Drugs Used in Cardiac Arrhythmias Flashcards

1
Q

Class 1 Sodium Channel-blocking Drugs: 1A

A

– Quinidine (Cardioquin)
– Procainamide (Pronestyl)
– Disopyramide (Norpace)

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2
Q

Class 1 Sodium Channel-blocking Drugs: 1B

A

– Lidocaine (Xylocaine)

– Mexiletine (Mexitil)

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3
Q

Class 1 Sodium Channel-blocking Drugs: 1C

A

– Flecainide (Tambocor)

– Propafenone (Rythmol)

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4
Q

Class 2 Beta Blockers

A

– Esmolol (Brevibloc)

– Propranolol (Inderal)

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5
Q

Class 3 Potassium Channel-blocking Drugs

A

– Amiodarone (Cordarone)
– Sotalol (Betapace)
– Dofetilide (Tikosyn)
– Ibutilide (Corvert)

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6
Q

Class 4 Cardioactive Calcium Channel Blockers

A

– Verapamil (Isoptin)

– Diltiazem (Cardizem)

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7
Q

Miscellaneous agents

A

Adenosine (Adenocard)

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8
Q

Fast action potential in cardiac muscle: Which phase?

  • Voltage-dependent fast Na+ channels open as a result of depolarization; Na+ enters the cells down its electrochemical gradient
A

Phase 0

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9
Q

Fast action potential in cardiac muscle: Which phase?

  • K+ exits cells down its gradient, while fast Na+ channels close, resulting in some repolarization
A

Phase 1

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10
Q

Fast action potential in cardiac muscle: Which phase?

  • plateau phase results from K+ exiting cells offset by and Ca2+ entering through slow voltage-
    dependent Ca2+ channels
A

Phase 2

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11
Q

Fast action potential in cardiac muscle: Which phase?

  • Ca2+ channels close and K+ begins to exit more rapidly resulting in repolarization
A

Phase 3

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12
Q

Fast action potential in cardiac muscle: Which phase?

  • Resting membrane potential is gradually restored by Na+/K+ ATPase and the Na+/Ca2+
    exchanger
A

Phase 4

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13
Q

Effects of Class 1A drugs

A
  • Block sodium channels
  • Bind to open (ACTIVATED) sodium channels
  • Dissociate from channel with INTERMEDIATE kinetics
  • Block POTASSIUM channels
  • PROLONG AP duration **
  • Prolong QRS and QT intervals of the ECG **
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14
Q

Class 1A: Procainamide

Clinical Use?

A

• Used infrequently (frequent dosing is required,
common occurrence of lupus-related side effects)

• Is effective in sustained VENTRICULAR TACHYCARDIAS and arrhythmias associated with myocardial infarction (not
a first choice drug for these indications)

• Sidenote: it directly depresses the activities of SA and AV nodes

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15
Q

Class 1A: Procainamide

Adverse effects?

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

• Extracardiac
– Lupus erythematosus syndrome with arthritis, pleuritis, pulmonary disease, hepatitis and fever
– Nausea, diarrhea
– Agranulocytosis

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16
Q

Class 1A: Quinidine

Pharmacodynamics and clinical use?

A

– Affords antimuscarinic effect on the heart –> may ENHANCE AV conductance

– Exhibits beta-blocking activity (effect on PR interval is
variable)

– May cause HYPOTENSION –> tachycardia

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17
Q

Class 1A: Quinidine

Clinical use?

A

Rarely used because of cardiac and extracardiac adverse

effects and the availability of better-tolerated antiarrhythmic drugs

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18
Q

Class 1A: Quinidine

Adverse effects?

A

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

• Extracardiac:
– GI side effects (diarrhea, nausea, vomiting)
– Headache, dizziness, tinnitus (cinchonism)
– Thrombocytopenia, hepatitis, fever

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19
Q

Class 1A: Disopyramide

Clinical use?

A

Recurrent ventricular arrhythmias

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20
Q

Class 1A: 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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21
Q

Effect of Class 1B Drugs

A
  • Block sodium channels
  • Bind to INACTIVATED sodium channels (bind to depolarized cells)
  • Dissociate from channel with fast kinetics
  • SHORTEN the AP
  • Do NOT block potassium channels
  • Do NOT prolong AP or QT duration
22
Q

Class 1B: Lidocaine

Clinical use?

A

Termination of ventricular tachycardia in the setting

of acute myocardial ischemia

23
Q

Class 1B: 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

24
Q

Class 1B: Mexiletine

Clinical use?

A

• Ventricular arrhythmias

• To relieve chronic pain, especially pain due to
diabetic neuropathy and nerve injury

25
Q

Class 1B: Mexiletine

Adverse effects?

A
  • Tremor
  • Blurred vision
  • Nausea
  • Lethargy
26
Q

Effect of Class 1C Drugs

A
  • Block sodium channels
  • Bind to open (ACTIVATED) sodium channels
  • Dissociate from channel with SLOW kinetics
  • Block certain potassium channels **
  • Do NOT prolong AP duration and QT interval duration of the ECG **
  • Prolong QRS interval duration **
27
Q

Class 1C : Flecainide

What channels does it block?

