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Pharm Test 4 > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

1
Q

Class 1A Antiarrhythmics- Available Drugs

A

Procainamide
Quinidine
Disopyramide

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2
Q

Class 1A Antiarrhythmics- Mech of Action (Procainamide, Quinidine, Disopyramide)

A

Blocks Na and K channels= prolongation of action potential

Intermediate kinetics

Anti-Cholinergic effects:
disopyramide»quinidine>procainamide

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3
Q

Class 1A Antiarrhythmics- Effect (Procainamide, Quinidine, Disopyramide)

A
  • slows upstroke of AP and conduction
  • prolongs QRS complex
  • direct depressant actions on SA/AV nodes
  • use/state-dependent action
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4
Q

Class 1A Antiarrhythmics- Clinical Application (Procainamide, Quinidine, Disopyramide)

A
  • atrial and ventricular arrhythmias

- 2nd choice for ventricular arrhythmias after acute myocardial infarction (Procainamide)

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5
Q

Procainamide- Pharmakokinetics, toxicities, interactions

A
  • PO, IV, IM
  • half-life= 3-4 hours
  • metabolized to NAPA

Side effects:

  • torsades des pointes (from NAPA)
  • ganglion blocking properties
  • hypotension
  • anticholinergic effects
  • lupus syndrome w/ long-term use
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6
Q

Quinidine- Pharmakokinetics, toxicities, interactions

A

Side Effects:

  • torsade des pointes!!
  • ganglion blocking properties (»procainamide)
  • hypotension (»procainamide)
  • antichoinergic effects
  • increases sinus rate and AV conduction
  • may require co-administration of drugs that slow AV conduction
  • induction of V-fib
  • Cinchonism: headache, dizziness, tinnitus
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7
Q

Class 1B Antiarrhythmics- available drugs

A

Lidocaine

Mexiletine

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8
Q

Class 1B Antiarrhythmics- Mech of Action (Lidocaine, Mexiletine)

A
  • Na channel blockade
  • use/state-dependent drug action
  • fast kinetics
  • reduction of action potential duration
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9
Q

Class 1B Antiarrhythmics- Effect (Lidocaine, Mexiletine)

A
  • rapid kinetics
  • at normal action potential= no effect on conduction, recovery from block between action potential
  • selective depression of conduction in depolarized (ischemic) cells
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10
Q

Class 1B Antiarrhythmics- Clinical Application (Lidocaine, Mexiletine)

A
  • highly effective for ventricular arrhythmias after myocardial infarction
  • drug of 1st choice for treatment of ventricular tachycardia and fibrillation after cardioversion in the setting of ischemia/infarction
  • prophylactic treatment not recommended (may increase mortality)
  • off-label use: chronic pain (mexiletine)
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11
Q

Lidocaine- Pharmakokinetics, toxicities, interactions

A
  • I.V. only, extensive 1st pass metabolism
  • half-life= 1-2 hrs (>3-6 hrs. w/ liver disease)
  • least cardiotoxic drug among Class I drugs
  • neurological side effects due to local anesthetic properties
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12
Q

Mexiletine- Pharmakokinetics, toxicities, interactions

A
  • oral
  • half-life= 8-20 hrs
  • neurological side effects due to local anesthetic properties
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13
Q

Class 1C Antiarrhythmics- Available Drugs

A

Fecainamide

Propafenone

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14
Q

Class 1C Antiarrhythmics- Mech of Action (Fecainamide, Propafenone)

A
  • Na and K channel blockade
  • propafenone: potent blocker of Na channels, may also block K channels, weak B-blocking activity
  • slow kinetics
  • no effect on action potential duration
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15
Q

Class 1C Antiarrhythmics- Effect (Fecainamide, Propafenone)

A
  • no effect on action potential duration

- no anticholinergic effects

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16
Q

Class 1C Antiarrhythmics- Clinical Application (Fecainamide, Propafenone)

A

supraventricular arrhythmias in patients w/ otherwise normal hearts

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17
Q

Fecainamide- Pharmakokinetics, toxicities, interactions

A
  • well-absorbed
  • half-life= 20 hrs
  • elimination: liver and kidney
  • increases mortality in patients w/ ventricular tachyarrhythmias, myocardial infarction and ventricular ectopy = CONTRAINDICATION
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18
Q

