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Pharma: Cardiovascular System > Chapter 17: Antiarrhythmic Drugs > Flashcards

Chapter 17: Antiarrhythmic Drugs Flashcards

1
Q

What are class I (Na+ channel blockers)? (7)

A 
Disopyramide (IA)
Procainamide (IA)
Quinidine (IA)
Lidocaine (IB)
Mexiletine (IB)
Flecainidine (IC)
Propafenone (IC)
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2
Q

What are class II (B-adrenoreceptor blockers)? (3)

A

Esmolol
Metoprolol
Propranolol

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3
Q

What are class III (K+ channel blockers)? (4)

A

Amiodarone
Dofetilide
Dronedarone
Sotalol

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4
Q

What are class IV ( Ca2+ channel blockers)?

A

Diltiazem

Verapamil

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5
Q

What are other anti-arrhythmic drugs?

A

Adenosine

Digoxin

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6
Q

What are causes of arrhythmias?

A
  1. Abnormal automaticity: cardiac sites other than the SA node showing enchanced automaticity generating competing stimuli; also damaged cardiomyocytes which may remain depolarized during diastole and reach the firing threshold earlier than normal SA cells
    Effects of drugs on automaticity: suppress automaticity by blocking Na+ or Ca2+ channels to reduce ratio of these ions to K+, this decreases slope of phase 4 depolarization and lowers the threshold to a less negative voltage
2. Abnormalities in impulse conduction: reentry can occur if unidirectional block caused by myocardial injury to prolonged refractory period  results in abnormal confuction; most common cause of arrhythmias 
Effects of drugs on conduction abnormalities: prevent reentry by slowing conduction (class I) or increasing the refractory period (class III), converting the unidirectional block into a bidirectional block
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7
Q

What is the mechanism of class I antiarrhythmic drugs?

A

-block voltage sensitive sodium channels via the same mechanism as local anesthetics, decrease rate of entry of Na+ slows rate of rise of Phase 0 of the action potential

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8
Q

What is the use dependence of class I drugs? IA, IB, IC

A

Class I drugs bind to open or inactivated Na+ channels than to channels that are fully repolarized; these drugs show more effect in tissues that are rapidly repolarzing
-these drugs are use dependent: they blocks cells that are discharging at an abnormally high frequency without interfering with the normal low frequency beating of the heart

Class IA: slow rate of rise of action potentian and prolong action potential, increase ventricular refractory period

Class IB: little effect on rate of depolarization; they decrease duration of action potential by shortening repolarization; rapidly interact with Na+ channels

Class IC: depress rate of rise of the action potential; they cause slowing of confuction but have little effect on duration of membrane action potential

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9
Q

What is the use dependence of class I drugs? IA, IB, IC

A

Class I drugs bind to open or inactivated Na+ channels than to channels that are fully repolarized; these drugs show more effect in tissues that are rapidly repolarzing
-these drugs are use dependent: they blocks cells that are discharging at an abnormally high frequency without interfering with the normal low frequency beating of the heart

Class IA: slow rate of rise of action potentian and prolong action potential, increase ventricular refractory period

Class IB: little effect on rate of depolarization; they decrease duration of action potential by shortening repolarization; rapidly interact with Na+ channels

Class IC: depress rate of rise of the action potential; they cause slowing of confuction but have little effect on duration of membrane action potential or ventricular effective refractory period; bind slowly to Na+ channels

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10
Q

What is the MOA, indications, pharmokinetics, and adverse effects of quinidine?

A

MOA: binds to open and inactivated Na+ channels and prevents Na+ influx (slows upstroke of phase 0); also decreases slope of phase 4 and inhibits K+ channels

indications: atrial, AV junctional and ventricular tachyarrhythmias
pharmokinetics: oral administration, hepatic cytochrome P450 enzymes

adverse effects: development of an arrhythamia

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11
Q

What is the MOA, indications, pharmokinetics, and adverse effects of quinidine?

A

MOA: binds to open and inactivated Na+ channels and prevents Na+ influx (slows upstroke of phase 0); also decreases slope of phase 4 and inhibits K+ channels

indications: atrial, AV junctional and ventricular tachyarrhythmias
pharmokinetics: oral administration, hepatic cytochrome P450 enzymes

adverse effects: development of an arrhythmia

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12
Q

What is the MOA, indications, pharmokinetics, and adverse effects of procainamide?

