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Yr2 - Advanced Concepts > Cardio Respiratory - Week 2 Cardiac Excitation and Function > Flashcards

Cardio Respiratory - Week 2 Cardiac Excitation and Function Flashcards

1
Q

What is Excitation-contraction coupling (ECC)? (1)

A

The physiological process of converting an electrical stimulus to a mechanical response

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2
Q

Describe the physiological process of Excitation-Contraction Coupling (3)

A

Action Potential (electrical stimulus) —> Increased Cytosolic Calcium (messenger release) —> Muscle Contraction (mechanical response)

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3
Q

Draw and describe the graph for the main events during a cardiac cycle (5)

A

Look at notes - week 2 cardiorespiratory

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4
Q

Changes in the cytoplasmic [Ca2+]i is determined by what? (1)

A

The electrical activation

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5
Q

What is a function of [Ca2+]i? (1)

A

Force and time course of contraction is a function of [Ca2+]i

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6
Q

What are transverse tubules? (2)

A

Extensions of the plasma membrane which invaginate into the centre of cardiac cells (typically around z-discs)

Extracellular fluid can flow freely down these tubules

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7
Q

Describe the structure of the sarcoplasmic reticulum (1)

A

Made up of longitudinal and terminal elements

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8
Q

Describe the function of the sarcoplasmic reticulum (1)

A

The internal store of Ca within the cell are contained within the Sarcoplasmic reticulum

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9
Q

Where is the terminal cisternae of the SR located? (1)

A

Located close to the t-tubules

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10
Q

Why is the terminal cisternae important? (1)

A

Where calcium is released

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11
Q

How can structure of the t-tubules vary between different species? (1)

A

Smaller animals which typically exhibit a higher heart rate have more intricate t-tubules compared to larger animals with a slower heart rate

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12
Q

How can T-tubules vary depending on the location of the cell within the heart? (1)

A

Atrial myocytes which are not required to produce as much force can lack t-tubules

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13
Q

Why can atrial myocytes lack t-tubules? (1)

A

Not required to produce much force

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14
Q

SR junctions contain Ca2+ release channels. What are they called? (1)

A

Ryanodine receptors (RYR)
Also known as foot proteins

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15
Q

Which Ca2+ channels are located in the walls of the t-tubule? (1)

A

L-type Ca2+ channels (DHPR)

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16
Q

What junction do the L-type Ca2+ channels and Ryanodine receptors (RYR) form? (1)

A

DYAD junction

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17
Q

Why is the DYAD junction important? (1)

A

Allow intracellular and extracellular coupling to facilitate event of calcium induced calcium release

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18
Q

Describe overview calcium induced calcium release occur and how does this link to excitation contraction coupling (4)

A

Action potential travels across the surface membrane of ventricular cell and down the T-tubules

This depolarises the T-tubular membrane and result in opening of the L-type Ca2+ channels

Calcium enters intracellular space between the t-tubues and SR, where the Ca2+ release units the (RYRs) are located

Calcium causes Ca to be released through the RYR out of the SR and contributes for the majority of the rise in intracellular calcium concentration

If calcium is released from just one of these units it causes a calcium spark

It is the spatio-temportal summation of these Ca sparks that give rise to the Ca transient activating a uniform and forceful contraction of the cell

Arrangement of RyR2 causes a wave of Ca2+ release from the SR which spreads along the musculature

Increased cytosolic Ca2+ binds to the contractile myofilaments, causing sarcomere shortening and cardiac contraction

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19
Q

What is Ca induced Ca release? (1)

A

Small amount of Calcium entering the cell causes a release of a larger amount of Ca from the intracellular stores

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20
Q

What is hierarchical structure of the cardiac muscle (4)

A

Muscle Fibre
Myofibrils
Sarcomeres
Myofilaments

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21
Q

Describe muscle fibres (2)

A

Individual myocyte (≈25 µm in diameter, ≈100 µm in length).

