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Cardio II Final > Drugs Used in Cardiac Arrhythmias - DSA > Flashcards

Drugs Used in Cardiac Arrhythmias - DSA Flashcards

1
Q

Class 1 Sodium Channel-Blocking drugs

A

1A drugs:
Quinidine
Procainamide
Disopyramide

1B drugs:
Lidocaine
Mexiletine

1C drugs:
Flecainide
Propafenone

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2
Q

Class 2 Beta Blockers

A

Esmolol

Propranolol

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3
Q

Class 3 Potassium channel-blocking drugs

A 
Amiodarone
Dronedarone
Sotalol
Dofetilide
Ibutilide
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4
Q

Class 4 Cardioactive Calcium channel blockers

A

Verapamil

Diltiazem

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5
Q

Misc. agents

A

adenosine

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6
Q

Class 1 A drugs

A

– Block sodium channels, slow impulse conduction, reduce automatism of latent (ectopic) pacemakers

– Use-dependent block – preferentially bind to open (activated) sodium channels
• Ectopic pacemaker cells with faster rhythms will be preferentially targeted

– Dissociate from channel with intermediate kinetics

– Block potassium channels

– Prolong action potential duration

– Prolong QRS and QT intervals of the ECG

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7
Q

Procainamide

A

– Used to treat sustained ventricular tachycardias, may be used in
arrhythmias associated with myocardial infarction
– Directly depresses the activities of SA and AV nodes
– Possesses antimuscarinic activity

– Has ganglion-blocking properties, reduces peripheral vascular resistance – may cause hypotension

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8
Q

Procainamide pharmacokinetics

A

Active metabolite N-acetylprocainamide has Class 3 activity, has longer half-life, accumulates in renal dysfunction – measurements of both parent drug and metabolite are necessary in pharmacokinetic studies

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9
Q

Procainamide adverse effects

A

Cardiac:
• QT interval prolongation
• Induction of torsade de pointes arrhythmias and syncope
• Excessive inhibition of conduction

Extra cardiac:
• Lupus erythematosus syndrome with arthritis, pleuritis,
pulmonary disease, hepatitis and fever
• Nausea, diarrhea
• Agranulocytosis
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10
Q

Quinidine

A

Natural alkaloid from Cinchona bark

– Used occasionally for restoring rhythm in atrial flutter/fibrillation patients with normal (but arrhythmic) hearts
– Sustained ventricular arrhythmia
– In clinical trials patients on quinidine twice as likely have normal sinus
rhythm, but the risk of death is increased two to three-fold
– Affords antimuscarinic effect on the heart – may enhance AV conductance
– May cause hypotension  tachycardia

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11
Q

Quinidine adverse effects

A

Cardiac:
• QT interval prolongation
• Induction of torsade de pointes arrhythmia and syncope
• Excessive slowing of conduction throughout the heart

Extra cardiac:
• GI side effects (diarrhea, nausea, vomiting)
• Headache, dizziness, tinnitus (cinchonism)
• Thrombocytopenia, Hepatitis, Fever

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12
Q

Disopyramide

A

– Used for the treatment of
• Recurrent ventricular arrhythmias
– Affords potent antimuscarinic effect on the heart

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13
Q

Disopyramide adverse effects

A

Cardiac: QT interval prolongation, induction of torsade de pointes arrhythmia and syncope, negative inotropic effect – may precipitate heart failure, excessive depression of cardiac conduction

Extracardaic: atropine-like symptoms – urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma

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14
Q

Class 1B drugs

A

– Block sodium channels

– Use-dependent block – bind to inactivated sodium channels
• Preferentially bind to depolarized cells

– Dissociate from channel with fast kinetics – no effect on conduction in
normal tissue

– May shorten action potential

– More specific action on sodium channels – do not block potassium
channels, do not prolong action potential or QT duration on ECG

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15
Q

Lidocaine

A

– Blocks inactivated sodium channels (use-dependence) – selectively
blocks conduction in depolarized tissue, making damaged tissue
completely “electrically silent”
– Rapid kinetics results in recovery from block between AP, with no effect
on cardiac conductivity in normal tissue
– Used in mono- and polymorphic ventricular tachycardias
• Very efficient in arrhythmias associated with acute myocardial infarction

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16
Q

Lidocaine pharmacokinetics

A

extensive first-pass metabolism – used only by the intravenous route

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17
Q

Lidocaine adverse effects

A

• The least toxic of all Class 1 drugs
• Cardiovascular: may cause hypotension in patients with heart
failure by inhibiting cardiac contractility, proarrhythmic effects are
uncommon
• Neurological effects: paresthesias, tremor, slurred speech,
convulsions

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18
Q

Mexiletine

A

– Orally active drug

– Electrophysiological and antiarrhythmic effects are similar to lidocaine

– Clinical use
• Ventricular arrhythmias
• To relieve chronic pain, especially the pain due to diabetic
neuropathy and nerve injury

