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Anti-Arrhythmia Drugs Flashcards

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1
Q

What are the Vaughn-William class 1 drugs we have to know?

A

1A- Quinidine (Na channel blocker)
1B- Lidocaine (Na channel blocker)
1C- Flecainide (Na channel blocker)

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2
Q

What are the Vaughn-William class 2 drugs?

A

They are the B-blockers.

  1. Metoprolol
  2. Propanolol
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3
Q

What are the Vaughn-William class 3 drugs?

A

These are the K-channel blockers.

  1. Amiodarone
  2. Dofetilide
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4
Q

What are the Vaughn William class 4 drugs?

A

Ca-channel blockers.

  1. Verapamil
  2. Diltiazem

Nifedipine does not have a strong affect on arrhythmias.

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5
Q

What are the 6 main types of antiarrhythmic drugs?

A
  1. Na channel blockers
  2. B blockers
  3. K channel blockers
  4. Calcium channel blockers
  5. Digoxin (cardiac glycoside)
  6. Adenosine
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6
Q

What are the 4 main goals of antiarrhythmia drugs?

A
  1. prevent SCD
  2. diminish symptoms
  3. diminish complications secondary to arrhythmias (emboli, syncope, hypotension)
  4. suppress arrhythmic events in patients with ICD to prevent excessive firing of the device
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7
Q

Treatment of arrhythmias uses a combination of invasive, non-invasive and pharmacological measures. _____________ and _______ therapy currently plats a more important role than __________ therapy.

A

Procudures and device-based play a more important role than drug-based.

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8
Q 
How are class I antiarrhythmic drugs subdivided?
Which is the most effective at terminating and preventing arrhythmias?
A

A- intermediate dissociation rate (Quinidine)
B- fast dissociation rates (lidocaine)
C- slow dissociation rates (flecainide)- MOST EFFECTIVE AT TREATING ARRHYTHMIA

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9
Q 
What is the method of action of quinidine? What class of drug is it? 
What are the electrophysiological effects?
A

It is a class 1A antiarrhythmic that blocks Na channels (predominantly) and K channels. It has intermediate dissociation.

  1. lengthen the QT interval
  2. widen QRS
  3. raise threshold
  4. increase effective refractory period
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10
Q

What is the main therapeutic use of Quinidine?

What are the adverse effects?

A

It maintains sinus rhythm in a patient with atrial flutter or fibrillation to prevent V tach and V fib.
It is RARELY used.
Adversely- since it prolongs QT it can lead to Torsades des Pointes.

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11
Q 
What is class of Lidocaine?
What is the mechanism of action?
What are the electrophysiological effects?
A 
It is a class 1B antiarrythmic.
It blocks Na channels exclusively. (has a fast dissociation)
  1. raise threshold
  2. decrease automaticity
  3. increase effective refractory period
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12
Q

Why doesn’t lidocaine work for atrial arrhythmias?

A

It has a fast dissociation rates, so it only is able to inhibit Na channels for a brief period.

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13
Q

What are the therapeutic uses of lidocaine? What are the adverse effects?

A

Therapy-
1. acute IV therapy for ventricular arrhythmia
Adverse Effect-
Survival was found to be WORSE with lidocaine

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14
Q 
What class of drug is flecainide?
What is the mechanism of action?
What are the electrophysiological effects?
A 
It is a class IC antiarrhythmia drug.
It binds Na channels to block AND K channels. It may also weakly block Ca channels
  1. increased threshold
  2. increased effective refractory period
  3. slowed conduction (Na block)
  4. slowed repolarization (K block)
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15
Q

What changes would you see on an EKG of someone taking flecainide?

A
  1. Prolonged PR
  2. Wide QRS
  3. Long QT interval
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16
Q

What is the therapeutic use for flecainide?

What are the adverse effects?

A
  1. PSVT
  2. Atrial flutter and A. fib in patients WITHOUT structural heart disease

Adverse effects:

  1. new or worse arrhythmia (VT, VF, torsade de pointes)
  2. Increase ventricular rate in a patient with Atrial flutter
  3. worsen CHF, MI
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17
Q 
What class of drug is amiodarone? 
What is the mechanism of action?
A 
It is a class III drug and blocks K channels (mainly) but has slight effect on Na and Ca channels.
It also non-competitively blocks adrenergic receptors.
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18
Q

What are the electrophysiological effects of amiodarone? What is seen on the EKG?

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A
  1. slows conduction (Na block) which increases QRS
    2 Slows AV-nodal conduction (Ca Block and adrenergic) which increases PR
    3.Increases AP duration and increases QT (K block)
19
Q

What are the therapeutic uses for amiodarone?

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A
  1. Recurrent VT or VF resistant to other drugs

2. Maintain sinus rhythm with AF

20
Q

What are the 3 most important adverse effects of IV amiodarone?

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A
  1. Cause sinus bradycardia and inhibit automaticity (AV block)
  2. Hypotension due to vasodilation
  3. worsen arrhythmias and create new (long QT can lead to VT and Torsades des pointes)
    3.
21
Q

What are the 4 most important negative effects of oral amiodarone?

