S1W1 L2 Electrical activity of the heart Flashcards
extracellular and intracellular conc of Na (mM)
140, 10
extracellular and intracellular conc of K (mM)
4, 140
extracellular and intracellular conc of Ca (mM)
1.2, 0.0001
equilibrium potential/ Nernst potential
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
Na, Ca, K equilibrium potentials
+70mV
+12mV
-94mV
So, if cell is held at -94mV,
no net K movement in or out of cell
what is resting membrane potential
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
what are the electrical properties of a tissue dependant on
which ion channels are expressed in the membrane
when does the fast voltage gated Na+ channels open and effect
-70mV
activated and inactivated rapidly
inward membrane current generated
two ion channels which move Na+ back out of the cell
Na+/K+ pump
Na+/ Ca2+ exchanger
2 types of cardiac Ca2+ channels
T-type and L-type
T type Ca2+ channel
tiny conductance and transient openings
opens at -55mV, inactivate fairly rapidly
L type calcium channel
large conductance and long lasting openings
found throughout heart
open at -40mV and inactivate more slowly
direction and effect of K current
outward
make cell more negative inside
helps with repolarisation
why does K+ exert most control over resting and action potential duration
cell at rest is more permeable to K+
three main K+ currents:
background K+ current
delayed K+ currents transient outward K+ currents
what controls background K+ current
inward rectifying channel (Kir)
resting outward current (I kin/ Ik1)
when do background K+ channels open and their function
- voltages
help set stable - resting membrane potential of atria and ventricular myocyte
when do delayed K+ current and transient outward k+ current channels close
and function
close at negative voltages
open when cell becomes more +
open to help repolarise cell after AP
is the current voltage relationship for background current linear
no
why do efflux of K+ ions not occur as cell becomes more positive past equilibrium potential
regulation by ion channel itself
magnesium ions
polyamines
why is it important K+ doesn’t efflux out of cell
many consequences of K+ loss from cell
background current ib
inward background current of mostly Na+
causes cell to be slightly higher than Ek
funny current if
permeable to Na and K
activated at hyperpolarisation
ventricular myocyte resting potential
-85/-90mV
stable
ventricular myocyte AP: what channels are open at negative potentials and set resting membrane potential close to Ek
ik1
ikir
ventricular myocyte AP: what is the rapid depolarisation due to
opening of voltage gated Na+ channels
ventricular myocyte AP: what channels close as Na+ permeability increases
background K+ channels
ventricular myocyte AP: as cell becomes more positive due to Na+ influx, what channels transiently open
ito
voltage gated K+ channels
ventricular myocyte AP: what channels open when membrane potential reaches -40mV and effect
L type Ca2+
calcium enters cell
causing plateau phase
ventricular myocyte AP: when the cell is the most pearmeable to Ca2+, it is least permeable to
K+
ventricular myocyte AP: what is repolarisation brought about by
K+ permeability increases
ikr, iks
voltage gated delayed K+ channels
ventricular myocyte AP: when membrane potential is close to resting level, what occurs
background K+ channels open again to keep resting membrane stable
conducting system AP: how is AP initiated
autorhythmic/ pacemaker cells
conducting system AP: dominant pacemaker cell?
SAN
SAN AP: why is there no stable resting membrane potential
background K+ channels are absent
SAN AP: max diastolic potential?
-60mV
SAN AP: what is known as pacemaker potential?
slow depolarisation towards threshold of -40mV
SAN AP: three phases
upstroke
repolarisation
period between AP
SAN AP: what four overlapping currents make up SAN AP
funny current (if)
T type Ca2+ current
L type Ca2+ current
decay of delayed K+ channel permeability
SAN AP: what currents are occurring in phase 4 (period between APs)
iCa (T)
if
SAN AP: what channels open at -40mV
L type Ca2+
depolarises cell
SAN AP: what is repolarisation induced by
closure of L type Ca2+ channels
opening of delayed K+ channels
what is the pacemaker potential of the when SAN isolated
100 beats per min
what is the pacemaker potential of the AVN when isolated
40 beats per min
what is the pacemaker potential of the purkinje fibres when isolated
20 beats per min
what cells can initiate a heartbeat
any cardiac cell with pacemaker ability
how long does it roughly take for SAN to initiate AP in the rest of the heart
150-200ms
what is the absolute refractory period of the SAN AP driven by
inactivation of Na+ channels,
almost as long as contraction phase,
can change depending on AP duration
