Electrical activity of the heart Flashcards
(71 cards)
1
Q
driving forces
A
difference between the membrane potential (Em) and the ions equilibrium potential (Ex)
2
Q
ion current Ix
A
occurs when there is movement of an ion across the cell membrane
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
4
Q
resting membrane potential
A
potential difference that exists across the membrane of excitable cells at rest
5
Q
what is the value of resting membrane potential
A
-70mV to -80mV
6
Q
what is membrane potential expressed as
A
intracellular potential relative to extracellular potential
7
Q
what do you need to know for Nerst. equation
A
-95 for potassium
+65 for sodium
+120 for calcium
8
Q
most predominant intracellular ion
A
potassium
9
Q
potassium movement in chemical gradient
A
diffuses down the chemical gradient
diffuses out
10
Q
potassium movement in electrical gradient
A
diffuses into the cell
11
Q
calcium chemical gradient
A
into the cell
12
Q
calcium electrical gradient
A
out of the cell
13
Q
sodium chemical gradient
A
into the cell
14
Q
sodium electrical gradient
A
out of the cell
15
Q
calculating ion current
A
Ix= Gx (Em-Ex)
Gx= ion conductance (1/ohm)
Em-Ex= driving force on ion
16
Q
ohms law
A
V=IR
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
18
Q
action potential positive terms
A
depolarisation
inward current
threshold potential
overshoot
19
Q
depolarisation
A
less negative
20
Q
negative action potential terminology
A
hyperpolarisation
outward current
undershoot/repolarisation
refractory period
21
Q
hyperpolarisation
A
more negative
22
Q
threshold potential
A
point where action potential occurs
23
Q
refractory period
A
no action potential
24
Q
absolute refractory period
A
overlaps with almost entire duration of the action potential
25
why can no more action potentials occur in refractory period
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
26
relative refractory period
begins at the end of the absolute refractory period and overlaps primarily with period of the hyperpolarisation
27
what occurs during relative refractory period
action potential can be elicited but only if a greater than usual depolarisation current is applied
28
basis of relative refractory
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
29
propagation
wave of depolarisation spreads via gap junctions
30
types of muscle cells in heart
contractile cells
conducting cells
31
SA node
primary pacemaker
32
AV node
slow conduction
33
bundle of his, pukinje system, ventricles
fast
34
sinoatrial node
AP duration 150 ms
upstroke: inward Ca current with inward Ca channels
no plateau
phase 4 depolarisation: inward Na current, normal pacemaker
35
atrium
action potential duration: 150 ms
inward Na current
plateau: inward Ca current, slow inward current, L-type ca channels
no phase 4 depolarisation
36
ventricle
250ms
inward na current
plateau: slow inward ca current, L-type ca channels
no phase 4 depolarisation
37
purkinje fibres
300ms
inward na current
plateau: inward ca current, slow, l-type channels
latent pacemaker
38
phase 0
upstroke, rapid
depolarization, Na+ influx
39
phase 1
nitial repolarization, Na+
influx stops & K+ efflux
40
phase 2
plateau, stable
depolarization, Ca2+ influx & K+
efflux
41
phase 3
repolarization, Ca2+ influx
stops & K+ efflux
42
phase 4
esting membrane
potential, or electrical diastole,
43
features of the Sa node action potential
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
cardiac action potential Sa node
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
sinoatrial node, pacemaker action potential
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
latent pacemaker
cells in Sa aren't only myocardial cells with intrinsic automaticity
latent pacemakers also have capacity for spontaneous phase 4 depolarisation
47
latent pacemakers
opportunity to drive heart rate only if SA is suppressed or intrinsic firing rate of latent pacemaker becomes faster than the SA node
48
effects of autonomic nervous system on heart rate
chronotropic effects
49
what is in the image q
positive chronotropic
50
what is in the image
negative chronotropic effects
51
positive dromotropic effect
increase in conduction velocity through AV node
52
negative dromotropic effect
decrease in condition velocity through AV node
53
what are dromotropic effects
effects of the autonomic nervous system on conduction velocity
54
myocardial cell structure
55
contractility
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
amount of Ca released from SR depends on what
the size of the inward Ca2+ current
the amount of Ca2+ previously stored in the SR for release
57
what are inotropic effects
effects of the autonomic nervous system on contractility
58
positive inotropic effect
increase in contractility
59
negative inotropic effect
decrease in contractility
60
sympathetic action receptor and mechanism on the heart rate
increases
beta 1 receptor
increases If and ICa
61
sympathetic action receptor and mechanism on conduction velocity
increases
beta 1
increases ICa
62
sympathetic action receptor and mechanism on contractility
increases
beta 1
increased Ica and phosphorylation of phospholamban
63
sympathetic action receptor and mechanism on vascular Smooth muscle (skin renal and splanchnic)
constriction
alpha 1
64
sympathetic action receptor and mechanism on vascular smooth muscle (skeletal)
dilation with B2
and constriction with alpha 1
65
parasympathetic action receptor and mechanism on heart rate
decreased
m2
decreased If and increased K.ACh and decreased ICa
66
parasympathetic action receptor and mechanism on conduciton velocity
decreased
m2
decreased Ica and increased Ik.Ach
67
parasympathetic action receptor and mechanism on contractility
decreased in atria only
m2
decreased ICa
increased IKAch
68
all vascular smooth muscle parasympathetic action receptor
dilation releasing EDRF
M3
69
EDRF, ICa, If, IK-Ach
endothelial derived relaxing factor
inward calcium ion current
inward sodium ion current
outward potassium ion current
70
mechanism of action of cardiac glycosides
1. The Na + -K + ATPase is located in the cell membrane of the myocardial cell. Cardiac glycosides inhibit Na + -K + ATPase at the extracellular K + -binding site.
2. When the Na + -K + ATPase is inhibited, less Na + is pumped out of the cell, increasing the intracellular Na + concentration.
3. The increase in intracellular Na + concentration alters the Na + gradient across the myocardial cell membrane, thereby altering the function of a Ca 2+ -Na + exchanger. This exchanger pumps Ca 2+ out of the cell against an electrochemical gradient in exchange for Na + moving into the cell down an electrochemical gradient. (Recall that Ca 2+ -Na + exchange is one of the mechanisms that extrudes the Ca 2+ that entered the cell during the plateau of the myocardial cell action potential.) The energy for pumping Ca 2+ uphill comes from the downhill Na + 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, Ca 2+ -Na + exchange decreases because it depends on the Na + gradient for its energy source.
4. As less Ca 2+ is pumped out of the cell by the Ca 2+ -Na + exchanger, the intracellular Ca 2+ concentration increases.
5. Since tension is directly proportional to the intracellular Ca 2+ concentration, cardiac glycosides produce an increase in tension by increasing intracellular Ca 2+ concentration—a positive inotropic effect.
71
excitation-contraction coupling
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
