Antiarrhythmics Flashcards

(37 cards)

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
mechanism of class IB drugs
- slows phase 0 - shortens phase 3 repolarization - decrease slope of phase 4
26
clinical applications of class IB drugs
ventricular tachyarrhythmias | mexiletine used with v-tachy and lidocaine in digitalis induced arrhythmias
27
adverse effects of class IB drugs
lidocaine - convulsions/seizures and coma if in toxic range mexiletine - CNS and GI effects
28
what are the class IC drugs
Flecainide Propafenone Can i have Fries Please
29
mechanism of class IC drugs
-blocks sodium channels and due to its slow kinetics has a much higher increase in QRS propafenone also has beta blocking activity
30
clinical applications of class IC drugs
- life threatening supraventricular tachyarrhythmias - ventricular tachyarrhythmias - prevention of paraoxysmal a-fib - maintenance of normal sinus rhythm - used exclusively for atrial arrhythmias
31
adverse effects of flecainide and propafenone
- 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
what are class II drugs and name them
they are beta blockers | metoprolol, propanolol, and esmolol
33
mechanism of class II drugs
- inhibit sympathetic tone which affects slow response tissues - slows conduction of impulses - reduce rate of spontaneous depolarization in cells with pacemaker activity
34
clinical uses of class II drugs
- supraventricular arrhythmias (a-fib, a-flutter, AV nodal re-entrant tachycardia) - ventricular tachyarrhythmias - reduce incidence of sudden arrhythmic death after MI
35
useful in tx of acute arrhythmias occuring during surgery or in emergency situations
esmolol
36
adverse effects of beta blockers
sleep disturbances GI upset bradycardia hypotension
37
contraindications of beta blockers
acute CHF severe bradycardia heart block severe hyperactive airway disease