Antiarrhythmics Flashcards

1
Q

what is cardiac arrhythmia

A

loss of cardiac rhythm

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2
Q

what are the two types of cardiac action potentials

A
  • those characteristic of atrial and ventricular muscle such as purkinje fibers are called fast response action potentials
  • those observed in the sinoatrial (SA) node and atrioventricular (AV) node are called slow response action potentials
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3
Q

resting potential in most myocardial cells

A

80 - 95 mV

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4
Q

how are arrhythmias classified

A

supraventricular (atrial or AV junctional)

ventricular

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5
Q

what are all arrhythmias a result of

A
  • disturbances in impulse formation
  • disturbances in impulse conduction
  • or both
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6
Q

what are the different types of arrhythmias

A
  • premature atrial contractions
  • premature ventricular contractions (PVCs)
  • atrial fibrillation
  • atrial flutter
  • paroxysmal supraventricular tachycardia (PSVTs)
  • ventricular tachycardia (V-Tach)
  • ventricular fibrillation (V-fib)
  • sinus node dysfunction
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7
Q

describe premature atrial contraction, premature ventricular contractions, and atrial fibrillation

A
  • premature atrial contraction is an early extra beat that originates in the atria and is harmless
  • premature ventricular contraction is most common arrhythmias. it is a skipped beat caused by stress, exercise, nicotine, heart disease and etc and does not require treatment
  • atrial fibrillation is irregular heart rhythm causing the atria to contract abnormally
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8
Q

describe atrial flutter, paroxysmal supraventricular tachycardia, ventricular tachycardia

A
  • atrial flutter is caused by one or more rapid circuits in the atrium. it is more regular than a-fib
  • paroxysmal supraventricular tachycardia is a rapid heart rate with regular rhythm originating from above the ventricles
  • v-tach is a rapid heart rhythm originating in ventricles and requires treatment immediately
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9
Q

describe v-fib and sinus node dysfunction

A
  • v fib is erratic disorganized firing of impulses from ventricle that prevents it from contracting and pumping out blood to the body and requires immediate response
  • sinus node dysfunction is a slow heart rhythm due to abnormal SA node and requires treatment with a pace maker
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10
Q

what is an electrical cardioversion

A

if drugs not controlling irregular heart rhythm, this is used to deliver electrical shock that synchronizes the heart and allows normal rhythms to restart

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11
Q

why are the class I drugs classified into different subgroup and how does each subgroup differ?

A

classified based on their rate of drug binding and dissociation from the channel receptor

  • class IA: intermediate in speed of binding and dissociation from receptor
  • class IB: most rapid for both
  • class IC: slowest for both
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12
Q

mechanism of class I drugs

A
  • blocks Na channels –> automaticity (ability to generate action potential) is decreased by shifting threshold to more positive potentials and decreasing slope of phase 4 depolarization
  • basically it raises the threshold for action potential and slows the rate of depolarization
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13
Q

what types of cells are not affects by class I drugs

A

nodal tissues because they do not rely on Na channels for depolarization

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14
Q

what is the class IA drug and what do they do

A

QUinidine, PROCainamide, DISOPYRAMIDe

the QUeen PROClaims DISO’s PYRAMID

  • they are sodium channel blockers thereby inhibiting phase 0 depolarization hence increased action potential duration
  • they also block K channels in phase 3 (rectifying K channels) resulting in prolongation of the refractory period (unable to initiate another action potential) in atria and ventricles —-> increased QT interval
  • antimuscarinic properties
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15
Q

what is a big difference between the class IA drugs

A

quinidine and procainamide decrease vascular resistance while disopyramide increases vascular resistance

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16
Q

what is the effect of a metabolite of procainamide called NAPA (n-acetyl procainamide)

A

it has little effect on sodium channels but still blocks the K channels so acts more like a class III drug

17
Q

clinical uses of class IA drugs

A

atrial fibrillation, supraventricular and ventricular arrhythmias

18
Q

adverse effects of quinidine

A
  • precipitate arrhythmias
  • increases toxicity of digoxin by decreasing its renal clearance
  • Cinchonism (blurred vision, tinnitus, headache, tinnitus)
  • thrombocytopenia purpura
  • hemolytic anemia
19
Q

adverse effects of procainamide

A
  • reversible lupus like syndrome
  • aggravation of underlying HF
  • induction of ventricular arrhythmias
20
Q

adverse effects of disopyramide

A
  • heart failure
  • hypotension
  • severe antimuscarinic effects
21
Q

contraindications for quinidine

A
  • complete heart block
  • watch those with increased QT interval, history of torsades de pointes, incomplete heart block, uncompensated heart failure, myocarditis, severe myocardial damage
22
Q

contraindication for procainamide

A
  • hypersensitivity
  • complete heart block
  • 2nd degree block
  • SLE
  • torsades de pointes
  • heart failure and hypertension
23
Q

contraindication for disopyramide

A

-uncompensated heart failure

24
Q

what are the class IB drugs

A

Lidocaine
Mexiletine

I’d Buy LIDdy’s MEXican Tacos

25
Q

mechanism of class IB drugs

A
  • slows phase 0
  • shortens phase 3 repolarization
  • decrease slope of phase 4
26
Q

clinical applications of class IB drugs

A

ventricular tachyarrhythmias

mexiletine used with v-tachy and lidocaine in digitalis induced arrhythmias

27
Q

adverse effects of class IB drugs

A

lidocaine - convulsions/seizures and coma if in toxic range

mexiletine - CNS and GI effects

28
Q

what are the class IC drugs

A

Flecainide
Propafenone

Can i have Fries Please

29
Q

mechanism of class IC drugs

A

-blocks sodium channels and due to its slow kinetics has a much higher increase in QRS

propafenone also has beta blocking activity

30
Q

clinical applications of class IC drugs

A
  • life threatening supraventricular tachyarrhythmias
  • ventricular tachyarrhythmias
  • prevention of paraoxysmal a-fib
  • maintenance of normal sinus rhythm
  • used exclusively for atrial arrhythmias
31
Q

adverse effects of flecainide and propafenone

A
  • negative inotropic effects
  • CNS effects (headaches etc)
  • life threatening arrhythmias and ventricular tachycardia

propafenone also has beta blocking activity so bronchospasm and aggravation of underlying heart failure

32
Q

what are class II drugs and name them

A

they are beta blockers

metoprolol, propanolol, and esmolol

33
Q

mechanism of class II drugs

A
  • inhibit sympathetic tone which affects slow response tissues
  • slows conduction of impulses
  • reduce rate of spontaneous depolarization in cells with pacemaker activity
34
Q

clinical uses of class II drugs

A
  • supraventricular arrhythmias (a-fib, a-flutter, AV nodal re-entrant tachycardia)
  • ventricular tachyarrhythmias
  • reduce incidence of sudden arrhythmic death after MI
35
Q

useful in tx of acute arrhythmias occuring during surgery or in emergency situations

A

esmolol

36
Q

adverse effects of beta blockers

A

sleep disturbances
GI upset
bradycardia
hypotension

37
Q

contraindications of beta blockers

A

acute CHF
severe bradycardia
heart block
severe hyperactive airway disease