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Medicine Unit 4 > Electrical activity of the heart > Flashcards

Electrical activity of the heart Flashcards

1
Q

driving forces

A

difference between the membrane potential (Em) and the ions equilibrium potential (Ex)

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2
Q

ion current Ix

A

occurs when there is movement of an ion across the cell membrane

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3
Q

conditions for ions to move across membrane through ion channels

A

driving force on the ion
membrane has a conductance to that ion

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4
Q

resting membrane potential

A

potential difference that exists across the membrane of excitable cells at rest

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5
Q

what is the value of resting membrane potential

A

-70mV to -80mV

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6
Q

what is membrane potential expressed as

A

intracellular potential relative to extracellular potential

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7
Q

what do you need to know for Nerst. equation

A

-95 for potassium
+65 for sodium
+120 for calcium

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8
Q

most predominant intracellular ion

A

potassium

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9
Q

potassium movement in chemical gradient

A

diffuses down the chemical gradient
diffuses out

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10
Q

potassium movement in electrical gradient

A

diffuses into the cell

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11
Q

calcium chemical gradient

A

into the cell

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12
Q

calcium electrical gradient

A

out of the cell

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13
Q

sodium chemical gradient

A

into the cell

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14
Q

sodium electrical gradient

A

out of the cell

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15
Q

calculating ion current

A

Ix= Gx (Em-Ex)

Gx= ion conductance (1/ohm)
Em-Ex= driving force on ion

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16
Q

ohms law

A

V=IR

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17
Q

relationship between ionic current and ohms law

A

is a rearrangement
V=E
G is reciprocal of R
I is current
I=GV

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18
Q

action potential positive terms

A

depolarisation
inward current
threshold potential
overshoot

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19
Q

depolarisation

A

less negative

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20
Q

negative action potential terminology

A

hyperpolarisation
outward current
undershoot/repolarisation
refractory period

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21
Q

hyperpolarisation

A

more negative

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22
Q

threshold potential

A

point where action potential occurs

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23
Q

refractory period

A

no action potential

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24
Q

absolute refractory period

A

overlaps with almost entire duration of the action potential

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25
Q

why can no more action potentials occur in refractory period

A

closure of inactivation gates of sodium channel in response to depolarisation
gates closed position until cell is depolarised back to resting membrane potential and Na+ have recovered to closed but available state

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26
Q

relative refractory period

A

begins at the end of the absolute refractory period and overlaps primarily with period of the hyperpolarisation

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27
Q

what occurs during relative refractory period

A

action potential can be elicited but only if a greater than usual depolarisation current is applied

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28
Q

basis of relative refractory

A

higher K+ conductance than is present at rest
membrane potential is closer to K+ equilibrium potential, more inwards current needed to bring membrane to threshold for next action potential to be initiated

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29
Q

propagation

A

wave of depolarisation spreads via gap junctions

30
Q

types of muscle cells in heart

A

contractile cells
conducting cells

31
Q

SA node

A

primary pacemaker

32
Q

AV node

A

slow conduction

33
Q

bundle of his, pukinje system, ventricles

A

fast

34
Q

sinoatrial node

A

AP duration 150 ms
upstroke: inward Ca current with inward Ca channels
no plateau
phase 4 depolarisation: inward Na current, normal pacemaker

35
Q

atrium

A

action potential duration: 150 ms
inward Na current
plateau: inward Ca current, slow inward current, L-type ca channels
no phase 4 depolarisation

36
Q

ventricle

A

250ms
inward na current
plateau: slow inward ca current, L-type ca channels
no phase 4 depolarisation

37
Q

purkinje fibres

A

300ms
inward na current
plateau: inward ca current, slow, l-type channels
latent pacemaker

38
Q

phase 0

A

upstroke, rapid
depolarization, Na+ influx

39
Q

phase 1

A

nitial repolarization, Na+
influx stops & K+ efflux

40
Q

phase 2

A

plateau, stable
depolarization, Ca2+ influx & K+
efflux

41
Q

phase 3

A

repolarization, Ca2+ influx
stops & K+ efflux

42
Q

phase 4

A

esting membrane
potential, or electrical diastole,

43
Q

features of the Sa node action potential

A

automaticity: SA node can spontaneously generate AP without neural input
SA node has unstable resting membrane potential in contrast to other cardiac cells
SA node AP has no sustained plateau

44
Q

cardiac action potential Sa node

A

Phase 0: upstroke, rapid
depolarization, Ca2+ influx
* Phase 3: repolarization, Ca2+
influx stops & K+ efflux
* Phase 4: Na+ influx (funny),
Ca2+ channels recover,
gradient restored
* The rate of phase 4 decides
the HR

