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Pharm 3 test 4 > Antiarrhythmic Agents > Flashcards

Antiarrhythmic Agents Flashcards

1
Q

What is the greatest ADE of antiarrhythmic agents?

A

Arrhythmias

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2
Q

What is the refractory period in the cardiac cells?

A

The time between phase 0 and sufficient recovery of na channels in phase 3 to permit a new propagated response to external stimulus

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3
Q

What is the name of the late rectifier K current?

A

Human either Ago Go

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4
Q

All arrhythmias result from _____

A

Disturbances in impulse formation, disturbances in impulse conduction, or both

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5
Q

What causes depolarization of funny channels?

A

Opening of Ca slowly because they lack Na channels

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6
Q

What is the phase 4 depolarization slope susceptible to?

A

Parasympathetic outflow and drugs like BBs that slow the rate

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7
Q

What are EADS or DADS?

A

Early afterdepolarizations

Delayed afterdepolarizations

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8
Q

What type of disturbances are EADS or DADS?

A

Disturbances in electrical impulse formation

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9
Q

What are examples of disturbances in electrical impulse cunduction?

A

Heart blocks-usually in AV node or BBB

Reentry Arrhythmias- One impulse reenters and excites areas of the heart more than once

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10
Q

What is the usual treatment for reentry arrhythmias?

A

Drugs that slow conduction by blocking Na or Ca because they lengthen the refractory period

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11
Q

What three things need to be corrected before relying on drugs to correct arrhythmias?

A

Ensure ischemia is not present, correct electrolyte imbalances, change drugs that are possibly causing arrhythmias

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12
Q

What drugs can cause torsades?

A

Quinidine, sotalol, macrolides

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13
Q

What are the mentioned patient specific contraindications to antiarrhythmics?

A

HF and Dronedarone

Amiodarone can cause ILD and pulmonary fibrosis

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14
Q

What is the Singh/Vaughan-Williams classification for antiarrhythmic agents?

A

Class 1A-1C- Na channel blockers
Class 2- Blocking sympathetic autonomic effects-BBs
Class 3- Prolongation of AP duration and the effective refractory period
Class 4- Ca channel blockade

Lidocaine
Esmolol
Amiodarone
Diltiazem

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15
Q

Where on the ion channels do most antiarrhythmic drugs bind exactly?

A

Below the activation gate

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16
Q

What channel state do channel blocking agents have a low affinity to?

A

Resting

17
Q

So why are hyperactive cardiac channels more susceptible to channel blockers?

A

Channels that are more frequently in the activated state, or inactivated state, are more likely to become blocked due to the channel blockers high affinity to them.

18
Q

Why is antiarrhythmic agents such a gamble?

A

Because they can still cause inactivation of normal cardiac cells, but are just more likely to affect the abnormally firing cells. The “Do the math” concept

19
Q

What are the class 1a na chanel blocking drugs?

A

Quinidines, procainamide, Disopyramide

20
Q

What is quinidines MOA?

A

Blocks Na channels and prolongs potential duration (Through blocking K channels)

21
Q

What is quinidines ADE?

A

Toxicity that causes prolonged QT and torsades

22
Q

What are the class 1B blockers?

A

Lidocaine, mexiletine

23
Q

What is an important pharmacokinetic point to understand about lidocaine?

A

It has extensive first pass metabolism, so poor oral bioavailability

24
Q

What are the class 1C blockers?

A

Flecainide, propafenone

25
Q

What makes class 1B and 1C different?

A

Class 1B dissociates rapidly from the channel, where 1C dissociates slowly

26
Q

What is the main difference between class 1A and class 1B blockers?

A

1A blocks Na AND K, 1B is only a Na blocker

27
Q

What is the MOA of class 2 drugs (beta blockers)?

A

They block B1, causing a decrease in Ca, reduced HR slows AV node conduction, and inhibits formation of afterdepolarization

28
Q

What are the class 2 beta blockers to know?

A

Propanolol, sotalol, Acebutolol, and esmolol

APES

29
Q

What makes esmolol unique?

A

It has significant K blockade in addition to beta, so high risk for torsades

30
Q

What is class 3 blockers MOA?

A

Blocks K channels

31
Q

What are the class 3 blockers?

A

Amiodarone, sotalol?, dronedarone, dofetilide, ibutilide

32
Q

What are the class 4 blockers?

A

CCB

33
Q

What is adenosines MOA?

A

Activates K current to shorten AP duration and cause hyperpolarization

34
Q

What is digoxins MOA?

A

Increases parasympathetic outflow and influence on the heart, decreases sympathetic outflow
Slows AV nodal conduction

Pharm 3 test 4 (5 decks)

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