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Pharmacology > Antiarryhthmics > Flashcards

Antiarryhthmics Flashcards

0
Q

Quinidine Adverse

A

Class 1 Sodium channel blocker
**Cinchonism (named after tree that anti malarials come from-Quinines-so seen in any antimalarials only BUZZ WORD) - Tinnitus, ocular dysfunction (cannot tell if miosis or mydriasis because it is both a muscarinic and alpha blocker), CNS excitation, GI disturbances (same as eyes explanation)
Hypotension
Prolongation of QRS and QT interval - Torsades *****

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1
Q

Quinidine General

A

Class IA Sodium channel blocker

  • muscarinic receptor blocker
  • alpha bloc (possible reflex tachycardia)
  • wide clinical use in many arrhthymias; in atrial fibrillation, need initial digitalization (to slow AV conduction)
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2
Q

Quinidine drug interactions

A

Class 1 sodium channel blocker

  • Hyperkalemia enhances effects and vice versa
  • Displaces digoxin from tissue binding sites
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3
Q

Procainamide Description

A

Class 1A Sodium channel blocker

  • Less muscarinic receptor block than quinidine
  • Metabolized through conjugation by N-acetyltransferase
  • -therefore affected by slow/fast metabolizers
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4
Q

Procainamide Adverse

A

Class 1 Sodium channel blockers
SLE like syndrome
Hematotoxicity
CV effects (torsades)

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5
Q

Torsades caused by what type of drugs?

A

Anti muscarinic

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6
Q

SLE like syndrome is caused by what drugs?

A

Procainamide
Hydralazine (anti HTN)
Isoniazid (anti TB)
-seen in slow acetylators

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7
Q

Drug induced SLE lab results

A

Positive anti ANA
Positive anti histone** (specific to drug induced)
Negative anti dsDNA

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8
Q

Disopyramide

A

Class 1A sodium channel blocker

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9
Q

Class 1B Drugs

A

Sodium channel blockers
-Block fast sodium channels (decrease
-Block inactivated channels (slow conduction in hypoxic and ischemic heart) -slows cells ability to go back to resting
-Decrease APD - due to block of the slow sodium “window” currents
Lidocaine, Mexiletine

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10
Q

Lidocaine cardio uses

A

Class1 B

  • post MI
  • Open heart surgery
  • Digoxin toxicity*
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11
Q

Lidocaine adverse

A 
Class 1B
CNS toxicity (seizures); least cardiotoxic of conventional anti arrhythmics
***IV only*** (due to first pass metabolism)
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12
Q

Mexiletine and Tocainide

A

Class 1B drugs
Same as lidocaine
Oral formulations

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13
Q

Class 1C

A

Second choice drug (only use if nothing else worked)

  • block fast sodium channels especially His-Purinje tissue
  • No effect on APD
  • No ANS effect
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14
Q

Flecainide

A

Class 1C
Limited use becase of its proarrhthymic effects leading to sudden cardiac death
Last ditch drug … some will be saved but many may die too
Flecainide, Propafenone

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15
Q

Class II

A

Beta blockers (see ANS)

  • decrease SA and AV nodal activity (parasymp dominance)
  • decrease slope of phase 4
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16
Q

Class II Drugs

A 
Beta blockers 
Non selective  (propranolol) and selective (acebutolol, esmolol)
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17
Q

Class II Uses

A

Beta blockers

  • negative inotropic effect decreases O2 demand so helpful to reduce reccurence of MI or prevent MI in general
  • Prophylaxis post MI, supraventricular tachyarrhythmias (SVT)
  • Esmolol (IV) is used in acute SVTs
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18
Q

Which beta blocker is used in treatment of acute supraventricular tachycardias but not for prophylaxis?

A

Esmolol

19
Q

Esmolol is indicated for use in what?

A

Supraventricular tachycardia

Indicated for the rapid control of supraventricular tachycardias in patients with atrial fibrillation or atrial flutter in the peri or post operative setting where rapid, short term control of ventricular rate with an ultra short acting agent is indicated

20
Q

The beta blockers have what as part of their antiarrhythmic mechanism of action?

