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Physiology > Electrical Activity of the Heart > Flashcards

Electrical Activity of the Heart Flashcards

1
Q

What is the driving force of ions?

A

Diff between memb pot (Em) & ion’s equ potential (Ex)
(ions “want” memb potential to = its equ potential)

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2
Q

What is the equilibrium potentials of K+, Na+, Ca2+?

A

-85mV = K+
+65mV = Na+
+120mV = Ca2+

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3
Q

What happens is there is a difference between memb pot & equ pot (i.e., a driving force)?

A

Ions will move to bring about equ (then will stop - i.e., there is no driving force)

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4
Q

How to calculate equilibrium potential of ions?

A

Use Nernst equation

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5
Q

What is ion current?

A

Occurs when ion moves across cell memb

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6
Q

What are the 2 factors needed for ions to move across the cell memb?

A

-Driving force of ion
-Memb has a conductance to the ion - i.e., specific channels which are open
(as phospholipoid bilayer = impermeable to ions - need channels)

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7
Q

What is resting membrane potential?

A

Potential difference - exists across memb of excitable cells at rest

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8
Q

What is the resting membrane potential of most excitable cells?

A

-70 –> -80 mV

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9
Q

How is membrane potential expressed?

A

As intracellular potential relative to extracellular potential

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10
Q

Compare the intracellular vs the extracellular potential at rest & when depolarised?

A

-Int = -ve (at rest)
-Ext = +ve (at rest)
-Int = +ve (dep)
-Ext = -ve (dep)

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11
Q

What are the 3 ions and their ion channels involved in resting membrane potential?

A

K+
Ca2+
Na+

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12
Q

Describe K+ involvement in resting membrane potential?

A

-Intracellular [K+] is highest
-K+ diffuses down its chemical grad out cell
= inc conc out cell - more +ve extracellular
–> causes K+ to diffuse down its electrical grad (built up prev) into cell
-Until reach equ (balance) for both chem & elect
(Electrochemical grads)

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13
Q

Describe Ca2+ involvement in resting membrane potential?

A

-Extracellular [Ca2+] is highest
-Ca2+ diffuses down its chemical grad into cell
= inc conc in cell - more +ve in cell
–> causes Ca2+ to diffuse down its electrical grad (build up prev) out cell
-Until reach equ (balance) for both chem & elect
(Electrochemical grads)

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14
Q

Describe Na+ involvement in resting membrane potential?

A

-Extracellular [Na+] is highest
-Na+ diffuses down its chemical grad into cell
= inc conc in cell - more +ve in cell
–> causes Na+ to diffuse down its electrical grad (build up prev) out cell
-Until reach equ (balance) for both chem & elect
(Electrochemical grads)

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15
Q

What sets up & maintains the chemical gradients of Na+ & K+ in resting membrane potential?

A

Na+/K+ ATPase pump

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16
Q

Give 4 words associated with +ve membrane potential?

A

-Depolarisation
-Inward current
-Threshold potential
-Overshoot

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17
Q

Define depolarisation (+ve associated words).

A

Less -ve (NOT +ve yet!)

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18
Q

Define inward current (+ve associated words).

A

Flow of +ve charge (Na+ & K+ influx) into the cell –> depolarisation

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19
Q

Define threshold potential (+ve associated words).

A

Memb pot at which occurrence of the action potential is definite (will occur)

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20
Q

Define overshoot (+ve associated words).

A

Portion of action potential where memb pot is +ve

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21
Q

Give 4 words associated with -ve membrane potential?

A

-Hyperpolarisation
-Outward current
-Undershoot/repolarisation
-Refractory period

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22
Q

Define hyperpolarisation (-ve associated words).

A

More -ve

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23
Q

Define outward current (-ve associated words).

A

Flow of +ve charge (Na+ K+) out of cell

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24
Q

Define undershoot/repolarisation (-ve associated words).

A

Portion of action potential where memb returns to -ve (restore polarity)

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25
Q

Define refractory period (-ve associated words).

A

Period when another normal action potential cannot be elicited in an excitable cell

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26
Q

2 types of refractory period?

A

-Absolute
-Relative
(In cardiac muscle cells = additional category called effective refractory period)

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27
Q

Simplify this graph.

A
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28
Q

Symbols for membrane potential?

A

Em or Vm

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29
Q

What is the absolute refractory period?

A

-Overlaps almost fully w/ action pot
-In this - can’t generate action pot - no matter how great the stimulus

30
Q

Why can’t another action potential be elicited during the absolute refractory period?

A

-Inactivation gates of Na+ channel = closed (due to depolarisation)
–> closed until cell is repolarised back to resting memb pot
-& Na+ channels need to recover to “closed, but available” state

31
Q

What is the relative refractory period?

