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Cardio II Exam 3 > Pharm: Antiarrythmics > Flashcards

Pharm: Antiarrythmics Flashcards

1
Q

what causes arrhythmias?

A
  1. abnormal impulse generation: early afterdepolarization, delayed afterdepolarization, disturbances in impulse formation
  2. abnormal conduction: can result from depressed conduction (blocks) or reentry mechanisms
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2
Q

what is reqd for a reenry mechanism

A

obstacle that establishes circuit

unidirectional block

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

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3
Q

refractoriness

A

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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4
Q

Type 1A

A

procainamide*

Na+ channel blocker
Dissociates with intermediate kinetics

↓conduction velocity
↑refractoriness
↓autonomic properties

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5
Q

Type 1B

A

lidocaine

Na+ channel blocker
Dissociates with rapid kinetics

No effect on velocity
May ↓refractoriness

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6
Q

Type 1C

A

Flecainide

Na+ channel blocker
Dissociates with slow kinetics

↓conduction velocity
No effect on refractoriness

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7
Q

Type III

A

amiodarone and sotalol

K+ channel blocker

↑refractoriness
↑action potential duration

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8
Q

Type II

A

Beta-blockers, esmolol, metoprolol, propanolol

↓conduction velocity
↑refractoriness
↓autonomic properties

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9
Q

Type IV

A

diltiazem/verapamil
non-DHP CCB’s

↓conduction velocity
↑refractoriness
↓autonomic properties

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10
Q

Procainamide

A

** 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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11
Q

Quinidine

A

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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12
Q

Disopyramide

A

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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13
Q

Lidocaine

A

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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14
Q

Tocainide

A

Class 1B

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15
Q

Mexiletine

A

Class 1B

Varr.

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16
Q

Flecainide

A

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

17
Q

Moricizine

A

Class 1C Na+ channel blocker

18
Q

Propafenone

A

Class 1C Na+ channel blocker

19
Q

-olol

A

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)

20
Q

Amidiorone

A

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!

21
Q

Dofetilide

A

Class III K+ Channel Blocker

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

can cause dose related TdP

22
Q

Sotalol

A

Class III K+ Channel Blocker

has QT prolonging effects thus must be initiated in the hospital

23
Q

Verapamil

A

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

24
Q

Diltiazem

A

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

25
Q

Adenosine

A

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

26
Q

atropine

A

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

27
Q

Digoxin

A

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

28
Q

↑ repolarization time, QTc interval, and risk of TdP

A

Class 1a and III

29
Q

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

A

Class II and IV

30
Q

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

A

Class 1b

31
Q

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

A

Class 1C

32
Q

supraventricular arrhthmias

A

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
33
Q

ventricular arr.

A 
all originate below the Bundle of 
His
 Premature ventricular contractions
 Ventricular tachycardia
 Ventricular fibrillation
34
Q

acute tx of atrial fibrillation?

A

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.

  1. Non-DHP CCB’s (verapamil, diltiazem) IV produce
    rapid effects 4-5 minutes.
  2. Digoxin has much slower onset (max effect 6-8
    hours), less effective than BB/CCB in increased
    sympathetic tone
35
Q

chronic tx of A fib?

A

oral BB, CCB - not digoxin

long term strategy is rate control > rythym control

36
Q

PAROXYSMAL SUPRAVENTRICULAR

TACHYCARDIA (PSVT) tx

A

AV nodal re-entry

Acute treatment: IV adenosine (DOC), verapamil,
or diltiazem

Chronic: radiofrequency catheter ablation
potentially curative

37
Q

premature ventricular contractions (PVCs) tx

A

Ventricular arrhythmias arise from irritable foci
within ventricular myocardium

blockers within first 24 hours after MI if no
contraindications (improves survival)

38
Q

sustained V tach tx

A

Hemodynamic instability: synchronous cardioversion

Stable VT patients: procainamide, sotalol,
amiodarone

Implantable cardioverter/defibrillator for:

39
Q

torsades de pointes tx

A

Hemodynamic compromise: electrical
cardioversion

Hemodynamically stable: Mg

Cardio II Exam 3 (15 decks)

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