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CTB Block 2 > B2 W3 - The Heart as an Electrical Pump > Flashcards

B2 W3 - The Heart as an Electrical Pump Flashcards

1
Q

What is the heart’s primary function, and why is this function significant?

A
  • The heart is a muscular organ responsible for pumping blood throughout the body.
  • This is crucial because it delivers oxygen and nutrients to the body’s tissues and removes waste products.
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2
Q

How does the heart compare to other muscles in the body in terms of workload?

A
  • The heart is one of the most heavily used muscles in the body
  • Constantly working to maintain blood circulation.
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3
Q

Approximately how many times does the heart beat in an average human lifetime?

A

3 billion times

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4
Q

What is the estimated volume of blood pumped by the heart over an average human lifespan?

A

200,000,000 litres.

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5
Q

What is the cardiac cycle, and why is it important for efficient heart function?

A
  • The coordinated sequence of events, driven by electrical impulses, that ensures the heart pumps blood efficiently.
  • It involves a precise timing of contraction and relaxation of the heart chambers.
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6
Q

What is the cardiac conduction system?

A

It’s a specialised network of cells within the heart responsible for generating and conducting electrical impulses that coordinate the contraction of the heart muscle.

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7
Q

What is the role of electrical activity in the heart’s pumping function?

A
  • Coordinated electrical activity ensures that the heart contracts in a specific sequence, allowing for efficient blood pumping.
  • The electrical impulses act as signals, triggering the contraction of the heart chambers in a synchronised manner.
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8
Q

What is the primary role of the cardiac conduction system?

A
  • Ensures the organised and coordinated contraction of the heart chambers for efficient pumping.
  • It achieves this by generating and propagating electrical impulses throughout the heart muscle.
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9
Q

What are the key components of the cardiac conduction system, and where are they located in the heart?

A

The main components are:

  • The sinoatrial (SA) node in the right atrium
  • The intermodal pathways within the atria
  • The atrioventricular (AV) node between the atria and ventricles
  • The Bundle of His, branching into left and right bundle branches running down the septum
  • Purkinje fibres extending from the bundle branches into the ventricular muscle
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10
Q

What is the function of the SA node, and why is it referred to as the pacemaker of the heart?

A
  • The SA node initiates the heartbeat by spontaneously generating electrical impulses at a rate of about 70 to 80 beats per minute.
  • This intrinsic automaticity earns it the title of the heart’s pacemaker.
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11
Q

Describe the path of the electrical impulse through the cardiac conduction system.

A

The impulse originates in the SA node
→ Spreads through the atria via internodal pathways, causing atrial contraction.
→ It then reaches the AV node and experiences a slight delay
→ Following the delay (100 milliseconds) it travels down the Bundle of His and bundle branches to the Purkinje fibres, finally causing ventricular contraction.

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12
Q

How long is the slight delay in impulse at the AV node?

A

Around 100 milliseconds

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13
Q

Why is there a delay in impulse conduction at the AV node, and what is its significance for the heart’s pumping function?

A

To allow the atria to contract and fully empty blood into the ventricles before the ventricles contract, ensuring efficient pumping.

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14
Q

What prevents the electrical impulse from directly travelling from the atria to the ventricles?

A
  • The atrioventricular ring, a layer of fibrous connective tissue, acts as an electrical insulator, preventing direct propagation of the impulse from atria to ventricles.
  • This necessitates conduction through the AV node.
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15
Q

How do the bundle branches and Purkinje fibres contribute to coordinated ventricular contraction?

A
  • They rapidly conduct the electrical impulse throughout the ventricular muscle mass, ensuring near-simultaneous contraction of the ventricles.
  • This coordinated contraction starts at the apex and spreads upwards, effectively pumping blood out of the heart.
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16
Q

Where does the near-simultaneous contraction of the ventricular muscle mass start? How does it spread?

A
  • Starts at the apex
  • Spreads upwards, effectively pumping blood out of the heart.
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17
Q

What is the significance of varying conduction velocities within the heart?

A

Ensures the timely and coordinated contraction of heart chambers - facilitating efficient blood pumping.

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18
Q

What characteristic of the heart allows it to continue beating even when separated from nervous system input?

A
  • Intrinsic automaticity
  • It can generate its own electrical impulses for contraction, independent of external nerve stimulation.
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19
Q

Which cells within the heart are responsible for initiating the heartbeat?