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22
Q

Describe myofibrils (2)

A

Densely bundled structures which contain sarcomeres repeated in series

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23
Q

Describe sarcomeres (2)

A

The functional contractile unit of muscle (Z disc ↔ Z disc)

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24
Q

Describe myofilaments (2)

A

Protein strands which slide over each other to shorten the sarcomere

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25
Q

How is the diffusion distance of Ca minimised in the contractile units? (3)

A

T-tubules are usually spaced along the z-lines

This places the Ca release sites intimately around the myofibrils

The maximum diffusion distance to activate myofilaments is ~ 500 nm

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26
Q

Despite the large size of a cell, how does a synchronised contraction of each contractile unit occur? (1)

A

Due to the diffusion distance of Ca minimised in the contractile units due to placement of T-tubules close to myofibrils

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27
Q

Describe the ultrastructure of sarcomeres (4)

A

The myofibrils are composed of two sets of interdigitating filaments

Contains A-bands and I-band which contain thick and thin filaments

The A-bands contain thick filaments

Thick filaments are composed mainly of the protein myosin

The I-bands contain thin filaments

The thin filaments are composed primarily of the protein actin

Titin is a filamentous protein spanning the half-sarcomere, with spring-like properties in the I-band region

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28
Q

Describe the roles of Titin (2)

A

Align the myosin filaments and contribute elasticity to the heart wall

Also thought to play a role in active and passive force regulation in the muscle

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29
Q

Describe the arrangement of filaments in the sarcomere in a cross-sectional view (3)

A

The thick and thin filaments overlap and interdigitate

Thin filaments attached to Z-disc and arranged in hexagonal array

Myosin filaments organised by M-line- also in a hexagonal arrangement.

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30
Q

Describe thin filament structure (5)

A

The actin filament has a double stranded rope-like structure

Associated with the actin filament is a long protein called tropomyosin

This protein lies in the groove made by the two strands of the actin filament

Each strand of the actin filament has a repeating structure composed of 7 actin monomers polymerised together and associated with that is one tropomyosin protein unit. This can be know as an actin tropomyosin filament

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31
Q

What is an actin tropomyosin filament (2)

A

Each strand of the actin filament has a repeating structure composed of 7 actin monomers polymerised together and associated with that is one tropomyosin protein unit

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32
Q

Describe the troponin complex (4)

A

Every 38.5 nm there is a troponin complex:
Every 38.5 nm there is a troponin complex:
Troponin-C (Tn-C)
Troponin-I (Tn-I)
Troponin T (Tn-T)

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33
Q

Describe Troponin-C (Tn-C) and its function? (2)

A

mol. wt, 18,000
Binds Ca2+ ions

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34
Q

Describe Troponin-I (Tn-I) and its function? (2)

A

mol. wt, 25,000
Binds to actin & inhibit the binding of myosin to actin

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35
Q

Describe Troponin-T (Tn-T) and its function? (2)

A

mol. wt. of 42,000
Binds Tropomyosin

36
Q

Describe thick filament structure (5)

A

Mainly composed of Myosin

The head is made up of 2 identical sub-units

The heads of the molecules are known as cross bridges and are the site of ATP hydrolysis and consequent tension generation

Each thick filament is at the centre of a hexagonal array of thin filaments

37
Q

Describe Actin-myosin interaction (2)

A

Activation of the heart muscle cells via the action potential is transduced into a rise of Ca2+ in the cytoplasm.

Then Ca2+ binds to troponin-C, which acts as a molecular switch to allow cross bridge cycling to occur.

38
Q

Describe the Troponin complex in absence of Ca2+ (5)

A

Tropomyosin (Tm) is bound to the actin filament

Troponin-T (TnT) is bound to tropomyosin and Troponin-I (TnI)

TnI also binds strongly to actin in the absence of Ca2+

Troponin-C (TnC) is bound weakly to TnI

Tn-I binds to actin and covers up the actin-myosin binding site

As a result, the myosin head cannot bind to actin to form acto-myosin.

39
Q

What can’t form without Ca2+ (1)

A

Cross bridges cannot form

40
Q

Describe the Troponin complex in presence of Ca2+ (5)

A

When the levels Ca2+ rises in the cytoplasm, Calcium binds to the Troponin C and causes TnC to bind strongly to TnI

When there is a strong interaction between Troponin I and Troponin C then Troponin I can no longer bind to actin

This also then follows a cascade of changes in binding, causing a change in the binding of TnI to TnT and subsequent changes in the binding of TnT to tropomyosin and tropomyosin to actin

41
Q

Explain the cross-bridge cycle (5)

A

Look at notes - week 2 cardiorespiratory

42
Q

What needs to happen for relaxation? (1)

A

Ca2+ must be removed from the cytoplasm by one of three pathways

43
Q

What are the three pathways by which Ca2+ must be removed from the cytoplasm? (3)

A

Pumped back into the SR (80%)

Via the Na+-Ca2+ exchanger (NCX) (18-19%)

Via the sarcolemmal Ca2+ ATPase (1-2%)

44
Q

How is a steady state level of Ca2+ in cells maintained? (1)

A

The amount of Ca2+ that entered the cell during excitation is removed from the cell before the next beat

45
Q

How does NCX remove Ca2+ from the cell? (3)

A

Uses the power of the inwardly directed electro-chemical gradient for Na+ to extrude Ca2+ from the cell against its concentration gradient

3 Na+ ions are required to remove one Ca2+ ion from the cell

Therefore, NCX is electrogenic.