A

-At end of absolute refractory period - overlaps w/ hyperpolarisation
-Can generate action pot - IF greater than usual depolarising (inward) current is applied (strong/large stimuli)

32
Q

What is the cause of the relative refractory period?

A

-Higher K+ conductance than at rest
-As memb pot - closer to K+ equ potential - more inward current needed to reach threshold to initiate action pot

33
Q

What is propagation?

A

Process of exciting cells one after another - through gap junctions - so only 1 cell has to have an action potential generated in it
(not every cell has to have action pot - will start in 1 cell & spread though gap junctions between adjacent cells)

34
Q

TRUE OR FALSE?
1 = Resting membrane potential is the potential difference that exists across the membrane of excitable cells at rest
2 = Depolarisation is when the cell becomes positive.
3 = During absolute refractory period, AP can be elicited when enough stimulus is applied.

A

1 = True
2 = False
3 = False

35
Q

What are the 2 muscle cell types in the heart?

A

-Contractile muscle cells
-Conducting muscle cells

36
Q

Describe the process of cardiac action potentials from the SAN.

A

-SAN generates action pot (phases 4,0,3)
-Action pot/excitatory wave passes across both atria & atrial internodal tracts (but not to vs - due to fibrous ring between as & vs - non-conducting tissue)
= atria contract (phases 0,1,2,3,4) - valves open - blood into vs
-Excitatory wave passes to AV node
-Then is a pause/delay in impulse - before AV node conducts - allows time for ventricular filling
-Wave passes down Bundle of His - down R&L branches down purkinje fibres to ventricles = fast (so vs contract simultaneously)
-Ventricles contract (phases 0,1,2,3,4) from apex up- SL valves open - blood ejected

37
Q

Importance of the fibrous ring in being non-conducting tissue?

A

So atria & ventricles do not contact at same time

38
Q

What is the SAN’s role in cardiac action potentials?

A

As a primary pacemaker/action potential generator

39
Q

What are the phases: 0,1,2,3,4 for atria & ventricular cardiac action potentials?

A

0 = upstroke, rapid depolarization, Na+ influx - makes int cell +ve
1= initial repolarization, Na+ influx stops (channels close) & K+ efflux (channels open)
2 = plateau, stable depolarization, Ca2+ influx (channels open) & K+ efflux (a sort of equ)
3 = repolarization, Ca2+ influx stops (channels close) & K+ efflux (get more -ve than @ resting)
4 = resting membrane potential, or electrical diastole:
–> memb pot = stable - influx & efflux currents are same - resting membrane potential is very close to but not equal to K+ equ pot

40
Q

What type of Ca2+ channels involved in atria & ventricular cardiac action potentials?

A

L-type channels

41
Q

What drugs can target Ca2+ L-type channels?

A

Channel blockers:
-Nifedipine
-Diltiazem
-Verapamil

42
Q

3 features of SA node (cardiac) action potentials?

A

-Automaticity - spontaneously generates action pots - no neural input
-Unstable resting memb pot compared to other cardiac cells
-No sustained plateau (phase 2) - as continually signals/fires to stimulate heart contraction

43
Q

What are the phases 4,0,3 for SAN cardiac action potentials?

A

0 = upstroke, rapid depolarization, Ca2+ influx (not as steep/rapid as in other cardiac tissues) - upstroke inactivates HCN (stops funny current until phase 3)
3 = repolarization, Ca2+ influx stops & K+ efflux - hyperpolarisation caused
4 = HCN mediates funny current: Na+ influx & K+ efflux, Ca2+ channels recover, gradient restored - depolarises back to threshold
-Rate of phase 4 decides HR

44
Q

What is a channel only found in pacemaker cells e.g., SAN?

A

HCN channel that mediates funny current - Na+ influx & K+ efflux –> to bring memb pot back to threshold (in phase 4) after hyperpolarisation (in phase 3)

45
Q

Summarise stage 4 (pre-potential) of SAN cardiac action potentials in more detail.

A

= key to automaticity of SA nodal cells
-Pacemaker cells contain HCN gated channels (non-spec) - activated by hyperpolarisation - stage 3
-HCN causes a funny current (If)
-If = simultaneous K+ efflux & Na+ influx
-Na+ influx dominates & memb slowly depolarises to threshold
-Ca2+ upstroke = inactivates HCN until end of Phase 3 (hyperpolarisation)

46
Q

What is a key determinant of heart rate?

A

Rate of phase 4 depolarisation in SAN

47
Q

Summarise atrial & ventricular cardiac action potentials.

A
48
Q

What are latent pacemakers?

A

= Myocardial cells other than SAN w/ intrinsic automaticity
-Have capacity for spontaneous phase 4 depolarisation
-Can drive HR if SAN = suppressed or intrinsic firing rate of one of these other cells becomes faster than SAN
-AV node = next fastest
-Bundle of His = next fastest
-Purkinje fibres = next fastest

49
Q

What is the name of what suppresses latent pacemakers when SAN drives heart rate?

