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Pharmacology > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

• Class I - fast channel blockers (Na+)?

A
  • (IA) Quinidine, procainamide, disopyramide
  • (IB) Lidocaine, mexiletine
  • (IC) Flecainide, propafenone
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2
Q

• Class II - b-blockers?

A

Propranolol, metoprolol, esmolol

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3
Q

• Class III - inhibitors of repolarization (K+)?

A

• Amiodarone, sotalol, dofetilide

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4
Q

• Class IV - calcium channel blockers (Ca2+) used for antiarrhythmics?

A

• Verapamil, diltiazem

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5
Q

• Miscellaneous drugs used for antiarrhythmics?

A

• Digoxin, adenosine, magnesium, atropine

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6
Q

MOA of sodium channel blockers?

A

• Block fast inward Na+ channels
• Decreased Na+ entry slows rate of rise of Phase 0
depolarization
• Cause decrease in excitability and conduction velocity
• Different properties depending on their affinity for Na+
channel
• Possess use / state-dependence

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7
Q

What is state dependence?

A

• Drugs bind more rapidly to open or inactivated Na+
channels
• Drugs have greater effect in tissues more freq.
depolarizing
Basically:
Use/state dependence = cells discharging at
abnormally high frequency are preferentially blocked

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8
Q

MOA of class 1A sodium channel blockers?

A

• Slow rate of change of phase 0
• Slowing conduction, prolonging action potential &
increasing ventricular effective refractory period
• Prolong phase 3 by an inhibiting K+ channels
• Intermediate speed of association with activated /
inactivated Na+ channels & intermediate rate of
dissociation
Increase QRS and QT intervals( moderate and significant respectively)

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9
Q

Quinidine MOA?

A

• Concomitant Class III activity (block K+ channels)
• Pro-arrhythmic
• Due to toxicity is being replaced by Ca2+ antagonists
Clinical Applications
• Suppression of supraventricular and ventricular
arrhythmias
Replaced by more effective/safer antiarrhythmic agents

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10
Q

Quinidine PK?

A

Pharmacokinetics
• Quinidine sulfate = rapid oral absorption
• Forms active metabolites (CYP 3A4)
• Inhibits CYP 2D6, 3A4 & P-glycoprotein

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11
Q

Quinidine AE?

A

• Arrhythmias (torsades de pointes)
• SA & AV block or asystole
• Nausea, vomiting & diarrhea (30-50%)
• Thrombocytopenic purpura
• Toxic doses – ventricular tachycardia (exacerbated by
hyperkalemia)
• Cinchonism (blurred vision, tinnitus, headache,
psychosis)
• Mixed a-adrenergic block & antimuscarinic properties
• Can increase [digoxin] by decreasing renal clearance

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12
Q

Quinidine contraindications?

A
  • Do not use in patients with:
  • Complete heart block
  • Use with extreme caution in patients with:
  • Prolonged QT interval
  • History of Torsades de Pointes
  • Incomplete heart block
  • Uncompensated heart failure
  • Myocarditis
  • Severe myocardial damage
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13
Q

Procainamide MOA?

A

• Derivative of local anesthetic procaine
• Similar actions to quinidine
• Blockade of Na+ channels in activated state
• Blockade of K+ channels
• Antimuscarinic properties
Clinical Applications
• Suppression of supraventricular and ventricular
arrhythmias
Due to proarrhythmic effects use should be reserved
for life-threatening arrhythmias

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14
Q

Procainamide PK?

A
  • IV
  • Metabolized by CYP 2D6
  • Partly acetylated to N-acetylprocainamide (NAPA) which prolongs duration of action potential (class III)
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15
Q

Procainamide AE?

A

Chronic use = high incidence of AE
• Reversible lupus-like syndrome (25-30%)
• Toxic doses: asystole, induction of ventricular
arrhythmias
• CNS effects (depression, hallucination, psychosis)
• Weak anticholingeric effects
• Hypotension

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16
Q

Procainamide contraindications?

A
  • Hypersensitivity
  • Complete heart block
  • 2nd degree AV block
  • Systemic lupus erythematosus (SLE)
  • Torsades de Pointes
  • Heart failure & hypertension (use with caution)
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17
Q

Disopyramide MOA and clinical applications?

A 
• Strong negative inotropic effect (> quinidine &
procainamide)
• Strong antimuscarinic properties
• Causes peripheral vasoconstriction
• Blocks K+ channels
Clinical Applications
• Suppression of supraventricular and ventricular
arrhythmias
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18
Q

Disopyramide AE?

A

• Pronounced negative inotropic effects
• Severe antimuscarinic effects (dry-mouth, urinary
retention, blurred vision, constipation)
• May induce hypotension & cardiac failure without preexisting
myocardial dysfunction

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19
Q

Class 1b moa?

A

• Slow Phase 0 & decrease slope of Phase 4
• Shorten Phase 3 repolarization
• Little effect on depolarization phase of action
potential in normal cells
• Rapidly associate and dissociate with Na+ channels
Increase QRS and decrease QT intervals(both mild)

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20
Q

Lidocaine MOA and PK?

A

• Local anesthetic
• More effect on ischemic or diseased tissue
• Particularly useful in treating ventricular arrhythmias
• LITTLE EFFECT on K+ channels
Pharmacokinetics
• IV only (extensive first-pass metabolism)

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21
Q

Lidocaine Clinical applications?

A

• Acute treatment of ventricular arrhythmias from
myocardial infarction or cardiac manipulation (eg,
cardiac surgery)
• Treatment of digitalis-induced arrhythmias
• Lidocaine’s use for VT has declined as a consequence of
trials showing IV amiodarone to be superior
• Little effect on atrial or AV junction arrhythmias

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22
Q

Lidocaine AE?