Propafenone- Pharmakokinetics, toxicities, interactions

A
  • arrhythmogenic
  • sinus bradycardia/bronchospasm (B-blockade)
  • metallic taste
  • constipation
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19
Q

Class 2 Anti-Arrhythmics: B-Adrenoceptor blockers- Available Drugs

A

Propranolol

Esmolol

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20
Q

Propranolol- Mech of Action

A
  • inhibits normal sympathetic effects that act through B-adrenoceptors
  • non- selective B-blocker
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21
Q

Esmolol- Mech of Action

A
  • cardioselective B-blocker, only affects B1 receptors
  • IV only
  • half-life= 9 min.
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22
Q

Class 2 Anti-Arrhythmics: B-Adrenoceptor blockers- Effect (Propranolol, Esmolol)

A
  • inhibits sympathetic influences on cardiac electrical activity
  • reduces heart rate
  • decreases pacemaker currents (SA node automaticity)
  • reduces conduction
  • decreases catecholamine induced DAD and EAD mediated arrhythmias
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23
Q

Propranolol- Clinical Application

A
  • prevention of recurrent infarction and sudden death after myocardial infarction
  • also used for atrial fibrillation, atrial flutter, and AV nodal reentry
24
Q

Esmolol- Clinical Application

A

supraventricular tachycardia (acute only)

25
Q

Class 3 Anti-Arrhythmics: Prolongation of action potential duration- Available Drugs

A

amiodarone
dronedarone
sotalol

26
Q

Class 2 Anti-Arrhythmics: B-Adrenoceptor blockers- Pharmakokinetics, toxicities, interactions (Propranolol, Esmolol)

A
  • bradycardia
  • reduced exercise capacity
  • heart failure
  • hypotension
  • AV block
  • bronchospasm, caution in patients w/ asthma or chronic obstructive pulmonary disease
  • may mask tachycardia associated w/ hypoglycemia in diabetic patients
  • contraindicated in patients w/ sinus bradycardia and partial AV block
27
Q

Amiodarone- Mech of Action

A
  • blocks K channels

- also blocks Na & Ca channels, B-receptors

28
Q

Dronedarone- Mech of Action

A
  • blocks K channels

- also blocks Na & Ca channels, B-receptors

29
Q

Class 3 Anti-Arrhythmics: Prolongation of action potential duration- Effect

A
  • prolongation of action potential duration
  • prolongs refractoriness and slows conduction
  • suppresses abnormal automaticity and can slow normal sinus automaticity
  • prolongs QT interval and QRS complex
30
Q

Sotalol- Mech of Action

A
  • non-selective B-adrenoceptor blocker that inhibits delayed rectifyer and possibly other K currents
  • racemic mixture of D- and L-sotalol
  • B- blocking activity due to L-isomer only
  • B- blocking activity at doses below effects on action potential duration
31
Q

Amiodarone- Clinical Application

A

Oral:

  • recurrent ventricular tachycardia or fibrillation resistant to other drugs
  • also used for atrial fibrillation (maintains sinus rhythm)

IV:
- 1st choice drug for out-of-hospital cardiac arrest, termination of ventricular tachycardia, or fibrillation

32
Q

Dronedarone- Clinical Application

A

atrial fibrillation/flutter

33
Q

Sotalol- Clinical Application

A
  • Ventricular and supraventricular arrhythmias

- maintenance of sinus rhythm in patients w/ atrial fibrillation

34
Q

Amiodarone- Pharmakokinetics, toxicities, interactions

A
  • Oral bioavailability: 30-60%
  • highly lipophilic, accumulation in several organs (heart, lung, liver, cornea)
  • structural analogue of thyroid hormone: blocks conversion of T4 to T3
  • source of inorganic iodine: hypo- and hyperthyroidisms

Side Effects:

  • bradycardia and heart block in patients w/ SA/AV node disease
  • pulmonary and hepatic toxicity
  • photodermatitis
  • cornea microdeposits
35
Q

Dronedarone- Contraindications

A

severe or recently decompensated symptomatic heart failure

36
Q

Class 4: Ca Channel blockers- available drugs

A

verapamil

diltiazem

37
Q

Class 4: Ca Channel blockers- Mech of Action (Verapamil, Diltiazem)

A
  • blocks activated and inactivated Ca channels (L-type) primarily in the heart
  • use/state-dependent action
  • diltiazem has lower cardioselectivity
38
Q

Class 4: Ca Channel blockers- Effect (Verapamil, Diltiazem)