A

Specialised cells known as pacemaker cells, located in the sinoatrial (SA) node

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20
Q

Where is the sinoatrial (SA) node situated?

A
  • Posterior wall of the right atrium
  • Near the superior vena cava.
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21
Q

Describe the intrinsic automaticity of the SA node.

A
  • The SA node can spontaneously generate action potentials at a rate of approximately one per second
  • Leading to a heart rate of around 60-80 beats per minute.
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22
Q

What is sinus rhythm?

A

Normal heart rhythm driven by the SA node

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23
Q

Aside from the SA node, are there other potential pacemakers in the heart?

A
  • Yes
  • Other areas of the heart, such as the atrioventricular (AV) node and Purkinje fibres, also possess pacemaker capabilities, but they are typically overridden by the faster rate of the SA node.
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24
Q

What are latent pacemakers?

A
  • Latent pacemakers refer to potential pacemaker sites in the heart, like the AV node and Purkinje fibres
  • They have slower intrinsic firing rates than the SA node and are usually suppressed under normal conditions.
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25
Q

Under what circumstances might a latent pacemaker take over the control of heart rhythm?

A
  • If the SA node is damaged or its function is compromised, a latent pacemaker, typically the AV node, can take over
  • Leading to a slower heart rate.
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26
Q

Why would relying on the Purkinje fibres as a pacemaker be problematic?

A

The Purkinje fibres have a very slow intrinsic firing rate (around 20 beats per minute), which is insufficient to maintain adequate cardiac output for survival.

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27
Q

What is an ectopic pacemaker?

A

An ectopic pacemaker refers to any pacemaker originating from a site other than the SA node, often causing disruptions in the coordinated electrical activity of the heart, potentially leading to impaired pump function.

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28
Q

How does the autonomic nervous system exert control over the SA node?

A

Both the sympathetic and parasympathetic branches of the autonomic nervous system can influence the firing rate of the SA node, thereby modulating heart rate.

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29
Q

Which neurotransmitters are involved in the autonomic regulation of heart rate?

A
  • Acetylcholine, released by the parasympathetic nervous system, acts to slow heart rate
  • Noradrenaline, released by the sympathetic nervous system, accelerates heart rate.
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30
Q

Acetylcholine is released by the which branch of the nervous system?

A

Parasympathetic nervous system

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31
Q

Noradrenaline is released by the which branch of the nervous system?

A

Sympathetic Nervous system

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32
Q

Explain how the parasympathetic nervous system slows down heart rate.

A
  • Parasympathetic stimulation, primarily via the vagus nerve, decreases inward currents through calcium and HCN channels
  • Leading to a less steep phase 4 depolarization, thereby reducing the frequency of action potentials generated by the SA node.
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33
Q

What is vagal tone?

A

Vagal tone refers to the predominant influence of the parasympathetic nervous system on the heart at rest, keeping the heart rate relatively low.

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34
Q

Describe how the sympathetic nervous system increases heart rate.

A
  • Sympathetic stimulation increases the conductance of both the funny current and the voltage-gated calcium current in SA node cells
  • Leading to a steeper phase 4 depolarization and a faster heart rate.
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35
Q

What are positive chronotropy?

A
  • Positive chronotropy refers to an increase in heart rate
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36
Q

What is positive dromotropy?

A

Positive dromotropy describes an increase in the speed of electrical conduction, typically through the AV node.

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37
Q

What are the two main types of cardiac action potentials?

A

The two types are:

  • Slow response or pacemaker potentials, found in the SA and AV nodes
  • Fast response action potentials, characteristic of atrial and ventricular myocytes and Purkinje fibres.
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38
Q

What are the key characteristics that distinguish slow response (pacemaker) potentials from fast response action potentials?

A
  • Slow response potentials exhibit a slowly depolarising resting membrane potential, leading to spontaneous action potentials.
  • Fast response potentials show rapid depolarisation and have a stable resting membrane potential.
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39
Q

How many phases are typically observed in cardiac action potentials, and what do these phases represent?

A
  • Up to five phases (0-4)
  • Each reflect changes in membrane potential due to the activity of various ion channels throughout the action potential.
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40
Q

When is the “funny current” (If) activated?

A
  • At negative membrane potentials
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41
Q

What is the role of the “funny current” (If) in slow response potentials?

