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Y2S1 Advanced concepts in Human Physiology and Health- Cardiorespiratory Physiology and Pharmacology: Cardiorespiratory Physiology and Pharmacology > S1W1 L2 Electrical activity of the heart > Flashcards

S1W1 L2 Electrical activity of the heart Flashcards

1
Q

extracellular and intracellular conc of Na (mM)

A

140, 10

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2
Q

extracellular and intracellular conc of K (mM)

A

4, 140

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3
Q

extracellular and intracellular conc of Ca (mM)

A

1.2, 0.0001

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4
Q

equilibrium potential/ Nernst potential

A

potential gradient across the membrane to maintain concentration gradient, calculated by Nernst equation, tells us what electrical potential is needed to stop diffusion of ions down their chemical gradient

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5
Q

Na, Ca, K equilibrium potentials

A

+70mV
+12mV
-94mV

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6
Q

So, if cell is held at -94mV,

A

no net K movement in or out of cell

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7
Q

what is resting membrane potential

A

potential difference between the inside and outside of the cell, represents voltage difference inside and outside cell
result of differences in ion conc across membrane
sum of different ions equilibrium potential x electrical conductance

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8
Q

what are the electrical properties of a tissue dependant on

A

which ion channels are expressed in the membrane

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9
Q

when does the fast voltage gated Na+ channels open and effect

A

-70mV
activated and inactivated rapidly
inward membrane current generated

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10
Q

two ion channels which move Na+ back out of the cell

A

Na+/K+ pump
Na+/ Ca2+ exchanger

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11
Q

2 types of cardiac Ca2+ channels

A

T-type and L-type

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12
Q

T type Ca2+ channel

A

tiny conductance and transient openings
opens at -55mV, inactivate fairly rapidly

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13
Q

L type calcium channel

A

large conductance and long lasting openings
found throughout heart
open at -40mV and inactivate more slowly

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14
Q

direction and effect of K current

A

outward
make cell more negative inside
helps with repolarisation

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15
Q

why does K+ exert most control over resting and action potential duration

A

cell at rest is more permeable to K+

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16
Q

three main K+ currents:

A

background K+ current
delayed K+ currents transient outward K+ currents

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17
Q

what controls background K+ current

A

inward rectifying channel (Kir)
resting outward current (I kin/ Ik1)

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18
Q

when do background K+ channels open and their function

A
  • voltages
    help set stable - resting membrane potential of atria and ventricular myocyte
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19
Q

when do delayed K+ current and transient outward k+ current channels close
and function

A

close at negative voltages
open when cell becomes more +
open to help repolarise cell after AP

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20
Q

is the current voltage relationship for background current linear

A

no

21
Q

why do efflux of K+ ions not occur as cell becomes more positive past equilibrium potential

A

regulation by ion channel itself
magnesium ions
polyamines

22
Q

why is it important K+ doesn’t efflux out of cell

A

many consequences of K+ loss from cell

23
Q

background current ib

A

inward background current of mostly Na+
causes cell to be slightly higher than Ek

24
Q

funny current if

A

permeable to Na and K
activated at hyperpolarisation

25
Q

ventricular myocyte resting potential

A

-85/-90mV
stable

26
Q

ventricular myocyte AP: what channels are open at negative potentials and set resting membrane potential close to Ek

A

ik1
ikir

27
Q

ventricular myocyte AP: what is the rapid depolarisation due to

A

opening of voltage gated Na+ channels

28
Q

ventricular myocyte AP: what channels close as Na+ permeability increases

A

background K+ channels

29
Q

ventricular myocyte AP: as cell becomes more positive due to Na+ influx, what channels transiently open

A

ito
voltage gated K+ channels

30
Q

ventricular myocyte AP: what channels open when membrane potential reaches -40mV and effect

A

L type Ca2+
calcium enters cell
causing plateau phase

31
Q

ventricular myocyte AP: when the cell is the most pearmeable to Ca2+, it is least permeable to

A

K+

32
Q

ventricular myocyte AP: what is repolarisation brought about by

A

K+ permeability increases
ikr, iks
voltage gated delayed K+ channels

33
Q

ventricular myocyte AP: when membrane potential is close to resting level, what occurs

A

background K+ channels open again to keep resting membrane stable

34
Q

conducting system AP: how is AP initiated

A

autorhythmic/ pacemaker cells

35
Q

conducting system AP: dominant pacemaker cell?

A

SAN

36
Q

SAN AP: why is there no stable resting membrane potential

A

background K+ channels are absent

37
Q

SAN AP: max diastolic potential?

A

-60mV

38
Q

SAN AP: what is known as pacemaker potential?

A

slow depolarisation towards threshold of -40mV

39
Q

SAN AP: three phases

A

upstroke
repolarisation
period between AP

40
Q

SAN AP: what four overlapping currents make up SAN AP

A

funny current (if)
T type Ca2+ current
L type Ca2+ current
decay of delayed K+ channel permeability

41
Q

SAN AP: what currents are occurring in phase 4 (period between APs)

A

iCa (T)
if

42
Q

SAN AP: what channels open at -40mV

A

L type Ca2+
depolarises cell

43
Q

SAN AP: what is repolarisation induced by

A

closure of L type Ca2+ channels
opening of delayed K+ channels

44
Q

what is the pacemaker potential of the when SAN isolated

A

100 beats per min

45
Q

what is the pacemaker potential of the AVN when isolated

A

40 beats per min

46
Q

what is the pacemaker potential of the purkinje fibres when isolated

A

20 beats per min

47
Q

what cells can initiate a heartbeat

A

any cardiac cell with pacemaker ability

48
Q

how long does it roughly take for SAN to initiate AP in the rest of the heart

A

150-200ms

49
Q

what is the absolute refractory period of the SAN AP driven by

A

inactivation of Na+ channels,
almost as long as contraction phase,
can change depending on AP duration

Y2S1 Advanced concepts in Human Physiology and Health- Cardiorespiratory Physiology and Pharmacology: Cardiorespiratory Physiology and Pharmacology (6 decks)

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