A

Overdrive suppression

50
Q

What is meant by the automaticity of the SAN (& other latent pacemakers)?

A

Spontaneously generate action pots without neural input (spontaneous phase 4 depolarisation)

51
Q

TRUE OR FALSE?
1 = The AV node is the primary pacemaker
2 = The SA node has the longest AP duration
3 = The SA node has the fastest firing rate
4 = Inward Ca2+ causes upstroke in:
a = SA node
b = Atria
c =Ventricles
d = Purkinje fibres

A

1 = False
2 = False
3 = True
4
a = True
b = False
c = False
d = False

52
Q

What is the sympathetic nervous system responsible for in heart & blood vs?

A

‘Fight or Flight’
Increase in HR, conduction velocity & contractility
-All by β1 rec
-HR = involves funny & Ca2+ channels
-Conduction velocity & contractility = involves Ca2+ channels

53
Q

What is the parasympathetic nervous system responsible for in heart & blood vs?

A

‘Rest & Digest’
Decrease in HR, conduction velocity & contractility
-All by M2 rec

54
Q

Where are β1 and β2 receptors (& how to remember this)?

A

β1 = heart (1 heart)
β2 = lungs (have 2 lungs)

55
Q

What are chronotropic effects?

A

The effects of the nervous system on HR

56
Q

What do +ve chronotropic effects cause, & what part of the autonomic NS causes this?

A

-Increase/faster HR
-Sympathetic NS (‘fight or flight’)

57
Q

What do -ve chronotropic effects cause, & what part of the autonomic NS causes this?

A

-Decrease/slower HR
-Parasympathetic NS (‘rest & digest’)

58
Q

What are dromotropic effects?

A

The effects of the nervous system on conduction velocity of heart

59
Q

What do +ve dromotropic effects cause, & what parts of the autonomic NS causes this?

A

-Increase in conduction velocity - through AV node
-Sympathetic NS (‘fight or flight’)

60
Q

What do -ve dromotropic effects cause, & what parts of the autonomic NS causes this?

A

-Decrease in conduction velocity - through AV node
-Parasympathetic NS (‘rest & digest)

61
Q

TRUE OR FALSE?
1 = Positive chronotropic effects occur via parasympathetic NS.
2 = Positive chronotropic effect means increasing conduction velocity.
3 = Positive dromotropic effect means increasing heart rate.
4 = Sympathetic nervous system exerts its effects on the heart via beta 2 receptors.

A

1 = False
2 = False
3 = False
4 = False

62
Q

Myocardial cell structure - sarcomere?

A
63
Q

What is excitation-contraction coupling?

A

The link (transduction) between action pot generated in sarcolemma & the start of a muscle contraction (in cardiac muscle! not skeletal!!)

64
Q

Process of excitatory-contraction coupling?

A

-Cardiac action pot generated in phase 0
-Ca2+ enters cell during plateau (between phase 1 & 2)
–> causes Ca2+ induced Ca2+ release from sarcoplasmic reticulum of cell
-Ca2+ bind to troponin C
-Sliding filament theory occurs - myosin heads pull actin towards centre of sarcomere = shortens sarcomere (in all sarcomeres = how muscles contract)
–> cross-bridge cycling caused = tension
(when Ca2+ lowers - as reaccumulates in SR - cardiac muscle relaxes)

65
Q

What is contractility (inotropism)?

A

= Intrinsic ability of myocardial cells to develop force at a given muscle cell length
-Correlates directly w/ intracellular [Ca2+]

66
Q

What does the amount of Ca2+ released from sarcoplasmic reticulum depend on?

A

-Size of inward Ca2+ current
-Amount of Ca2+ previously stored in SR for release

67
Q

What are inotropic effects?

A

Effects of the autonomic nervous system on contractility

68
Q

What do +ve inotropic effects cause, & what part of the autonomic NS causes this?

A

-Increase in contractility = stimulates & increases contraction force of myocardial cells
-Sympathetic NS (‘fight or flight’)

69
Q

What do -ve inotropic effects cause, & what part of the autonomic NS causes this?

A

-Decrease in contractility = stimulates & decreases/weakens contraction force of myocardial cells
-Parasympathetic NS (‘rest & digest’)

70
Q

What are cardiac glycosides?

A

Drug class - act as +ve inotropic agents

71
Q

How are cardiac glycoside’s affects used?

A

To treat congestive heart failure - decreased contractility of ventricular muscle (i.e., negative inotropism) - so these drugs will do the opposite & elicit a +ve inotropic effect (increase contractility)

Physiology (10 decks)

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