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19
Q

Mexiletine adverse effects

A
  • Tremor
  • Blurred vision • Nausea
  • Lethargy
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20
Q

Class 1C drugs

A

– Block sodium channels, slow impulse conduction
– Preferentially bind to open (activated) sodium channels
– Dissociate from channel with slow kinetics
– Block certain potassium channels
– Do not prolong action potential duration and QT interval duration of the ECG
– Prolong QRS interval duration

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21
Q

Flecainide

A

– Blocks sodium and potassium channels

– Has no antimuscarinic effects

– Clinical use
• In patients with normal hearts
• Treatment of supraventricular arrhythmias including AF,
paroxysmal SVT (AVNRT, AVRT)
• Life-threatening ventricular arrhythmias, such as sustained
ventricular tachycardia

22
Q

Flecainide adverse effects

A

May be very effective in suppressing premature ventricular contractions, but may cause severe exacerbation of ventricular arrhythmias when administered to
• Patients with preexisting ventricular tachyarrhythmias
• Patients with a previous myocardial infarction
• Patients with ventricular ectopic rhythms

23
Q

Propafenone

A

– Possesses weak -blocking activity

– Used
• To prevent paroxysmal AF and SVT in patients without structural
disease
• In sustained ventricular arrhythmias

24
Q

Propafenone adverse effects

A

• Exacerbation of ventricular arrhythmias
• A metallic taste
• Constipation
• Do not combine with the CYP2D6 and CYP3A4 inhibitors as the
risk of proarrhythmia may be increased

25
Q

Class 2 drugs

A

• Pacemaker action potential
– Sinoatrial node – decrease HR (increase RR interval)
– AV node – decrease AV conductance (Increase PR interval

• Ventricular myocardium
– Decrease Ca2+ overload, prevent delayed after depolarizations

26
Q

Propranolol

A

Clinical indications for use in cardiac arrhythmias
• Arrhythmias associated with stress

• Re-entrant arrhythmias that involve AV node
– AV nodal reentrant tachycardia (AVNRT)
– AV reentrant tachycardia (AVRT)

• Atrial fibrillation and flutter

• Arrhythmias associated with MI
– Decrease mortality in patients with acute MI

27
Q

Esmolol

A
  • Short-acting selective beta-1 blocker
  • Half-life is 10 min because of hydrolysis by blood esterases
  • Used as a continuous i.v. infusion, with rapid onset and termination of its action

• Clinical use
– Supraventricular arrhythmias
– Arrhythmias associated with thyrotoxicosis
– Myocardial ischemia or acute myocardial infarction with arrhythmias
– As an adjunct drug in general anesthesia to control arrhythmias in
perioperative period

28
Q

Class 3 drugs

A

– Block potassium channels
– Prolong action potential duration and QT interval on ECG
– APD prolongation is rate-dependent, with the most marked effect at slow
heart rates
– Prolong refractory period

29
Q

Amiodarone

A

– Blocks potassium channels
– Prolongs QT interval and APD uniformly over a wide range of heart rates
– Blocks inactivated sodium channels
– Possesses adrenolytic activity
– Has calcium channel blocking activities
– Causes bradycardia and slows AV conduction
– Causes peripheral vasodilation (effect may be related to the action of the
vehicle)

– Clinical use
• Treatment of ventricular arrhythmias
• Atrial fibrillation (not an FDA approved indication)

30
Q

Amiodarone pharmacokinetics

A
  • Metabolized by CYP3A4 – its half-life is affected by drugs that inhibit CYP3A4 (cimetidine), or induce it (rifampin)
  • Major metabolite is active, with very long elimination half-life (weeks-months)
  • Effects are maintained 1 to 3 months after discontinuation, and metabolites are found in the tissues 1 year after discontinuation
  • Inhibits many CYP enzymes – may affect the metabolism of many other drugs
  • All medications should be carefully reviewed in patients on amiodarone – dose adjustments may be necessary
31
Q

Amiodarone adverse effects

A
  • Cardiac
  • AV block and bradycardia
  • Incidence of torsade de pointes is low as compared to other Class 3 drugs

• Extracardiac
• Fatal pulmonary fibrosis
• Hepatitis
• Photodermatitis, deposits in the skin, gives blue-grey skin discoloration in sun-exposed areas
• Deposits of drug in cornea and other eye tissues, optical
neuritis
• Blocks the peripheral conversion of thyroxine to
triiodothyronine, also a source of inorganic iodine in the body – may cause hypo- or hyperthyroidism

32
Q

Dronedarone

A

• Amiodarone derivative (but without the iodine moiety)
• Blocks multiple K+ channels
– Prolongation of repolarization, action potential duration, and refractory period
• Blocks Na+ current
• Blocks L-type Ca2+ current
– Decreased nodal conduction
– Causes bradycardia
– Prolongs AV refractory period and P-R interval
• Has stronger antiadrenergic effects than Amiodarone