A
  • Allows sodium influx, causing the slow depolarisation of the resting membrane potential, (also known as the pacemaker potential.
  • This instability enables the spontaneous generation of action potentials.
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42
Q

Which phases are present in slow response potentials, and which are absent?

A
  • Only exhibit phases 0, 3, and 4.
  • No 1 or 2
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43
Q

Which ion primarily drives the depolarisation phase (phase 0) in slow response potentials, in contrast to neuronal action potentials?

A
  • Calcium
  • This is slower when compared to the sodium-driven depolarisation in neuronal action potentials.
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44
Q

How does parasympathetic stimulation affect heart rate and conduction velocity?

A

Parasympathetic activation, via the vagus nerve, releases acetylcholine which slows heart rate (negative chronotropy) and reduces conduction velocity through the AV node (negative dromotropy).

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45
Q

What are the mechanisms by which parasympathetic stimulation slows the heart rate at the SA node level?

A
  • Parasympathetic stimulation reduces inward calcium and funny currents
  • This leads to a less steep phase 4 and slower depolarisation.
  • It also increases outward potassium current, hyperpolarising the resting membrane potential.
  • It also modulates calcium channels, increasing the threshold for action potential activation.
46
Q

How does sympathetic stimulation impact heart rate and conduction velocity?

A

Sympathetic activation, through the release of noradrenaline, increases heart rate (positive chronotropy) and speeds up conduction velocity through the AV node (positive dromotropy).

47
Q

What are the cellular effects of sympathetic stimulation on SA node action potentials?

A

Sympathetic stimulation:

  • Enhances the conductance of the funny current and voltage-gated calcium current:
    → a steeper phase 4
    → faster depolarisation
    → a shorter action potential duration.
  • It also reduces the threshold for calcium channel activation.
48
Q

What is the refractory period in cardiac action potentials, and what are its two distinct phases?

A

The refractory period is the time following an action potential during which it’s difficult or impossible to initiate another action potential. It comprises the absolute refractory period (where no stimulus can elicit another action potential) and the relative refractory period (where a stronger than usual stimulus is needed).

49
Q

What is the significance of the plateau phase (phase 2) in fast response action potentials?

A

The plateau phase, resulting from a balance between calcium influx and potassium efflux, prolongs the action potential, allowing sufficient time for calcium entry to trigger contraction and ensuring adequate relaxation and ventricular filling before the next heartbeat.

50
Q

Which ion channels contribute significantly to the morphology of fast response action potentials?

A
  • Voltage-gated sodium channels (phase 0)
  • Voltage-gated potassium channels (phases 1 and 3)
  • Voltage-gated calcium channels (phase 2).
51
Q

What causes the plateau phase (phase 2) in fast response action potentials?

A
  • A balance between calcium influx and potassium efflux
52
Q

What is the physiological importance of the refractory period in cardiac muscle?

A
  • Ensures unidirectional propagation of the action potential
  • Prevents excessively rapid heart rates that would compromise ventricular filling and efficient pumping.
53
Q

How are cardiac myocytes structurally interconnected to facilitate coordinated contraction?

A
  • Cardiac myocytes are connected end-to-end by intercalated discs, which contain gap junctions and desmosomes.
  • Gap junctions allow rapid electrical communication between cells
  • Desmosomes provide mechanical strength.
54
Q

How do gap junctions contribute to the propagation of electrical impulses through cardiac tissue?

A

Gap junctions form channels between adjacent myocytes, enabling the passage of ions, particularly sodium and calcium, from a depolarised cell to a resting cell, thus spreading the electrical impulse and coordinating contraction.

55
Q

What is excitation-contraction coupling (EC coupling) in cardiac muscle?

A

The process by which the electrical excitation of a cardiac myocyte, via the action potential, triggers the release of calcium ions from the sarcoplasmic reticulum (SR), leading to muscle contraction.

56
Q

Explain the role of “trigger calcium” in EC coupling.

A
  • Depolarisation of the T-tubule membrane activates voltage-gated calcium channels, allowing a small amount of “trigger calcium” to enter the cell.
  • This trigger calcium activates ryanodine receptors on the SR membrane, releasing a larger amount of calcium into the cytoplasm.
57
Q

What is “calcium-induced calcium release” in cardiac muscle?

A

The entry of a small amount of trigger calcium triggers the release of a much larger amount of calcium from the SR stores through ryanodine receptors, amplifying the calcium signal and initiating contraction.