45
Q

sinoatrial node, pacemaker action potential

A

Phase 4: Prepotential (distinguishing feature of
a pacemaker action potential)
* The key to automaticity
* Pacemaker cell membranes contain HCN-gated
channels (non-specific cation channels)
* Activated by hyperpolarisation (from Phase 3)
* HCN mediates a ‘funny current’ (If);
pacemaker current
* If is a simultaneous K+ efflux and Na+ influx
* Na influx dominates and membrane slowly
depolarises to threshold
* Upstroke inactivates HCN until end of Phase 3
(hyperpolarisation)

46
Q

latent pacemaker

A

cells in Sa aren’t only myocardial cells with intrinsic automaticity
latent pacemakers also have capacity for spontaneous phase 4 depolarisation

47
Q

latent pacemakers

A

opportunity to drive heart rate only if SA is suppressed or intrinsic firing rate of latent pacemaker becomes faster than the SA node

48
Q

effects of autonomic nervous system on heart rate

A

chronotropic effects

49
Q

what is in the image q

A

positive chronotropic

50
Q

what is in the image

A

negative chronotropic effects

51
Q

positive dromotropic effect

A

increase in conduction velocity through AV node

52
Q

negative dromotropic effect

A

decrease in condition velocity through AV node

53
Q

what are dromotropic effects

A

effects of the autonomic nervous system on conduction velocity

54
Q

myocardial cell structure

A
55
Q

contractility

A

inotropism
It is the intrinsic ability of myocardial cells to develop force
at a given muscle cell length.
* Contractility correlates directly with the intracellular Ca2+
concentration.

56
Q

amount of Ca released from SR depends on what

A

the size of the inward Ca2+ current
the amount of Ca2+ previously stored in the SR for release

57
Q

what are inotropic effects

A

effects of the autonomic nervous system on contractility

58
Q

positive inotropic effect

A

increase in contractility

59
Q

negative inotropic effect

A

decrease in contractility

60
Q

sympathetic action receptor and mechanism on the heart rate

A

increases
beta 1 receptor
increases If and ICa

61
Q

sympathetic action receptor and mechanism on conduction velocity

A

increases
beta 1
increases ICa

62
Q

sympathetic action receptor and mechanism on contractility

A

increases
beta 1
increased Ica and phosphorylation of phospholamban

63
Q

sympathetic action receptor and mechanism on vascular Smooth muscle (skin renal and splanchnic)

A

constriction
alpha 1

64
Q

sympathetic action receptor and mechanism on vascular smooth muscle (skeletal)

A

dilation with B2
and constriction with alpha 1

65
Q

parasympathetic action receptor and mechanism on heart rate

A

decreased
m2
decreased If and increased K.ACh and decreased ICa

66
Q

parasympathetic action receptor and mechanism on conduciton velocity

A

decreased
m2
decreased Ica and increased Ik.Ach

67
Q

parasympathetic action receptor and mechanism on contractility

A

decreased in atria only
m2
decreased ICa
increased IKAch

68
Q

all vascular smooth muscle parasympathetic action receptor

A

dilation releasing EDRF
M3

69
Q

EDRF, ICa, If, IK-Ach

A

endothelial derived relaxing factor
inward calcium ion current
inward sodium ion current
outward potassium ion current

70
Q

mechanism of action of cardiac glycosides

A

1.The Na+-K+ATPase is located in the cell membrane of the myocardial cell. Cardiac glycosidesinhibit Na+-K+ATPaseat the extracellular K+-binding site.
2.When the Na+-K+ATPase is inhibited, less Na+is pumped out of the cell, increasing theintracellular Na+concentration.
3.The increase in intracellular Na+concentration alters the Na+gradient across the myocardial cell membrane, thereby altering the function of aCa2+-Na+exchanger.This exchanger pumps Ca2+out of the cell against an electrochemical gradient in exchange for Na+moving into the cell down an electrochemical gradient. (Recall that Ca2+-Na+exchange is one of the mechanisms that extrudes the Ca2+that entered the cell during the plateau of the myocardial cell action potential.) The energy for pumping Ca2+uphillcomes from thedownhillNa+gradient, which is normally maintained by the Na+-K+ATPase. When the intracellular Na+concentration increases, the inwardly directed Na+gradient decreases. As a result, Ca2+-Na+exchange decreases because it depends on the Na+gradient for its energy source.
4.As less Ca2+is pumped out of the cell by the Ca2+-Na+exchanger, theintracellular Ca2+concentration increases.
5.Since tension is directly proportional to the intracellular Ca2+concentration, cardiac glycosides produce an increase in tension by increasing intracellular Ca2+concentration—apositive inotropic effect.

71
Q

excitation-contraction coupling

A

cardiac action potential
Ca2+ enters cell during plateau
Ca2+ induced Ca2+ release from SR
Ca2+ binds to troponin C
cross bridge cycling so could lead to Ca2+ reaccumulated in SR then relaxation
or leads to tension

Medicine Unit 4 (19 decks)

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