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

Antiarrhythmetic Drugs #1 Flashcards

1
Q

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

A

PM cells normally sit at a more depolarized resting potential

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2
Q

PM action potentials are dependent on __ influx

A

Ca

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3
Q

Talk through the ion motion in a PM cell

A

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

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4
Q

beta adrenergic receptor stimularion results in….

A

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

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5
Q

What does acetylcholine do to the heart

A
  • 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
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6
Q

Phases of a myocyte action potential

A

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

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7
Q

Explain how the voltage gated Na Channels/Refractory Period works

A

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

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8
Q

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

A

Stronger depolarization

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9
Q

Scale used to classify anti-arrhythmic drugs?

A

Vaugn-Williams-Singh Scale

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10
Q

Talk trough the Vaugn-Williams-Singh Scale

A

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

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11
Q

Effects of Class II antiarythmics?

A

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

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12
Q

Effects of Class IV antiarythmetics (AAs)?

A

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

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13
Q

Beta blockers typically used to treat arythmia

A

Esmolol, Acebutolol, Propanolol

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14
Q

Important Esmolol details

A

Cardioselective with a short half life

IV

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15
Q

Important Acebutolol details

A

Cardioselective
Sympathetomimetic Partical Agonist
Weak Na channel Blockade

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16
Q

Important propanolol details

A

non-selective, weak Na blockage

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17
Q

Why would you pick beta blockers to treat an arrythmia?

A

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

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18
Q

Two Ca blockers used as AAs?

A

Verapamil

Diltiazem

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19
Q

Verapamil Mechanism of Action

A

Frequency Dependent Block of Calcium Channels

Accumulation of blockade in rapidly depolarizing tissues (tachy)

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20
Q

Diltiazem mechanism of action

A

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

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21
Q

Ca channel blockers are used chiefly to…

A

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

22
Q

Which classes of drugs influence myocyte action potentials

A

Class 1 – Na channel blockers

Class 3 – K channel blockers

23
Q

Review the appearance of the curves on page 26

A

pretty please

24
Q

Effects of Class 1A

A

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

25
Q

Effects of Class 1B

A

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

26
Q

Effects of Class 1C

A

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

27
Q

Important examples of 1A

A

Quinidine
Procainamide
Disopyramide

28
Q

Important examples of 1B

A

Lidocaine
Tocainide
Mexilitine

29
Q

Important examples of 1C

A

Propafenone

Flecainide

30
Q

Risks of Class 1A drugs

A

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

31
Q

Risks of Class 1B drugs

A

Lidocaine - IV, rapidly control of vent. arr.

32
Q

Risks of Class 1C

A

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

33
Q

How do class 3 AAs work?

A

Block K channels, prolonging action potential + QT interval

Increase in Effective Refractory Period, which can terminate reentry in a re-entrant circuit

34
Q

Significance of Torsade de pointes (TDP)

A

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

35
Q

Early after depolarizations (EAD) are capable of…

A

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

36
Q

The five given Class 3 anti-arrhythmetic drugs

A 
Amiodarone
Dronedarone
Ibutilide
Sotalol
Dofertilide
37
Q

Important details for Amiodarone/Dronedarone

A

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
Q

Important Ibutilide details

A

Can cause TDP

Rapid Conversation of A Fib/Flut to normal rhy

39
Q

Important details for Sotalol

A

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

40
Q

Important details about dofetilide

A

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

41
Q

Sources of Long QT Syndrome (LQTS)

A

Drug Induced
Electrolyte Imbalances
Bock of HERG Channel

42
Q

Some drugs that are associated witi TDP

A

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

43
Q

Clinical use of Amiodarone

A

A-fib

Suppression post-MI vent arr.

44
Q

Clinical use of Dronedarone

A

A fib

45
Q

Clinical use of Sotalol

A

Prevent A fib reoccurance

46
Q

Clinical use of Ibutilide

A

Convert A fib to sinus rhythm

47
Q

Important digoxin details?

A

Direct inhibition os AV node

48
Q

Important Magnesium Chloride details?

A

Treat hypomagnesemia
Convert TDP
Prevent MI and Digoxin Arr.

49
Q

Important details of Potassium Chloride

A

Hypokalemia reduces Ikr current

Prolong action potentials and can be proarrhythmetic

50
Q

Important details of Adenosine

A

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

Pharmacology - Test #4 (9 decks)

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