Na Channels blockers

Question 1

What does ischemia lead to on a cellular level?

Answer 1

Decreased O2 in tissue

• Cellular Hypoxia
• Mitochondria damage
• Diminished Intracellular ATP

Question 2

Why is ATP so important for cardiac function?

Answer 2

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

Question 3

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

Answer 3

Pumps more 3:2 Na:K ions out than K ions in.

• Net loss of + charge
• leads to increasing negativity
• Repolarization happens

Question 4

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

Answer 4

cells stays more positive and doesnt repolarize

Question 5

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

Answer 5

Activates K+ATP channels which open at reduced values of ATp

- Allows outflow of K+ so cells can depolarize

Question 6

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

Answer 6

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+

Question 7

What does decrease in ATP do the Action Potential curve?

Answer 7

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

-shape determined by specific perm to diff ions

Question 8

What does decrease in ATP do to the sodium channels?

Answer 8

Channel is dependent on membrane potential

• More positive membrane means channels become inactivated
• Slower channel recovery

Question 9

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

Answer 9

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

• Decrease CONDUCTION velocity

** Altered impulse conduction

Question 10

What does slowed conduction lead to?

Answer 10

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

Fixed: scarring or fibrosis replaces myocyte

Question 11

What is accommodation?

Answer 11

Fast response action potential begins to looks like slow response AP

-Leads to altered impulse formation

Question 12

What can the altered impulse formation lead to?

Answer 12

Display spontaneous depolarization and automaticity

• Thus can lead to ectopic beats or arrhythmia

Question 13

What can ischemia thus lead to?

Answer 13

Depolarized membrane potential that can potentially create arrhythmias

Question 14

What are the MOA of antiarrhythmics?

Answer 14

Reduced pacemaker activity

- modify conduction/refractoriness

Question 15

How doe we deal with reentry?

Answer 15

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

Question 16

What are the Class 1 drugs MOA?

Answer 16

Na Channel blockage

- Alters AP duration and kinetics of Na Channel blockage

Question 17

What are the Class II drugs and their MOA?

Answer 17

Beta-Andrenoceptor Blockade

-Blocks the SNS effects on the heart

Question 18

What are the Class II drugs and their MOA?

Answer 18

K channel blockage

- Prolongation of the effective refractory period

Question 19

What are the Class IV drugs?

Answer 19

Ca channel blockade

- slows conduction where depole is Ca dependent

Question 20

What do Na channel blockers do the AP curve?

Answer 20

Elongates phase 0

• Slows conduction
• binds to channels in the the inactivated state

Question 21

What doe K channel blockers do the AP curve?

Answer 21

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

Question 22

How do we deal with accommodation?

Answer 22

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

Question 23

What do Ca channel blockers do the AP curve?

Answer 23

Slows influx of Ca by blocking L-type channels

- allows Na to take back over for repole

Question 24

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

Answer 24

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

• only affect non-nodal tissues

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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

Question 27

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

Answer 27

C>A>B

Question 28

Which class 1 subdivision is best at increase the ERP?

Answer 28

A>C>B

Question 29

Class 1A kinetics with Na channel and effect?

Answer 29

Intermediate rate

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

Question 30

Class 1B kinetics with Na Channel and effect?

Answer 30

Rapid rate

• Shorten refractory period (phase 3)
• Decreases duration of AP

Question 31

Class 1C kinetics with Na channel and effect?

Answer 31

Slow rate

• Markedly slows phase 0 Depole
• No effect on refractory

Question 32

What are class II Beta Andrenoceptor blockers mainly used for?

Answer 32

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

Question 33

What are Beta blocker effects?

Answer 33

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

Question 34

What suffix do beta blockers end in?

Answer 34

olol

Question 35

What is propranolol AE’s?

Answer 35

Adverse effects include bronchospasm, bradycardia, fatigue

Question 36

What is Acebutolol mainly used for?

Answer 36

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

Question 37

What is Esmolol used for?

Answer 37

short acting blocker used primarily for intraoperative and acute arrhythmias

Question 38

What is Sotalol for?

Answer 38

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