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CVS > Lecture 9 > Flashcards

Lecture 9 Flashcards

1
Q

What sets up the resting membrane potential in cardiac myocytes?

A

K+ permeability (K+ channels open all the time)

  • permable to K+ ions at rest, so they move out the cell down their concentration gradient
  • this sets up an electrical gradient making the inside negative
  • this pushes K+ back into the cell
  • net outflow of K+ until Ek is reached
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2
Q

Why does RMP never equal Ek?

A

Because the membrane is permeable to other ions at rest

usually -90/-85, rather than -95

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3
Q

When does contraction occur?

excitation -> contraction

A

When every AP is fired,because AP triggers increase in cytosolic Ca2+, allowing contraction due to actin & myosin interaction.
(cardiac myocytes are electrically active-fire AP’s)

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4
Q

What is unusual about a cardiac AP?

A

It is very long, 280 ms.

compared to AP of an axon= 0.5ms

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5
Q

What are the stages of the cardiac action potential?

A

Resting potential: -85mV

  • opening of V gated Na channels due to depolaristion, mV move towards Ena (+70mV) (these fast Na+ channels that cause the AP are very different to HCN’s causing pacemaker potential)
  • transient outward K+ current (rapid & short lived)
  • PLATEU PHASE: opening of L type voltage gated Ca2+ channels (also require some K+ channels opening to maintain the membrane potential)
  • Ca2+ channels deactivate and voltage gated potassium channels open
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6
Q

What is special about L type voltage gated Ca2+ channels?

A

They stay open for a long time, hence why they are part of the plateu phase.

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7
Q

Why do each cardiac myocyte behave in a different way?

A

They have lots of different types of K+ channels.

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8
Q

What is the SA/AV node AP? (the pacemaker potential)

A

Resting potential: -60mV

  • long slow depolarisation (PACEMAKER POTENTIAL) due to influx of Na+ (funny current: If) vis HCN channels
  • spontaneous depolaristion without any nervous input
  • T type (transient) Ca2+ channels open to reach TV (not Na+!!)
  • opening of voltagegated K+ channels cause repolarisation
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9
Q

Does the AV/SA node depolarise more slowly?

A

AV node

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10
Q

What do SA node/pacemaker cells lack?

A

They have little Na+ channels

no plateau, AP is triangular, as soon as membrane is depolarised over TV, it starts to repolarise

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11
Q

When is the pacemaker potential activated?

A

At membrane potentials that are more -ve than -50mV

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12
Q

What are HCN channels?

A

Hyperpolarisation-activated, Cyclic Nucleotide-gated

  • allow the influx of Na+ ions
  • cAMP activates these channels
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13
Q

How do the SA node AP fire?

A

Natural automacity.

No nervous input, they do it automatically due to a mixture of ion channels giving an unstable membrane potential.

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14
Q

What is the purpose of the SAN?

A

Set the HR/rhythm

-it is the pacemaker

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15
Q

How does the purkinje fibres AP differ from the ventricular AP?

A

There is a slight depolarisation before the upstroke.

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16
Q

What is bradycardia/tachycardia?

A

Bradycardia- AP’s fire too slow (below 60)

Tachycardia- AP’s fire too quickly (above 100)

17
Q

What is asystole/filbrillation?

A

Asystole- AP’s fail

Fibrillation- electrical activity becomes random

18
Q

What is the plasma K+ concentration range?

A

3.5-5.5 mmol/L

19
Q

Why are cardiomyocytes sensitive to changes in K+?

A
  • heart has many different types of K+ channels

- K+ permeability dominates resting membrane potential

20
Q

What is hyperkalaemia and its effects?

A

> 5.5 mmol/L

  • raise plasma K+
  • resting potential not as low
  • inactivates some voltage gated Na+ channels, slowing the upstroke

Effects:

  • asystole
  • increased excitability
21
Q

What are the different extents of hyperkalaemia?

A

Mild: 5.5-5.9 mmol/L (increased excitability)
Moderate: 6-6.4 mmol/L
Severe: 6.5 mmol/L +
Moderate and severe lead to asystole

22
Q

How would you stop the heart for surgery?

A

Bathe in high potassium solution, and ice cold so doesn’t require oxygen.

23
Q

What is the treatment for hyperkalaemia?

A

-calcium gluconate
-insulin/glucose (moves K+ into cell)
These don’t work if heart has already stopped because they can’t be transported around the blood.

24
Q

What is hypokalaemia and its effects?

A
  • K+ channels respond to low levels of plasma K+ by reducing its permeability to K+
  • lengthens the AP as it delays repolarisation
25
Q

Problem with hypokalaemia?

A
  • longer AP can lead to early after depolarisations (EADs)
  • leads to oscillations in the membrane potential
  • results in ventricular fibrillation
26
Q

How does excitation cause contraction of the muscle?

A

-depolarisation of T tubules opens L type Ca2+ channels
-Ca2+ entry opens Induced Calcium Release (CICR) channels in SR causing Ca2+ to be released into the muscle
-Ca2+ binds to troponin C
-conformational change causes tropomyosin to reveal myosin binding site on actin
= Reverse Sliding Filament Mechanism

27
Q

How much Ca2+ comes from the SR/sarcolemma?

A

SR: 75%

Sacrolemma (t tubule): 25%

28
Q

How do cardiac muscles relax?

A

Return to Ca2+ resting levels

  • most pumped back into SR via SERCA (raised Ca2+ stimulates the pumps)
  • some exits across cell membrane via Na+/Ca2+ exchanger, sarcolemmal Ca2+ ATPase
29
Q

How are the blood vessels controlled?

A

Contraction/relaxation of smooth muscle layer in the tunica media

30
Q

How does contraction of smooth vascular muscle occur?

A
  • depolarisation opens voltage gated calcium channels/ NA activates alpha 1 G protein coupled receptors (which cleaves to IP3 & DAG, IP3 stimulates release of Ca2+ from ER)
  • 4 Ca2+ bind to calmodulin, which activates MLCK
  • MLCK phophorylates regulatory light chain on myosin head, forming ADP, activating it and allowing the myosin to attach to actin
31
Q

What is MLCK & MLCP?

A

Myosin Light Chain Kinase

Myosin Light Chain Phosphatase

32
Q

How does smooth vascular muscle relax?

A
  • relaxation as Ca2+ levels decline

- MLCP removes phosphate from light chain to allow relaxation

33
Q

What effect does DAG have on vascular smooth muscle contraction?

A

-PKC from DAG has an inhibitory effect on MLCP, keeping myosin in active form

34
Q

What happens if MLCK is phosphorylated?

A
  • phosphorylated by PKA

- inhibits MLCK, inhibiting phosphorylation of myosin light chain, and therefore contraction

35
Q

What does increased tone of a vessel mean?

A

Refers to degree of constriction, so therefore narrowing the lumen in this case.

CVS (16 decks)

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