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CPR Exam 1 > Drugs to treat Cardiac Arrhythmias > Flashcards

Drugs to treat Cardiac Arrhythmias Flashcards

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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
What are adverse effects seen in procainamide
QT interval prolongation - torsades de pointes SLE Hypotension
26
What are the adverse effects of Quinidine?
QT prolongation GI (diarrhea, nausea, vomiting) Tinnitus, hearing loss, confusion Thrombocytopenia
27
In addition to the sodium block what other action does disopyramide have
strong antimuscarinic effect on the heart
28
What is the clinical use of disopyramide
recurrent ventricular arrhythmias
29
What are the adverse effects of disopyramide
- QT prolongation - negative inotropic effect - precipitate heart failure - Atropine like symptoms
30
describe the action of Class 1B drugs
block sodium channels only. targets depolarized tissue to slow conduction. Shortens AP
31
describe the clinical use of lidocaine
termination of vtach in AMI only IV due to extensive first pass metabolism
32
What are the adverse effects of lidocaine
least toxic of all class 1 drugs - hypotension in pts with heart failure - paresthesias, tremor, slurred speech, convulsions
33
How does mexiletine compare to lidocaine
it is orally active
34
Describe the clinical use of mexiletine
ventricular arrhythmias | relieve chronic pain especially in DM
35
What are the adverse effects of mexiletine
Tremor Blurred Vision Nausea Lethargy
36
Describe the actions of 1C drugs
block sodium channels and some potassium channels to slow impulse conduction without prolonging QT, only prolongs QRS
37
What is the clinical use of Flecainide
Normal hearts BUT with supraventricular arrhythmias | refractory ventricular arrhythmias that are life-threatening
38
What are the adverse effects of Flecainide
sever exacerbation of ventricular arrhythmias when given to - pre existing vtach - previous MI - ventricular ectopic rhythms
39
Describe the action of propafenone
sodium channel blocking kinetics is similar to flecainide. Weak B blocker
40
Describe the clinical use of propafenone
Supraventricular arrhythmias in patients without structural disease
41
What are the adverse effects of propafenone
exacerbation of ventricular arrhythmias
42
What is the effect of sympathetics on the pacemaker AP
increased slope due to If and T-type channels and reduce threshold
43
Describe the action of beta-blockers in prevention in their antiarrhythmic action
SA - decrease HR (increase RR interval) AV - decrease AV conduction (increase PR)
44
Describe the clinical use of propranolol
- Arrhythmias associated with stress and thyroid storm - Afib/flutter - paroxysmal supraventricular arrhythmias - arrhythmias associated with MI
45
Describe the action of Esmolol
short acting selective beta-1 blocker | only continuous IV admin (short half life)
46
Describe the clinical use of esmolol
- supraventricular arrhythmias - arrhythmias associated with thyrotoxicosis - myocardial ischemia - adjunct drug in general anesthesia to control arrhythmias in perioperative period
47
Describe adverse effects of beta blockers
reduced cardiac output bronchoconstriction impaired liver glucose metabolism - increase VLDL
48
What are contraindications for beta blockers
``` Asthma Peripheral vascular disease Raynauds T1DM on insulin Bradyarrhythmias ```
49
Describe the mechanism of action for class 3 drugs
Potassium channel blockers - limits the frequency of APs by regulating the duration of the refractory period
50
describe the pharmacodynamics of Amioderone
``` blocks potassium channels Proling QT Blocks inactivated Na channels adrenolytic activity ca blocking properties ```
51
What is the clinical use for amiodarone
recurrent v tach | a fib
52
what are the adverse effects of amioderone
``` bradycardia and AV block fatal Pulmonary fibrosis hepatitis photodermatitis - blue gray cause thyroid dysfunction ```
53
describe the mechanism of action of sotalol
has class 2 (nonselective B blocking) and class 3 (prolongs APD) activity
54
What is the clinical use of sotalol
treatment of life threatening ventricular arrhythmias | maintenance of sinus rhythm in patients with A fib
55
What are the adverse effects of sotalol
depression of cardiac function | provoked torsades
56
what is the mechanism of action for Dofetilide and Ibutilide
specifically block rapid component of the delayed rectifier potassium current
57
What is the clinical use of Dofetilide and Ibutilide
restore sinus rhythm in patients with a fib | Maintain sinus rhythm after cardioversion (dofetilide)
58
What are adverse effects of Dofetilide and ibutilide
QT interval prolongation and increased risk of ventricular arrhythmias
59
describe the mechanism of action of type 4 drugs
block Ca channels active in cells with pacemaker potential - -decrease slope of phase 0 - - increase L-type Ca threshold potential
60
What is the clinical use of Verapamil and Diltiazem
termination and prevention of paroxysmal supraventricular tachy ventricular rate control in a fib and flutter
61
What are the adverse effects of Verapamil and Diltiazem
``` Negative inotropy AV block SA arrest Bradyarrhythmias verapamil can cause constipation ```
62
What is the mechanism of action of adenosine
enhances Potassium current causing hyperpolarization | inhibits AV conduction
63
what is the clinical use of adenosine
Conversion to sinus rhythm in paroxysmal supraventricular tachycardia
64
What are the adverse effects of adenosine
``` SOB bronchoconstriction chest burning AV block Hypotension ```
65
What was the outcome of the study using Flecainide and the other 1C drugs
the Cardiac Arrhythmia Suppression test was terminated prematurely because that combo increased mortality by 2.5 fold.
66
What are the important steps to take before initiation of antiarrhythmic therapy
Eliminate cause Firm diagnosis consider underlying cardiac conditions Consider nonpharmacological therapies
67
What are nonpharm approaches to cardiac arrhythmias
- catheter ablation - implantable cardioverter-defibrillator - Artificial cardiac pacemaker - direct current cardioversion
68
What combination of drugs can cause excessive repolarization and torsades des pointes
Class 1A and 3
69
What drug combo can cause excessive slowing of conduction -> persistent ventricular tachycardias
Class 1A and 1C
70
what is the most common arrhythmia
A fib
71
what is the main mechanism of A fib
reentry circuits - impulse re enters and excites areas of the heart more than once
72
What are the three conditions that lead reentry circuits
- must be obstacle to homogenous conduction - unidirectional block - conduction time must exceed effective refractory period
73
what drugs are prescribed in patients with minimal heart disease and Afib to maintain sinus rhythm
``` Flecainide propafenone sotalol amiodarone dofetilide ```
74
What drugs are used in patients with structural diseases and Afib?
Sotalol Amiodarone Dofetilide
75
What is the most common type of of PSVT
atrioventricular nodal reentrant tachycardia

CPR Exam 1 (19 decks)

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