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Pharm block 4 hemostasis and cardiac > Antiarrhythmai drugs > Flashcards

Antiarrhythmai drugs Flashcards

1
Q

what is an EAD and when does it occur

A

occur at slow heart rates, get an extra depolarization from the plateau of the membrane potential (during repolarization)

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2
Q

what is a DAD and when does it occur

A

occur at fast HRs, an extra depolarization occurs from the resting potential

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3
Q

what are the requirements for re-entry

A
  1. must be a block
  2. block must be unidirectional (allows conduction from other side)
  3. theres slow conduction through the block (slower than the depolarization of the cells on the other side allowing them to be reacitivated
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4
Q

what are the goals of anti-arrhythmic therapy

A

Aimed to reduce ectopic pacemaker activity and/or

modify conduction characteristics to disable re-entry circuits

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5
Q

what are possible anti-arrhythmic mechanisms

A

Na+ channel blockade

Blockade of sympathetic autonomic effects (β-receptors)

Prolongation of the effective refractory period
 (longer QT interval)
Ca++ channel blockade

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6
Q

Use-dependent or state-dependent drug action

A

channels that are used frequently or inactivated are more susceptible, e.g. during fast tachycardia (many channel activations/inactivations) or in ischemic or infarcted tissues (more positive resting potential)

whereas

channels in normal cells rapidly loose the drug during resting phase

Selective blockade of depolarized cells

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7
Q

why wouldn’t you give anti-arrhythmic drugs prophylactically

A

However, anti-arrhythmic drugs DO NOT ACT SPECIFICALLY and can also depress
conduction in normal cells, leading to drug-induced arrhythmia !!!!

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8
Q

do you treat an asymptomatic or mildly symptomatic arrhythmia?

A

NO

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9
Q

how are anti-arrhythmic drugs classified

A

Anti-arrhythmic drugs are classified by their PREDOMINANT effect on the action potential and/or PREDOMINANT cellular mechanism of action.

Many drugs have multiple effects that are related to different classes of drug action.

Metabolites of drugs also may be biological active via different mechanisms of action.

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10
Q

Vaughan Williams Classification of Anti-Arrhythmic Drug Actions Class I :

A

Class I : Na+ channel blockers

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11
Q

Vaughan Williams Classification of Anti-Arrhythmic Drug Actions Class II

A

Class II: β-adrenoceptor blockers

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12
Q

Vaughan Williams Classification of Anti-Arrhythmic Drug Actions Class III

A

Class III: Prolongation of action potential duration

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13
Q

Vaughan Williams Classification of Anti-Arrhythmic Drug Actions Class IV

A

Class IV: Ca++ channel blockers

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14
Q

what is the main function of class I drugs

A

Na+ channel blockers, local anesthetic action

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15
Q

what is the MOA of Na+ channel blockers

A

Block fast Na+ channels (Phase 0 in non-nodal cells, fast response action potential) (these are found in the heart and nerve endings)

Actions (therapeutic actions and side-effects) depend on heart rate, membrane potential and drug specific blocking kinetics

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16
Q

what are the subclasses of Na+ channel blockers

A

Class 1A: intermediate kinetics, APD increased
Class 1B: fast kinetics, APD decreased
Class 1C: slow kinetics, no effect on APD

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17
Q

what are the drugs in class 1A

A

Procainamide, Quinidine, Disopyramide

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18
Q

what are the drugs in class 1B

A

*Lidocaine, Mexiletine

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19
Q

what are the drugs in class 1C

A

Flecainide, Propafenone

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20
Q

Procainamide and quinidine effects

A

Slows upstroke of AP, conduction, prolongs QRS complex
Direct depressant actions on SA and AV nodes
More effective in depolarized cells (use/state-dependent action)

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21
Q

Procainamide and quinidine indications

A

Atrial and ventricular arrhythmias

Drug of second or third choice (after lidocaine and amiodarone) for ventricular arrhythmias after acute myocardial infarction

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22
Q

Procainamide pharmacokinetics

A
  • Administered i.v., i.m., p.o.
  • Metabolite N-acetylprocainamide (NAPA) has class 3 activity
  • Elimination via liver and kidney (NAPA), 
 dose reduction with renal failure
  • half-life: 3-4 hrs.
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23
Q

Procainamide adverse effects/toxicity

A
  • Ganglion blocking properties,
  • risk of hypotension
  • Anti-cholinergic effects
  • Induction of torsade de pointes arrhytmia (NAPA) !!
  • Long term: Lupus erythematosus syndrome (arthritis, pleuritis…)
  • in 30% of all patients
24
Q

Quinidine adverse effects

A

Rarely used because of cardiac and extra-cardiac
adverse effects

Ganglion blocking properties, risk of hypotension
(» procainamide)

Anti-cholinergic effects, increases sinus rate and AV conduction, may require co-administration of drugs that slow AV conduction

Induction of ventricular fibrillation and torsade de pointes !!

