13. Cardiac AP & Conduction Flashcards
what is the order an AP spreads in the heart
SA node
AV node
bundle of his
R/L bundle branches
purkinje fibers
where is AP generated most frequently in the heart
SA node
= pacemaker
what is overdrive suppression
higher freq of SA node firing suppress other pacemakers (like AV node)
aka: SA node trigger AP in AV before it can fire itself
*something wrong with the SA node- then AV node will take over
what are the pacemaker qualities of the AV node & purkinje fibers
AV node: less freq that SA node
purkinje fibers: least freq, asynchronous contraction
rate the velocity of the fibers of the heart
purkinje > atrial/ventricular M > AV
depends on fiber diameters - larger = faster
which part of the heart contracts milisecs before the other side
RA before LA
endocardium before epicardium
RV epicardium before LV epicadium
why is it preferred that the endocardium contract prior to the epicardium
b/c want to push blood up and out
what is the current at phase 0 & 1
Na current
-Vg Na channels open for depol
what is the reason for the rapid/partial repol at the peak of phase 1
transient outward K+ current
what phase is a result of L-type Ca channels opening
phase 2 & 3
slow to open and reapin open for specific amount of time & then close (–> causing transition to phase 3)
what is inward rectifying current
Vg-K channels that are open at RMP & close and particular Vg (phase 2)
-open again in phase 3 & slow to close
What current denotes phase 3 only
rapid K & slow K current
Vg gated contribute to repol
what current accounts for phase 4
K leak channels
what is the funny Na current
rise in mem potential
open after certain repol vg reached & close at threshold
-lead to continous, rhythmic firing
what are the characteristics of the Vg Na channels
quick to open & quick to close at threshold
have activation gate (opened at threshold)
& inactivation gate (close quickly after activation gate opens –> will not allow another AP until it opens again = Abs refractory period)
when do L type Ca channels open and clsoe
open at threshold - high current
-and slow down (start closing) –> complete closure at end of phase 2
when does transient outward K current happen
K channels open at phase 0 & close rapidly to get the peak at phase 1
-makes sure mem. potential doesnt overshoot
What happens when vg K channel current peaks
transition from phase 2 to phase 3
What are the steps of the inward rectifying current (starting from before threshold)
- open - let K out of cell
- —> cell depol & channels close in phase 0 to help maintain phase 2
- —> open again at particular Vg to help with phase 3
What currents contribute to phase 2
=Ca current in
K current out
inward rectifying current (closed channels)
when does contraction happen in relation to AP
slightly delayed - so happens after AP
to help get Ca to M cells, etc
what happens to K leak channels during phase 2
increased outward current
how is phase 4 of SA/AV nodes different from other APs
gradually depol unti reaching threshold (funny Na current)
= intrinsic, spontaneous depol –> = pace maker
what happens in phase 0 of the SA/AV nodes
Vg Ca open –> depol (NOT Na)
close rectifiers (Vg K channels)
what channels are open/closed during phase 3 of the SA/AV node
close - Vg Ca
open- Vg K (rectifier & traditional)
what is the cause of the absolute refactory period (ARP)
inactivation gates of Na channel closed
when can you have an AP during RRP? What will the AP look like
w/ greater stimulus
= smaller/weaker
what is SNP
as you repolarize, inactivation gates eventually reset - so these channels can fire even if not completley repolarized
==> dont need as much stimulus bc youre already close to threshold
-AP will still be smaller/weaker tho
how can arrythmias occur
in beats are happening too closely
-rapid firing of APs
what is the chonotropic effect determined by
depolarization of phase 4
faster = + chonotropic
slower = - chonotropic
=effect changes in HR
what can be determined by slope of phase 0
dromotropic effects
= effect speed of conduction
steeper slope = quicker conduction
what is inotropic
effect strength of M contraction
what is lusitropic
effect rate of M relaxation
what occurs in parasym stimuluation of the SA/AV node
neg chronotropic effect: slower funny Na current & hyperpol of SA node by increasing outward K current (Ach K channels)
neg dromotropic effect: decrease inward Ca current & increase outward K current (Ach K channels)
what happens with sym stimulus of the SA/AV nodes
pos chronotropic effect: more rapid opening of funny Na channels
pos dromotropic effect: increased inward Ca current
