S4) Cellular & Molecular Events in the CVS Flashcards Preview

(LUSUMA) Cardiovascular System > S4) Cellular & Molecular Events in the CVS > Flashcards

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

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

 

2

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

3

State the RMP for the following:

- Axon

- Skeletal muscle

- SAN

- Cardiac ventricle

A image thumb
4

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

A image thumb
5

Describe the 3 different stages in the SAN action potential 

A image thumb
6

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

A image thumb
7

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

A image thumb
8

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

- SAN

- Purkinje fibres 

- Atrial muscle 

- Ventricular muscle 

- AVN

A image thumb
9

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

10

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

3.5 – 5.5 mmol L-1

11

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

12

In 5 steps, describe the effects of hyperkalaemia

Q image thumb

⇒ 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

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

14

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

15

How can hyperkalaemia be treated?

- Calcium gluconate

- Insulin + glucose

Ineffective if the heart already stopped

16

In 4 steps, describe the effects of hypokalaemia

Q image thumb

 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

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

A image thumb
18

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 

A image thumb
19

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

20

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 

21

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

A image thumb
22

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

A image thumb