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cardiovascular lectures > electrical activation of the heart > Flashcards

electrical activation of the heart Flashcards

1
Q

define membrane potential

A

the difference in electric potential between the interior and the exterior of a cell.

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2
Q

if there is a charge outside the cell is that positive or negative membrane potential

A

negative

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3
Q

if there is a charge inside the cell is that positive or negative membrane potential

A

positive

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4
Q

how to calculate membrane potential

A

interior potential - exterior potential

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5
Q

what is the membrane potential of a cardiac myocyte at rest

A

-90mV

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6
Q

what are the units for membrane potential

A

mV

millivolts

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7
Q

compare action potentials of the heart to action potentials of skeletal muscle

A

the action potential of the heart is 100x longer than skeletal muscle.

because cardiac muscle has slow calcium channels

skeletal muscle cells: 2-5ms duration

cardiac muscle cells: 200-400ms duration

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8
Q

what are the phases of myocyte action potential

A
  1. resting state
  2. depolarisation
  3. partial depolarisation
  4. plateau
  5. repolarisation
  6. resting state
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9
Q

what is phase 4 of myocyte action potential

A

it is resting state
pd is -90 mv

SAN generates action potential

causes depolarisation

if threshold is reached

phase 0 starts

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10
Q

what is phase 0 of myocyte action potential

A

depolarisation

action potential arrives

threshold potential (-60mV) reached

Na+ channels open.
inflow of Na+

causes slightly positive pd

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11
Q

what is phase 1 of myocyte action potential

A

partial repolarization

At +30mV, Na+ channels close and transient K+ channels open.

slightly negative pd due to K+

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12
Q

what is phase 2 of myocyte action potential

A

plateau

L-type Ca2+ channels allow a slow influx of Ca2+ to balance K+ efflux.

so pd remains constant

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13
Q

what is phase 3 of myocyte action potential

A

repolarisation

the Ca2+ channels close allowing repolarisation.

K+ channels open allowing influx of K+

causes pd to become more negative

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14
Q

2 types of refractory period

A

abolsute

relative

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15
Q

what is the absolute refractory period

A
  • period after an action potential where the cell is completely unexcitable so second impulse CANNOT cause a second contraction of cardiac muscle
  • longer for cardiomyocytes
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16
Q

what is the relative refractory period

A

when a greater than normal stimulus can depolarise the cell

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17
Q

purpose of refractory period

A
  1. to prevent excessive FREQUENT
    contraction
  2. To allow adequate filling time
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18
Q

how is resting potential of cardiac myocyte membrane maintained

A

by Na+ & K+ ATPase pumps

pumping 3Na+ ions OUT
for every
2K+ ions pumped IN

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19
Q

why is resting membrane potential much closer to the K+ equilibrium potential (-90mV) than to the Na+
equilibrium potential (+60mV)

A

The resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+ than to Na+ - meaning the resting membrane potential is much closer to the K+ equilibrium potential (-90mV) than to the Na+ equilibrium potential (+60mV)

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20
Q

what is K+ equilibrium potential

A

-90mv

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21
Q

what is Na+ equilibrium potential

A

+60mv

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22
Q

why is resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+

A

since K+ channels are open meaning K+ is leaving the cell -

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23
Q

what happens when an action potential arrives in myocardial cell

A
  • Na+ voltage gated ion channels are OPENED
  • Na+ entry depolarises the cell
  • triggering more Na+ channels to open
    -positive feedback effect
  • At the same time that the Na+ voltage gated ion channels are triggered to open Ca2+ voltage gated ion channels are ALSO triggered
  • however these channels open much more slowly than the Na+ channels.
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24
Q

what happens when the potential in cell is positive (+52)

A

voltage gated Na+ channels CLOSE,
at the same time voltage gated K+ channels OPEN - partially REPOLARISING the cell

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25
Q

what happens during the partial repolarisation causes by the outflow of K+

A
  • Ca2+ voltage gated channels finally OPEN at T-TUBULES which are part of the sarcolemma
  • resulting in the INFLOW of Ca2+ into the cell
  • since these channels remain open for a long duration of time they are often referred to as Ltype Ca2+ channels (L=long lasting), these channels are modified versions of the
    dihydropyridine (DHP) receptors that function as voltage sensors in excitationcontraction coupling of skeletal muscles
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26
Q

why are Ca2+ voltage-gatted channels located in t-tubules called L-type Ca2+

A

because these channels remain open for a long duration of time

they are modified versions of the
dihydropyridine (DHP) receptors that function as voltage sensors in excitation-contraction coupling of skeletal muscle

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27
Q

what keeps the membrane DEPOLARISED at the PLATEAU VALUE of roughly 0mV.

