Pharm: Antiarrythmics Flashcards by Caitlin miller

what causes arrhythmias?

abnormal impulse generation: early afterdepolarization, delayed afterdepolarization, disturbances in impulse formation
abnormal conduction: can result from depressed conduction (blocks) or reentry mechanisms

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what is reqd for a reenry mechanism

obstacle that establishes circuit

unidirectional block

conduction time must be long enough that retrograde impulse does not encounter refractor times

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refractoriness

shorten refractoriness and facilitate conduction: results in removal of the unidirectional block allowing signal to continue normally

prolong refractoriness/depress conduction: causes a bidirectional block such that the loop can no longer continue due to tissue still being refractory and being unable to respond

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Type 1A

procainamide*

Na+ channel blocker
Dissociates with intermediate kinetics

↓conduction velocity
↑refractoriness
↓autonomic properties

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Type 1B

lidocaine

Na+ channel blocker
Dissociates with rapid kinetics

No effect on velocity
May ↓refractoriness

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Type 1C

Flecainide

Na+ channel blocker
Dissociates with slow kinetics

↓conduction velocity
No effect on refractoriness

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Type III

amiodarone and sotalol

K+ channel blocker

↑refractoriness
↑action potential duration

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Type II

Beta-blockers, esmolol, metoprolol, propanolol

↓conduction velocity
↑refractoriness
↓autonomic properties

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Type IV

diltiazem/verapamil
non-DHP CCB’s

↓conduction velocity
↑refractoriness
↓autonomic properties

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Procainamide

** prototype ** Class 1A NA+ Channel Blocker

MOA: Slows upstroke of action potential (Phase 0), slows conduction, prolongs QRS, prolongs action potential duration

Use: rarely used, but used for atrial and ventricular arr.

SE: excessive potential prolongation, reversible lupus, nausea, diarrhea, hypotension

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Quinidine

Class 1A NA+ Channel Blocker

MOA: Slows upstroke of action potential (Phase 0), slows conduction, prolongs QRS, prolongs action potential duration

rarely used

toxicity GI [diarrhea, nausea, vomiting (33-50%)], cinchonism (headache, dizziness, tinnitus)

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Disopyramide

Class 1A NA+ Channel Blocker

MOA: Slows upstroke of action potential (Phase 0), slows conduction, prolongs QRS, prolongs action potential duration

Antimuscarinic effects, precipitates heart failure, urinary retention, dry mouth, blurred vision, constipation

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Lidocaine

Class 1B Na+ Channel Blocker

* cannot use to tx atrial arrhythmias*

MOA: Shortens Phase 3 repolarization, and decreases duration of AP in ventricular mm. fibers

given IV

Toxicity: Least cardiotoxic of Na+ channel blockers! Hypotension, neurologic (paresthesias, tremor, nausea, lightheadedness)

Note: highly effective in tx. of arrythmias assoc. w/ acute MI

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Tocainide

Class 1B

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Mexiletine

Class 1B

Varr.

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Flecainide

Class 1C Na+ channel blocker

high incidence of drug induced arrythmias
cannot be used in structural heart disease

MOA: slows Phase 0 depolarization in ventricular mm. fibers more than class 1A: Blocks both Na+ and K+ channels but does not prolong action potential or QT interval, depresses rate of rise of membrane action potential,

Use: supraventricular arrythmias

Moricizine

Class 1C Na+ channel blocker

Propafenone

Class 1C Na+ channel blocker

-olol

Beta blockers: propanolol, esmolol (short acting), metoprolol (B1 selective)

MOA: inhibit phase 4 depolarization in SA and AV nodes thus prolonging conduction, decreasing HR and contractility, and decreasing myocardial O2 demand

uses: Tachyarrhythmias, AF, AFib, AV nodal re-entrant tachycardia, hypertension, heart failure, ischemic heart disease
toxicity: Bradycardia, heart block, potential worsening reactive airway disease (as nonselective)

Amidiorone

Class III K+ Channel Blocker

Diminish outward K+ during repolarization, increased duration of AP, prolong effective refractory period

Use: AFib, recurrent VT, adjunct to ICD to reduce uncomfortable discharges

Toxicity: accumulates in tissues, heart, lung, liver, skin, tears, can cause skin deposits and gray-blue skin color and thyroid problems

MANY DRUG INTERACTIONS!

