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Pharm: Pre Midterm 1 > Antiarrhythmic Drug Therapy > Flashcards

Antiarrhythmic Drug Therapy Flashcards

1
Q

What are the two main goals of antiarrhythmic drugs?

A
  1. Termination of an ongoing arrhythmia and/or

2. prevention of an arrhythmia

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2
Q

Antiarrhythmic drugs exert their effect by doing what?

A

Decreasing the automaticity of ectopic pacemakers more than that of the SA node.
–reduce conduction and excitability and increase the refractory period to a greater extent in depolarized tissue than in normally polarized tissue

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3
Q

Drugs used to treat arrhythmias fall into classes I-IV and miscellaneous. First up are the class I (Na channel blockers). In general what is the action of these drugs?

A

Modulate or block sodium channels
–inhibiting phase 0 depolarization
Blocking Na channels
–automaticity is decreased by shifting the threshold to more positive potentials and decrease the slope of phase 4 depolarization
–leaves fewer channels available to open in response to membrane depolarization therefore this raises the threshold for action potential firing and slowing the rate of depolarization

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4
Q

Now within class I are three different group A,B,C. These subgroups have been identified because their mechanism of action is different due to variable rates of drug binding to and dissociation from the channel receptor. Describe briefly the differences

A

IA: intermediate in terms of the speed of binding and dissociation from the receptor
IB: the most rapid binding and dissociation from the receptor
IC: slowest binding and dissociated from the receptor

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5
Q

Class IA anti-arrhythmics include: Quinidine, Procainamide and Disopyramide. What are some features?

A
  • -May or may not affect conduction
  • -block K channels (phase 3) leading to prolongation of the refractory period in both the atria and ventricles
  • -excitability is reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
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6
Q

Does class IA drugs have inotropic and chrontropic effects?

A

Anticholinergic and negative inotropic actions

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7
Q

What are some differences in the class IA drugs?

A

Quinidine: moderate anticholinergic properties, decrease vascular resistance
Procainamide: weak anticholinergic properties, decrease vascular resistance, little Na channel blocking activity
Disopyramide: strong anticholinergic effects, increases vascular resistance

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8
Q

What are the clinical applications of the class IA drugs?

A

A-fib
Supraventricular
Ventricular tachyarrhythmias
–these drugs arent used to much anymore due to the proarrhythmic risk

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9
Q

What are side effects of Quinidine?

A

1 .Precipitate Arrhythmias such as torsades de pointes

  1. Enhance digoxin toxicity by decreasing its renal clearance
  2. Cinchonism (blurred vision, tinnitus, headache and psychosis)
  3. Thrombocytopenic purpura and hemolytic anemia
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10
Q

What are the side effects of Procainamide?

A
  1. Reversible lupus like syndrome
  2. Depression, hallucinations and psychosis
  3. Contraindicated in presence of QT prolongation or CHF
  4. Induction of ventricular arrhythmias
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11
Q

What are the side effects of Disopyramide?

A
  1. Negative inotropic effects
  2. Induce hypotension and cardiac failure
  3. Severe antimuscarinic effects
  4. Proarrhythmic
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12
Q

What are the contraindications for Quinidine?

A

Complete heart block – dont use in patients with this
use in caution with:
–prolonged QT, history of torsades de pointes, incomplete heart block, uncompensated heart failure, myocarditis, and severe myocardial damage

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13
Q

What are the contraindications of procainamide?

A

Hypersensitivity, complete heart block, 2nd degree AV block, SLE, torsades de pointes
Caution
heart failure and HTN

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14
Q

What are the contraindications of Disopyramide?

A

Uncompensated heart failure

–due to the negative inotropic actions

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15
Q

Moving on to the class IB drugs, Lidocaine and Mexiletine, what is the general action of these drugs?

A

Increase the electrical stimulation threshold of the ventricle and His-Purkinje system

  • -block Na channels in depolarized tissues
  • -in ischemic tissue, cells are partly depolarized because they lack sufficient ATP to operate the sodium pump
  • -as a result sodium channels in ischemic tissues spend more time in the inactivated state than do channels in nonischemic tissues
  • -therefore class IB drugs have a greater affinity for inactivated channels, they suppress conduction more in ischemic tissue than in normal tissue
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16
Q

What is the clinical application of class IB drugs?

A

Ventricular tachyarrhythmias

  • -lidocaine use to be the drug of choice for termination of v-tach and prevention of v-fib after cardioversion in the setting of acute ischemia.
  • -lidocaine is also used in tx of digitalis -induced arrhythmias
17
Q

What are the adverse effects of Lidocaine?

