2: Force generation by the heart Flashcards Preview

Cardiovascular Week 1 & 2 2016/17 > 2: Force generation by the heart > Flashcards

Flashcards in 2: Force generation by the heart Deck (65)
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1
Q

Cardiac muscle has a streaky appearance - what are these streaks called?

A

Striations

So cardiac muscle is described as 'striated'

2
Q

Why is cardiac muscle striated?

A

Alternating actin and myosin proteins

(Actin has a lighter colour and myosin has a darker colour)

3
Q

Do muscles have a nerve supply?

Why?

A

No

Autorhythmicity - heart can generate its own nerve impulses

4
Q

What allows for cell-to-cell conduction of impulses between cardiac myocytes?

A

Gap junctions

5
Q

What property of gap junctions allows for electrical communication between cardiac myocytes?

A

Low resistance

6
Q

What is the All-or-none Law of the Heart?

A

All cardiac myocytes will respond to an action potential, no matter its strength

7
Q

The low resistance of gap junctions ensures that excitation reaches ___ cardiac myocytes.

A

all

8
Q

What is the function of desmosomes?

A

Provide mechanical adhesion - sticks cardiac myocytes together so they all tense up together

9
Q

Within a muscle fibre, fascicles contain ___ which are made up of sarcomeres.

A

myofibrils

10
Q

Myofibrils have alternating __ and __ protein segments.

A

thick , thin

11
Q

What is the smallest unit of contractile muscle?

A

Sarcomere

12
Q

What are the thin, lighter segments of myofibril made of?

A

Actin

13
Q

What are the thicker, darker sections of myofibril called?

A

Myosin

14
Q

What are the smaller functional units found within myofibrils called?

A

Sarcomeres

15
Q

Actin filaments ___ along myosin filaments to cause muscle ___.

A

slide along

muscle contraction

16
Q

The interactions between actin and myosin are dependent on what two molecules?

A

ATP

Ca2+

17
Q

ATP binds to myosin to trigger what?

A

Detachment of myosin cross bridge from actin

Cross bridge then slides along actin and rebinds

18
Q

Ca2+ triggers (binding / detachment) of myosin-actin.

A

Binding

19
Q

What ion is required to switch on myosin cross-bridge formation?

A

Ca2+

So ATP binds to myosin to detach it from actin, it then slides forward and if calcium is present, it rebinds (and the muscle has contracted)

20
Q

Name the two regulatory proteins found on actin filaments.

A

Tropomyosin

Troponin

21
Q

What is the name of the rope-like protein structure found on actin filaments?

A

Tropomyosin

22
Q

What protein blocks myosin binding sites on actin filaments until it is disabled by calcium ions?

A

Troponin

23
Q

Calcium binds to troponin causing a _____ change, moving the protein away and exposing the ___ binding sites on the ___ filaments.

A

conformational change

myosin-binding sites on actin filaments

24
Q

Ca2+ is released from the ____ ____ depending on the extracellular presence of Ca2+.

A

sarcoplasmic reticulum

25
Q

What triggers the release of Ca2+ ions from the sarcoplasmic reticulum of myofibrils?

A

Extracellular calcium - i.e Calcium-dependent Calcium release

26
Q

During systole...

1. Contractile machinery activated

2. Ca2+ influx during plateau phase of action potential

3. Ca2+ released from the sarcoplasmic reticulum

4. Ca2+ binds to troponin and allows myosin-actin cross-bridge binding

Arrange these statements in the correct order.

A

2 → 3 → 4 → 1

27
Q

What is the refractory period?

A

The period following an action potential in which it is not possible to produce another action potential

28
Q

During the plateau phase, how do Nachannels ensure that another action potential (i.e depolarisation) does not take place?

A

They close

29
Q

In the descending phase, how do K+ channels ensure that another depolarisation does not take place?

A

They open

bringing membrane back down to K levels

30
Q

Why is the refractory period of the heart important?

A

It prevents generation of tetanic contractions of cardiac muscle (i.e constant heartbeats)

31
Q

What are tetanic contractions of the heart?

A

Sustained muscle contraction when the rate of action potentials in cardiac muscle is too high

32
Q

Contraction of ventricular muscle ejects the ___ volume.

A

stroke

33
Q

What is the definition of stroke volume?

A

The volume of blood ejected by each ventricle per heart beat

34
Q

What is the equation for stroke volume?

A

Stroke volume (SV) = End diastolic volume (EDV) - End systolic volume (ESV)

SV = EDV - ESV

35
Q

Which two types of mechanism regulate the stroke volume of the heart?

