <> Strong contractions of the heart require a strong substance to hold muscle cells together

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10
Q

What is the structure of intercalated discs?

A

Desmosomes and gap junctions bridging cardiac cells

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11
Q

What is the function of the desmosomes and gap junction in intercalated discs?

A

Desmosomes - prevents the cells from separating during contraction <> Gap junctions - allow action potential to be carried form one cell to the next

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12
Q

What do the intercalated discs allow?

A

Allows for the co-oridanted contraction of all the muscle cells

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13
Q

What is the main difference between a ventricular muscle action potential and a nerve/skeletal muscle cell?

A

Nerve/skeletal muscle cells produce a very short action potential (1-2ms) while a ventricular cell produce an action potential lasting 100ms +

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14
Q

What causes the ventricular cell to produce a longer action potential?

A

There is a sustained and slower Ca2+ current due to the slow opening and closing Ca2+ channels

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15
Q

Why is it important to have a sustained Ca2+ current in the heart?

A

It prevent tetanus as it makes for a longer absolute refractory period allowing the heart chambers to fill up with blood

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16
Q

What are the fours stages of an action potential in a cardiac muscle cell?

A

1 - Rapid depolarisation: voltage-gated Na+ channel opens causing depolarisation (Na comes into cell) <> 2 - Hyperpolarisation (not a major component of cardiac muscle tissue): Na+ channels close and K+ moves out of the cell <> 3 - Plateau phase: slow voltage gated Ca2+ channels opening slowly allowing Ca2+ to move into the cell maintaining depolarised state and then closing slowly <> 4 - Depolarisation: Ca2+ closes and the K+ channels are opened causing depolarisation back to the RMP

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17
Q

As you exercise, how does the action potential change?

A

It becomes shorter

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18
Q

What causes the tetanus (combining of multiple AP) of cardiac muscle to be unlikely?

A

The membrane potential is depolarising through most of the heart beat therefore the absolute refractory period is extending to almost the point the heart is relaxed

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19
Q

If there is an action potential generated during the relative refractory period (i.e. near the end of the heart beat), how does the next heart beat differ? Why?

A

It will be smaller because it has had less time to fill

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20
Q

What is a major difference in the T-tubule and sarcoplasmic reticulum between cardiac and skeletal muscle?

A

Cardiac muscle has calcium release channel on SR that are not physically linked onto the T-tubles like skeletal muscle

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21
Q

What are the two types of Ca2+ channels that are found in a cardiac muscle cell?

A

Voltage sensitive and chemical sensitive

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22
Q

Where are the voltage sensitive Ca2+ channels found? What causes their stimulation?

A

Inside the T-tubule <> Action potential

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23
Q

Where are the chemical sensitive Ca2+ channels found? What cause their stimulation?

A

On the sarcoplasmic reticulum <> Ca2+ is the activation ion

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24
Q

How is relaxation of the cardiac muscle induced?

A

The calcium is transported back into the sarcoplasmic reticulum by calcium ATPase and also removing Ca2+ from the cell by a Ca2+ / Na+ anti-porter

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25
Q

What type of channel is the Ca2+ channels on the T-tubules?

A

L - type (i.e. long lasting types activation)

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26
Q

How is the Ca2+ influence balanced?

A

By a Ca2+/Na+ antiporter

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27
Q

What does the influx of Ca2+ from the L-types channels do?

A

It then stimulates a calcium induced calcium released from the sarcoplasmic reticulum by opening the chemical gated Ca2+ channel on the SR with Ca2+

28
Q

What are the methods of Ca2+ transport out of the cytosol?

A

Sarcoplasmic reticulum by Ca2+ ATPase <> Sarcolemmal Na/Ca2+ antiporter <> Sarcolemmal Ca2+ ATPase <> Mitochondrial Ca2+ uniport

29
Q

What is the trigger for contraction for skeletal and cardiac muscle?

A

Ca2+ release from sarcoplasmic reticulum

30
Q

What is the trigger for Ca2+ release from the SR in skeletal and cardiac cells?

A

Skeletal = Na+ influx which is voltage gated <> Cardiac = Ca2+ influx which is Ca2+ induced

31
Q

What is the effect of increasing Ca2+ inside skeletal and cardiac tissue? Why is this the response?

A

Skeletal = no effect, it is either all or no contraction due to their being so much Ca2+ released in an activation that the troponin becomes saturated <> Cardiac = graded concentration as the amount of Ca2+ that can enter into the cytosol can vary and the more that enters the more troponin is bound to therefore the more actin exposed therefore the stronger the contraction

32
Q

What is the cardiac output during rest?

A

5Lmin-1

33
Q

What is the cardiac output during a maximum effort?