A

Wide-toxic therapeutic ratio
–can include dizziness, sedation, slurred speech, blurred vision, paresthesia, muscle twitching, confusion, n/v, seizures, psychosis, sinus arrest, and aggravation of underlying conduction disturbances

18
Q

What are the adverse effects of Mexiletine?

A

Mainly CNS and GI side effects

19
Q

Finally class IC sodium channel blockers are Flecainide and Propafenone, what is their action?

A

Block open Na channels and slow conduction

  • -most potent
  • -produce a dose related decrease in intracardiac conduction in all parts of the heart
  • -works on the AV conduction time and intra-atrial conduction times
20
Q

What are the clinical applications of class IC drugs?

A

Life threatening supraventricular tachyarrhythmias and ventricular tachyarrhythmias
–prevention of paroxysmal a-fib and maintenance of normal sinus rhythm

21
Q

What are the adverse effects of Flecainide?

A

Proarrhythmia and potential for fatal ventricular arrhythmias in persons with structural heart disease

22
Q

What are the adverse effects of propafenone?

A

Slight B-blocking effect: dizziness and bronchospasm
Slight B-blocking and Slight CA2+ channel blocking activity: headache, taste disturbances and aggravation of underlying heart failure. conduction disturbances or arrhythmias.

23
Q

Moving on to the class II (B-blockers) include Esmolol, Metoprolol and Propranolol. What is their action?

A

Inhibit sympathetic tone which affects predominantly slow response tissues

24
Q

B-blockers slow the rate of discharge of the sinus and ectopic pacemakers and increase the effective refractory period of the AV node. Thus heart rate is slowed, PR interval is lengthened and repolarization is prolonged at the AV node. What actions do the b-blockers take to make this happen?

A
  1. An increase in automaticity due to enhancement of phase 4 spontaneous depolarization
  2. An increase in membrane excitability due to shortening in refractoriness
  3. An increase in the rate of impulse conduction through the myocardial membrane resulting from acceleration of phase 0 upstroke velocity or the rate of membrane depolarization
  4. An increase in delayed afterpotentials
25
Q

What is the clinical use of class II beta-blockers?

A

Supraventricular arrhythmias (atrial flutter and fibrillation)
Ventricular tachyarrhythmias
Reduce incidence of sudden arrhythmic death after MI

26
Q

Esmolol is a short acting beta 1 antagonist and is useful in treatment of what?

A

Acute arrhythmias occurring during surgery or in emergency situations

27
Q

What are the contraindications of class II beta blockers?

A

Acute CHF, severe bradycardia or heart block and severe hyperactive airway disease

28
Q

Moving on to the class III potassium channel blockers include Amiodarone, Ibutilide, Dofetilide and Sotalol. What is their action?

A

Block K channels

  • -prolong action potential duration and increase the effective refractory period in both fast and slow response tissues
  • -QT interval prolongation
29
Q

What is the MOA of amiodarone?

A

Shows Class I, II,III and IV activity

  • -decreases the slope of phase 4 and conduction velocity in addition to the effect on phase 3
  • -dominant effect is class IV
30
Q

What is the MOA of dofetilide and sotalol?

A

Dofetilide:
–potent K channel blocker and no extracardiac effects
Sotalol:
–weak beta blocking effects

31
Q

What is the clinical application of amiodarone?

A

Severe supraventricular and ventricular arrhythmias

  • -drug of choice for acute VT refractory to cardioversion shock or other antiarrhythmic agents
  • -maintain ventricular rate in patients with a-fib
32
Q

What are the clinical applications of Dofetilide and Sotalol?

A

Dofetilide:
–maintenance of normal sinus rhythm in patients with chronic a-fib of longer than 1 week duration who have been converted
–conversion of a-fib/flutter to normal sinus rhythm
Sotalol:
–tx of life threatening ventricular arrhythmias
–maintenance of sinus rhythm in patients with a-fib and flutter who are currently in sinus rhythm.

33
Q

What are the adverse effects associated with amiodarone?

A

Long term use

  • -tremor, ataxia, paresthesia, GI disturbances, bradycardia, AV block hyper or hypo-thyroidism
  • -Interstitial pulmonary fibrosis
  • -arrhythmias, lover toxicity, photosensitivity, corneal deposits
  • -blue grey skin discolorization and hypotensive
34
Q

What are the adverse effects of dofetilide and sotalol?

A

Dofetilide:
–headache, dizziness
–v-tach and torsades de pointes can also occur
Sotalol:
-lowest rate of adverse effects. similar adverse effects a beta blockers

35
Q

What are the cotraindications for amiodarone?

A 
bradycardia
SA or AV block 
severe hypotension 
severe resp failure 
--also able to alter concentrations of digoxin, theophylline, warfarin and quinidine.

Pharm: Pre Midterm 1 (30 decks)

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