58
Q

How does the calcium transient relate to the force of contraction in cardiac muscle?

A
  • The amplitude of the calcium transient, representing the amount of calcium released from the SR, directly correlates with the force of contraction.
  • A larger calcium transient results in a stronger contraction.
59
Q

How is calcium removed from the cytoplasm to facilitate relaxation of the cardiac muscle?

A

Calcium is pumped back into the SR by the SERCA pump (sarco/endoplasmic reticulum calcium ATPase), and a small amount is extruded from the cell by the sodium-calcium exchanger (NCX).

60
Q

How does sympathetic stimulation enhance the force of contraction in cardiac muscle?

A

Sympathetic activation, via beta-adrenergic receptors, increases cyclic AMP levels, activating protein kinase A, which phosphorylates various proteins involved in EC coupling, ultimately leading to a larger calcium transient and a stronger contraction (positive inotropy).

61
Q

What is the effect of sympathetic stimulation on the rate of relaxation in cardiac muscle?

A
  • Sympathetic stimulation accelerates the removal of calcium from the cytoplasm
  • → Faster relaxation of the cardiac muscle (positive lusitropy) →Allowing for a faster heart rate.
62
Q

Which division of the autonomic nervous system dominates the control of heart rate at rest?

A

The parasympathetic nervous system

A phenomenon known as vagal tone.

63
Q

Through which nerve does the parasympathetic nervous system primarily innervate the SA and AV nodes?

A

The vagus nerve (X)

64
Q

What is the primary neurotransmitter involved in parasympathetic modulation of heart rate?

A
  • Acetylcholine, released by the vagus nerve, binds to M2 muscarinic receptors on SA and AV node cells, leading to a decrease in heart rate.
65
Q

How does parasympathetic stimulation affect the pacemaker potential in SA node cells?

A

Reduces inward currents through calcium and HCN channels → Less steep phase 4 depolarization and a slower heart rate.

66
Q

Name two ways parasympathetic stimulation alters action potential characteristics to slow heart rate.

A
  • Hyperpolarizes the resting membrane potential
  • Increases the threshold for action potential generation.
67
Q

What term describes the parasympathetic nervous system’s effect on the frequency of action potentials in the SA node?

A

Negative chronotropy refers to the decrease in action potential frequency caused by parasympathetic stimulation.

68
Q

What is Negative chronotropy?

A

The decrease in action potential frequency caused by parasympathetic stimulation.

69
Q

Besides affecting the SA node, how else does the parasympathetic system influence heart rate?

A

It decreases conduction velocity through the AV node, delaying the transmission of the electrical impulse to the ventricles. This is termed negative dromotropy.

70
Q

What is negative dromotropy.

A
  • The decrease in conduction velocity through the AV node, delaying the transmission of the electrical impulse to the ventricles
  • Caused by the parasympathetic system
71
Q

What is the primary neurotransmitter involved in sympathetic modulation of heart rate?

A

Noradrenaline, released by sympathetic nerves, binds to beta-1 adrenergic receptors in the SA node, increasing heart rate.

72
Q

How does sympathetic stimulation affect the pacemaker potential in SA node cells?

A

Increases the conductance of both the funny current (If) and the voltage-gated calcium current (Ica) → A steeper phase 4 depolarization and a faster heart rate.

73
Q

What term describes the sympathetic nervous system’s effect on the frequency of action potentials in the SA node?

A

Positive chronotropy refers to the increase in action potential frequency caused by sympathetic stimulation.

74
Q

How does the sympathetic system influence the speed of electrical conduction through the AV node?

A
  • It increases conduction velocity through the AV node, accelerating the transmission of the electrical impulse to the ventricles.
  • This effect is termed positive dromotropy.
75
Q

What is excitation-contraction coupling (EC coupling)?

A

The process that links the electrical excitation of a cardiomyocyte (action potential) to the mechanical contraction of the heart.

76
Q

How do gap junctions contribute to the coordinated contraction of the heart?

A
  • Gap junctions allow the action potential to rapidly spread from cell to cell
  • Ensuring the heart muscle is excited in a synchronized manner.
77
Q

Explain the role of T-tubules in EC coupling.

A
  • T-tubules are invaginations of the cell membrane
  • They allow extracellular ions, including calcium, to rapidly reach the interior of the cardiomyocyte, which is essential for initiating contraction.
78
Q

What happens when the action potential reaches the T-tubule membrane?