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A
  1. Pulmonary toxicity/fibrosis (unusual at low dose)
  2. Worsens arrhythmias
  3. Liver injury (raised enzymes)- usually asymptomatic
  4. Hypo/Hyperthyroidism due to it blocking peripheral thyroxine (T4) to triiodothyronine (T3)
22
Q

What is important about the pharmacokinetics of amiodarone?

Study These Flashcards
A

It is metabolized in the liver and it interacts with drugs that are also metabolized by P450

23
Q 
What class of drug is Dofetilide?
What is the mechanism of action?
Study These Flashcards
A

It is a class III anti-arrhythmic that exclusively blocks K channels. Its action is specific to cardiac muscles

24
Q

What are the electrophysiological effects of dofetilide? What do you see on the EKG?

Study These Flashcards
A
  1. prolonged action potential (increased QT)
25
What are the therapeutic uses for dofetilide? | What are the adverse effects?
1. terminate re-entrant tachyarrythmias (AFib, AFlut, VT) It is used in patients with 1 wk symptoms and is ALWAYS initiated in the hospital. Adverse: 1. new or worsening arrhythmia (torsades des pointes)
26
What is the molecular mechanism of a B-blocker? What are the electrophysiological actions? (what would you see on an EKG?
They block B-adrenergic receptors and inhibit sympathetic stimulation of cardiac muscle 1. decrease Ca current in slow response tissue (SA and AV nodes) - increase PR 2. decrease pacemaker current 3. decrease afterdepolarization mediated arrythmias
27
What is the effect of using a B-blocker to treat arrhythmia?
1. Reduce HR 2. decrease intracellular Ca 3. inhibit after depolarization-mediated triggered activity. 4. terminate AVNRT 5. Control ventricle rate in AF and A flutter
28
``` What is the molecular mechanism of class IV drugs? What are the electrophysiological actions? ```
They block Ca channels and slow voltage-dependent recovery of the channels. they block Ca channels in the AV node, SA node so AV nodal conduction decreases (increased PR)
29
What are the effects of Ca channel blockers on arrhythmias?
1. HR is slowed (although hypotension can cause reflex sympathetic activation and tachycardia) 2. AV nodal conduction decreases (PR increases) 3. AV nodal block occurs 4. terminate AVNRT and AVRT 5. reduce ventricle rate in A flutter and A fib
30
What is the mechanism of action of adenosine? What are the pharmacological effects? What is it used to treat?
It is an agonist for adenosine receptors (G coupled that increase K, decrease Ca and antagonize cAMP) 1 . shortens atrial action potential duration 2. blocks AV nodal conduction It treats supraventricular tachycardia
31
``` What class of drug is digoxin? What are the pharmacological effects? ```
It is a cardiac glycoside that hyperpolarizes the atrium, shortens atrial action potentials and increases AV refractoriness. It is used to control ventricle rate in Afib and terminate reentry arrhythmias involving the AV node
32
Generally speaking, what is acute management for an AVNRT or AVRT?
1. Rate control 2. chemical or electrical cardioversion 3. rhythm control
33
What are indications for electrical cardioverison?
acute arrhythmia associated with hemodynamic instability
34
What are the three drug choices for chemical cardioversion to slow conduction through the AV node to terminate reentrant tachycardia?
1. B-blocker 2. Ca channel blocker 3. Adenosine (ABC for AVRT)
35
How can adenosine be diagnostic? | How can it be therapeutic?
Diagnostic- it will bring out flutter waves if there is atrial flutter, and will bring out P waves in focal atrial tachycardia Therapeutic- it will stop AVNRT or AVRT involving the AV node
36
What are the 2 ways to chronically manage AVRT?
1. drug therapy (IC antiarrhythmia, b-blocker, calcium channel blocker) 2. Catheter ablation
37
What 3 drugs are used to chronically manage AVRT? (stop the recurrence)
1. B-blocker 2. Ca channel blocker 3. IC anti-arrhythmic (Flecainide)
38
What are the two types of catheter ablation? | What are risks associated with the procedure?
1. Radiofrequency - heat 2. Cryoablation -cold This causes permanenr injury to myocardium to interrupt the reentry pathway or to eliminate ecoptic pulse. Risks: 1. perforation of the heard 2. interrupt normal conduction 3. damage intracardiac structures
39
What are the 5 drugs used for acute control of atrial fibrillation?
1. Ca channel blocker 2. Digoxin 3. B-blocker 4. Amiodarone (K channel blocker)
40
What is the chronic management for someone with atrial fibrillation?
1. Determine need for anticoagulation (CHADS score) | 2. Rate and rhythm controls (drugs/cardioversion)
41
What are the 4 drugs used for RATE control of atrial fibrillation? What are the procedural options for treatment?
1. amiodarone, b-blocker, ca channel blocker, digoxin or a combo 2. AV ablation and placement of a ventricular pacemaker
42
What 4 drugs are used for RHYTHM control of atrial fibrillation?
1. IC- flecainide 2. III- Amiodarone 3. III- dronedarone 4. III- dofetilide
43
What anti-arrhythmic drugs can be used for ventricular arrhythmias in someone with CAD and past MIs?
1. B-blocker (good choice) 2. IB (lidocaine)- not really used 3. IC (flecainide) - CONTRAINDICATED TO TO STRUCTURAL DEFECT 4. III (amiodarone) - first choice 5. Digoxin

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