A

Blocks sodium and potassium channels

28
Q

Class 1C : Flecainide

Clinical use?

A

In patients with otherwise normal hearts who have

supraventricular arrhythmias

29
Q

Class 1C : 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

30
Q

Class 1C : Propafenone

Clinical use?

A

Supraventricular arrhythmias in patients without structural disease

31
Q

Class 1C : Propafenone

Adverse effects?

A
  • Exacerbation of ventricular arrhythmias
  • A metallic taste
  • Constipation
32
Q

Class 2 Beta-Blockers

Effect on AP?

A

• Slow action potential
– Sinoatrial node – decrease HR (increase RR interval)

– AV node – decrease AV conductance (increase
PR interval)

33
Q

Class 2 Beta-Blockers:

Clinical use of propranolol in cardiac arrhythmias?

A
  • Arrhythmias associated with stress and THYROID storm
  • Atrial fibrillation and flutter
  • Paroxysmal supraventricular arrhythmias

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

34
Q

Class 2 Beta-Blockers: Esmolol

Clinical use?

A
  • 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

35
Q

Adverse effects of Beta-blockers?

A
– Reduced cardiac output
– Bronchoconstriction
– Impaired liver glucose mobilization
– Produce an unfavorable blood lipoprotein profile (increase VLDL
and decrease HDL) 
– Sedation, depression 
– Withdrawal syndrome associated with sympathetic
hyperresponsiveness
36
Q

Contraindications to Beta-blockers?

A
– Asthma
– Peripheral vascular disease
– Raynaud’s syndrome
– Type 1 diabetics on insulin
– Bradyarrhythmias and AV conduction abnormalities
– Severe depression of cardiac function
37
Q

Class 3 Potassium Channel Blockers:

Effects of Class 3 drugs?

A

– Block potassium channels
– Prolong action potential duration
– Prolong QT interval on ECG
– Prolong refractory period

38
Q

Class 3 Potassium Channel Blockers: Amiodarone

Clinical use?

A
  • Recurrent ventricular tachycardia

* Atrial fibrillation

39
Q

Class 3 Potassium Channel Blockers: Amiodarone

Effects on heart rate and conduction?

A
  • Has calcium channel blocking activities
  • Causes bradycardia and slows AV conduction
  • Causes peripheral vasodilation (effect may be related to the action of the vehicle)
40
Q

Class 3 Potassium Channel Blockers: 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

41
Q

Class 3 Potassium Channel Blockers: Sotalol

Clinical use?

A

• Treatment of life-threatening ventricular
arrhythmias

• Maintenance of sinus rhythm in patients with atrial
fibrillation

42
Q

Class 3 Potassium Channel Blockers: Sotalol

Adverse effects?

A
  • Depression of cardiac function

* Provokes torsade de pointes

43
Q

Class 3 Potassium Channel Blockers: Dofetilide

Clinical use?

A

• Restore sinus rhythm in patients with atrial
fibrillation

• Maintain the sinus rhythm after cardioversion in
patients with atrial fibrillation

44
Q

Class 3 Potassium Channel Blockers: Dofetilide

Adverse effects?

A

QT interval prolongation and increased risk of

ventricular arrhythmias

45
Q

Class 3 Potassium Channel Blockers: Ibutilide

Clinical use?

A

Conversion of atrial flutter and atrial fibrillation to sinus rhythm

46
Q

Class 3 Potassium Channel Blockers: Ibutilide

Adverse effects?

A

QT interval prolongation and increased risk of ventricular arrhythmias (patients require continuous ECG monitoring until QTc returns to baseline)

47
Q

Effect of Class 4 L-type calcium channel blockers

A

• Block both ACTIVATED AND INACTIVATED L-type
calcium channels

• Active in slow response cells

  • Decrease the slope of phase 0 depolarization
  • Increase L-type Ca2+ channel threshold potential
  • Prolong refractory period in AV node

• Slow sinoatrial node depolarization, cause
bradycardia

• Prolong action potential duration and conduction time in AV node

48
Q

Effect of Class 4 L-type calcium channel blockers:

Clinical use?

A
  • Termination and prevention of paroxysmal supraventricular tachycardia
  • Ventricular rate control in atrial fibrillation and flutter
49
Q

Effect of Class 4 L-type calcium channel blockers:

Adverse effects?

A
• Cardiac
– Negative inotropy 
– AV block 
– Sinoatrial node arrest 
– Bradyarrhythmias 
– Hypotension

• Extracardiac
– Constipation (Verapamil)

50
Q

Miscellaneous: Adenosine

Effects of Adenosine

A

– Activates potassium current and inhibits Ca2+ and
Funny currents, causing marked hyperpolarization and suppression of action potentials in slow cells

– Inhibits AV conduction and increases nodal refractory period

51
Q

Miscellaneous: Adenosine

Clinical use?

A

Conversion to sinus rhythm in paroxysmal supraventricular tachycardia

52
Q

Miscellaneous: Adenosine

Adverse effects?

A

• Shortness of breath

• Bronchoconstriction (both A1
and A2B adenosine receptors cause bronchoconstriction)

  • Chest burning
  • AV block
  • Hypotension