A

900Lmin-1

34
Q

What is the cardiac output formula?

A

CO = SV * HR <> CO = cardiac output <> SV = stroke volume <> HR = heart rate

35
Q

What structure in the heart sets the heart rate?

A

The sinoatrial node

36
Q

How can the sinoatrial node be modified to change the heart rate?

A

By neurotransmitters and automatic nerves

37
Q

How can the stroke volume be changed?

A

Increasing the street of the ventricles <> Increasing the heart rate <> Neurotransmitters (can increase stroke power)

38
Q

Where is the sinoatrial node located?

A

In the right atrium

39
Q

Why does the SA node control the heart rate?

A

It has the shortest plateau period so it generates an AP the quickest and this spreads throughout the organ

40
Q

How does the AP from the SA node spread?

A

By the AV node which connects to nerves which run throughout the heart

41
Q

Why does the AP from the SA node travel via a nerve and not cell to cell?

A

It is much quicker to conduct along a nerve than cell to cell

42
Q

What is different between the SA node cells and other nervous and muscular cells?

A

The SA node does not have a stable RMP

43
Q

What is it meant by an unstable resting potential?

A

After hyper polarisation from AP generation the potential of the cell increases slowly to the threshold potential, it doesn’t remain stable

44
Q

Why is the Sinoatrial node’s RMP not stable?

A

It is more leaky to cations especially Na+ which causes its RMP to constantly change

45
Q

What is the section of a SA node change in potential which is below the threshold potential but it is increasing?

A

The pacemaker potential

46
Q

Does a heart need nerves? Why?

A

No <> The SA Node automatically produces an action potential which can spread throughout the cell

47
Q

Does the heart have nerves?

A

Yes

48
Q

What nerves connect to the heart?

A

The vagus nerve (i.e. parasympathetic) and the sympathetic cardiac nerve

49
Q

What does the vagus nerve do?

A

Slows down the heart rate

50
Q

What does the sympathetic cardiac nerve do?

A

Increases the heart rate and increase the force of connection

51
Q

How does the vagus nerve slow the heart rate?

A

Releases ACh

52
Q

How does the sympathetic cardiac nerve increase your heart rate?

A

With noradrenaline

53
Q

What are the three methods which can control the heart rate?

A

Neural control <> Length - tension relationship <> Automicity

54
Q

What is the normal heart rate of a heart where there is no stimulation from any nerve?

A

~100 beats min-1

55
Q

How does the ACh decrease the heart rate?

A

Cause slight hyper polarisation of the SA node RMP which means that the pacemaker potential has to take longer to reach threshold therefore activate an AP an cause a heart beat

56
Q

How does noradrenalin increase the heart rate?

A

It causes slight depolarisation of the SA node RMP which means that the pacemaker potential doesn’t take as long to reach threshold and produce AP, it also decreases the time taken for hyper polarisation to reach the RMP again for another AP produced

57
Q

How is the heart able to stretch its ventricle more?

A

By putting more blood into it

58
Q

How is more blood put into the heart?

A

The skeletal muscle cells during exercise help pump blood around the body and vasoconstriction of the blood vessels increases blood pressure

59
Q

How much more resting tension can be developed in cardiac cells compared to skeletal muscle relative to the maximum active tension? Why is this the case?

A

Skeletal = ~150-200% <> Cardiac = 300% + <> Cardiac tissue has a lot more collagen and connective tissue

60
Q

Why is there more collagen and connective tissue in the heart?

A

It makes the heart a lot stiffer preventing it from getting a strain and gives the heart more elasticity creating greater passive tension

61
Q

What law describes the amount of blood that is pumped by the heart?

A

Starlings law of the heart: “as the resting ventricular volume is increased the force of the contraction is increased”

62
Q

How does increasing the heart rate affect the concentration of Ca2+ inside the cardiac cells and why? How does this affect the contraction strength and why?

A

It increases the concentration of Ca2+ inside the cytosol as there is less time for it to be removed <> Causes a stronger contraction as more troponin is bonded to resulting in more actin being exposed causing a stronger contraction

63
Q

What neural control affects stroke volume?

A

Noradrenaline released by the sympathetic nerve

64
Q

How does noradrenaline increase the stroke volume on the heart cell?

A

It opens up the L-type Ca2+ channels more and for longer increasing the amount of Ca2+ that goes into the cytosol AND it makes the Ca2+ pump in the sarcoplasmic reticulum work more realising more Ca2+ from the SR into the cytosol AND the contraction period is faster <> This causes a stronger contraction of the heart muscles

65
Q

What does increased noradrenalin do to the force developed per given length? What is this called?

A

It increases the force developed per given length <> Increase inotropy