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Flashcards in Na Channels blockers Deck (38):

What does ischemia lead to on a cellular level?

Decreased O2 in tissue
- Cellular Hypoxia
- Mitochondria damage
- Diminished Intracellular ATP


Why is ATP so important for cardiac function?

Provided energy needed for the Na+/K+/ATPase transport pump


What is the purpose of the Na/K/ATPase pump?

Pumps more 3:2 Na:K ions out than K ions in.
- Net loss of + charge
- leads to increasing negativity
- Repolarization happens


What happens when this Na/K/ATPase pump goes out?

cells stays more positive and doesnt repolarize


What do the cells do the compensate for the loss of ATP?

Activates K+ATP channels which open at reduced values of ATp
- Allows outflow of K+ so cells can depolarize


What is the net effect of the K+ATP channels?

Too much extracellular K+ and Too much Na+ intracellulary (backwards)

- More positive (less negative) and thus depolarized
- Leads to delayed depolarization and quicker repole
- High intracellular Ca 2+


What does decrease in ATP do the Action Potential curve?

Depolarization slope is less steep and the repole (refractory period) shortens

-shape determined by specific perm to diff ions


What does decrease in ATP do to the sodium channels?

Channel is dependent on membrane potential
- More positive membrane means channels become inactivated
-Slower channel recovery


How does the affect sodium channels due to decreased ATP lead to Action potential curve changes?

Less sodium channels open to cause the depolarization (curve is less steep)

- Decrease CONDUCTION velocity

** Altered impulse conduction


What does slowed conduction lead to?

Unidirectional block
If functional: Impulse reaches tissue that is still in refractory state from previous stimulation

Fixed: scarring or fibrosis replaces myocyte


What is accommodation?

Fast response action potential begins to looks like slow response AP

-Leads to altered impulse formation


What can the altered impulse formation lead to?

Display spontaneous depolarization and automaticity

- Thus can lead to ectopic beats or arrhythmia


What can ischemia thus lead to?

Depolarized membrane potential that can potentially create arrhythmias


What are the MOA of antiarrhythmics?

Reduced pacemaker activity
- modify conduction/refractoriness


How doe we deal with reentry?

-Slow conduction further
-Speed conduction
-Alter effective refractory period


What are the Class 1 drugs MOA?

Na Channel blockage
- Alters AP duration and kinetics of Na Channel blockage


What are the Class II drugs and their MOA?

Beta-Andrenoceptor Blockade
-Blocks the SNS effects on the heart


What are the Class II drugs and their MOA?

K channel blockage
- Prolongation of the effective refractory period


What are the Class IV drugs?

Ca channel blockade
- slows conduction where depole is Ca dependent


What do Na channel blockers do the AP curve?

Elongates phase 0
- Slows conduction
- binds to channels in the the inactivated state


What doe K channel blockers do the AP curve?

Slows the efflux of K during phase 3 prolonging the refractory time of the cell
- Repole takes longer


How do we deal with accommodation?

Change cell from altered Ca dependent back to Na dependent depole by altering Ca2+ perm.


What do Ca channel blockers do the AP curve?

Slows influx of Ca by blocking L-type channels
- allows Na to take back over for repole


What are Class 1 useful for? Which tissues do they affect?

treating tachycardias
- increases type needed for phase 0 (decreases slope and amplitude)

- only affect non-nodal tissues


What is the reason for subclasses of Class 1 Na blockers?

Affects action potential duration (APD) and effective refractory period (ERP)
- Diff affects on slope of phase 0


What is the effects of ERP from Na channel blockers from?

specific secondary activity of these drugs on efflux of K+ in phase 3


Which subdivision of class one is best at Na channel blockage?



Which class 1 subdivision is best at increase the ERP?



Class 1A kinetics with Na channel and effect?

Intermediate rate
- slow rate of rise of AP (phase 0)
- Prolongs AP (increase refractory)


Class 1B kinetics with Na Channel and effect?

Rapid rate
- Shorten refractory period (phase 3)
-Decreases duration of AP


Class 1C kinetics with Na channel and effect?

Slow rate
- Markedly slows phase 0 Depole
-No effect on refractory


What are class II Beta Andrenoceptor blockers mainly used for?

Prevent and treat supraventicular arrhythmias and reduce ectopic depole and sudden death in pts with MI


What are Beta blocker effects?

-Slow heart
-Decrease AV node conduction
-Increase the AV node refractory period
-Little to no effect on ventricular conduction and repolarization


What suffix do beta blockers end in?



What is propranolol AE's?

Adverse effects include bronchospasm, bradycardia, fatigue


What is Acebutolol mainly used for?

better for use in patients with asthma (to avoid the adverse effects such as bronchospasm


What is Esmolol used for?

short acting blocker used primarily for intraoperative and acute arrhythmias


What is Sotalol for?

nonselective β-blocking drug that prolongs the action potential (delays the slow outward current of K+)