Physiology of the heart 3 Flashcards

1
Q

What is the heart rate at rest?

A

75/min

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2
Q

What is stroke volume of heart at rest?

A

the difference between end diastolic volume (EDV) and end systolic volume (ESV) = EDV - ESV = 80 ml

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3
Q

Give the definition of ejection fraction?

A

a measurement of the percentage of blood leaving your heart each time it squeezes (contracts).

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4
Q

What is ejection fraction (EF) at rest?

A

= Stroke Volume (SV)/ End Diastolic Volume (EDV) = 0.5 - 0.75 (~60%)

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5
Q

What if ejection fraction (EF) is more than 60%?

A

Cardiac failure occur

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6
Q

Definition of cardiac output

A

the amount of blood the heart pumps from each ventricle per minute.

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7
Q

What is Cardiac Output (CO) at rest?

A

CO = Heart Rate (HR) x Stroke Volume (SV) = 6000 mL/min (at rest)

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8
Q

Will cardiac output increase or decrease during exercise?

A

Cardiac Output will increase

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9
Q

Cardiac output will increase during exercise
-> What is the max. value of CO?

A

25L/min

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10
Q

What are the 2 types of CO regulation?

A
  1. Heterometric (Change in sarcomere length)
  2. Homometric (No change in sarcomere length)
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11
Q

2 types of CO regulations are
1. Heterometric (Change in sarcomere length)
2. Homometric (No change in sarcomere length)
-> Which regulation is the intrinsic feature of the cardiac muscle? Why?

A

Heterometric regulation is the intrinsic feature of cardiac muscle
-> B/c there is no change in contractility

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12
Q

2 types of CO regulations are
1. Heterometric (Change in sarcomere length)
2. Homometric (No change in sarcomere length)
-> Which regulation type is the neuro-hormonal control mechanism? Why?

A

Homometric regulation is the neuro-hormonal control mechanism
-> B/c there is a change in contractility

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13
Q

What is the other name for “Starling’s law of the Heart”?

A

Frank Starling mechanism

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14
Q

Which type of CO regulation is related to Frank Starling mechanism?

A

Heterometric regulation

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15
Q

What does Staring’s law of the Heart state?

A

Work done by the heart depend on the volume of the ventricle

(Increased EDV => Increased Work done)

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16
Q

Draw the length-tension diagram

A
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17
Q

the length-tension diagram
-> What does the red line represent?

A

Active tension

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18
Q

the length-tension diagram
-> What does the green line represent?

A

Passive tension

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19
Q

the length-tension diagram
-> What does the blue line represent?

A

Sum of active and passive tension

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20
Q

What can you conclude about cardiac muscle in this graph?

A

Normal working range is at suboptimal fiber length

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21
Q

This is the graph W vs. EDV
-> What happen to the graph if we add more load?

A
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22
Q

Why does normal working shift to the right?

A

Because there is more load, leading to more work

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23
Q

HETEROMETRIC REGULATION - FRANK-STARLING MECHANISM

Draw the graph indicate what will happen to the atria and ventricle if there is an increasing preload?

A
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24
Q

Heterometric Regulation: Frank-Starling Mechanism

What happen if more blood arrives to the heart from the veins?

A

More blood coming from the veins
-> increasing preload
-> increasing venous return
-> increasing EDV
-> Increasing sarcomere length (to the optimal length)
-> stronger contraction
-> extra load (increasing work done on the heart)

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25
Q

Afterload of the heart is the characteristic of ___ (what?)

A

Resistant of arteries

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26
Q

Draw the graph if there is an increase in resistance of the arteries

A

Based on green line

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27
Q

What happen if there is an increase in resistance of arteries?

A

Increasing after load
-> Increasing total peripheral resistance (TPR) or arterial blood pressure (ABP)
[-> Increasing sarcomere length (to the optimal length)
-> stronger contraction
-> extra load (increasing work done on the heart)]

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28
Q

Describe Frank starling mechanism

A

if we increase venous return to the heart (preload) or if we increase the total peripheral resistance to the heart (afterload) the heart will adapt by. contracting more forcibly.

29
Q

What happen if the preload increases?

A

the atria forwards the extra blood to the ventricles, however this
extra blood will dilate the ventricles more.
-> This makes the walls and the fibres of the ventricular wall to stretch more allowing the cardiac muscles to reach optimal sarcomere length and function efficiently to compensate for the extra blood.
-> The heart will contract more forcibly.

30
Q

When the afterload increases, what will happen?

A

When the afterload increases which is an increase in arterious blood pressure (total peripheral resistance).

There is increased resistance against the blood flow towards the left ventricle.

This will cause the ventricles to not pump up enough blood at normal resting function, so blood remains in the left ventricle at the end cardiac cycle.

31
Q

In the next cardiac cycle more blood comes and this extra blood is added to the normal amount of blood
=> What is the end result?

A

The end result will be the dilation of the vessel leading to the stretch of the muscle fibers increasing the sarcomere length to optimal levels for stronger contractions.
=> In this case not just more blood is pumped out its also pumped at higher speed to counteract the resistance of the blood flow.

32
Q

How can increases in after load and preload affect the graph?

A

The increase in afterload and preload can affect the pressure-volume loop graph as work done will increase by the heart:

33
Q

How Homometric regulation works is due to change in ___

A

calcium sensitivity.

34
Q

What is inotropic effect?

A

inotropic effect which is defined by change in force of contraction based on changing calcium sensitivity

35
Q

What type of fibers involve in neurohormonal mechanism?

A

Sympathetic fibers (plexus cardiacus)

36
Q

____ are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are GS coupled receptors.
-> Name of the 2 hormones

A

Epinpherine and norepinephrine

37
Q

____ are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are GS coupled receptors.
-> Name of the 2 hormones

A

Epinpherine and norepinephrine

38
Q

Epinpherine and norepinephrine are released from ____ and they will act on the beta-1 adrenergic receptors which are GS coupled receptors.

