S4) Cellular & Molecular Events in the CVS Flashcards Preview

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Flashcards in S4) Cellular & Molecular Events in the CVS Deck (22)
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1
Q

In four steps, describe how the resting membrane potential of cardiac cells is generated

A

⇒ Cardiac myocytes are permeable to K+ at rest

K+ move out of the cell (down concentration gradient)

⇒ Inside becomes more negative relative to the outside

⇒ As charge builds up an electrical gradient is established

2
Q

In three steps, briefly explain how excitation leads to action

A

⇒ Cardiac myocytes are electrically active & fire action potentials

⇒ Action potential triggers increase in [Ca2+]i

Actin and myosin interact, triggering the contraction mechanism

3
Q

State the RMP for the following:

  • Axon
  • Skeletal muscle
  • SAN
  • Cardiac ventricle
A
4
Q

Describe the 4 different stages of the ventricular (cardiac) action potential

A
  • Depolarisation – Na+ influx
  • Initial repolarisation – K+ efflux
  • Plateau – Ca2+ influx
  • Proper repolarisation – K+ efflux
5
Q

Describe the 3 different stages in the SAN action potential

A
6
Q

Describe the mechanisms behind the slow depolarising pacemaker potential

A
  • Turning on of slow Na+ conductance (If – funny current)
  • Activated at membrane potentials more negative than - 50mV
  • HCN (Hyperpolarisation-activated Cyclic Nucleotide-gated) channels are activated which allow influx of Na+ for depolarisation
7
Q

Describe how the action potential waveform varies throughout the heart

A
  • SAN is fastest to depolarise, it is the pacemaker and sets rhythm
  • Other parts of the conducting system also have automaticity, but it’s slower
8
Q

Describe the action potential diagrams for different parts of the heart:

  • SAN
  • Purkinje fibres
  • Atrial muscle
  • Ventricular muscle
  • AVN
A
9
Q

Explain four problems that could occur during the process of excitation leading to contraction

A
  • Action potentials fire too slowly → bradycardia
  • Action potentials fail → asystole
  • Action potentials fire too quickly → tachycardia
  • Electrical activity becomes random → fibrillation
10
Q

What is the normal range of plasma [K+]?

A

3.5 – 5.5 mmol L-1

11
Q

If [K+] is too high or low it can cause problems, particularly for the heart.

In terms of plasma [K+] levels, define hyperkalaemia and hypokalaemia

A
  • Hyperkalaemia – plasma [K+] is too high > 5.5 mmol.L-1
  • Hypokalaemia – plasma [K+] is too low < 3.5 mmol.L-1
12
Q

In 5 steps, describe the effects of hyperkalaemia

A

EK becomes less negative (smaller concentration gradient)

Membrane potential becomes less negative and depolarises

⇒ Early depolarisation causes Na channels to open then inactivate (less steep uptake slope)

HCN channels are activated by hyperpolarisation (remain inactive)

Depolarisation is slow and over a long duration

13
Q

What are the risks associated with hyperkalaemia?

A
  • Pacemaker potential decreases, heart rate decreases/stops (asystole)
  • May initially get an increase in excitability but then conductance may cease
14
Q

Risks associated with hyperkalaemia depend on the extent and how quickly it develops.

Describe the severity of hyperkalaemia

A
  • Mild: 5.5 – 5.9 mmol/L
  • Moderate: 6.0 – 6.4 mmol/L
  • Severe: > 6.5 mmol/L
15
Q

How can hyperkalaemia be treated?

A
  • Calcium gluconate
  • Insulin + glucose

Ineffective if the heart already stopped

16
Q

In 4 steps, describe the effects of hypokalaemia

A

EK becomes more negative (greater concentration gradient)

Membrane potential becomes more negative

Action potential is prolonged as plateau phase is longer (Ca2+ channels remain open)

Repolarisation is delayed & slower

17
Q

What are the risks associated with hypokalaemia?

A
  • Longer action potentials lead to early after depolarisations (EADs)
  • Prolonged plateau phase provides greater opportunity to stimulate more action potentials and cause more contractions

⇒ Leads to oscillations in membrane potential which result in ventricular fibrillation

18
Q

In two steps, describe excitation-contraction coupling

A

⇒ Depolarisation opens L-type Ca2+ channels in the T-tubule system

⇒ Localised Ca2+ entry opens closely-linked CICR channels in the SR

25% enters across sarcolemma, 75% released from SR

19
Q

How does relaxation occur in cardiac myocytes?

A

[Ca2+]i must return to resting levels:

  • SERCA is stimulated and pumps calcium back into SR
  • PMCA & NCX remove calcium across the cell membrane
20
Q

What controls the tone of blood vessels?

A

Tone of blood vessels is controlled by contraction & relaxation of vascular smooth muscle cells:

  • Located in tunica media
  • Present in arteries, arterioles and veins
21
Q

In 5 steps, describe the cellular mechanism leading to the contraction of blood vessels

A

⇒ Ca2+ binds to calmodulin

⇒ Ca2+- calmodulin complex is formed

Myosin Light Chain Kinase is activated

⇒ MLCK phosphorylates myosin so it interacts with actin

Contraction mechanism is triggered

22
Q

In 5 steps, describe the cellular mechanism leading to the relaxation of blood vessels

A

Ca2+ levels decline

Myosin light chain phosphatase dephosphorylates myosin

PKA phosphorylates MLCK & inhibits its action

⇒ Myosin light chain is not phosphorylated

⇒ Contraction is inhibited