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Y1 - Cardiovascular > Physiology: Force Generation by the Heart > Flashcards

Physiology: Force Generation by the Heart Flashcards

1
Q

Describe the organisation of cardiac muscle

A
  • Striated, due to regular protein arrangement

- No neuromuscular junctions

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2
Q

List and describe the connections between cardiac myocytes

A

Gap junctions:

  • Protein channels
  • Allow low resistance electrical communication between neighbouring cells

Desmosomes:

  • Provide mechanical adhesion between cells
  • Ensure that tension produced by one cell is transmitted to the next
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3
Q

Describe the All-or-none Law of the heart

A

If the stimulus exceeds the threshold potential, heart will give a complete response, otherwise there is no response

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4
Q

Describe a myfibril

A
  • Contractile units of muscle

- Alternating segments of actin and myosin

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5
Q

Describe the appearance of actin filaments in a myofibril

A
  • Thin

- Lighter colour

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6
Q

Describe the appearance of myosin filaments in a myofibril

A
  • Thick

- Darker colour

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7
Q

Describe a sarcomere

A
  • A subunit of a myofibril
  • Smallest contractile subunit
  • From one Z line to the next
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8
Q

What is the basic principle of how muscle tension is produced?

A

By actin filaments sliding on myosin filaments

e.g. Sarcomeres shorten

This uses ATP

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9
Q

Describe the process by which myosin binds to actin

A
  • Troponin-tropomyosin blocks the myosin cross bridge binding sites
  • Ca2+ binds to troponin, causing a conformational change
  • Myosin binding sites exposed
  • Myosin cross bridge binds to actin via binding sites
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10
Q

Give another term for a muscle fibre

A

Muscle cell (myocyte)

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11
Q

Describe the sarcoplasmic reticulum (SR)

A
  • Stores Ca2+ for release during contraction mechanism
  • Forms a mesh enclosing the myofibrils
  • Has transverse tubules (T-tubule) connected by lateral sacks
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12
Q

Define the sarcolemma

A

The membrane that envelops myocytes

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13
Q

Define transverse tubules (T-tubules)

A

Extensions of the sarcolemma that penetrate into the centre of the myocyte

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14
Q

Describe the purpose of the transverse tubules (T-tubules)

A

To bring the membrane potential closer to the myofibrils (and thus sarcomeres)

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15
Q

Describe the mechanism by which adequate Ca2+ are acquired to free up the myosin cross bridge binding sites

A

Ca2+ induced Ca2+ release (CICR):

  • Ca2+ influx during phase 2 of action potential
  • Ca2+ influx induces Ca2+ stores in the Sarcoplasmic reticulum to be released
  • Enough Ca2+ present to full expose the myosin cross bridge binding sites
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16
Q

Is there enough Ca2+ influx during phase 2 of the action potential to allow the myosin cross bridge binding sites to move?

A

No, it requires Ca2+ release from the sarcoplasmic reticulum

This occurs via Ca2+ - induced Ca2+ release (CICR)

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17
Q

Define the refractory period of a cardiac myocyte

A

The period after an action potential in which it is impossible to produce another action potential

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18
Q

Describe the importance of the long refractory period of cardiac myocytes

A

Prevents tetanic contractions

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19
Q

Define tetanic contractions

A

Sustained muscle contraction due to very rapidly occurring action potentials

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20
Q

What factors contribute to the existence of the refractory period?

A
  • The Na+ channels are closed after phase 0, preventing further depolarisation
  • Phase 2 lasts a long time due to the slowly inactivating L-type Ca2+ channels
  • In phase 3 the outflux of K+ prevents another depolarisation
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21
Q

Define the stroke volume (SV) of the heart

A

The volume of blood ejected a ventricle during systole

22
Q

Give an equation for determining stroke volume from the end volumes of systole and diastole

A

SV = EDV - ESV

23
Q

Define the end diastolic volume (EDV)

A

The volume of blood within the ventricle at the end of diastole

i.e. the max volume of blood in the ventricle

24
Q

What determines the end diastolic volume?

