S4) Cellular & Molecular Events in the CVS Flashcards Preview

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

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

⇒ 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



In three steps, briefly explain how excitation leads to action

⇒ Cardiac myocytes are electrically active & fire action potentials

⇒ Action potential triggers increase in [Ca2+]i

⇒ Actin and myosin interact, triggering the contraction mechanism


State the RMP for the following:

- Axon

- Skeletal muscle


- Cardiac ventricle

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

Depolarisation – Na+ influx

- Initial repolarisation – K+ efflux

- Plateau – Ca2+ influx

- Proper repolarisation – K+ efflux

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Describe the 3 different stages in the SAN action potential 

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Describe the mechanisms behind the slow depolarising pacemaker potential

- 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

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Describe how the action potential waveform varies throughout the heart

- 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

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


- Purkinje fibres 

- Atrial muscle 

- Ventricular muscle 


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

- Action potentials fire too slowly → bradycardia

- Action potentials fail → asystole

- Action potentials fire too quickly → tachycardia

- Electrical activity becomes random → fibrillation


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

3.5 – 5.5 mmol L-1


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

- Hyperkalaemia – plasma [K+] is too high > 5.5 mmol.L-1

- Hypokalaemia – plasma [K+] is too low < 3.5 mmol.L-1


In 5 steps, describe the effects of hyperkalaemia

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⇒ 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


What are the risks associated with hyperkalaemia?

- Pacemaker potential decreases, heart rate decreases/stops (asystole)

- May initially get an increase in excitability but then conductance may cease


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

Describe the severity of hyperkalaemia

- Mild: 5.5 – 5.9 mmol/L

- Moderate: 6.0 – 6.4 mmol/L

- Severe: > 6.5 mmol/L


How can hyperkalaemia be treated?

- Calcium gluconate

- Insulin + glucose

Ineffective if the heart already stopped


In 4 steps, describe the effects of hypokalaemia

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 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


What are the risks associated with hypokalaemia?

- 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

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In two steps, describe excitation-contraction coupling

⇒ 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 

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How does relaxation occur in cardiac myocytes?

[Ca2+]i must return to resting levels:

- SERCA is stimulated and pumps calcium back into SR

- PMCA & NCX remove calcium across the cell membrane


What controls the tone of blood vessels?

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

- Located in tunica media

- Present in arteries, arterioles and veins 


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

⇒ 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

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

⇒ Ca2+ levels decline

⇒ Myosin light chain phosphatase dephosphorylates myosin

PKA phosphorylates MLCK & inhibits its action

⇒ Myosin light chain is not phosphorylated

⇒ Contraction is inhibited

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