Antiarrhythmics 3 Flashcards

(49 cards)

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.

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

23
Q

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

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
What is the clinical application of Verapamil?
**\*\*AV nodal arrhythmias, especially in prophylaxis**
26
What is the clinical application of diltiazem (class 4-CCB)?
**\*\*Rate control in A-fib\*\***
27
Which 2 meds have the following toxicities: 1. Cardiac depression **2. \*\*Constipation** **3. \*\*Hypotension**
Verapamil and diltiazem (class 4- CCB)
28
Which group of meds are calcium channel blockers but are not useful in arrhythmias; sometimes precipitate them
Dihydropyridines (group 4- CCBs)
29
MOA of which drug? **\*\*interacts with Na+/K+-ATPase, K+, and Ca2+ channels\*\*** (poorly understood)
Magnesium
30
which drug normalizes or increases plasma Mg?
Magnesium
31
Which drug has the following clinical application: ## Footnote **\*\*Torsades de pointes** **\*\*Digitalis-induced arrhythmias**
Magnesium
32
Pharmacokinetics of which med? ## Footnote IV • duration dependent on dosage
Magnesium
33
What is the toxicity of Magnesium?
Muscle weakness in overdose
34
Which med **increases K+ permeability, K+ currents\*\***
Potassium
35
What are 2 effects of potassium?
1. Slows ectopic pacemakers 2. slows conduction velocity in heart
36
What are the 2 clinical applications of Potassium?
1. Digitalis-induced arrhythmias 2. **\*\*arrhythmias associated with hypokalemia**
37
what 2 toxicities can occur with potassium in the tx of arrhythmias?
**1. \*\*Reentrant arrhythmias** **2. \*\*Fibrillation or arrest in overdose**
38
MOA of which drug? 1. **\*\*Activates inward rectifier IK** 2. **\*\*blocks ICa**
Adenosine
39
What is the effect of Adenosine?
Very brief, usually complete AV blockade
40
What is the clinical application of Adenosine?
**\*\*Paroxysmal supraventricular tachycardias (PSVTs)\*\*** (stops heart with hopes it will reset at normal rhythm)
41
Which med? ## Footnote **\*\*IV only--\> duration 10-15 seconds\*\***
Adenosine
42
What are the 3 toxicities of Adenosine?
**1. \*\*Flushing** **2. \*\*Chest tightness** **3. \*\*Dizziness**
43
In patients with A-fib, therapy is traditionally aimed at what 3 things?
1. Controlling ventricular rate 2. Preventing thromboembolic complications 3. Restoring and maintaining sinus rhythm
44
In patients with A-fib, what 4 meds are used to control ventricular rate?
1. Digoxin 2. Nondihydropyridines 3. CCBs 4. Beta Blockers
45
In patients with A-fib, what 2 meds are used to prevent thromboembolic complications
1. Warfarin 2. Aspirin
46
In patients with A-fib, what 2 meds are used to restore and maintain sinus rhythm?
1. AADs 2. Direct-current cardioversion (DCC)
47
What have studies shown about tx of A-fib?
- 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
T/F: the use of antiarrhythmic drugs in the US has declined
TRUE because: - some trials show increased mortality w/ AADs - Proarrhythmia is a significant side effect - Advances in technology such as- Ablations and ICDs
49
What technologies are now being used to tx arrhythmias instead of antiarrhythmic drugs?
**ICD** (reduced mortality in EF\<30%) **radiofrequency catheter ablation or cryoablation** (for arrhythmias w/ defined anatomic pathways)