A
  • major effects in slow-response tissues (SA/AV node)
  • directly slows AV node conduction and increases AV node refractoriness, slows SA node automaticity
  • lowers heart rate and increases PR-interval
39
Q

Class 4: Ca Channel blockers- Clinical Application (Verapamil, Diltiazem)

A
  • supraventricular arrhythmias (verapamil drug of 1st choice)
  • re-entry arrhythmias/tachycardias involving the AV node
  • slows ventricular rate in atrial flutter/fibrillation
  • hypertension & angina pectoris (diltiazem)
40
Q

Class 4: Ca Channel blockers- Pharmakokinetics, toxicities, interactions (Verapamil, Diltiazem)

A
  • oral bioavailability= 20%
  • extensively metabolized in liver (caution: liver dysfunction)
  • half-life= 7 hours

Side effects:

  • vasodilation (particularly after IV injection) and negative inotropic effects
  • hypotension & fibrillation in patients w/ ventricular tachycardia or left ventricular dysfunction
  • AV block in patients with AV nodal disease or in high doses (to be treated with atropine or B-receptor stimulants)
  • heart block in patients w/ B-adrenoceptor blockers!!!
  • constipation, lassitude, nervousness, peripheral edema
41
Q

Adenosine- Mech of Action

A

increases K conductance (hyperpolarization) and inhibits Ca currents via purinergic receptors

42
Q

Adenosine- Effect

A
  • primarily acts on atrial tissues
  • slows AV node conduction and increases AV node refractoriness
  • produces transient cardiac arrest
43
Q

Adenosine- Clinical Application

A
  • drug of choice for conversion of paroxysmal supraventricular tachycardia to sinus rhythm
44
Q

Adenosine- Pharmakokinetics, toxicities, interactions

A
  • half-life: seconds
  • rapid IV bolus dose required
  • less effective w/ theophylline/caffeine
  • potentiated by dipyridamole

Side effects:
- flushing and shortness of breath

45
Q

Magnesium- Mech of Action

A

unknown MOA

  • influences/inhibits Na-K pump, Na, K, Ca channels
  • alters membrane surface charge
46
Q

Magnesium- Effect

A
  • anti-arrhythmic effects in some patients w/ normal Mg levels
  • may inhibit afterdepolarizations
47
Q

Magnesium- Clinical Application

A
  • digitalis induced arrhythmias w/ hypomagnesemia

- may be effective against torsade des pointes

48
Q

Magnesium- Pharmakokinetics, toxicities, interactions

A
  • IV
49
Q

Potassium- Mech of Action

A

Hyperkalemia:
- depolarizes resting membrane potential

Hypokalemia:
- decreases K permeability

50
Q

Potassium- Effect

A

Hyperkalemia:
- slows conduction (may lead to re-entrant arrhythmias and AV nodal block)

Hypokalemia:

  • enhances ectopic automaticity
  • lengthens action potential duration which can lead to EADs (torsades de pointes)
51
Q

Potassium- Clinical Application

A

maintain normal plasma K

52
Q

Potassium- Pharmakokinetics, toxicites, interactions

A
  • IV, PO
53
Q

Cardiac Glycosides (digitalis)- Mech of Action

A
  • inhibits Na-K pump thereby affecting Na-Ca exchange

- increase intracellular Ca

54
Q

Cardiac Glycosides (digitalis)- Effect

A
  • positive inotropic actions (used widely in heart failure)

- parasympathomimetic effects: increase AV nodal refractoriness and slow AV node conduction

55
Q

Cardiac Glycosides (digitalis)- Clinical Application

A
  • atrial arrhythmias
  • in atrial flutter or fibrillation parasympathomimetic effects slow AV nodal conduction, thereby slowing excessively high ventricular rates
56
Q

Cardiac Glycosides (digitalis)- Pharmakokinetics, toxicities, interactions

A
  • half-life: long, 40hrs, 160hrs
  • eliminated by the kidney
  • narrow therapeutic window
  • development of arrhythmias (DAD)
  • many drug interactions (amiodarone, verapamil, flecainide)!!!!
  • hypokalemia/magnesemia enhance toxic effects

Side effects:

  • loss of appetite
  • nausea
  • blurred vision
  • visual disturbances (yellow-green)
  • drowsiness
  • depression
  • severe digitalis toxicity can be reversed by digoxin antibodies

Pharm Test 4 (6 decks)

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