Cinchonism: headache, dizziness, tinnitus

25
Q

Lidocaine pharmacokinetics

A

Use/state-dependent drug action
rapid kinetics at normal resting potential: No effect on conduction, recovery from block between action potential

selective depression of conduction in depolarized (ischemic) cells

I.v. only, extensive first-pass hepatic metabolism
half-life 1-2 hrs, > 3-6 hrs with liver diseases

26
Q

Lidocaine indications

A

High degree if effectiveness in arrhythmias after myocardial infarction

Drug of 1st choice for treatment of ventricular tachycardia and fibrillation after cardioversion in the setting of ischemia/infarction

But: prophylactic treatment not recommended (may increase mortality

27
Q

Mexiletine’s off label use

A

Off-label use: chronic pain (diabetic neuropathy, nerve injury)

28
Q

what is an orally active lidocaine analogue

A

Mexiletine (actions and side effects the same as lidocaine)

29
Q

Flecainide MOA

A

Potent blocker of Na+ and K+ channels with slow kinetics
No anti-cholinergic effects

class 1C

30
Q

Flecainide indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

31
Q

Flecainide pharmacokinetics

A

Well absorbed, half-life 20 hrs, elimination: liver and kidney

32
Q

Flecainide adverse effects

A

Increases mortality in patients with ventricular tachyarrhythmias, myocardial infarction and ventricular ectopy

33
Q

Propafenone MOA

A

Potent blocker of Na+ channels with slow kinetics, may also block K+ channels
Structural similarity to propranolol with weak β-blocking activity

34
Q

Propafenone Indications

A

Supraventricular arrhythmias in patients with otherwise normal hearts

35
Q

Propafenone adverse effects/toxicity

A

Probably same as flecainide (arrhythmogenic)
Sinus bradycardia/bronchospasm (β-blockade)
Metallic taste and constipation

36
Q

β-adrenoceptor blockers MOA

A

inhibit normal sympathetic effects that act through

β-adrenoceptors

37
Q

non-selective blockers

A

block β1and β2 receptors

Typical drug: Propranolol (other: Sotalol, Timolol)

38
Q

cardioselective B-blockers

A

relatively selective β1 blockers

Typical drug: Esmolol (other: Acebutolol)

39
Q

actions of B-Blockers

A

inhibit sympathetic influences on cardiac electrical activity
reduce heart rate
decrease intracellular Ca++ overload
decrease pacemaker currents (SA node automaticity)
reduce conduction velocity
decrease catecholamine induced DAD and EAD mediated arrhythmias

40
Q

indications for B-Blockers

A

Prevention of recurrent infarction and sudden death
after myocardial infarction
Exercise-induced arrhythmias
Also used for atrial fibrillation, atrial flutter and AV nodal reentry

41
Q

adverse affects/toxicity of B-blockers

A

Bradycardia, reduced exercise capacity, heart failure, hypotension, AV block - contraindicated in patients with sinus bradycardia and partial AV block

Bronchospasm, contraindicated in patients with asthma or chronic obstructive pulmonary disease.

Blocking β2-adrenoceptors lowers plasma glucose and β1-blockers lower heart rate - thus tachycardia associated with hypoglycemia in diabetic patients may be masked

42
Q

Adenosine MOA

A
  • Endogenous purine nucleoside
  • Acts via purinergic receptors (GPCR), increases K+ conductance (hyperpolarization) and inhibits cAMP-mediated Ca++ currents
  • Primarily acts on atrial tissues (actions similar to acetylcholine only via different receptors)
  • Slows AV node conduction and increases AV node refractoriness
  • Produces transient cardiac arrest
43
Q

Adenosine indications

A

Drug of choice for conversion of paroxysmal supraventricular tachycardia to sinus rhythm !!

44
Q

Adenosine adverse effects/toxicity

A

Flushing and shortness of breath, sinus bradycardia, sinus pauses, AV block, decrease in blood pressure

45
Q

Adenosine pharmacokinetics

A

Half-life of seconds, rapid i.v. bolus dose required (initially 6 mg i.v.)
Less effective with theophylline/caffein, potentiated by dipyridamole

46
Q

Vagal maneuvers

A
  • carotid sinus message, diving reflex (cold water on face), Valsalva maneuver.
    • slows conduction through AV node. Acute treatment for paroxysmal supraventricular tachycardia (PSVT)
47
Q

Radiofrequency ablation / Cryoablation

A
  • interrupts reentrant / accessory pathway

- used more frequently to replace anti-arrhythmic drug therapies

48
Q

Electrical cardioversion can be used for what rhythms

A
  • atrial fibrillation

- ventricular tachycardia and fibrillation

49
Q

Implantable Cardioverter-Defibrillator (ICD) is used for what rhythm

A

ventricular fibrillation

50
Q

what drugs should be used for Conversion to sinus rhythm

A

Adenosine / Amiodarone

Flecainide

51
Q

what drugs should be used for Maintenance of sinus rhythm

A

Amiodarone / Dronedarone

Flecainide / Propafenone

52
Q

what drugs should be used for Ventricular rate control:

A

Diltiazem/Verapamil

Propranolol/Esmolol

53
Q

what drugs should be used for ventricular tachycardia in pts without heart disease

A

Amiodarone

Lidocaine

54
Q

what should be done for Ventricular fibrillation

A

Defibrillation
w/wo Amiodarone
or Lidocaine

55
Q

what should be done for Atrial fibrillation

A

Diltiazem/Verapamil

Propranolol

56
Q

what should be done for Paroxysmal supraventricular tachycardia

A

Adenosine/Amiodarone
Verapamil/Diltiazem/
Propranolol

Pharm block 4 hemostasis and cardiac (12 decks)

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