46
Q

How does sarcolemmal Ca ATPase remove Ca2+ from the cell? (3)

A

A high affinity pump but has a slow turnover rate compared to its distant cousin in the SR membrane

Relaxation of a single beat using this mechanism alone would take almost 60 seconds

As such, only ~1-2 % of calcium involved in contraction is extruded via this route

47
Q

Compare cardiac and skeletal muscles (6)

A

Look at notes - week 2 cardiorespiratory

48
Q

What is cardiac output? (1)

A

The amount of blood pumped by each ventricle of the heart in 1 minute.

49
Q

How to calculate cardiac output? (1)

A

Heart rate (HR) x Stroke volume (SV)

50
Q

How to calculate SV? (1)

A

EDV – ESV
(EDV: volume of blood in ventricle just before contraction)
(ESV: volume of blood left in ventricle after contraction)

51
Q

What is ejection fraction? (1)

A

SV/EDV

52
Q

Give typical resting values for HR, EDV, ESV (3)

A

HR, 70 bpm
EDV, 120 mL
ESV, 45 mL

53
Q

What can CO exceed to during exercise? (1)

A

25 L/min

54
Q

What are the factors affecting heart rate? (4)

A

Autonomic innervation
Hormones
Fitness levels
Age

55
Q

What are the factors affecting SV? (7)

A

Heart size
Fitness levels
Gender
Contractility
Duration of contraction
Preload (EDV)
Afterload (resistance)

56
Q

What are the intrinsic factors affecting regulation of cardiac output? (3)

A

Preload
Afterload
Inotropic state (contractility)

57
Q

What are the extrinsic factors affecting regulation of cardiac output? (2)

A

Neurotransmitters/neural input
Hormones

58
Q

What is preload how does it affect CO? (5)

A

Degree of filling of a ventricle

EDV determines the preload on the heart, i.e. the volume load on the ventricles before ventricular contraction begins.

Filling pressure (i.e. venous return)

Filling time (note: as heart rate increases, less time is spent in diastole and therefore filling time decreases)

Affects Cardiac Output because:
Preload increases which increases SV which increases CO

59
Q

How is preload linked to cardiac muscle? (2)

A

An increase in preload (i.e. increasing the volume of blood in the ventricle) stretches the muscle cells before they contract

Increases the number of cross bridges formed between actin and myosin filaments and increases strength of contraction

60
Q

What is the Frank-Starling law? (2)

A

Relationship between EDV and ESV

i.e. as the degree of stretch on the heart increases so does the force of contraction.

61
Q

What is afterload? (6)

A

Pressure that needs to be overcome (in arteries) in order to eject blood from the ventricles

Afterload (on the left ventricle) is the diastolic aortic pressure

Left ventricular pressure has to exceed the afterload before any blood can be ejected from the ventricle

If afterload increases, e.g. in patients with high blood pressure, less blood will be ejected from the ventricle, increasing ESV

As a consequence SV and CO will fall at a constant heart rate

As a consequence, the heart muscle hypertrophies and the left ventricular wall of the heart becomes thicker

62
Q

What is inotropic state and contractility? (3)

A

Inotropic state - The ionic basis of contraction
Contractility - How well ventricles can contract (i.e. speed, force, duration)

Is related to the degree of activation of the contractile proteins by Ca2+

63
Q

What is positive inotropic influence (or increased contractility)? (1)

A

Cardiac muscle can generate more tension from an unchanged resting length

64
Q

How does action potential impact inotropic state? (3)

A

Increase AP plateau length causes increased Ca2+ influx which increases inotropic state

65
Q

How does external ion concentration impact inotropic state? (7)

A

Increasing external Ca2+
Increases influx
Increases inotropic state

Lower external Na+
Slows Na+/Ca2+ exchange
Ca2+ accumulates inside
Increases inotropic state

