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Cardiovascular system > Lecture 9- Electrical and molecular mechanisms in the hearts > Flashcards

Lecture 9- Electrical and molecular mechanisms in the hearts Flashcards

1
Q

which ion set shte resting membrane potential

A

K+ permeability

  • high conc of K+ intracellularly
  • lower conc of Na+ intracellularly
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2
Q

At rest the cardiomyocyte are permeable to

A

K+ ions

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3
Q

at rest K+ ions move out of the cell

A

down conc gradient

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4
Q

what makes the inside negative with respect to the outside at rest

A

small movement of ions

  • as charge builds up an electrical gradient established–> K+ moves back in
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5
Q

When chemical and electrical gradients are equal but opposite- no movement

A
  • RMP

Net outflow of K+ until Ek reached

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6
Q

why is resting potential not equal to Ek

A

small permeability to other ion species at rest

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7
Q

Excitation contraction coupling

A
  1. Cardiac myocytes are electrically active- fire AP
  2. AP triggers release of calcium into cytosol
  3. A rise in calcium is required to allow actin and myosin interaction
  4. Generate tension-contraction
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8
Q

Different types of APs in different tissues - have different features such as

A

Different lengths

Cardiac myocyte lasts 280ms (much longer than axonal or skeletal)

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9
Q

4 types of AP

A

axonal

skeletal muscle

SAN

Cardiac ventricle

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10
Q

APs are measured using

A

microelectrode

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11
Q

How is the equilibrium potential of potassium (resting potential) set up?

A

Chemical diffusion and electrical gradients

1) Chemical diffusion: Potassium flows out of the cell down its concentration gradient via diffusion

2) Electrical gradient: causes potassium to flow back in due to the negativity created by K+ initially leaving the cell down its conc gradient (and also intracellular anions)

When these forces are equal and opposite- no net movement of potassium - negative membrane potential due to anions

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12
Q

resting membrane potential of axon

A

-70mV

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13
Q

resting membrane potential of skeletal muscle

A

-90

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14
Q

resting membrane potential of SAN

A

-60mV

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15
Q

resting membrane potential of cardiac ventricle

A

-90mV

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16
Q

what is membrane potential

A

Membrane potential is the electrical charge that exists across a membrane

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17
Q

draw and label the ventricular (cardiac) AP

A
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18
Q

Ek of the cardiac AP

A

-90-95mV

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19
Q

ENa of Cardiac AP

A

+70 mV

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20
Q

phases of the cardiac AP

A
  1. RMP due to background K+ channels (not V-gated)
  2. Upstroke due to opening of voltage-gated sodium channels- Na+ influx
  3. Initial repolarisation due to transient outward K+ channel (V-gated)
  4. Plateau due to opening of voltage gated Ca2+ channels (L-type)- influx of calcium
  5. Balanced with K+ efflux
  6. Inactivation of calcium channels. Repolarisation due to efflux of K+ through voltage gated K+ channels and other
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21
Q

which type of voltage gates calcium channesl

A

L type

22
Q

draw and label the SAN AP

A
23
Q

the SAN is knwon as the

A

pacemaker- where the electrical activity originates

24
Q

outline the SA node action potential

A
  1. Long slow depolarisation to threshold (starting at -60mV)- due to funny current
  2. Upstroke- Opening of V-gated calcium channels
  3. V-gated Sodium channels not involved (would make them all inactive)
  4. Downstroke- Opening of V-gates K+ channels
25
Q

Funny current- If

A

HCN channels

  1. Hyperpolarisation-activated cyclic nucleotide-gated channels (responsible for spontaenous depolarisation)
  2. Allow influx of Na+ ions which depolarises the cells
  3. Upstroke
26
Q

SAN AP is similar to

A

AV AP

27
Q

IF SAN not working the

A

AVN would take over as the pacemaker (just slower than the SAN)

28
Q

Aps throughout the heart

A
  • SA and AVN both have unstable resting membrane potential
  • Atrial muscle fibres-like ventricular muscle
  • Purkunjee- in-betweens SA and ventricular muscle AP
    • Slight If (funny current- incline at the beginning)
29
Q

Purkunjee fibres

A
  • in-betweens SA and ventricular muscle AP

Slight If (funny current- incline at the beginning)

30
Q

If AP fires too slowly

A
  • bradycardia
31
Q

If AP potential fail

A

asystole

is the most serious form of cardiac arrest and is usually irreversible. A cardiac flatline is the state of total cessation of electrical activity from the heart, which means no tissue contraction from the heart muscle and therefore no blood flow to the rest of the body.

