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MJ- Pharm exam 2 > Antiarrhythmics 3 > Flashcards

Antiarrhythmics 3 Flashcards

1
Q

Effects of which class of drugs?

  1. Prolong the AP duration by reducing the outward (repolarizing) phase 3 potassium current
  2. ***Main effect is to prolong the effective refractory period (ERP)
  3. Note - phase 4 diastolic potassium current (IK1) is not affected by these drugs.
A

class 3

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2
Q

Which drug’s MOA:

  • Blocks IKr, INa, ICa-L channels,
  • β adrenoceptors
A

Amiodarone

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3
Q

Effects of which drug?

  1. **Prolongs action potential duration and QT interval
  2. slows HR and AV node conduction
  3. low incidence of torsades de pointes
A

Amiodarone (class 3)

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4
Q

What are the clinical applications of Amiodarone (class 3)

A

1.** Serious ventricular Arrhythmias

2. **Supraventricular arrhythmias

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5
Q

What is the most commonly prescribed AAD?

A

Amiodarone (Class 3)

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6
Q

Pharmacokinetic of which drug?

  1. Oral, IV
  2. variable absorption and tissue accumulation
  3. hepatic metabolism, elimination complex and slow
A

Amiodarone (class 3)

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7
Q

Which drug has the following toxicities?

  1. Bradycardia and heart block in diseased heart,
  2. peripheral vasodilation
  3. **pulmonary fibrosis
  4. hepatic toxicity
  5. **hyper- or hypothyroidism
A

Amiodarone (class 3)

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8
Q

Which drug has many interactions, based on CYP metabolism

A

Amiodarone (class 3)

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9
Q

The impressive effectiveness of ________ coupled with its low proarrhythmic potential has challenged the notion that selective ion channel blockade by AADs is preferable

A

Amiodarone

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10
Q

What is the MOA of Dofetillide (class 3)?

A

IKr block

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11
Q

What are the 2 effects of Dofetillide (class 3)?

A
  1. prolongs action potential
  2. Prolongs effective refractory period
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12
Q

Clinical application of which med?

Maintenance or restoration of sinus rhythm in A-fib

A

Dofetillide (group 3)

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13
Q

PK of which drug?

Oral

• renal excretion

A

Dofetillide (class 3)

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14
Q

What is the toxicity of Dofetillide (class 3)?

A

***Torsades de pointes

(initiate in hospital)

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15
Q

Interaction of which class 3 med?

Additive with other QT-prolonging drugs

A

Dofetillide

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16
Q

Which class 3 med is used for ventricular arrhythmias and A-fib?

A

Sotalol

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17
Q

Which class 3 med is used for conversion of atrial flutter and A-fib?

A

Ibutillide

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18
Q

Which class 3 drug reduces mortality in patients with A-fib?

A

Dronedarone

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19
Q

Which drug prolongs atrial refractoriness and is effective in A-fib

A

Vernakalant

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20
Q

Effects of which class of drugs?)

•**Reduce inward calcium current during the AP and during phase 4

•**Result= conduction velocity is slowed in the AV node and refractoriness is prolonged

•Pacemaker depolarization is slowed during this phase as well if caused by excessive calcium current.

A

Class 4

21
Q

Ca2+ channel blockers (L-Type) decrease excitability of SA nodal cells and prolong AV nodal conduction, primarily by slowing the ______ upstroke in nodal tissue.

A

actional potential

22
Q

Which class of meds are useful in tx of arrhythmias that involve re-entry through the AV node

A

Class 4

23
Q

High doses of Ca2+ channel blockers can prolong AV nodal conduction to such an extent that______ results

A

heart block

24
Q

MOA of which 2 drugs?

  1. **Dependent ICa block slows conduction in AV node and pacemaker activity
  2. PR interval prolongation
A

Verapamil

Diltiazem

25
Q

What is the clinical application of Verapamil?

A

**AV nodal arrhythmias, especially in prophylaxis

26
Q

What is the clinical application of diltiazem (class 4-CCB)?

A

**Rate control in A-fib**

27
Q

Which 2 meds have the following toxicities:

  1. Cardiac depression

2. **Constipation

3. **Hypotension

A

Verapamil and diltiazem (class 4- CCB)

28
Q

Which group of meds are calcium channel blockers but are not useful in arrhythmias; sometimes precipitate them

A

Dihydropyridines (group 4- CCBs)

29
Q

MOA of which drug?

**interacts with Na+/K+-ATPase, K+, and Ca2+ channels**

(poorly understood)

A

Magnesium

30
Q

which drug normalizes or increases plasma Mg?

A

Magnesium

31
Q

Which drug has the following clinical application:

**Torsades de pointes

**Digitalis-induced arrhythmias

A

Magnesium

32
Q

Pharmacokinetics of which med?

IV

• duration dependent on dosage

A

Magnesium

33
Q

What is the toxicity of Magnesium?

A

Muscle weakness in overdose

34
Q

Which med increases K+ permeability, K+ currents**

A

Potassium

35
Q

What are 2 effects of potassium?

A
  1. Slows ectopic pacemakers
  2. slows conduction velocity in heart
36
Q

What are the 2 clinical applications of Potassium?

A
  1. Digitalis-induced arrhythmias
  2. **arrhythmias associated with hypokalemia
37
Q

what 2 toxicities can occur with potassium in the tx of arrhythmias?

A

1. **Reentrant arrhythmias

2. **Fibrillation or arrest in overdose

38
Q

MOA of which drug?

  1. **Activates inward rectifier IK
  2. **blocks ICa
A

Adenosine

39
Q

What is the effect of Adenosine?

A

Very brief, usually complete AV blockade

40
Q

What is the clinical application of Adenosine?

A

**Paroxysmal supraventricular tachycardias (PSVTs)**

(stops heart with hopes it will reset at normal rhythm)

41
Q

Which med?

**IV only–> duration 10-15 seconds**

A

Adenosine

42
Q

What are the 3 toxicities of Adenosine?

A

1. **Flushing

2. **Chest tightness

3. **Dizziness

43
Q

In patients with A-fib, therapy is traditionally aimed at what 3 things?

A
  1. Controlling ventricular rate
  2. Preventing thromboembolic complications
  3. Restoring and maintaining sinus rhythm
44
Q

In patients with A-fib, what 4 meds are used to control ventricular rate?

A
  1. Digoxin
  2. Nondihydropyridines
  3. CCBs
  4. Beta Blockers
45
Q

In patients with A-fib, what 2 meds are used to prevent thromboembolic complications

A
  1. Warfarin
  2. Aspirin
46
Q

In patients with A-fib, what 2 meds are used to restore and maintain sinus rhythm?

A
  1. AADs
  2. Direct-current cardioversion (DCC)
47
Q

What have studies shown about tx of A-fib?

A
  • no need to try to maintain SR
  • Rate control alone is often good enough
  • Chronic AAD therapy may still be needed in pts who continue to have sxs despite good rate control
48
Q

T/F: the use of antiarrhythmic drugs in the US has declined

A

TRUE because:

  • some trials show increased mortality w/ AADs
  • Proarrhythmia is a significant side effect
  • Advances in technology such as- Ablations and ICDs
49
Q

What technologies are now being used to tx arrhythmias instead of antiarrhythmic drugs?

A

ICD (reduced mortality in EF<30%)

radiofrequency catheter ablation or cryoablation (for arrhythmias w/ defined anatomic pathways)

MJ- Pharm exam 2 (19 decks)

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