A
  • Wide toxic-therapeutic ratio
  • CNS effects (drowsiness, slurred speech, agitation etc.)
  • Little impairment of left ventricular function
  • NO negative inotropic effect
  • Cardiac arrhythmias (<10%)
  • Toxic doses: convulsions, coma
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23
Q

Mexiletine Clinical applications and adverse effects

A
  • Orally active derivative of lidocaine
  • Can be used both orally and IV

Clinical Applications
Management of severe ventricular arrhythmias

Adverse Effects
Mainly CNS & GI

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24
Q

Class 1C MOA?

A

• 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
Marked Increase in the QRS interval

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25
Q

Flecainide clinical applications?

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.

26
Q

Flecainide AE?

A
  • Negative inotropic efffect (aggravates CHF)
  • CNS effects: dizziness, blurred vision, headache
  • GI effects: nausea, vomiting, diarrhea
  • Life-threatening arrhythmias & ventricular tachycardia
27
Q

Propafenone clinical application and adverse effect?

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.

28
Q

EKG changes with Class 1 drugs?

A

Quinidine, procainamide, disopyramide
Block both Na+ and K+ channels
Increase both QRS and QT

Lidocaine, mexiletine
Block Na+ channels
Small increase in QRS. Clinically insignificant
decrease in QT

Flecainide, propafenone
Block Na+ channels
Significant increase in QRS

29
Q

Class 2 drug moa?

A

Beta 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
Increase the PR interval

30
Q

Propranolol and 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)

31
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

32
Q

Class 2 antiarrhythmics AE?

A

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

33
Q

Class 3 antiarrhythmics MOA?

A

• 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

34
Q

Amiodarone MOA?

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

35
Q

Amiodarone Clinical 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

36
Q

Amiodarone PK?

A

• Oral (very well absorbed) and IV
• t1/2 = several weeks (extensively distributed in adipose
tissue), loading dose required
• Full clinical effects (& adverse effects) may take 6 weeks
to achieve

37
Q

Amiodarone AE?

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.

38
Q

Amiodarone contraindications?

A
  • Patients taking:
  • Digoxin, theophylline, warfarin, quinidine
  • Patients with:
  • Bradycardia
  • SA or AV block
  • Severe hypotension
  • Severe respiratory failure
39
Q

Sotalol MOA?

A
  • Potent non-selective b-blocker
  • Inhibits rapid outward K+ current
  • Prolongs repolarization & duration of action potential
  • Lengthens refractory period
40
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

41
Q

Sotalol AE?

A

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

42
Q

Dofetilide clinical 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

43
Q

Dofetilide PK and AE?

A

Pharmacokinetics
• Excreted in urine (~80 % unchanged)
Adverse Effects
• Headache, chest pain, dizziness, ventricular tachycardia
• Torsade de Pointes (prolongs QT interval)

44
Q

Class 4 calcium channel blockers?

A

• 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
Increase PR interval

45
Q

Verapamil and diltiazem selectivity 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)

46
Q

Verapamil and diltiazem MOA?

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

47
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

48
Q

Verapamil and diltiazem AE 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

49
Q

Digoxin clinical application and effect on refractory period?

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

50
Q

Digoxin MOA?

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
51
Q

Digoxin action and use in atria?

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)

52
Q

Digoxin AE in regards to antiarrhythmics?

A

Toxic doses
• Ectopic ventricular beats → ventricular tachycardia
& fibrillation

53
Q

Adenosine PK, moa?

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)

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

54
Q

Adenosine AE?

A 
Low toxicity
• Flushing
• Burning
• Chest pain
• Hypotension
• Bronchoconstriction in asthmatics (may persist up to
30 min)
55
Q

Magnesium clinical uses? Atropine use?

A 
• Functional Ca2+ antagonist
Used for treatment of:
• Torsades de pointes
• Digitalis-induced arrhythmia
• Prophylaxis of arrhythmia in acute MI

Atropine:
• Used in bradyarrhythmias to decrease vagal tone

56
Q

Drugs used for SA node,AV, node, atrial myocytes, ventricular myocytes, and accessory pathways?

A

SA Node- b-blockers (II), calcium-channel blockers (IV)
& digoxin

AV Node- Calcium-channel blockers (IV), b-blockers (II)
& digoxin

Atrial myocytes Class’s IA & IC & K+ channels blockers (III)

Ventricular myocytes - Na+ channel blockers (I) & K+ channel blockers (III)

Accessory Pathways - Class IA & K+ channel blockers (III)

57
Q

Drugs used for these three areas: Ventricular & supraventricular, Mainly Ventricular, Mainly Supraventricular

A

Ventricular & supraventricular
Class’s IA & IC & K+ channels blockers (III)

Mainly Ventricular Lidocaine (IB) & mexiletine (IB)

Mainly Supraventricular Calcium-channel blockers (IV) & b-blockers (II)

58
Q

How to approach atrial flutter?

A

• Commonest arrhythmia encountered clinically
• 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)

59
Q

consequence of rate vs rhythm control of atrial flutter?

A

Studies show little difference between two strategies in
terms of symptom control or clinical events
Choice depends on patient characteristics &
preference
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)

60
Q

Drugs used in rate control?

Drugs used in rhythm 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)
  2. Rhythm control (induction / maintenance of sinus
    rhythm)
    • Class IC antiarrhythmics, (flecainide, propafenone)
    • Class III antiarrhythmics, (amiodarone, dofetilide)
61
Q

How to prevent 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

Pharmacology (49 decks)

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