32
Q

If AP fire too quickly

A

tachycardia

33
Q

If electrical activity become random

A

–> fibrillation

34
Q

Plasma [K+] must be controlled within tight range

A

– 3.5-5.5 mmol/l-1

35
Q

hyperkalaemia

A

>5.5 mmol L-1

36
Q

Hypokalaemia

A

<3.5 mmol L-1

37
Q

Why are cardiac myocytes so sensitive to changes in [K+]?

A

K+ permeability dominates RMP

The heart has many different kinds of K+ channels –> some behave in peculiar ways

38
Q

hyperkalaemia effect on the heart

A

Hyperkalaemia depolarises the myocytes and slows down the upstroke of the action potential

39
Q

why does hyperkalaemia depolarises the myocytes and slows down the upstroke of the action potential

A
  • EK = 61.5mV Log [K+]o / [K+]i
  • If you raise plasma K+ then EK gets less negative so the membrane potential depolarises a bit
  • This inactivates some of the voltage-gated Na+ channels
  • Slows upstroke

*dotted line= hyperkalaemia*

40
Q

risk of hyperkalaemia

A
  • Heart can stop- asystole
  • May initially get an increase in excitability
  • Depends on the extent and how quickly it develops
    • Mild 5.5-5.9 mmol/L
    • Moderate 6-6.3 mmol/l
    • Severe >6.5mmol/l
41
Q

treatment of hyperkalaemia

A
  • Calcium gluconate
    • Calcium makes the membrane less excitable
  • Insulin and glucose
  • Wont work if hearts already stopped
42
Q

hypokalaemia and cardiac AP

A
  • Lengthens the action potential
  • Delays repolarisation

More brown line =effect of hypokalaemia

43
Q

hypokalaemia can lead to

A

early after depolarisation (EAD)–> this can lead to oscillations in mem potential–> Can result in ventricular fibrillation

44
Q

outline Excitation contraction coupling in the heart

A
  1. Depolarisation opens L-type calcium channels in T-tubule system
  2. Localised entry of calcium (25% of total calcium influx into cytosol) opens Calcium induced calcium release (CICR) channels in the SR (75%)
  3. Close link between L-type channels and Ca2+ release channels

Regulation of cardiac myocyte contraction

  1. Calcium binds to troponin C
  2. Conformational change shifts tropomyosin to reveal myosin binding site on actin filament

Relaxation of cardiac myocytes

  1. Must return (Ca+2) to resting levels
  2. Most is pumped back into SR (via SERCA)
    1. Raised calcium stimulates the pump
  3. Some exit across cell membrane
    1. Sarcolemmal Ca2+ ATPase
    2. Na+/Ca2+ exchanger
45
Q

Tone of blood vessel is controlled by contraction and relaxation of vascular smooth muscle cells

A
  • Located in tunica media
  • Present in arteries, arterioles and veins
46
Q

E-C coupling in smooth muscle

A
  1. Opening of VOCC or activation of GalphaQ ( Alpha 1 receptors)
  2. Calcium influx from extracellular space or SR
  3. Calcium binds to Calmodulin (x4 calcium ions)
  4. Activated calmodulin activates to Myosin light chain kinase (MLCK)
  5. MLCK now phosphorylates the myosin light chain
    • If phosphate isn’t bound- wont bind to actin
  6. When activated (with phosphate) myosin light chain can bind to actin
  7. Myosin light chain phosphatase removes phosphate form myosin which allows relaxation
  8. DAG – produced via GalphaQ will activates PKC- PKC has inhibitory effect on MLCP- keeps Myosin light chain in active form
47
Q

Myosin light chain must be ………… to enable actin-myosin interaction

A

phosphorylated

48
Q

Relaxation of smooth muscle as….

A
  • Calcium levels decline
  • Myosin light chain phosphatase dephosphorylates the myosin light chain
49
Q

Phosphorylation of MLCK by

A

PKA inhibits the action of MLCK

Inhibits phosphorylation of the myosin chain and inhibits contraction

50
Q

Difference between cardiac muscle and smooth muscle

A

Contraction of heart initiated by spread of AP from SA node

No neural input needed

Cardiac myocyte action potential allow calcium entry

  • Further calcium released from SR
  • Calcium binding to troponin C

Contraction of vascular smooth muscle cells initiated by depolarisation or activation of alpha-adrenoreceptors

  • Increased intracellular calcium
  • Calcium binding to calmodulin
  • Activation of MLK- phosphorylates myosin light chain

Cardiovascular system (30 decks)

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