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CPR Exam 1 > Drugs to treat Cardiac Arrhythmias > Flashcards

Drugs to treat Cardiac Arrhythmias Flashcards

1
Q

What is the function of Class 1 drugs?

A

Sodium channel blockers

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2
Q

What drugs belong to class 1A

A

Quinidine
Procainamide
Disopyramide

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3
Q

What drugs belong to class 1B

A

Lidocaine

Mexiletine

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4
Q

What drugs belong to class 1C

A

Flecainide

Propafenone

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5
Q

What is the function of class 2 drugs?

A

Beta blockers

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6
Q

What drugs belong to class 2

A

Esmolol

Propranolol

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7
Q

What is the function of Class 3 drugs

A

Potassium channel-blocking drugs

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8
Q

What drugs belong to class 3

A

Amiodarone
Sotalol
dofetilide
Ibutilide

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9
Q

What is the function of class 4 drugs

A

Cardioactive calcium channel blockers

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10
Q

What drugs belong to class 4

A

verapamil

diltiazem

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11
Q

What is the miscellaneous agent

A

Adenosine

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12
Q

What tissues use fast cardiac action potentials

A

Ventricular contractile cardiomyocytes
Atrial cardiomyocytes
Purkinje fibers

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13
Q

What tissues use the slow (pacemaker action potentials)

A

SA node cells

Atrioventricular node cells

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14
Q

What occurs in phase 0 of the cardiac cycle

A

voltage-dependent fast Na+ channels open as a result of depolarization; Na enters the cells down its electrochemical gradient

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15
Q

What occurs in phase 1 of the fast action potential cardiac cycle

A

K+ exits cells down its gradient while Na+ channels close -> some repolarization

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16
Q

What occurs in phase 2 of the fast action potential cardiac cycle

A

plateau phase results from K+ exiting cells offset by and Ca2+ entering through slow voltage-dependent Ca2+ channels

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17
Q

What occurs in phase 3 of the fast action potential cardiac cycle

A

Ca2+ channels close and K+ begins to exit more rapidly resulting in repolarization.

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18
Q

What occurs in phase 4 of the fast action potential cardiac cycle

A

resting membrane potential is gradually restored by Na/K ATPase and Na/Ca exchanger

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19
Q

Describe phase 4 of the slow pacemaker action potential

A
  • poor selective ionic influx (pacemaker or funny current) - activated by hyperpolarization
  • slow Ca influx via T (transient) channels
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20
Q

Describe phase 0 of the pacemaker action potential

A

upstroke of AP

-Ca2+ through slow L-type Ca channels

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21
Q

Describe phase 3 of the pacemaker action potential

A

repolarization

  • inactivation of calcium channels with increased K+ efflux
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22
Q

Describe the mechanism of 1A drugs

A

block sodium channels - slow impulse conduction, reduce automatism of ectopic pacemakers

Block potassium channels - prolong AP duration, prolong QT

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23
Q

In addition to sodium blocking capacity, what other characteristics does procainamide posses that make it effective?

A

Depresses SA and AV node
antimuscarinic activity
ganglion blocking properties

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24
Q

What are the main clinical uses for procainamide?

A

used infrequently

best in sustained Vtach and MI arrhythmias

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25
Q

What are adverse effects seen in procainamide

A

QT interval prolongation - torsades de pointes
SLE
Hypotension

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26
Q

What are the adverse effects of Quinidine?

A

QT prolongation
GI (diarrhea, nausea, vomiting)
Tinnitus, hearing loss, confusion
Thrombocytopenia

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27
Q

In addition to the sodium block what other action does disopyramide have

A

strong antimuscarinic effect on the heart

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28
Q

What is the clinical use of disopyramide

A

recurrent ventricular arrhythmias

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29
Q

What are the adverse effects of disopyramide

A
  • QT prolongation
  • negative inotropic effect - precipitate heart failure
  • Atropine like symptoms
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30
Q

describe the action of Class 1B drugs

A

block sodium channels only. targets depolarized tissue to slow conduction. Shortens AP

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31
Q

describe the clinical use of lidocaine

A

termination of vtach in AMI

only IV due to extensive first pass metabolism

32
Q

What are the adverse effects of lidocaine

A

least toxic of all class 1 drugs

  • hypotension in pts with heart failure
  • paresthesias, tremor, slurred speech, convulsions
33
Q

How does mexiletine compare to lidocaine

A

it is orally active

34
Q

Describe the clinical use of mexiletine

A

ventricular arrhythmias

relieve chronic pain especially in DM

35
Q

What are the adverse effects of mexiletine

A

Tremor
Blurred Vision
Nausea
Lethargy

36
Q

Describe the actions of 1C drugs

A

block sodium channels and some potassium channels to slow impulse conduction without prolonging QT, only prolongs QRS

37
Q

What is the clinical use of Flecainide

A

Normal hearts BUT with supraventricular arrhythmias

refractory ventricular arrhythmias that are life-threatening

38
Q

What are the adverse effects of Flecainide

A

sever exacerbation of ventricular arrhythmias when given to

  • pre existing vtach
  • previous MI
  • ventricular ectopic rhythms
39
Q

Describe the action of propafenone

A

sodium channel blocking kinetics is similar to flecainide.

