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PCM Exam 2 Pharm > Antiarrhythmic 2 > Flashcards

Antiarrhythmic 2 Flashcards

1
Q

What are the Class IC drugs and what is their effect?

A

Flecainide / Propafenone

• Markedly depress Phase 0 of action potential

→ marked slowing of conduction of action potential but, little effect on duration or ventricular effective refractory period

  • Associate and re-associate slowly with Na+ channels
  • Show prominent effects even at normal heart rates
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2
Q

Class 1C Drug Map

A
  • no effect on potassium channels
  • only effect by blocking sodium channels: increase QRS
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3
Q

What are the clincial Applications of Flecainide?

A

Severe symptomatic ventricular arrhythmias, premature ventricular contraction or ventricular tachycardia resistant to other therapy

Severe symptomatic supraventricular arrhythmias & prevention of paroxysmal atrial fibrillation

Flecainide and propafenone are associated with the potential for fatal ventricular arrhythmias in persons with structural heart disease.

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4
Q

What are the adverse effects of Flecainide?

A
  • Negative inotropic efffect (aggravates CHF)
  • CNS effects: dizziness, blurred vision, headache
  • GI effects: nausea, vomiting, diarrhea
  • Life-threatening arrhythmias & ventricular tachycardia
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5
Q

What is the Clinical Applications and adverse effects of Propafenone?

A

• Used for treatment of life-threatening ventricular arrhythmias and the maintenance of normal sinus rhythm in patients with symptomatic atrial fibrillation

Adverse Effects

  • Similar to flecainide
  • Also has b-blocking activity therefore bronchospasm, aggravation of underlying heart failure etc.
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6
Q

Class 1 a,b,c Summary:

A
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7
Q

What are the common features of Class II antiarrhythmic drugs?

A

b-blockers

• Reduce both heart rate & myocardial contractility (b1)

  • Slow conduction of impulses through myocardial conducting system
  • Reduce rate of spontaneous depolarization in cells with pacemaker activity (block of adrenergic release)

• Little effect on action potential in most myocardial cells

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8
Q

Class II Map

A
  • prolong repolarization through the av node
  • Slow conduction through the AV node
  • increase in PR
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9
Q

Propranolo, Metoprolol Clinical Applications

A
  • Reduce incidence of sudden arrhythmic death after MI
  • Control of supraventricular tachycardias (atrial fibrillation & flutter, AV nodal re-entrant tachycardias)
  • Ventricular tachycardias (catecholamine-induced arrhythmias, digoxin toxicity)
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10
Q

Esmolol Clinical applications:

A
  • Short-acting b1-selective antagonist
  • t1/2 = ~ 9 min
  • Used IV for treatment of acute arrhythmias occurring during surgery or in emergency situations
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11
Q

Class II adverse effects:

A

Propranolol / Metoprolol / Esmolol

  • Bradycardia, hypotension, CNS effects etc.
  • Contraindicated in acute CHF, severe bradycardia or heart block and severe hyperactive airway disease
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12
Q

Common features of class III

A

K+ channel blockers

  • Block repolarizing K+ channels
  • Prolong action potential (and QT interval) without altering Phase 0 or resting membrane potential
  • Prolong effective refractory period
  • All have potential to induce arrhythmias
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13
Q

Class III map

A
  • prolong repolarization
  • Increase in QT
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14
Q

Amiodarone Mechanism of Action?

A
  • Related structurally to thyroxine (contains iodine)
  • Complex MOA showing Class I, II and III (& some IV) effects
  • Dominant effect = K+ channel blockade.
  • Decreases AV conduction & sinus node function.
  • Blocks mostly inactivated Na+ channels
  • Weak Ca2+ channel blocker
  • Inhibits adrenergic stimulation (a & b-blocking properties)

• Antianginal & antiarrhythmic activity

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15
Q

Amiodarone Clincal Applications

A
  • One of most commonly employed antiarrhythmics(despite side-effect profile)
  • Used in the management of ventricular & supraventricular arrhythmias
  • Amiodarone is the drug of choice for acute VT refractory to cardioversion shock.
  • Low doses for maintaining normal sinus rhythm in patients with atrial fibrillation
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16
Q

Amiodarone Adverse Effects?