A

MOA: class IA drug, derivative of local anesthetic procaine, shows actions simliar to quinidine

pharmokinetics: oral; prolongs duration of the action potential, eliminated renally

adverse effects: high incidence (with chronic use) of reversible lupus syndrome
CNS side effects: depression, hallucination, psychosis

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13
Q

What is the MOA, indications, pharmokinetics, and adverse effects of disopyramide?

A

MOA: actions similar to quinidine, produces negative inotropic effect, causes peripheral vasoconstriction

indications: treatment of ventricular arrhythmias as an alternate to procainamide or quinidine
pharmokinetics: excreted renally and liver

adverse effects: may produce important decrease in myocardial contractility in patients with preexisting impairment of left ventricular function; anticholinergic activity

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14
Q

What is the MOA, indications, pharmokinetics, and adverse effects of lidocaine? IB drug (IB drugs rapidly associate and dissociate from sodium channels)

A

MOA: shortens phase 3 repolarization in ventricular muscle and decreases duration of action potential; work when cardiac cell is depolarzied and firing rapidly

indications: ventricular arrhythamias (in emergency situation) in MI
pharmokinetics: IV

adverse effects: wide toxic-to-therapeutic ratio

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15
Q

What are indications of mexiletine and tocainide?

A

Class IB drugs with similar action to lidocaine

Mexiletine: chronic treatment of ventricular arrhythmias associated with previous MI
Tocainide: treatment of ventricular tachyarrhythmias; has pulmonary toxicity which may lead to pulmonary fibrosis

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16
Q

What is the MOA, indications, pharmokinetics, and adverse effects of lidocaine? IB drug (IB drugs rapidly associate and dissociate from sodium channels)

A

MOA: shortens phase 3 repolarization in ventricular muscle and decreases duration of action potential; work when cardiac cell is depolarzied and firing rapidly

indications: ventricular arrhythamias (in emergency situation) in MI
pharmokinetics: IV

adverse effects: wide toxic-to-therapeutic ratio

17
Q

What is the MOA, indications, pharmokinetics, and adverse effects of flecainide? IC drug

A

MOA: IC drug-slowly dissociate from resting Na+ channels; suppresses phase 0 upstroke in Purkinje and myocardial fibres which causes slowing of conduction in all cardiac tissue

indications: treatment of refractory ventricular arrhythmias; partially useful in suppressing premature ventricular contraction

18
Q

What is the MOA, indications, pharmokinetics, and adverse effects of flecainide? IC drug

A

MOA: IC drug-slowly dissociate from resting Na+ channels; suppresses phase 0 upstroke in Purkinje and myocardial fibres which causes slowing of conduction in all cardiac tissue

indications: treatment of refractory ventricular arrhythmias; partially useful in suppressing premature ventricular contraction
pharmokinetics: absorbed orally

adverse effects: like all other class IC drugs, can aggrevate preexisting arrhythmias or induce life threatening ventricular tachycardia that is resistant to treatment

19
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Class II antiarrhythmic drugs?
ex: propanolol, metoprolol, esmolol

A

MOA: these drugs are B adrenergic antagonists; diminish phase 4 depolarization which depresses automaticity, prolongs AV conduction, decreases HR and contractility

indications: treatment of tachyarrhythmias caused by increased sympathetic activity

20
Q

What is the MOA, indications, pharmokinetics, and adverse effects of Class II antiarrhythmic drugs?
ex: propanolol, metoprolol, esmolol

A

MOA: these drugs are B adrenergic antagonists; diminish phase 4 depolarization which depresses automaticity, prolongs AV conduction, decreases HR and contractility

indications: treatment of tachyarrhythmias caused by increased sympathetic activity; useful in atrial flutter and fibrillation

Ex: Propanolol- reduces sudden arrhythmic death after MI by preventing ventricular arrhythmias

Metaprolol- widely used to treat cardiac arrhythmias; reduces risk of bronchospasm

Esmolol- very short acting used in acute arrhythmias that occur after surgery or during an emergency

21
Q

What is the mechanism of Class III antiarrhythmic drugs? ex: Aminodarone, Dronedarone, Sotalol, Dofetilide

A
  • block K+ channels which diminishes the outward K+ current during repolarization of cardiac cells
  • prolong the effective refractory period
  • all class III drugs have the potential to induce arrhythmias
22
Q

What is the MOA, indications, pharmokinetics, and adverse effects of amiodarone?