A

Intrinsic and extrinsic mechanisms

36
Q

What is intrinsic control of stroke volume?

A

Controls found within the heart muscle itself

37
Q

What is extrinsic control of stroke volume?

A

Control by the nervous system and hormones

38
Q

Intrinsic changes in stroke volume are brought about by...

A

end diastolic length of myocardial fibres (preload)

39
Q

Which volume determines the preload of myocardial fibres?

A

End Diastolic Volume (EDV)

40
Q

What is the cardiac preload?

A

The stretching of myocardial fibres at the end of diastole (which determines the stroke volume of the next heart beat)

41
Q

What determines the end diastolic volume?

 

A

Venous return

42
Q

1. End diastolic volume

determines

2. Diastolic length of myocardial fibres

determines

3. Venous return

determines

4. Cardiac preload

Arrange the numbers 1-4 in the correct order.

A

→ → → 4

43
Q

What is Starling's Law of the Heart?

A

The more the ventricle fills with blood during diastole (greater end diastolic volume) the greater the volume of ejected blood will be (greater stroke volume) during the resulting systolic contraction

i.e greater EDV = greater stroke volume

44
Q

Which law does this graph show?

A

Starling's Law of the Heart

(increased EDV = increased stroke volume)

45
Q

Increased stretch has an effect on a regulatory protein found on actin.

What is this effect?

A

Increased stretch > increased affinity of troponin for Ca2+

 

46
Q

According to Starling's Law of the Heart, optimum length in cardiac muscle is achieved by _____ the muscle.

A

stretching

47
Q

1.  Increased stroke volume into the pulmonary artery by Starling's Law

2. Increased venous return to left atrium from pulmonary vein 

3. Increased venous return to right atrium

4. EDV of left ventricle increases

5. EDV of right ventricle increases

...causing increased stroke volume into the aorta by Starling's Law.

Arrange 1-5 in the correct order.

A

3 → 5 → 1 → 2 → 4

48
Q

What is afterload?

A

The resistance into which the heart is pumping, imposed after the heart has contracted

Determined by TPR

49
Q

What happens if afterload increases?

A

1. The heart is unable is eject its full stroke volume, so some is left over

2. Thus EDV of the ventricles increases

3. So force of contraction increases by Starling's Law

4. If chronic, ventricular hypertrophy may occur to overcome the resistance

50
Q

Which autonomic nervous division supplies ventricular muscle?

A

Sympathetic

(remember that parasympathetic impulses have no effect on contractility)

51
Q

Which post-synaptic neurotransmitter acts on ventricular muscle?

A

Noradrenaline (sympathetic division supplies heart muscle)

52
Q

Stimulation of sympathetic nerves (increases / decreases) force of contraction.

A

increases

53
Q

Sympathetic stimulation increases the force of contraction of ventricular muscle. What name can be given to this effect?

A

Positive inotropic effect

54
Q

Stimulation of the sympathetic nerves in the heart produces two different effects, what are they called?

A

Positive chronotropic effect (increased heart rate)

Postivie inotropic effect (increased force of contraction)

Remember sympathetic stimulation also reduces AV nodal delay

55
Q

Why does sympathetic stimulation increase the force of contraction of ventricular muscle?

A

Activation of Ca2+ channels causes greater Ca2+ influx

56
Q

What molecule mediates the activation of calcium channels associated with sympathetic stimulation of the heart?

A

cAMP

57
Q

The activation of calcium channels associated with sympathetic stimulation of the heart also reduces the durations of ___ and ___.

A

systole and diastole

(Thus increasing heart rate)

58
Q

What effect does sympathetic stimulation have on the Frank-Starling curve and why?

A

Shifts curve to the left

Contractility of the heart at a given EDV increases

59
Q

Explain the trends seen on this Frank-Starling curve.

A

Positive inotropic effect is an increase in the force of contraction so stroke volume increases

and the opposite

60
Q

Heart failure causes a shift to the ___ on a Frank-Starling curve.

A

right

61
Q

What effect does parasympathetic stimulation have on the force of contraction?

A

No effect

Parasympathetic stimulation influences rate, not force, of contraction

62
Q

Where in the body are adrenaline and nonadrenaline released?

A

Adrenal medulla

63
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute

64
Q

Write an equation for cardiac output.

A

Cardiac output = Stroke volume x Heart rate

CO = SV x HR

65
Q

What is the resting cardiac output in a healthy adult?

A

Approx. 5L

70ml SV x 70bpm = 4900ml CO