B4.017 Prework 2 Electrophysiology of AV Node and EADs Flashcards
what does the magnitude of the L-type Ca current in the SA and AV nodes determine?
- threshold potential
- amplitude of the action potential
- rate of rise of the action potential
- conduction velocity: how quickly the AP propagates through the tissue (CV in the AV node determines the duration of the PR segment)
why do low ATP conditions impair Ca current?
L-type Ca channels must be phosphorylated during each AP (ATP dependent step)
impairment can occur with ischemia or hypoxia
effects of decreased Ca current in the AV node
reduce excitability of the AV node
decrease CV of the action potential in the tissue
underlying cause of AV node conduction blocks
discuss the 2 gates on a L-type Ca channel
- activation gate (opens and closes rapidly)
2. inactivation gate (opens and closes slowly)
what is the orientation of the Ca channel at rest
closed activation gate
open inactivation gate
what is a Ca window
overlap of calcium inactivation and calcium activation gate curves (time when both are open)
how does SYM stimulation affect the Ca window
increases Ca current by shifting activation curve towards more negative potentials
this means the activation gates open sooner during depolarization
larger Ca window
sequence of calcium channel gates
- resting w activation closed and inactivation open
- upon depolarization activation open and inactivation close slowly (ions flow)
- closure of inactivation ends phase 2
- activation and inactivation both closed
- inactivation opens after repolarization
when does the calcium window begin?
membrane potential corresponding to late phase 2 or early phase 3 of the ventricular AP
what is a potential problem created by the calcium window
inactivation gates may begin to open before all activation gates have closed
Ca2+ can move into the cell through those channels
this creates a depolarizing current and moves membrane potential more positive
consequences of EADs (early after depolarizations)
if Ca levels increase sufficiently , Ca could move through gap junctions to trigger abnormal depolarization in adjacent myocytes
are EADs normal?
no
normally the ventricle repolarizes (K+ current) quickly enough through the Ca window that activation gates close before there is enough time for inactivation gates to reopen
what happens if there is a suppression of the K+ repolarizing current?
EADs can occur more often due to the Ca window
what are some reasons for suppressed K+ current?
cocaine blocks delayed rectifier K channels, slowing the rate of repolarization
-also impairs reuptake of NE by SYM nerves, which increases Ca window
hypokalemia also decreases K+ and slows phase 3 repolarization
normal extracellular K+ conc
2.5-5 mEq/liter
