Anti-Arrythmics General Flashcards
What is the general “goal” of anti-arrythmic drugs?
We want to slow down the HR and lengthen the action potentials. The idea here is, since it is impossible to trigger a second action potential when the first one is still active, if the HR is slow and the AP is wide, we reduce the chances of triggering a second AP.
What is Effective Refractory Period (ERP)?
This is the time between just when depolarization begins all the way through when repolarization ends.
What is happening to the Na gates at -90 mV?
The M gate is closed, the H gate is open, and therefore there is 0 conductance of sodium through the channel at -90.
How does the fast Na gate go from -90 to -70 if there is no conductance of Na through the channel? (In cardiac myocytes) What happens at -70 mV>
The SA and AV nodes will allow for the slight depolarization through their seperate APs, and at -70 the threshold potential is reached, the M gate quickly snaps open and H gate remains open, allowing sodium conductance.
What happens at threshold potential (-70 mV) to fast gated sodium channels?
M gate snaps open, H gates remain open. Na can rush into the cell to cause depol.
What happens once the M gates open in the fast gated sodium channels while still in depol?
The h gates slowly closes, which prevents Na from entering the cell so once again conductance to Na becomes 0.
What happens to the H gates when it closes?
It stays closed throughout the cycle until the Na/K pump kicks in and pumps 3 Na out and 2K in and brings the cell potential to about -85 mV.
At what voltage does the M gates closes? When does it open?
Around -50 mV it closes at repol, at threshold (-70 mV) it opens during depol.
What causes the H gates to open and close?
It opens at -85 mV and when the cell remains depol it slowly starts to close.
Why are cells in the heart “refractory?”
Once the Na channels are inactivated it will remain so until another action potential is fired during depol.
Describe the Resting/Ready, Open/Active, and Inactive/Refractory states of the fast gated sodium channels.
Resting/Ready: M gates closed, H gates open, Open/Active: M and H gates open, Inactive/Refractory: M open H closed.
What are Class 1 drugs, and specifically 1A, 1B, 1C?
Class 1 are “Voltage dependant Na channel Blockers.” 1A hits the active, 1B blocks the inactive, and 1C hits the ready states of the sodium channels, however 1C is not specific it can also hit the open and inactive.
What happens in hypoxic tissues (with respect to cardiac tissues). How are the sodium channels in this state? Which class of anti-arrythmics (of class 1) help?
The sodium pump requires ATP to work so if hypoxic, sodium pump doesnt work, Na stays in the cell and the cell remains depolarized. And so, the channels will be in the inactive form and thus we want type 1b.
What is the fundamental effect on the cardiac myocytes that Class 1A drugs will do?
Increase action potential duration and thus increase effective refractory period. It will make the slope of phase 0 less steep (decrease the slope).
What is the secondary effect of class 1A drug besides blocking the open state of the fast gated Na channels?
Block K channels so it would increase the duration of repolarization.