Weak B blocker

40
Q

Describe the clinical use of propafenone

A

Supraventricular arrhythmias in patients without structural disease

41
Q

What are the adverse effects of propafenone

A

exacerbation of ventricular arrhythmias

42
Q

What is the effect of sympathetics on the pacemaker AP

A

increased slope due to If and T-type channels and reduce threshold

43
Q

Describe the action of beta-blockers in prevention in their antiarrhythmic action

A

SA - decrease HR (increase RR interval)

AV - decrease AV conduction (increase PR)

44
Q

Describe the clinical use of propranolol

A
  • Arrhythmias associated with stress and thyroid storm
  • Afib/flutter
  • paroxysmal supraventricular arrhythmias
  • arrhythmias associated with MI
45
Q

Describe the action of Esmolol

A

short acting selective beta-1 blocker

only continuous IV admin (short half life)

46
Q

Describe the clinical use of esmolol

A
  • supraventricular arrhythmias
  • arrhythmias associated with thyrotoxicosis
  • myocardial ischemia
  • adjunct drug in general anesthesia to control arrhythmias in perioperative period
47
Q

Describe adverse effects of beta blockers

A

reduced cardiac output
bronchoconstriction
impaired liver glucose metabolism
- increase VLDL

48
Q

What are contraindications for beta blockers

A 
Asthma
Peripheral vascular disease 
Raynauds 
T1DM on insulin 
Bradyarrhythmias
49
Q

Describe the mechanism of action for class 3 drugs

A

Potassium channel blockers - limits the frequency of APs by regulating the duration of the refractory period

50
Q

describe the pharmacodynamics of Amioderone

A 
blocks potassium channels 
Proling QT 
Blocks inactivated Na channels 
adrenolytic activity 
ca blocking properties
51
Q

What is the clinical use for amiodarone

A

recurrent v tach

a fib

52
Q

what are the adverse effects of amioderone

A 
bradycardia and AV block 
fatal Pulmonary fibrosis 
hepatitis 
photodermatitis - blue gray 
cause thyroid dysfunction
53
Q

describe the mechanism of action of sotalol

A

has class 2 (nonselective B blocking) and class 3 (prolongs APD) activity

54
Q

What is the clinical use of sotalol

A

treatment of life threatening ventricular arrhythmias

maintenance of sinus rhythm in patients with A fib

55
Q

What are the adverse effects of sotalol

A

depression of cardiac function

provoked torsades

56
Q

what is the mechanism of action for Dofetilide and Ibutilide

A

specifically block rapid component of the delayed rectifier potassium current

57
Q

What is the clinical use of Dofetilide and Ibutilide

A

restore sinus rhythm in patients with a fib

Maintain sinus rhythm after cardioversion (dofetilide)

58
Q

What are adverse effects of Dofetilide and ibutilide

A

QT interval prolongation and increased risk of ventricular arrhythmias

59
Q

describe the mechanism of action of type 4 drugs

A

block Ca channels

active in cells with pacemaker potential

  • -decrease slope of phase 0
    • increase L-type Ca threshold potential
60
Q

What is the clinical use of Verapamil and Diltiazem

A

termination and prevention of paroxysmal supraventricular tachy

ventricular rate control in a fib and flutter

61
Q

What are the adverse effects of Verapamil and Diltiazem

A 
Negative inotropy
AV block 
SA arrest
Bradyarrhythmias 
verapamil can cause constipation
62
Q

What is the mechanism of action of adenosine

A

enhances Potassium current causing hyperpolarization

inhibits AV conduction

63
Q

what is the clinical use of adenosine

A

Conversion to sinus rhythm in paroxysmal supraventricular tachycardia

64
Q

What are the adverse effects of adenosine

A 
SOB
bronchoconstriction 
chest burning 
AV block 
Hypotension
65
Q

What was the outcome of the study using Flecainide and the other 1C drugs

A

the Cardiac Arrhythmia Suppression test was terminated prematurely because that combo increased mortality by 2.5 fold.

66
Q

What are the important steps to take before initiation of antiarrhythmic therapy

A

Eliminate cause
Firm diagnosis
consider underlying cardiac conditions
Consider nonpharmacological therapies

67
Q

What are nonpharm approaches to cardiac arrhythmias

A
  • catheter ablation
  • implantable cardioverter-defibrillator
  • Artificial cardiac pacemaker
  • direct current cardioversion
68
Q

What combination of drugs can cause excessive repolarization and torsades des pointes

A

Class 1A and 3

69
Q

What drug combo can cause excessive slowing of conduction -> persistent ventricular tachycardias

A

Class 1A and 1C

70
Q

what is the most common arrhythmia

A

A fib

71
Q

what is the main mechanism of A fib

A

reentry circuits - impulse re enters and excites areas of the heart more than once

72
Q

What are the three conditions that lead reentry circuits

A
  • must be obstacle to homogenous conduction
  • unidirectional block
  • conduction time must exceed effective refractory period
73
Q

what drugs are prescribed in patients with minimal heart disease and Afib to maintain sinus rhythm

A 
Flecainide 
propafenone 
sotalol 
amiodarone
dofetilide
74
Q

What drugs are used in patients with structural diseases and Afib?

A

Sotalol
Amiodarone
Dofetilide

75
Q

What is the most common type of of PSVT

A

atrioventricular nodal reentrant tachycardia

CPR Exam 1 (19 decks)

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