A

2 reasons:

  1. because the flow of Ca2+ ions into the cell just balances the flow of K+ ions out of the cell
  2. the K+ channels open at the start close as well - maintaining depolarisation
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28
Q

what causes repolarisation to eventually occur

A

the eventual closure of the L-type Ca2+
channels
and
the reopening of the K+ channels (the ones open at the start) - these
are similar to the ones in neurons & skeletal muscle;
they open in response to depolarisation (after a delay) and close once the K+ current has depolarised the
membrane back to negative values

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29
Q

which ions are responsible for rapid depolarisation in phase 0

A

Na+ inflow

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30
Q

which ions are responsible for partial repolarisation in phase 1

A

K+ outflow
Inflow of Na+ stops

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31
Q

which ions are responsible for plateau in phase 2

A

Ca2+ slow inflow

32
Q

which ions are responsible for repolarisation in phase 3

A

K+ outflow
Inflow of Ca2+ stops

33
Q

which ions are responsible for pacemaker potential in phase 4

A

Na+ inflow
Slowing of K+ outflow

34
Q

what is excitation-contraction coupling

A

refers to the series of events that link the action potential (excitation) of the muscle cell membrane (the sarcolemma) to muscular contraction

35
Q

describe excitation - contraction coupling process

A
  1. wave of depolarisation/AP spreads into myocardial cells via T tubules
  2. L-type Ca2+ channels open –> Ca2+ enters the muscle cell
  3. causing small increase in cytosolic Ca2+ concentration
  4. the small amount of Ca2+ ions bind to ryanodine receptors on the sarcoplasmic reticulum
  5. this causes sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell
  6. this initiates cardiac muscle contraction - the start of the cross bridge cycle
  7. Ca2+ binds to Ca2+ binding site on troponin on actin
  8. troponin changes shape and displaces tropmyosin, exposing myosin binding sites
  9. mysoin head binds to actin via myosin binding site
  10. inorganic phosphate is dropped in order for mysoin head to bind to actin but the ADP is still attached to the head - this is cross bridge formation
  11. myosin head then drops ADP to contract and pull actin over mysoin
  12. this decreases the Z lines resulting in muscle contraction - the power stroke
  13. ATP binds to myosin head, detaching the head from actin and moving it to its start position
  14. ATPase in myosin head hydrolyses ATP into ADP and Pi ready for next contraction if the mysoin binding sites remain open
  15. contraction stops when cytosolic Ca2+ conc is restored to is original extremely low resting value by primary active Ca2+ - ATPase pumps in the sarcoplasmic reticulum and sarcolemma AND Na+/Ca2+ counter transporters in the sarcolemma
  16. the amount of Ca2+ returned to extracellular fluid and sarcoplasmic reticulum exactly matches the amounts that entered the cytosol during excitation
36
Q

how are myocardial cells supplied with blood

A

by the coronary ateries

the coronary arteries exit from behind the aortic valve cusps in the very first part of the aorta

most of the coronary arteries drain into a single vein called the coronary sinus, which empties into the right atrium

37
Q

what is the force of contraction directly proportional to

A

levels of cytosolicic Ca2+

38
Q

what is the effect of drugs and chemicals that c

A

increased cytosolic calcium levels

39
Q

examples of drugs that increase myocardial contractility

A

Adrenaline

Digoxin

cardiac glycosides

40
Q

what happens in rigour mortis

A

person is dead

no ATP

myosin head cannot detach from actin

resulting in stiffness of skeletal muscles

41
Q

what is the conducting system of the heart

A

approx 1% of cardiac cells dont function in contraction

instead they have specialised features essential for normal heart excitation

they form the conducting system of the heart and are in electrical contact with cardiac myocytes via gap junction

42
Q

what does the conducting system do

A

initiates the heartbeat & helps spread the action potential rapidly throughout the heart

43
Q

what do gap junctions do

A

interconnect myocardial cells and allow action potentials to spread from one cell to another

44
Q

how does the initial excitation of one cardiac celleventually result in the excitation of all cardiac cells

A

the action potential spreads over cell membranes,

the positive charge from the Na+ affects adjacent cells, resulting in depolarisation,

the newly depolarised cells can cause further depolarisation,

and the gap junctions enable ions to travel directly to other cells.

45
Q

where is the sinoatrial node (SAN)

A

right atrium

near entrance of superior vena cava

46
Q

how does action potential spread to ventricles

A

it arises in SAN

spreads from SAN throughout atria and into and throughout ventricles

47
Q

what is the SAN

A

the natural pacemaker of the heart

determines heart rate in mammals - tho no. of times the heart contracts per minute

characterized by the ability to generate spontaneous action potentials that serve to excite the surrounding atrial myocardium

48
Q

what is resting membrane potential of SAN

A

-55 to -60 mV

this is closer to the threshold of depolarisation so it depolarises first

its closer to depolarisation threshold because of it’s slow Na+ inflow not found anywhere else in the body