A
  • Long term use = > 50% patients show adverse effects severe enough for discontinuation
  • Many are dose-related and reversible on decreasing dose eg, interstitial pulmonary fibrosis, GI intolerance, tremor, ataxia, dizziness, hyper- or hypothyroidism, liver toxicity, photosensitivity, neuropathy, muscle weakness, hypotension, bradycardia, AV block, arrhythmias
  • blue skin discoloration (iodine accumulation)
  • despite prolonging the QT interval, has low incidence of Torsades de Pointes.
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17
Q

Amiodarone Contraindications:

A

• Patients taking: Digoxin, theophylline, warfarin, quinidine

  • Patients with:
  • Bradycardia
  • SA or AV block
  • Severe hypotension
  • Severe respiratory failure
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18
Q

Sotalol Mechanism of Action?

A
  • Potent non-selective b-blocker
  • Inhibits rapid outward K+ current
  • Prolongs repolarization & duration of action potential

• Lengthens refractory period

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19
Q

Sotalol Clinical Applications:

A
  • Treatment of life-threatening ventricular arrhythmias
  • Maintenance of sinus rhythm in patients with atrial fibrillation & flutter who are currently in sinus rhythm
  • Due to pro-arrhythmic effects – do not use for asymptomatic arrhythmias
20
Q

Sotalol Adverse effects?

A
  • As for b-blockers
  • Lowest rate (of antiarrhythmics) of acute or long-term adverse effect
  • Torsades de pointes (prolongs QT interval)
  • Use with caution in patients with renal impairment
21
Q
A
22
Q

Dofetilide clincal applications:

A

• Potent and pure K+ channel blocker

Clinical Applications

Conversion of atrial fibrillation / flutter to normal sinus rhythm

Maintenance of normal sinus rhythm in patients with chronic atrial fibrillation / flutter of longer than one week duration who have been converted to normal sinus rhythm

23
Q

Dofetililde?

A

Adverse Effects

  • Headache, chest pain, dizziness, ventricular tachycardia
  • Torsade de Pointes (prolongs QT interval)
24
Q

What are the common features of Class 4?

A
  • Ca2+ channel blockers
  • Decrease inward Ca2+ current leads to decreased rate of Phase 0 depolarization
  • Slow conduction in tissues dependent on Ca2+ current (SA & AV nodes)
  • Major effects on both vascular & cardiac smooth muscle
25
Q

Class 4 Map

A
  • increase PR
26
Q

Verapamil and Diltiazem features and major effects?

A
  • Verapamil = relatively selective for the myocardium and is less effective as a systemic vasodilator drug
  • Diltiazem = intermediate selectivity for the myocardium between verapamil and the dihydropyridines

Major Effects:
• Decrease contractility (negative inotropy)
• Decrease heart rate (negative chronotropy)
• Decrease conduction velocity (negative dromotropy)

27
Q

Verapamil and diltiazem mechanism of action?

A
  • Inhibit voltage-sensitive Ca2+ channels → decrease in slow inward current that triggers cardiac contraction
  • Bind only to open, depolarized channels, preventing repolarization before drug dissociates
  • Use/state-dependent
  • Slow conduction & prolong effective refractory period
28
Q

Verapamil and diltiazem clinical applications?

A

• More effective against atrial than ventricular arrhythmias

• Supraventricular tachycardia is major arrhythmia indication

• Reduction of ventricular rate in atrial fibrillation & flutter

• Hypertension, angina

29
Q

Verapamil and diltiazem adverse effects and contraindications?

A
  • Negative inotropes
  • Transient decrease in BP
  • CNS effects (headache, fatigue, dizziness)• GI effects (constipation, nausea)

Contraindications: Verapamil can increase the concentrations of other cardiovascular drugs such as digoxin, dofetilide, simvastatin, & lovastatin

30
Q

Digoxin common features:

A
  • Shortens refractory period in atrial & ventricular myocardial cells
  • Prolongs effective refractory period & diminishes conduction velocity in AV node

Clinical Applications: Control of ventricular response rate in atrial fibrillation & flutter with impaired left ventricular function or heart failure

31
Q

Digoxin mechanism of action?

