Chapter 52: Antidysrhythmic Drugs Flashcards

(57 cards)

1
Q

what is an dysrhythmia

A
  • abnormality in the rhythm of the heartbeat
  • arises from electrical impulse formation disturbances
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2
Q

pathway of conduction of electrical impulses in a heathy hear

A

SA –> atria –> AV –> ventricles

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3
Q

sinoatrial (SA) node

A

pacemarker of the heart

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4
Q

Atrioventricular (AV) node

A
  • slow enough to allow ventricles to fill with blood
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5
Q

His-Purkinje system

A

rapid ejection of blood

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6
Q

fast potentials occur

A

in fibers of the His-Purkinje and the atrial and ventricular muscle

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7
Q

what are the 5 phases of fast potentials

A

phase 0: depolarization
phase 1: (partial) depolarization
phase 2: plateau
phase 3: repolarization
phase 4: stable potential

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8
Q

slow potentials occur

A

in the SA and AV node

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9
Q

Phases of slow potentials

A

Phase 0: slow depolarization (mediated by calcium influx)
Phase 1: absent
phase 2 and 3: not significant
phase 4: depolarization

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10
Q

P wave

A

depolarization in the atria

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11
Q

QRS complex

A

depolarization of the ventricles

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12
Q

T wave

A

repolarization of the ventricles

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13
Q

what are the 2 fundamental causes of dysrhythmias

A
  • disturbances of automaticity
  • disturbances of conductions (AV block, reentry)
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14
Q

what are antidysrhythmic drugs classified by

A

Vaughan Williams classification

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15
Q

Class I

A

sodium channel blockers
- slow impulse conduction

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16
Q

Class II

A

beta blockers
- depress depolarization

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17
Q

Class III

A

Potassium channel blockers
- delay repolarization

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18
Q

Class IV

A

Calcium channel blockers
- similar to beta blockers

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19
Q

Antidysrhythmic drugs should be used only when

A

dysrhythmias are symptomatically significant and only when the potential benefits clearly outweigh the risks

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20
Q

Prodysrhythmic effects of antidysrhythmic drugs

A
  • prolongation of the QT interval
  • Torsades de pointes
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21
Q

Supraventricular dysrhythmias

A

Impulse arises above the ventricle
- atrial fibrilation
- atrial flutter
- sustained supraventricular tachycardia (SVT)

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22
Q

Ventricular dysrhythmias

A
  • sustained ventricular tachycardia
  • ventricular fibrilation
  • premature ventricular complexxes
  • digoxin induced ventricular dysrhythmias
  • torsades de pointes
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23
Q

example of class IA agents

A

Quinidine
- Procainamide (procan)
- Disopyramide (Norpace)

24
Q

Quinidine effects on the heart

A
  • blocks sodium channel blockers
  • slows impulse conduction
  • delays repolarization
  • blocks vagal input to the heart
25
Quinidine effects on ECG
- widens the QRS complex - prolongs QT interval
26
Quinidine therapeutic uses
- used for supraventricular and ventricular dysrhythmias
27
Quinidine side effects
- diarrhea, hypersensitivity, carditoxicity
28
Class IB agents examples
Lidocaine [Xylocaine] - mexiletine - phenytoin
29
Lidocaine [Xylocaine] effects on the heart
- blocks sodium channels (slows conduction) - reduces automaticity in the ventricles and His-Purkinje system (accelerates repolarization)
30
Lidocaine [Xylocaine] is used for
ventricular dysrhythmias
31
Lidocaine [Xylocaine] side/adverse effects
- drowsiness - confusion - paresthesia - toxic doses produce seizures and respiratory arrest
32
Lidocaine [Xylocaine] administration
IV use only - rapid hepatic metabolism
33
Class IC agents
- block cardiaac sodium channels - delay ventricular repolarization
34
all class IC agents negative effects
- exacerbate existing dysrhythmias and create new ones
35
what are the two class IC agents
- Flecainide [Tambocor] - Propafenone [Rhythmol]
36
what are the main beta blockers used to treat dysrhythmias
- propranolol [inderal] - Acebutolol [Sectral] - Sotalol [Sotacor] - Bidoprolol [Monocor]
37
Propranolol [Inderal] effects on the heart
- decreased automacity of the SA node - decreased velocity of conduction through AV node - decreased myocardial contracility
38
Propranolol therapeutic use
- dysrhythmias caused by excessive sympathetic stimulation - supra ventricular tachydysrhythmias (suppression of excessive discharge, slowing of ventricular rate)
39
Amiodarone [Cordarone] therapeutic uses
life threatening ventricular dysrhythmias only
40
Amiodarone [Cordarone] effects on the heart
- reduced automaticity in the SA node; contracilirty; reduced conduction velocity - QRS widening; prolongation of PR and QT intervals
41
Amiodarone [Cordarone] toxicity
- protracted half life (25-110 days) - pulmonary toxicity - cardiotoxicity - toxicity in pregnancy and breat feeding - corneal microdeposits - optic neuropathy - liver toxicity
42
Amiodarone [Cordarone] adverse effects
- photosensitivity - skin discoloration - GI upset - thyroid toxicity
43
Amiodarone [Cordarone] loading dose
6 weels
44
Amiodarone [Cordarone] drug interactions
- Quinidine - Diltiazem '- cyclosporine - digoxin - procainamide - diltiazem - phenytoin - warfarin - Lovastatin, simvastatin, atorcastatin
45
Amiodarone levels can be increased by
grapefruit juice and inhibirots of CTP3A4
46
Amiodarone levels can be reduced by
Cholestyramine
47
(potassium channel blockers) the risk of severe dysrhythmias is increased by
diuretics
48
combining amiodarone with a beta blocker, verapamil, or diltiazem can lead to
excessive slowing of the heart
49
Calcium channel blockers examples
- Verapamil [Isoptin] - Diltiazem [Cardizem]
50
calcium channel blockers effects
- reduce Sa modal automaticity - delay AV nodal conduction - reduce myocardial contractility
51
calcium channel blockers therapeutic uses
- slow ventricular rate (atrial fibrillation or atrial flutter) - terminate SVT caused by an AV nodal reentrant circuit
52
Adenosine [Adenocard] effects on the heart
- decreases automaticity in the SA node - slows conduction through AV node - Prolongs PR interval
53
Adenosine [Adenocard] therapeutic use
termination of paroxysmal SVT
54
Adenosine [Adenocard] adverse effects
- sinus bradycardia - dyspnea - hypotension - facial flushing - chest discomfort
55
Digoxin is primarily used in
heart failure
56
Digoxin is used in
- heart failure - treat supraventricular dysrhythmias
57
Digoxin [Lanoxin] adverse effects
Cardiotoxicity - risk increased by hypokalemia