49
Q

what are the phases for pacemaker action potential

A

phase 4

phase 0

phase 3

50
Q

what is pacemaker potential

A

SA node has no steady resting potential

instead it undergoes slow depolarisation

this is pacemaker potential

it brings membrane potential to a threshold at which ap occurs

51
Q

which 3 ion channel mechanisms contribute to pacemaker potential

A
  1. K+ channels
  2. F - type channels
  3. Ca2+ channels
52
Q

how do k+ channels affect pacemaker potential

A
  • the K+ channels that opened during the repolarisation phase of the previous action potential gradually
    close due to the membrane returning to negative potentials
  • leads to progressive reduction in K+ permeability.
53
Q

how do F type channels affect pacemaker potential

A
  • these open when the membrane potential is at NEGATIVE values - these nonspecific cation (positive ions) conduct mainly an inward Na+ current
  • since this is not normal these channels are referred to as “funny” and are thus
    called F-type channels
54
Q

how do Ca2+ channels affect pacemaker potential

A
  • these open VERY BRIEFLY but contribute to an inward current of Ca2+ which acts as an important final depolarising boost to the pacemaker potential.
  • Since the channel is only opened briefly it can be called transient so these channels are known as T-type Ca2+ channels
55
Q

compare action potentials in SA node and AV node

A

both similar in shape

but

pacemaker currents in SA node bring them to threshold more rapidly than the AV node

this is why the SA node normally initiates action potentials and determines the pace of the heart

56
Q

why is cardiac excitation slow in AV node

A

because the depolarising phase is caused by Ca2+ influx through L type Ca2+ channels instead of Na+

the Ca2+ currents depolarise the membrane more slowly than voltage gated Na+ channels

so the ap propagate ire slowly along nodal cells than in other cardiac cells

57
Q

what does the pacemaker potential provide the SA node with

A

automaticity

  • the ability for spontaneous, rhythmic self excitation
58
Q

how is ap spread to ventricles

A

using the atrioventricular node

the ap is conducted relatively fast from the SA node to the V node via internodal pathways

59
Q

where is the atrioventricular node (AVN)

A

Located at the base of the right atrium

60
Q

what does AVN do

A

transmits cardiac impulse from atria to
ventricles

61
Q

structure of AVN

A

Consists of modified cardiac cells that have lost contractile capability but conduct action potentials with LOW RESISTANCE

Elongated structure with an important
feature; the propagation of action potentials through the AV node is RELATIVELY SLOW (requiring approximately 0.1 secs) - this is
IMPORTANT since it enables the atria to
EMPTY BLOOD into the ventricles, enables atrial contraction to be completed before ventricular excitation occurs

62
Q

what happens after the AV node has been excited

A

the action potential progresses down the interventricular septum
- this pathway of conducting fibres is called the bundle of His

63
Q

what is the only electrical connection between the atria and ventricles

A

The AV node and the bundle of His constitute the ONLY electrical connection between the atria and ventricles -

except from THIS PATHWAY the atria are completely isolated from the ventricles by a layer of nonconducting connective tissue

64
Q

describe structure of bundle of His

A

Within the interventricular septum, the bundle of His divides into right & left bundle branches, conducting fibers that separate at the bottom (apex) of the heart and enter the walls of both ventricles

These fibers in turn make contact with Purkinje fibers, large-diameter conducting
cells that rapidly distribute the impulse throughout much of the ventricles
* Finally the Purkinje fibres make contact with ventricular myocardial cells - which spread the action potential through the rest of the ventricles

65
Q

why is conduction from the AV node to the ventricles is RAPID

A

to enable coordinate ventricular contraction

66
Q

rate of discharge in SAN

A

60-100/min

highest rate of discharge

thats why its the primary pacemaker

67
Q

how is the heart innervated

A

via a rich supply of parasympathetic (rest & digest) & sympathetic
(fight or flight) nerve fibres

68
Q

what is sympathetic stimulation

A

Sympathetic postganglionic fibers innervate the entire heart

69
Q

what is sympathetic stimulation controlled by

A

controlled by adrenaline & noradrenaline

70
Q

effect of sympathetic stimulation

A

*Increases heart rate (positively chronotropic)
* Increases force of contraction (positively inotropic)
* Increases cardiac output (by up to 200%

71
Q

what happens if there’s decreased sympathetic stimulation

A

decreased heart rate & force of
contraction and a decrease in cardiac output by up to 30%

72
Q

what does noradrenaline do

A

increases Ca2+ channel opening
= faster depolarisation

73
Q

what is parasympathetic stimulation

A

Fibers are transmitted via the vagus nerve (CN10)

74
Q

what is parasympathetic stimulation controlled by

A

by acetylcholine which bind to muscarinic receptors

75
Q

effect of parasympathetic stimulation

A
  • Decreases heart rate (negatively chronotropic)
  • Decreases force of contraction (negatively inotropic)
  • Decreases cardiac output (by up to 50%)
76
Q

what happens if there’s decreased parasympathetic stimulation

A

an increased heart rate

77
Q

what does ACH do (acetylcholine)

A

ACH activates potassium channels = Hyperpolarizes membrane = longer to reach TP

Also decreases calcium influx= decreases slope of pacemaker potential

cardiovascular lectures (15 decks)

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