33
Q

Dronedarone clinical indication

A

– Approved for the treatment of atrial fibrillation/flutter
– Not as effective as Amiodarone in maintaining sinus rhythm in these
patients

34
Q

Dronedarone adverse effects

A

– Worsening HF
– GI manifestations abdominal pain, nausea, vomiting, diarrhea
– Less side effects as compared with Amiodarone (no iodine moiety, shorter
half-life, less drug interactions)

35
Q

Dronedarone contraindication

A

– Black Box FDA warning: Increases risk of mortality in patients with decompensated HF (Class IV) and in patients with a recent decompensation of heart failure requiring hospitalization

36
Q

Sotalol

A

– Class 2 (non-selective beta-blocker) and class 3 agent (prolongs APD)
– Clinical use
• Treatment of life-threatening ventricular arrhythmias
• Maintenance of sinus rhythm in patients with atrial fibrillation
– Adverse effects

  • Depression of cardiac function
  • Provokes torsade de pointes
37
Q

Dofetilide

A

– Specifically blocks rapid component of the delayed rectifier potassium
current – effect is more pronounced at lower heart rates
– Eliminated by kidneys, has very narrow therapeutic window – dose has to
be adjusted based on creatinine clearance
– Used to convert AF to the sinus rhythm and maintain the sinus rhythm
after cardioversion
– Adverse effects
• QT interval prolongation and increased risk of ventricular arrhythmias

38
Q

Class 4 drugs

A

• Block both activated and inactivated L-type calcium channels
• Active in slow response cells – decrease the slope of phase 0 depolarization
• Slow sinoatrial node depolarization, cause bradycardia
• Prolong action potential duration and refractory period in AV node
• Prolong AV node conduction time
• May suppress delayed afterdepolarizations – may be effective in DAD-induced
ventricular arrhythmias

39
Q

Clinical use of verapamil and diltiazem

A

– Prevention of paroxysmal SVT

– Rate control in AF and atrial flutter

40
Q

Adverse effects of verapamil and diltiazem

A 
– Cardiac
• Negative inotropy
• AV block
• Sinoatrial node arrest
• Bradyarrhythmias
• Hypotension
– Extracardiac
• Constipation (Verapamil)
41
Q

Adenosine

A

– Activates potassium current and inhibits Ca2+ and Funny currents,
causing marked hyperpolarization and suppression of action potentials in
pacemaker cells
– Inhibits AV conduction and increases nodal refractory period
– Clinical use
• Conversion to sinus rhythm in paroxysmal SVT

42
Q

Adenosine adverse effects

A
  • Shortness of breath
  • Bronchoconstriction (both A1 and A2B adenosine receptors cause bronchoconstriction)
  • Chest burning
  • AV block
  • Hypotension
43
Q

Proarrhythmia

A

drug-induced significant new arrhythmia or worsening of an existing
arrhythmia.

44
Q

Drugs causing long QT syndrome and torsade de pointes arrhythmias

A
  • Antiarrhythmic drugs – classes 1A and 3 (amiodarone very rarely induces TdPs)
  • Antipsychotics
  • Antihistamines
  • Antibiotics
  • Antidepressants
45
Q

Drug-induced torsade de pointes

A 
A rapid form of polymorphic VT associated with the evidence of prolonged
ventricular repolarization (long QT syndrome).
46
Q

Mechanism of TdPs arrhythmias

A

A type of a triggered activity resulting from
early afterdepolarizations

– Triggered activity are depolarizing oscillations in the membrane potential
induced by the preceding action potentials

– Early afterdepolarizations
• Often associated with the impaired function of potassium channels leading to a prolonged period of repolarization
• Abnormal depolarizations that occur during phase 2 or phase 3 of AP are due to the opening of Ca2+ or Na+ channels, respectively

47
Q

Prevention of drug-induced torsade de pointes

A

– Monitoring of QTc is necessary

– Do not give TdP-inducing drugs if QTc is >450 ms

48
Q

Digoxin-induced tachyarrythmias and ectopic rhythms

A

• Mechanism: A type of a triggered activity resulting from delayed
afterdepolarization
• Occur during phase 4 as a result of increased cytosolic Ca2+ due to Ca2+ overload
• Spontaneous Ca release from SR activates 3Na+/Ca2+ exchange leading to a net
depolarizing current

49
Q

Digoxin-induced bradyarrhythmias and AV blocks

A

Mechanism: central parasympathomimetic activity and accentuation of vagal
effects on the heart

50
Q

Tx of digoxin-induced arrhythmias

A
  • Cancel digoxin
  • Anti-digoxin antibodies (Digibind, Digifab)
  • Potassium supplementation to upper normal levels
51
Q

Class 1C drugs

A

• Cause ventricular arrhythmias, such as PVCs, sustained VT, and VF
• Cardiac Arrhythmia Suppression Trial (CAST) was terminated prematurely
because Flecainide and other class 1C drugs increased the mortality by 2.5-fold

Cardio II Final (15 decks)

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