66
Q

How does force-frequency relationship impact inotropic state? (3)

A

Increase stimulation frequency of piece of papillary muscle
More Ca2+ entry (more APs)
Ca2+ accumulation

67
Q

What is an extrinsic mechanism for increasing CO? (1)

A

Sympathetic Stimulation through sympathetic fibres

68
Q

How do sympathetic fibres increase CO and why is this considered an extrinsic mechanism? (4)

A

Sympathetic fibres release noradrenaline, increases sympathetic activity of heart, increases force of contraction which increases cardiac output

Considered to be an extrinsic mechanism for increasing CO as it originates outside the heart muscle itself

69
Q

How does Sympathetic Stimulation Increase the Force of Contraction? (6)

A

Norepinephrine binds to β1 receptors in membrane causing a conformational change within the receptor

Releases G alpha s protein

The α-subunit of Gs activates Adenylate Cyclase

This increases cAMP production from ATP

This in turn activates protein kinase A (PKA)

PKA phosphorylates protein targets to affect function

70
Q

How does PKA target the L-type calcium channel? (3)

A

PKA phosphorylates L-type calcium channel
Increases L-type calcium channel flux
Increased calcium release from SR and therefore increases contraction force

71
Q

How does PKA target the Ryanodine Receptor? (3)

A

PKA phosphorylates RyR receptors
Increases RyR sensitivity to Ca2+ (trigger for release)
Increased calcium release from SR and therefore increases contraction force

72
Q

How does PKA target Phospholamban? (6)

A

PKA phosphorylates phospholamban
Removal of inhibition of SERCA
Increases calcium uptake in SR
Increases Calcium content in SR
Increases calcium release
Increases contraction force

73
Q

How does PKA target Troponin? (2)

A

PKA phosphorylates troponin
Decreases sensitivity to Ca2+
Quicker relaxation

74
Q

Describe Parasympathetic Stimulation (3)

A

Ach binds to muscarinic M2 receptors

Activates another G-protein Gi- this has an inhibitory effect on adenylate cyclase

Opposes effects of sympathetic stimulation via this mechanism

75
Q

How is the heart innervated? (2)

A

By the two branches of the autonomic nervous system

76
Q

How does the parasympathetic arm (the vagus nerve) innervate the heart? (2)

A

Innervates atrial muscle and the SA and AV nodes (+ Ventricles)

77
Q

How does the sympathetic arm innervate the heart? (1)

A

Innervates all parts of the heart.

78
Q

What is tachycardia? (1)

A

Increased activity in sympathetic NS leads to a faster heart rate - tachycardia

79
Q

What is bradycardia? (1)

A

Increased activity in parasympathetic NS leads to a slower heart rate – bradycardia

80
Q

Severing autonomic nerves leads to what? (2)

A

Severing autonomic nerves leads to an increase in heart rate to ~110 bpm (intrinsic rate of SA node)

81
Q

How does exercise affect activity in the Sympathetic NS (3)

A

When you begin exercising, the sympathetic arm of the ANS is stimulated and norepinephrine is released into the vicinity of the heart cells

82
Q

What happens when norepinephrine is released into the vicinity of the heart cells? (2)

A

Increases the strength of cardiac contractions

The SA node generates action potentials at a higher frequency and so heart rate increases

83
Q

What does a rise in cAMP do? (2)

A

Rise in cAMP increases If so pacemaker potential rate accelerated

84
Q

What does Reduction in K+ permeability do? (1)

A

Reduction in K+ permeability so MDP more positive

85
Q

What does increased L-type Ca2+ current do? (3)

A

Increased L-type Ca2+ current, so upstroke faster - more action potentials per unit time - tachycardia

86
Q

Describe the relationship between the strength of contraction and the action potential (4)

A

Action potentials are generated more frequently and propagated through the heart more rapidly

Action potentials are shorter in duration

The strength of contraction associated with each action potential is greater

The duration of each contraction is reduced

87
Q

Describe what happens when there is increased activity in the Parasympathetic NS (4)

A

Parasympathetic stimulation:
Acetylcholine (ACh)

ACh decreases If (inhibits adenylate cyclase and reduces cAMP)

ACh increases the K+ permeability of the SA node cells (via IK-ACh) which hyperpolarises the MDP

Fewer action potentials per unit time (bradycardia).

Yr2 - Advanced Concepts (12 decks)

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