093014 electrophysiology Flashcards
in non pacemaker cells of heart, what is responsible for the rapid upstroke of the action potential?
sodium entry-phase zero
calcium enters cell through calcium channel during what phase of muscle cell AP?
2
what contributes to the resting potential (phase 4) of nonpacemaker cells?
potassium
funny channel or HCN is activated during when
hyperpolarization in pacemaker cell–turned on by repolarization of membrane potential and you get increase in sodium conductance
after the inactivation gate on a sodium channel closes, what enables the activation gate to close and the inactivation gate to reopen again?
repolarization-as high negative membrane voltages are reachieved
resting potential of cardiac muscle cell is determined by
balance btwn concentration gradient and electrostatic forces for potassium b/c only potassium channels are open at rest
equilibrium potential of cardiomyocyte
-90mV
what is the major current passing through gap jxn in cardiomyoctyes?
Na+ current–spreads depolarization to neighboring cells
what contributes to the electrical delay btwn SA and AV nodes?
slower spread of depolarization by Ca2+ to neighboring cells
what can decreases pacemaker rate and slow conduction rate through AV node?
G protein activated K+ current (an inward K+ current mediated by GIRK K+ channels and regulated by acetycholine)
when is the If channel activated?
by hyperpolarization during phase 3 in pacemaker
delayed rectifier channels
allow potassium to flow out of cell and causes you to see the repolarization in phase 3 of cardiac cell AP
why is the SA node the dominant pacemaker?
because its cells have the fastest intrinsic spontaneous depolarization. normal resting rate sinus rhythm of 60-100 bpm
when does calcium influx occur in pacemaker action potential?
phase zero-once Na+ allows for reaching of threshold
why is upstroke of phase zero less rapid than in nonpacemaker cells?
because the current represents calcium influx through the relatively slow calcium channels
speed of action potential upstroke divides cardiac cells into two types
slow response cells (SA, AV nodal cells)
fast response cells (atrial and ventricular myocytes, Purkinje cells)
compare conduction velocities for fast response and slow response cells in heart
slow response has slow conduction velocity
fast response has faster conduction velocity
resting membrane potential of slow response cell
-40 to -70 mV
what causes spontaneous depolarization in SA node?
pacemaker channels (HCN channels)
these channels are modulated by ANS (Ach activates Gi inhibitory unit, so suppresses cAMP, so slow down or close off the channel)
Ito K+ channel
for early outward K+ current in atrial and ventricular cells. contributes to phase 1
effect of Ach on SA node
decreases If current, reducing steepness of phase 4
opens GIRK channels, increasing K+ conductance and making the diastolic potential more negative
reduces calcium current, reducing the steepness of phase zero and moves threshold to more positive value
norepinephrine effect on heart
increases calcium current, increases calcium influx, increases ca induced ca release from SR–so INOTROPIC EFFECT
increase If, increases ICa
mechanisms for altering heart rate
decrease rate of depolarization
decreas maximum diastolic potential
decrease calcium channel activity-changes upstroke of phase zero
effect of beta adrenergic/cholinergic on SA node
conduction velocity
pacemaker rate
cholinergics have little effect on what part of the heart?
atrial and ventricular muscle
effect of resting potential on speed of depolarization in muscle cardiac cell
if you have more inactivated sodium channels (so higher resting potential), then you have have a slower speed of depolarization
calcium channel blockers do what
decrease contractility of heart muscle
decrease entry of calcium and delay depoloarization of SA and AV nodal cells
beta blockers do what
prevent calcium entry into the cell–decreases heart rate, conduction velocity and strength of contraction
