Antiarrhythmetic Drugs #1 Flashcards Preview

Pharmacology - Test #4 > Antiarrhythmetic Drugs #1 > Flashcards

Flashcards in Antiarrhythmetic Drugs #1 Deck (50):
1

Difference between the resting potential of a pacemaker cell and a ventricular myocyte

PM cells normally sit at a more depolarized resting potential

2

PM action potentials are dependent on __ influx

Ca

3

Talk through the ion motion in a PM cell

Phase 0 - Upstroke from L-type Ca channels
Phase 3 - Repolarization by voltage gated K channels
Phase 4 - Depolarization by "funny currents" performed by HCN channels and ACh-gated K chanels

4

beta adrenergic receptor stimularion results in....

increased cAMP, increases HCN channel activity
Incrased PKA, more P of L-type Ca channels, lets channels open at more negative potentials and let more Ca thru

5

What does acetylcholine do to the heart

- Turns on M1, which inhibits cAMP, activated GIRK
- GIRK lets more K inward, hyperpolarizing, clamping membrane potential
- Less cAMP reduces HCN, less amp. of Ca dependent spikes

6

Phases of a myocyte action potential

Phase 0 -- Upstroke Potential (Na channels)
Phase 1 -- Brief Repo (transient outward notch)
Phase 2 -- Plateau (Inward Ca, some Na and K)
Phase 3 -- Repolarization (K currents dominate)
Phase 4 -- Time btw APs, slight depolarizationg units

7

Explain how the voltage gated Na Channels/Refractory Period works

Volatage gated channels have the m gate and the h gate
When hyperpolarized, M is closed and H is open
When first depolarized, M opens and Na rushes in
Shortly after opening, H gate closes, inactivating channel
Recovery -- Close the M, open the H

8

As you move later toward the end of a relative refractory period, a stimulus provides....

Stronger depolarization

9

Scale used to classify anti-arrhythmic drugs?

Vaugn-Williams-Singh Scale

10

Talk trough the Vaugn-Williams-Singh Scale

Class I -- Na Channel Blockers
Class II -- Beta adrenergic antag.
Class III -- K channel blockers, prolonging refrac. period
Class VI -- Ca Channel Blockers

11

Effects of Class II antiarythmics?

Beta Blockers slow PM and Ca currents in nodes
Increase the refractoriness of the nodes
Increase PR Interval (protecting vent. rate)
Stop arythmias involving catecholamines

12

Effects of Class IV antiarythmetics (AAs)?

Ca channel blockers increase frequency dependent block.
Increase the refractoriness of AV + PR interval
Protect vent. rate from atrial tachy

13

Beta blockers typically used to treat arythmia

Esmolol, Acebutolol, Propanolol

14

Important Esmolol details

Cardioselective with a short half life
IV

15

Important Acebutolol details

Cardioselective
Sympathetomimetic Partical Agonist
Weak Na channel Blockade

16

Important propanolol details

non-selective, weak Na blockage

17

Why would you pick beta blockers to treat an arrythmia?

Arrythmia involves catecholamines
Atrial Arrhythmia
Post MI -- Prevent Ventricular Arr.
Prophylaxis in long QT

18

Two Ca blockers used as AAs?

Verapamil
Diltiazem

19

Verapamil Mechanism of Action

Frequency Dependent Block of Calcium Channels
Accumulation of blockade in rapidly depolarizing tissues (tachy)

20

Diltiazem mechanism of action

Blocks reentrant arrythmias involving the AV (increases refractoriness)
Protects ventricular rate in A Flut and A Fib

21

Ca channel blockers are used chiefly to...

Protect ventricular rate in atrial flut and fib by increasing refrac. of the AV node

22

Which classes of drugs influence myocyte action potentials

Class 1 -- Na channel blockers
Class 3 -- K channel blockers

23

Review the appearance of the curves on page 26

pretty please

24

Effects of Class 1A

Mixed Na/K block
Blocks open state
Moderate, Incomplete dissociation
Widened QRS, Prolonged QT

25

Effects of Class 1B

Na channel Block
Blocks Open and Inactivated State
Rapid, Complete dissociation
Narrowed AP, normal EKG

26

Effects of Class 1C

Strong Na channel block
Blocks Open State
Very slow dissociation
Marked QRS widening

27

Important examples of 1A

Quinidine
Procainamide
Disopyramide

28

Important examples of 1B

Lidocaine
Tocainide
Mexilitine

29

Important examples of 1C

Propafenone
Flecainide

30

Risks of Class 1A drugs

Quinidine - Torsades de Pointes, Anti Musc.
Procainamide - Lupus-like, Gang. blocker
Disopyramide - Anti-musc.

31

Risks of Class 1B drugs

Lidocaine - IV, rapidly control of vent. arr.

32

Risks of Class 1C

Propafenone - Vent and Sup. vent use. beta-blocking activity

33

How do class 3 AAs work?

Block K channels, prolonging action potential + QT interval
Increase in Effective Refractory Period, which can terminate reentry in a re-entrant circuit

34

Significance of Torsade de pointes (TDP)

Arrhythmia that can develop because of Class 3 agent administration or use of a drug that blocks HERG channel.

35

Early after depolarizations (EAD) are capable of...

Giving Rise to triggered upstrokes and ectopic action potentials, potentially setting up a re-entry arrhyth.

36

The five given Class 3 anti-arrhythmetic drugs

Amiodarone
Dronedarone
Ibutilide
Sotalol
Dofertilide

37

Important details for Amiodarone/Dronedarone

Effects like all classes, but mostly 3
Used in emergency ventricular + atrial arr, A fib prev.
Long half life (weeks)
Amiodarone -- Can cause hypothyroid, pulm fibrosis
Dronedarone is similar, but with less toxicitiy

38

Important Ibutilide details

Can cause TDP
Rapid Conversation of A Fib/Flut to normal rhy

39

Important details for Sotalol

Can cause TDP
One isomer as beta-blocking activity
Life threatening vent. arr. or maintenence of normal rhy.

40

Important details about dofetilide

High risk of TDP, drug restricted, used infrequently
Atrial arrythmia
Requires special training/certification to administer/monitor

41

Sources of Long QT Syndrome (LQTS)

Drug Induced
Electrolyte Imbalances
Bock of HERG Channel

42

Some drugs that are associated witi TDP

antiarr, antibiotics, antineoplastics, Ca blockers, opiates, antihistamines, antipsychotics

43

Clinical use of Amiodarone

A-fib
Suppression post-MI vent arr.

44

Clinical use of Dronedarone

A fib

45

Clinical use of Sotalol

Prevent A fib reoccurance

46

Clinical use of Ibutilide

Convert A fib to sinus rhythm

47

Important digoxin details?

Direct inhibition os AV node

48

Important Magnesium Chloride details?

Treat hypomagnesemia
Convert TDP
Prevent MI and Digoxin Arr.

49

Important details of Potassium Chloride

Hypokalemia reduces Ikr current
Prolong action potentials and can be proarrhythmetic

50

Important details of Adenosine

Similar to M2 muscarinic activiation, depresses PM
Suppresses Atrial tachycardia
Short half-life, given IV