A

The venous return of to the heart

25
Q

Define cardiac preload

A

The initial stretching of the cardiac myocytes prior to contraction

It is determined by the end diastolic volume (how full the ventricle gets)

26
Q

Define the end systolic volume (ESV)

A

The volume of blood within the ventricle at the end of systole

27
Q

Describe the Frank-Starling Mechanism (Starling’s Law)

A
  • The relationship between end diastolic volume and stroke volume
  • The more blood in the ventricle during diastole (EDV), the greater the volume of blood ejected during systolic contraction (SV)
28
Q

What conditions are required to achieve optimal force generation from the heart?

A
  • Optimal fibre length
29
Q

Does the the myocyte fibre length increase past the optimal fibre length for maximising stroke volume

A

Not in a healthy heart

30
Q

Give the effect that myocyte fibre stretch has on troponin affinity for Ca2+

A

Fibre stretch increases the affinity of troponin for Ca2+

31
Q

Compare the optimum muscle fibre lengths of skeletal and cardiac muscle

A

Skeletal:
- Unstretched

Cardiac:
- After stretching

32
Q

Describe why the optimum muscle fibre length of cardiac muscle is achieved after stretch

A
  • As stretch increases the affinity of troponin for Ca2+
  • Leading to more cross bridge formation
  • More cross-bridges better contraction
33
Q

Define the venous return of to the heart

A

The blood that returns to the an atrium of the heart

Can refer to either the right or left atria

34
Q

Describe the effect of increased venous return into the right atrium on:

  • The EDV of the right ventricle
  • Stroke volume into the pulmonary artery
A

EDV increases
so
Stroke volume increases

35
Q

Describe the effect of increased venous return into the left atrium:

  • The EDV of the left ventricle
  • Stroke volume into the aorta on the EDV of the left ventricle
A

EDV increases
so
Stroke volume increases

36
Q

Define cardiac afterload

A

The resistance into which the heart is pumping

Is imposed after contraction

37
Q

Describe the heart’s response to an increased cardiac afterload

A
  • At first the heart cannot eject the full stroke volume
    So
  • EDV increases
    Then
  • The force on contraction increases via the Frank-Starling mechanism
38
Q

Describe the outcome of continued increases afterload

e.g. hypertension

A

Ventricular hypertrophy

To increase contractile force to overcome the increased afterload

39
Q

List the 2 types of extrinsic control of stroke volume

A
  • Hormonal

- Nervous

40
Q

Describe the role of sympathetic nervous stimulation in controlling stroke volume

A
  • Ventricular muscle is supplied by sympathetic nerves
  • Stimulation increases the contraction force (+ve inotropic effect)
  • Thus the peak ventricular pressure also increases
  • Causes increased rate of contraction and relaxation as well
41
Q

Describe the effect of sympathetic nervous stimulation on the rate of ventricular contraction and relaxation

A
  • Increased rate of contraction

- Increased rate of relaxation

42
Q

Describe the impact of increased rate of contraction and increased rate of relaxation

A

Increased rate of contraction:
- Reduces systole duration

Increased rate of relaxation:
- Reduces diastole duration

Thus it has a +ve chronotropic effect

43
Q

Why does sympathetic stimulation increase ventricular contraction force?

A
  • Activation of Ca2+ channels

- Greater influx of Ca2+

44
Q

Describe the effect sympathetic stimulation has on the the Frank-Starling Mechanism

A
  • Shifts the graph to the left and upwards

- A greater stroke volume is achieved at the same EDV

45
Q

Describe the impact of a +ve and a -ve inotropic effect on the the Frank-Starling Mechanism

A

A +ve inotropic effect:

  • A greater stroke volume is achieved at the same EDV
  • Graph moves upwards

A -ve inotropic effect:

  • A lower stroke volume is achieved at the same EDV
  • Graph moves downwards
46
Q

Describe the role of sympathetic nervous stimulation in controlling stroke volume

A
  • Very little innervation of ventricles by vagus nerve

- Therefore little effect of stroke volume

47
Q

Describe the role of hormones in controlling stroke volume

A
  • Adrenaline and noradrenaline have a +ve inotropic and chronotropic effect
  • They are released from the adrenal medulla
  • Have minor effects compared to that of sympathetic nerves
48
Q

Define cardiac output (CO)

A

The volume of blood pumped by each ventricle per minute

49
Q

Give an equation to calculate cardiac output from stroke volume and heart rate

A

CO = SV x HR

50
Q

What is an average healthy cardiac output?

A

~5 litres

Y1 - Cardiovascular (19 decks)

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