A

The T-tubule membrane depolarises, activating voltage-gated calcium channels.

79
Q

What is the function of the small amount of calcium that enters the cardiomyocyte through voltage-gated calcium channels?

A

This “trigger calcium” binds to and activates ryanodine receptors (RyR) located on the sarcoplasmic reticulum (SR) membrane.

80
Q

Describe the process of calcium-induced calcium release (CICR).

A
  • When trigger calcium binds to RyR, the RyR open, releasing a large amount of calcium from the SR stores into the cytoplasm.
  • This process amplifies the initial calcium signal.
81
Q

What is the calcium transient, and how does it relate to the force of contraction?

A
  • The rapid increase in cytoplasmic calcium concentration that occurs after calcium release from the SR.
  • The greater the amplitude of the calcium transient (i.e., the more calcium released), the stronger the force of contraction generated by the cardiomyocyte.
82
Q

How does the increased cytoplasmic calcium concentration lead to the contraction of the cardiomyocyte?

A
  • Calcium binds to the myofilaments, specifically to troponin C.
  • This binding initiates the sliding filament mechanism, causing the muscle fibres to shorten and generate force.
83
Q

What is the role of the sarco/endoplasmic reticulum calcium ATPase (SERCA) in muscle relaxation?

A
  • SERCA actively pumps calcium back into the SR, reducing cytoplasmic calcium levels and promoting relaxation.
  • This ensures the cardiomyocyte is ready for the next contraction cycle.
84
Q

How is the “trigger calcium” removed from the cytoplasm?

A

The sodium-calcium exchanger (NCX) uses the energy from the sodium gradient to extrude calcium from the cell back into the extracellular space.

85
Q

Explain how sympathetic stimulation leads to positive inotropy (increased force of contraction).

A

Sympathetic stimulation activates beta-1 adrenergic receptors on cardiomyocytes, activating a signalling cascade involving cyclic AMP (cAMP) and protein kinase A (PKA). PKA phosphorylates various proteins, including:

  • L-type calcium channels, increasing calcium influx during the action potential.
  • RyR, enhancing calcium release from the SR
  • SERCA, speeding up calcium reuptake into the SR.

These effects collectively increase the amplitude of the calcium transient, leading to a stronger contraction.

86
Q

How does sympathetic stimulation contribute to positive lusitropy (faster relaxation)?

A
  • By enhancing SERCA activity, sympathetic stimulation accelerates the removal of calcium from the cytoplasm.
  • This faster calcium reuptake into the SR leads to more rapid relaxation of the cardiomyocyte.
87
Q

What are cardiomyocytes?

A

Specialised muscle cells that make up the myocardium

88
Q

What is the myocardium?

A

The contractile middle layer of the heart wall.

89
Q

Describe the appearance of cardiomyocytes and explain why they look this way.

A
  • They appear Striated
  • This is due to the highly organised arrangement of thick and thin myofilaments (actin and myosin) that form the contractile units called sarcomeres.

Striated - Meaning they have a striped appearance

90
Q

What is the sarcolemma?

A

The plasma membrane of a cardiomyocyte, forming its outer boundary.

91
Q

What are T-tubules, and what is their importance in cardiomyocyte function?

A
  • T-tubules are invaginations (inward folds) of the sarcolemma that penetrate deep into the interior of the cardiomyocyte.
  • They allow rapid access of extracellular fluid, including ions like calcium, to the inner regions of the cell, which is crucial for initiating and synchronising contraction.
92
Q

Describe the structure and function of the sarcoplasmic reticulum (SR) in cardiomyocytes.

A
  • The sarcoplasmic reticulum (SR) is a specialised network of membranes within the cardiomyocyte that serves as a storage reservoir for calcium ions.
  • The controlled release of calcium from the SR is essential for triggering contraction.
93
Q

How are individual cardiomyocytes connected to form a functional syncytium?

A

Cardiomyocytes are connected end-to-end by specialised structures called intercalated discs.

94
Q

What are the two main components of intercalated discs, and what are their functions?

A

Intercalated discs contain:

  • Desmosomes
  • Gap junctions
95
Q

Function of desosomes in the intercalted discs?

A

Provide strong mechanical adhesion between adjacent cardiomyocytes, preventing them from separating during the stresses of contraction.

96
Q

Function of gap junctions in the intercalted discs?