A

MOA: prolongation of action potential duration and refractory period; antianginal and antiarrhythmic activity

indications: treatment of severe refractory supraventricular and ventricular tachyarrhythmias; main treatment of atrial fibrillation; effective in maintaining sinus rhythm
pharmokinetics: oral administration, prolonged halflife of several weeks and distributes in adipose tissue

adverse effects: high doses cause interstitial pulmonary fibrosis, GI intolerance, liver toxicity and blue skin discolouration
-iodine moieties responsible for thyroid dysfunction

23
Q

What is the MOA, indications, pharmokinetics, and adverse effects of dronedarone?

A
  • simliar to amiodarone but less toxic since it doesn’t have the iodine moiety
  • less effective than amiodarone in decreasing AF recurrance
24
Q

What is the MOA, indications, pharmokinetics, and adverse effects of sotalol?

A

MOA: potent class III drug that also has nonselective B-blocker activity; blocks rapid outward K+ current which prolongs repolarization and duration of action potential which prolongs the refractory period

25
Q

What is the MOA, indications, pharmokinetics, and adverse effects of sotalol?

A

MOA: potent class III drug that also has nonselective B-blocker activity; blocks rapid outward K+ current which prolongs repolarization and duration of action potential which prolongs the refractory period

indications: long term therapy to decrease rate of death in patients after a MI; suppress ectopic beats and reduce myocardial O2 demand; more effective in preventing arrhythmias than imipramine, mexiletine, procainamide, propafenone, and quinidine in patients with sustained ventricular tachycardia

adverse effects: prolong QT interval; torsades de pointes is a serious potential adverse effect

26
Q

What is the MOA, indications, pharmokinetics, and adverse effects of sotalol?

A

MOA: potent class III drug that also has nonselective B-blocker activity; blocks rapid outward K+ current which prolongs repolarization and duration of action potential which prolongs the refractory period

indications: long term therapy to decrease rate of death in patients after a MI; suppress ectopic beats and reduce myocardial O2 demand; more effective in preventing arrhythmias than imipramine, mexiletine, procainamide, propafenone, and quinidine in patients with sustained ventricular tachycardia

adverse effects: prolong QT interval; torsades de pointes is a serious potential adverse effect

27
Q

What is the MOA, indications, pharmokinetics, and adverse effects of dofetilide?

A

-can be used as first line antiarrhythmic drug in persistent AF and HF in patients with CAD with impaired left ventricular function

28
Q

What is the MOA, indications, pharmokinetics, and adverse effects of dofetilide?

A

MOA: class III antiarrhythmic drug; prolongs phase 3 repolarization in ventricular muscle fibres

indications: can be used as first line antiarrhythmic drug in persistent AF and HF in patients with CAD with impaired left ventricular function
pharmokinetics: renally excreted

adverse effects: risk of proarrhythmia

29
Q 
What is the mechanism of class IV antiarrhythmic drugs? 
Ex: Verapamil, Nifedipine, Diltiazem
A
  • Ca2+ channel blockers; decrease inward Ca2+ current resulting in decrease rate of phase 4 spontaneous depolarization; slow conduction in tissues dependent on Ca2+ currents
  • Verapamil has greater action on the heart than on vascular smooth muscle; Nifedipine(used to treat HT) has stronger effect on vascular smooth muscle than the heart; Diltiazem is intermediate in action

Verapamil, Diltiazem
MOA: effective against voltage sensitive channels causing a decrease in slow inward current that triggers cardiac contraction; prevent repolarization until drug dissociates from channel; slow conduction and prolong refractory period

indications: atrial arrhythmias; reentrant supraventricular tachycardia and reduce ventricular rate in atrial flutter and fibrillation; treat HT and angina
pharmokinetics: oral administration and metabolized by the liver

adverse effects:negative inotropic properties so contraindicated in patients with preexisting depressed cardiac function; both drugs can decrease BP because of peripheral vasodilation (beneficial in treating HT)

30
Q

What are the other antiarrhythmic drugs and their mechanisms?

A

Digoxin: shortens refractory period in atrial and ventricular myocardial cells while prolonging effective refractory period and diminishing conduction velocity in the AV node

  • used to control response rate in atrial fibrillation and flutter
  • at toxic concentrations: causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation

Adenosine: at high doses it decreases conduction velocity, prolongs refractory period and decreases automaticity in the AV node
-IV is drug of choice for abolishing acute supraventricular tachycardia

Pharma: Cardiovascular System (7 decks)

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