A

the plexus cardiacus

39
Q

____ are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are GS coupled receptors.
-> Name of the 2 hormones

A

Epinpherine and norepinephrine

40
Q

Epinpherine and norepinephrine are released from the plexus cardiacus and they will act on ___

A

the beta-1 adrenergic receptors which are GS coupled receptors.

41
Q

Epinpherine and norepinephrine are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are ___ (type of receptors?)

A

GS coupled receptors.

42
Q

The mechanism is a neurohormonal mechanism involving the sympathetic fibers (plexus cardiacus). Epinpherine and norepinephrine are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are GS coupled receptors.

=> What is the consequence?

A

This will lead to the activation of adenylyl cyclase which generates cAMP and cAMP levels will increase

43
Q

Epinpherine and norepinephrine are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are ___ (type of receptors?)

A

GS coupled receptors.

44
Q

The role of cAMP?

A

activates PKA

45
Q

Epinpherine and norepinephrine are released from the plexus cardiacus and they will act on the beta-1 adrenergic receptors which are ___ (type of receptors?)

A

GS coupled receptors.

46
Q

The role of PKA in homometric regulation?

A

PKA phosphorylates the cardiac muscles and the cardiac proteins will be phosphorylated and they are voltage dependent calcium channels (L-type).

47
Q

What are the 4 target molecules phosphorylated by PKA?

A
48
Q

PKA phosphorylates the cardiac muscles and the cardiac proteins will be phosphorylated and they are voltage dependent calcium channels (L-type).
-> The role of phosphorylated channels

A

The phosphorylated channels now are more open due to phosphorylation and more calcium can pass through the cardiac muscle cell.

49
Q

The phosphorylated channels now are more open due to phosphorylation and more calcium can pass through the cardiac muscle cell.
-> What is the role of ryanodine receptor?

A

. The ryanodine receptor will also get phosphorylated and its on the sarcoplasmic reticulum so it will liberating more calcium from the intracellular sources.

50
Q

Troponin subunit I will also get phosphorylated increasing troponin-myosin interactions which leads
-> Why does this happen? What is the consequence?

A

Troponin subunit I will also get phosphorylated increasing troponin-myosin interactions which leads to more easily developed contractions.

=> These effects all increase the calcium sensitivity.

51
Q

Regulation of cardiac function by the autonomic nervous system:
-> What are the 3 effects can be induced by sympathetic nervous system?

A

a positive chronotropic effect
a positive dromotropic effect
a positive ionotropic effect

52
Q

Sympathetic nervous system can induce a positive chronotropic effect
-> What is the consequence?

A

resulting in increase of heart rate.

53
Q

Regulation of cardiac function by the autonomic nervous system:
- Sympathetic nervous system can induce a positive chronotropic effect resulting in increase of heart rate.
=> Why does this happen?

A

This is due to the innervation of the sympathetic fibers to the SA node as the heart rate is regulated by the SA node.

54
Q

Regulation of cardiac function by the autonomic nervous system:
- Sympathetic nervous system releases Norepinephrine
=> What is the role of this hormone?

A

It activates adrenergic receptors leading to the activation of the cAMP and cAMP can activate the HCN(funny channel) and make it more active.

55
Q

Regulation of cardiac function by the autonomic nervous system:
- Sympathetic nervous system releases Norepinephrine which activates adrenergic receptors leading to the activation of the cAMP and cAMP can activate the HCN(funny channel) and make it more active
=> What will happen?

A

More action potentials will occur within the same period of time as a result of HCN and this results in faster heart rate.

56
Q

What is a positive dromotropic effect?

A

The effect that increases the conduction in the heart.

57
Q

The sympathetic nervous system can also induce a positive dromotropic effect which increases the conduction in the heart.
-> This effect is mediated by __

A

the stimulation of the AV node by the sympathetic fibers

58
Q

a positive dromotropic effect is mediated by the stimulation of the AV node by the sympathetic fibers.
=> How does this happen?

A

the voltage gated calcium channels (L-type) are phosphorylated by the PKA
-> leading to the calcium current responsible for the rapid upstroke in the action potential of the AV node becomes steeper
=> so earlier action potential occurs increasing the conduction velocity.

59
Q

The third effect of the sympathetic nervous system is the positive ionotropic effect
-> What does this effect do?

A

It increases the force of contraction

60
Q

Parasympathetic effects include ___
-> What is the prominent effect?

A

the negative chronotropic effect of the vagal nerves.

61
Q

Parasympathetic effects include the negative chronotropic effect of the vagal nerves
-> What is the consequence of this effect?

A

This decreases the heart rate upon parasympathetic stimulation and its an effect on the SA node.

62
Q

Parasympathetic effects include the negative chronotropic effect of the vagal nerves.
-> Which receptor can vagal nerve act on?

A

The vagal nerve can act on the muscarinic 2 acetylcholine receptor which is Gi coupled

63
Q

Type of receptor of the muscarinic 2 acetylcholine receptor?

A

GI coupled

64
Q

The vagal nerve can act on the muscarinic 2 acetylcholine receptor which is GI coupled
-> What is the consequence?

A

decreasing the levels of cAMP in the SA nodal cells and this will lead to less activity of the HCN channel which will make the action potentials slower and the heart rate will decrease.

65
Q

Drawing the graph that indicate adaptation by the heart to increased preload and afterload?

A
66
Q

Draw the graph that indicate regulation of heart function without changing EDV

A
67
Q

Draw the graph that indicate the effects of SNS

A
68
Q

Make a schematic drawing if regulation of the ventricles by the SNS

A