A
  • They form channels that directly connect the cytoplasm of neighbouring cells, allowing for rapid electrical communication and the passage of ions (like sodium and calcium) between cells.
  • This electrical coupling enables the heart to function as a coordinated unit.
97
Q

How do gap junctions contribute to the propagation of the electrical impulse through the heart muscle?

A
  • When an action potential depolarises one cardiomyocyte, ions flow through the gap junctions to the next cell, causing it to depolarise as well.
  • This wave of depolarisation spreads rapidly through the interconnected network of cardiomyocytes.
98
Q

Explain why the refractory period is important for the coordinated contraction of the heart.

A
  • The refractory period is a brief period following an action potential during which a cardiomyocyte is unable to generate another action potential.
  • This ensures that the electrical impulse propagates in one direction only, preventing the heart from contracting in an uncoordinated or chaotic manner.
99
Q

What is the primary relationship between the calcium transient amplitude and the force of contraction in a cardiomyocyte?

A
  • The force of contraction is directly proportional to the amplitude of the calcium transient.
  • A larger calcium transient leads to a stronger contraction.
100
Q

What is the definition of positive inotropy?

A

An increase in the force of contraction of the heart muscle.

101
Q

Which branch of the autonomic nervous system is primarily responsible for modulating contractile force in the heart?

A

The sympathetic nervous system

102
Q

Which specific receptor type on cardiomyocytes is activated by sympathetic stimulation to increase contractile force?

A

Beta-1 adrenergic receptors

103
Q

Briefly outline the intracellular signalling pathway that connects beta-1 adrenergic receptor activation to increased calcium transient amplitude?

A
  • Beta-1 adrenergic receptor activation stimulates the production of cyclic AMP (cAMP), which activates protein kinase A (PKA).
  • PKA then phosphorylates several key proteins involved in calcium handling, leading to an increased calcium transient amplitude.
104
Q

What are the specific actions of protein kinase A (PKA) that lead to an increase in the calcium transient amplitude?

A

PKA phosphorylates and activates:

  • L-type calcium channels, increasing calcium influx during the action potential plateau phase.
  • Ryanodine receptors (RyR), enhancing calcium release from the sarcoplasmic reticulum (SR).
  • SERCA, speeding up calcium reuptake into the SR, allowing for faster relaxation and a greater calcium store for subsequent release.
105
Q

What is the overall impact of sympathetic stimulation on the force and speed of cardiomyocyte contraction?

A
  • Increases both the force of contraction (positive inotropy) and the rate of relaxation (positive lusitropy).
106
Q

Explain how isoprenaline is used to demonstrate the effects of sympathetic stimulation on cardiomyocytes.

A
  • Isoprenaline is a beta-adrenergic receptor agonist, meaning it mimics the effects of sympathetic stimulation.
  • Experiments using isoprenaline show a marked increase in the amplitude and a faster decline of calcium transients in cardiomyocytes.
  • This results in an increased force of contraction and faster relaxation.
107
Q

Does the parasympathetic nervous system also play a role in modulating contractile force, and if so, how?

A
  • Yes,
  • The parasympathetic nervous system, via the vagus nerve, primarily influences atrial contractility.
  • It releases acetylcholine, which binds to M2 muscarinic receptors, leading to a decrease in cAMP levels and reduced PKA activity.
  • This results in decreased calcium influx through L-type calcium channels, leading to a decrease in contractile force, known as negative inotropy.
108
Q

Apart from the autonomic nervous system, what other factors can influence the force of contraction in cardiomyocytes?

A
  • The Frank-Starling mechanism: the force of contraction is proportional to the initial length of the muscle fibre, which is determined by the degree of ventricular filling. Increased stretching of the cardiomyocytes leads to a more forceful contraction.
  • Heart rate: faster heart rates can lead to a build-up of intracellular calcium due to reduced time for removal between beats, resulting in a more forceful contraction.
109
Q

What is the Frank-Starling mechanism?

A

The Frank-Starling mechanism:
* The force of contraction is proportional to the initial length of the muscle fibre, which is determined by the degree of ventricular filling.
* Increased stretching of the cardiomyocytes leads to a more forceful contraction.

110
Q

Can heart rate influence the force of contraction in cardiomyocytes?

A
  • Yes
  • Faster heart rates can lead to a build-up of intracellular calcium due to reduced time for removal between beats, resulting in a more forceful contraction.

CTB Block 2 (19 decks)

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