Dofetilide

Class III K+ Channel Blocker

Therapeutic Use:
Life-threatening ventricular arrhythmias, maintenance of sinus rhythm in AFib

can cause dose related TdP

Sotalol

Class III K+ Channel Blocker

has QT prolonging effects thus must be initiated in the hospital

Verapamil

Class IV Ca2+ channel blockers (non-DHP)

do not use in patients with VT –> will cause Vfib

MOA: decrease inward Ca2+ current, decrease rate of phase 4 depolarization, slows conduction in AV node (Ca2+ dependent tissues)

Use: SVT, decrease ventricular rate in AFib and AF, angina, HTN

Toxicity: ***Hypotension and ventricular fibrillation if given to a patient with VT misdiagnosed as SVT

Diltiazem

Class IV Ca2+ channel blockers (non-DHP)

MOA: decrease inward Ca2+ current, decrease rate of phase 4 depolarization, slows conduction in AV node (Ca2+ dependent tissues)

Use: SVT, angina, hypertension

toxicity: Edema, headache, AV block, bradycardia, hypotension

Adenosine

Nucleoside which activates inward rectifier K+ current and inhibits Ca2+ current resulting in marked hyperpolarization and increased refractory period Use: DOC for conversion of paroxysmal SVT t1/2 <10 seconds- given in IV flush toxicity: Flushing, shortness of breath, chest burning, high grade AV block, atrial fibrillation, headache, hypotension, nausea, paresthesias- all of these are short lived

atropine

MOA: Blocks actions of acetylcholine at parasympathetic sites, increases cardiac output use: Bradycardia, neuromuscular blockade reversal, cholinergic poisoning toxicity: Arrhythmia, tachycardia, dizziness, constipation, urinary retention

Digoxin

Inhibits Na+/K+ ATPase, results in positive inotropy, increased intracellular Na+, decreased Ca2+ expulsion, increased free Ca2+. Decreased HR, decreased refractory period, decreased conduction velocity Use: AFib, SVT, heart failure Toxicity: Nausea, vomiting, diarrhea, disorientation, visual disturbances, aberration of color perception, delayed afterdepolarization

↑ repolarization time, QTc interval, and risk of TdP

Class 1a and III

↓ HR (may cause bradycardia), force of contraction (may ↓ stroke volume), and ↑ PR interval (may cause 2nd or 3rd degree heart block)

Class II and IV

work only on ventricular tissue (cannot be used in AFib or AF)

Class 1b

should never be used after an MI or with CHF or severe LV hypertrophy (structural heart disease)

Class 1C

supraventricular arrhthmias

originate above the Bundle of His and characterized by normal QRS complexes ```  Sinus bradycardia  Sinus tachycardia  Paroxysmal supraventricular tachycardia  Atrial flutter  Atrial fibrillation  Wolff-Parkinson-White  Premature atrial contractions ```

ventricular arr.

``` all originate below the Bundle of His  Premature ventricular contractions  Ventricular tachycardia  Ventricular fibrillation ```

acute tx of atrial fibrillation?

Depolarization from ectopic focus or re-entrant circuit impact atria. No single pacemaker in control. “Irregularly irregular” 1, B-blockers (propranolol, metoprolol, esmolol) 1st choice in high catecholamine states. Should not be used acutely in systolic heart failure. 2. Non-DHP CCB’s (verapamil, diltiazem) IV produce rapid effects 4-5 minutes. 3. Digoxin has much slower onset (max effect 6-8 hours), less effective than BB/CCB in increased sympathetic tone

chronic tx of A fib?

oral BB, CCB - not digoxin long term strategy is rate control > rythym control

PAROXYSMAL SUPRAVENTRICULAR | TACHYCARDIA (PSVT) tx

AV nodal re-entry Acute treatment: IV adenosine (DOC), verapamil, or diltiazem Chronic: radiofrequency catheter ablation potentially curative

premature ventricular contractions (PVCs) tx

Ventricular arrhythmias arise from irritable foci within ventricular myocardium blockers within first 24 hours after MI if no contraindications (improves survival)

sustained V tach tx

Hemodynamic instability: synchronous cardioversion Stable VT patients: procainamide, sotalol, amiodarone Implantable cardioverter/defibrillator for:

torsades de pointes tx

Hemodynamic compromise: electrical cardioversion Hemodynamically stable: Mg