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Pharm Test 4 > Anti-Arrhythmic Drugs > Flashcards

Anti-Arrhythmic Drugs Flashcards

(56 cards)

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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

Study These Flashcards
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

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A

supraventricular tachycardia (acute only)

25
Class 3 Anti-Arrhythmics: Prolongation of action potential duration- Available Drugs
amiodarone dronedarone sotalol
26
Class 2 Anti-Arrhythmics: B-Adrenoceptor blockers- Pharmakokinetics, toxicities, interactions (Propranolol, Esmolol)
- 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
Amiodarone- Mech of Action
- blocks K channels | - also blocks Na & Ca channels, B-receptors
28
Dronedarone- Mech of Action
- blocks K channels | - also blocks Na & Ca channels, B-receptors
29
Class 3 Anti-Arrhythmics: Prolongation of action potential duration- Effect
- 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
Sotalol- Mech of Action
- 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
Amiodarone- Clinical Application
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
Dronedarone- Clinical Application
atrial fibrillation/flutter
33
Sotalol- Clinical Application
- Ventricular and supraventricular arrhythmias | - maintenance of sinus rhythm in patients w/ atrial fibrillation
34
Amiodarone- Pharmakokinetics, toxicities, interactions
- 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
Dronedarone- Contraindications
severe or recently decompensated symptomatic heart failure
36
Class 4: Ca Channel blockers- available drugs
verapamil | diltiazem
37
Class 4: Ca Channel blockers- Mech of Action (Verapamil, Diltiazem)
- blocks activated and inactivated Ca channels (L-type) primarily in the heart - use/state-dependent action - diltiazem has lower cardioselectivity
38
Class 4: Ca Channel blockers- Effect (Verapamil, Diltiazem)
- 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
Class 4: Ca Channel blockers- Clinical Application (Verapamil, Diltiazem)
- 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
Class 4: Ca Channel blockers- Pharmakokinetics, toxicities, interactions (Verapamil, Diltiazem)
- 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
Adenosine- Mech of Action
increases K conductance (hyperpolarization) and inhibits Ca currents via purinergic receptors
42
Adenosine- Effect
- primarily acts on atrial tissues - slows AV node conduction and increases AV node refractoriness - produces transient cardiac arrest
43
Adenosine- Clinical Application
- drug of choice for conversion of paroxysmal supraventricular tachycardia to sinus rhythm
44
Adenosine- Pharmakokinetics, toxicities, interactions
- half-life: seconds - rapid IV bolus dose required - less effective w/ theophylline/caffeine - potentiated by dipyridamole Side effects: - flushing and shortness of breath
45
Magnesium- Mech of Action
unknown MOA - influences/inhibits Na-K pump, Na, K, Ca channels - alters membrane surface charge
46
Magnesium- Effect
- anti-arrhythmic effects in some patients w/ normal Mg levels - may inhibit afterdepolarizations
47
Magnesium- Clinical Application
- digitalis induced arrhythmias w/ hypomagnesemia | - may be effective against torsade des pointes
48
Magnesium- Pharmakokinetics, toxicities, interactions
- IV
49
Potassium- Mech of Action
Hyperkalemia: - depolarizes resting membrane potential Hypokalemia: - decreases K permeability
50
Potassium- Effect
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
Potassium- Clinical Application
maintain normal plasma K
52
Potassium- Pharmakokinetics, toxicites, interactions
- IV, PO
53
Cardiac Glycosides (digitalis)- Mech of Action
- inhibits Na-K pump thereby affecting Na-Ca exchange | - increase intracellular Ca
54
Cardiac Glycosides (digitalis)- Effect
- positive inotropic actions (used widely in heart failure) | - parasympathomimetic effects: increase AV nodal refractoriness and slow AV node conduction
55
Cardiac Glycosides (digitalis)- Clinical Application
- atrial arrhythmias - in atrial flutter or fibrillation parasympathomimetic effects slow AV nodal conduction, thereby slowing excessively high ventricular rates
56
Cardiac Glycosides (digitalis)- Pharmakokinetics, toxicities, interactions
- 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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