A

Decrease cAMP levels

21
Q

A patient is diagnosed with congenital long QT syndrome. If this patient is to be treated for cardiac arrhthymias, drugs with which mechanism would most likely be contraindicated?

A 
Block potassium channels would be contraindicated
Congenital long QT syndrome predisposes patients to torsades, therefore those individuals should avoid drugs that May also precipitate torsades.  Both class 1A and Class III antiarrhythmic drugs may cause torsades because of their potassium channel blocking ability
22
Q

A patient on antiarrhthymic drug therapy yexperiences syncopal episodes associated with a prolonged QT interval. The patient also suffers from diarrhea and gastrointestinal upset and complains of ringing in his ears. What drug was prescribed for this patient?

A

Quinidine
Torsades-K channel blocks
Cinchonism- quinines

23
Q

Which antiarrhythmic drug is associated with an increase in mortality when usedprophylactically in ventricular tachycardia?

A

Flecainide

Class 1C antiarrhthymics -increased sudden death post MI

24
Q

What Class 1 oral drugs preferentially target ischemic areas of the heart?

A

Class 1B
Mexiletine and Tocainide
Lidocaine is only IV

25
Q 
Compared with procainamide, which of the following effects is unique to quinidine?
Hypotension
Prolongation of the action potential
Sodium channel block
Systemic lupus erythematosus
Torsades
A

Hypotension

26
Q

Class IA Mechanism

A

-Block fast sodium channels
-Preferentially in the open or activated state
-Increase APD and ERP
-Also block potassium channel (prolongs repolarization)
Quinidine, Procainamide, Dispyramide

27
Q

Class III Mechanism

A

Potassium channel blockers
-decreased I(k), slowing phase 3
-increase APD and ERP
Amiodarone, Ibutilide, Dofetilde, Sotalol “AIDS”

28
Q

Amiodarone general

A 
Class III Potassium Blocker
Mimic classes I, II, III and IV
Increases APD and ERP in all cardiac tissues
Use-any arrhythmia 
half life - greater than 80 days
29
Q

Amiodarone Side effects

A

High tissue and protein binding

  • Pulmonary fibrosis (restrictive pulmonary disease)
  • Blue pigmentation of the skin (smurf)
  • photo toxicity
  • corneal deposits
  • hepatic necrosis
  • thyroid dysfunction
30
Q

Sotalol

A

Decreases I(k), slowing phase III
Beta one blockade, leading to decrease heart rate, decrease AV conduction
Use-life threatening ventricular arrhythmia

31
Q

If a patient is prescribed sotalol for treatment of an arrhythmia, he was most likely diagnosed with what?

A

Ventricular fibrillation

32
Q

A patient with recurrent supraventricular tachycardia is started on a new medication that has a risk of causing pulmonary fibrosis. What drug?

A

Amiodarone

33
Q

The class III antiarrhythmics primarily slow what phase?

A

3

34
Q

Class IV

A

L type Calcium channel blockers

  • block slow cardiac Ca2+ channels
  • decrease phase 0, decrease phase IV
  • decrease SA, decrease AV nodal activity
35
Q

Class IV drugs

A

Calcium channel blockers

Verapamil and diltiazem

36
Q

Verapamil and Diltiazem Use

A

Supraventricular tachycardias

37
Q

Verapamil and Diltiazem Side effects

A

VERAPAMIL CONSTIPATION**

AV block

38
Q

Verapamil and Diltiazem Drug Interactions

A
  • Additive AV block with beta blockers, digoxin

- Verapamil displaces digoxin from tissue binding sites

39
Q

If a patient is prescribed verapamil for an arrhythmia she most likely has what?

A

Paroxysmal supraventricular tachycardia

40
Q

Diltiazem effects what phase as an antiarrhythmic?

A

Decreases phase 4

41
Q

Adenosine is antagonized by what?

A

Methylxanthines - theophylline (used in COPDs like asthma which can cause V-tach) and caffeine

42
Q

Magnesium is used for what?

A

Torsades

43
Q

Drugs that cause Torsades

A

Potassium channel blockers
Antimuscarinics -quinidine, antihistamines
Antipsychotics (Thioridazine)
Tricyclic antidepressants

44
Q

Magnesium works how?

A

By antagonizing calcium

Pharmacology (24 decks)

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