Cardiology 7.6 Flashcards
inward current do what to cell
depolarize
outward current do what to cell
repolarize
calcium current is voltage gated channel but modulated by
ligand gated channels
as AP is depolarizing what happens to the voltage channels
have a voltage threshold
what does calcium current do for plateau phase of AP
stays open
if you express calcium current in nerve cell can make it look like
cardiac cell
9:37
helps maintain
triggers relese of calcium from SR (calcium induced calcium release)
without calcium release cardiac cell will not
contract
sodium channels stay inactivated throughout
most of AP
what accounts for refractory period
sodium channels inactivated
depol cell and if nothing else happened what would happen to membrane potential if no potassium channels?
just shutting off sodium channels does not cause repol. so it wouldn’t repol.
whether membrane potential is depolarizing or repolarizing depends on net
ionic current
if inward current and outward currents whether big or small, if they are equal and opposite, membrane potential will be
stable
during depol net current ha to be
inward
during repol net current has to be
outward
Ito
potassium current
Ito accounts for what
accounts for phase 1 of AP
what happens to rate of phase 1 if you block Ito
slower
Ik
potassium current
Ik1
potassium current
Ik1 accounts for what when open
resting potential
if you have resting potential cell has to have open ____ channels
potassium
what happens to Ik1 to help depol cell
closes
what happens to AP if you block Ik
AP would get longer
longer AP b/c of blocked Ik what time interval would increase
QT
long QT syndrome are prone to
particular arhythmia
antihistamine blocked an Ik and what did it do
caused death! b/c it blocked the Ik
all drugs have to be tested to see if they block
Ik
b/c of that histamine that blocked Ik channel and killed ppl
anti-arthmia in too high a dose can be pro-
arthymic
how does HR affect AP duration
when you increase HR, AP duration (and refractory period) they are inversely proportional
increase HR what happens to diastolic interval
decreased but is still preserved
SA node and AV node are
pacemaker cells
phase 4 of SA node
spontaneously depols and fires AP
what don’t we see in SA node
the big sodium currents
calcium currents are smaller
upstroke of SA node is generated by acrtivation of
Ica
calcium current
If
“funny current”
sodium ion channel
draw out currents of SA node
pg 83
if you gave toxic dose of calcium channel blocker what will it do
block the Ica current and SA node will stop firing
SA node pacemaker activity is elicited by small sodium current, opens when it repolarizies, inward current dpols cell and brings it to thrshold. calcium current helps dpol towards end. activation of calcium current generates upstroke.
.
main way to regulate heart rate is by
autonomic nervous system
how does epi and noepi increase HR
increase rate of diastolic depol
increase If and Ica
block all beta receptors in heart and what happens to HR
wouldn’t go up
how does acetylcholine decrease heart rate
slows rate of diastolic depol & hyperpol Vm
decrease If & Ica
increase Ik, Ach
Ach does what to heart
slows rate of depol and hyperpolarizes cell so moves further away from calcium current threshold
if you stimulate the vagus nerve you can stop what from firing
SA node
stop vagus nerve, then after a few seconds what happens
heart starts firing again b/c another pacemaker takes over
when pt has high or low HR it might not have anything to do with SA node but could be due to
autonomic input
beta 1 blockers will block effect of
sympathetic tone on HR and will slow HR
HR goes down with exercise due to
increased vagal tone
when HR above 100 beats/min called
tachycardia
if HR less than 60 Beats/min called
bradycardia
sinus arhymia means
SA node is driving the heart
gatekeeper b/w atria and ventricles
AV node
normally AP cannot propegate across
CT barrier (see pg 87)
wants conduction veloctiy reaches his bundles
it is very fast
atrial systole and ventricular systole is delayed b/c
it cannot pss through the CT it is blockin AV node
if ventricles are firing super fast what does AV node do
electrical filter, only allows certain ones through
bypass track
AP can go through and bipass
echo
10:07
rentry
echo
rentry is one of the most common causes of
arrhythmias
heart cells are electrically connected to
gap junctions
if gap junctions are closed
AP will not propagate
what can close gap junctions
calcium inside cell too high
pH too low inside
gap junction close would happen when
ischemia - oxygen falls CO2 goes up ATP down, lactic acid produced. calcium goes up and tends to close gap junctions
how does AP propagate in cardiac
initial AP is what starts the whole thing, then the rest fire the same. individual cells connected by gap junctions
bigger cells decrease intracellular resistance
faster conduction velocity
in AV node cells are smaller and what is conduction velocity
much slower
conduction velocity
if things in numerator go up it goes faster
if things in denominator go up it slows down
if amplitude is bigger
goes faster
small cells have ____ conduction velocity
slow
if resistance increases
onduction velocity decreases
if gap junction resistance (it’s closed down) then
conduction velocity slows
if threshold voltage moves in positive direction what happens to conduction velocity
decreases
lidocaine does what
sodium channel blocker
used at dentist
can also be used to help some arhythmias
if you slowly depolarize a cell (like ventricular) sodium channels will directly from
ready to go closed state to inactivation state (hyperkalemia)
if you depolarize cell to -50 mv the heart cell will not
fire AP