A

• Heart Failure :Positive inotrope (increases intracellular [Ca2+]i)

  • Arrhythmias
  • Direct AV node blocking effects & vagomimetic properties:
  • Inhibition of Ca2+ currents in AV node
  • Activation of Ach-mediated K+ currents in atrium

• Major indirect actions
• Hyperpolarization

• Shortening of atrial action potentials• Increases in AV nodal refractoriness

32
Q

Digoxin Antiarrhythmic effect?

A

(1) Slows AV conduction,

and

(2) Prolongs effective refractory period of the AV node

thereby decreasing the fraction of atrial impulses that are conducted through the node and increasing PR interval

→ useful in treating atrial flutter / fibrillation (by controlling ventricular rate)

33
Q

Digoxin Adverse effect?

A

Toxic doses

• Ectopic ventricular beats → ventricular tachycardia & fibrillation

34
Q

Adenosine common feature?

A
  • Naturally occurring nucleoside (P1 receptor agonist)
  • High doses = decreases conduction velocity & prolongs refractory period as well as decreasing automaticity in AV node
  • Very short t1/2 (15 s)
35
Q

Adenosine mechanism of action

A
  • Enhances K+ conductance
  • Inhibits cAMP-mediated Ca2+ influx
  • Leads to hyperpolarization esp. in AV node

Clinical Applications: IV adenosine = drug of choice for abolishing acute supraventricular tachycardia

36
Q

Adenosine Adverse effect?

A

Low toxicity

  • Flushing
  • Burning
  • Chest pain
  • Hypotension

• Bronchoconstriction in asthmatics (may persist up to 30 min)

37
Q

Magnesium common feature?

A

• Functional Ca2+ antagonist

Used for treatment of:
• Torsades de pointes

  • Digitalis-induced arrhythmia
  • Prophylaxis of arrhythmia in acute MI
38
Q

Atropine effect?

A

Used in bradyarrhythmias to decrease vagal tone

39
Q

What are the Anti-Arrhythmic Drug Action Summary

A
40
Q

Anti-Arrhythmic Classified by Cardiac Tissue on which they act

A
41
Q

Anti-Arrhythmic Classified by Arrhythmia on which they are effective

A
42
Q

What is Atrial Fibrillations?

A
  • Can be paroxysmal (intermittent) or persistent (chronic)
  • For most patients is not immediately life-threatening, management is focused mainly on symptom control & prevention of long-term morbidity & mortality

Treatment Approaches:

  • Rhythm control (restore and maintain sinus rhythm)
  • Rate control (control of ventricular rate while allowing atrial fibrillation to continue)
43
Q

Rate vs Rhythm Control?

A

Rate control - Generally involves drugs that act on AV node to slow conduction

Rhythm control -Achieved either by synchronized direct current or by drugs (both methods must be preceded by anticoagulation)

44
Q

Drug Therapy in Rate Control?

A
  1. Rate control (slowing of ventricular rate) - negative dromotropic agents
  • Ca2+ channel blockers
  • b-blockers
  • Digoxin (in patients with reduced EF or CHF)
  • Amiodarone (when other agents can’t be used)
45
Q

Drug Therapy in Rhythm Control?

A
  1. Rhythm control (induction / maintenance of sinus rhythm)
  • Class IC antiarrhythmics, (flecainide, propafenone)
  • Class III antiarrhythmics, (amiodarone, dofetilide)
46
Q

What are the prevention methods used in Thromboembolic Events?

A
  • Heparin (IV) -Unstable patients who require immediate cardioversion
  • Warfarin (oral)- In stable patients cardioversion should be delayed for 3- 4 weeks until adequate anticoagulation has been achieved
  • Control of ventricular rate should be undertaken whilst patient is waiting for cardioversion
  • Oral anticoagulants usually continued for at least 4 weeks after procedure
47
Q
A

PCM Exam 2 Pharm (14 decks)

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