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Pharmacology II > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

(107 cards)

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1
Q

The two most general ways an arrhythmia forms is due to problems with what?

A
  1. impulse formation

2. impulse conduction

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2
Q

what involves physiological mechanisms alter automaticity causing arrhythmias?

A
  1. sympathetic stimulation

2. vagal stimulation

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3
Q

what are the 3 pathologic mechanisms that alter automaticity, causing arrhythmias

A
  1. escape beat
  2. ectopic beat
  3. direct tissue damage
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4
Q

how does direct tissue damage after a heart attack cause arrhythmias

A
  1. loss of ion gradient

2. loss of gap junction connectivity

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5
Q

what is the difference in escape beats and ectopic beats

A

escape beats are when latent pacemakers initiate impulse due to SA node firing too slow
Ectopic beats are when pacemakers are firing at a faster rate than SA node

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6
Q

what phase is interrupted by early afterdepolarizations?

A

phase 2 or 3

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7
Q

what phase is interrupted by delayed afterdepolarizations

A

phase 4

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8
Q

What are 3 ways arrhythmias are caused by disturbance in an impulse conduction

A
  1. re-entry
  2. conduction block
  3. accessory tract pathways
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9
Q

what arrhythmia can’t be seen on ECG because it happens to fast

A

Sinus Tachycardia

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10
Q

what is the MOA of sinus tachycardia arrhythmias?

A

altered automaticity (SA node firing fast)

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11
Q

what is the mechanism of paroxysmal supraventricular tachycardia

A

re-entry at AV node, SA node, or atrial tissue

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12
Q

what are the atrial firing rates in PSVT

A

140-250 bpm

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13
Q

what type of arrhythmia has no pattern?

what is it’s MOA

A

fibrillations

chaotic re-entrant impulses through myocardial cells

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14
Q

what is characterized by intermittent bouts of very high heart rates?

A

atrial flutter

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15
Q

what is considered re-entrant arrhythmias?

what is it’s MOA

A

ventricular tachycardia

3 or more extrasystoles at rates of 100-250 bpm

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16
Q

what is the MOA of torsades de pointes

A

afterdepolarizations in prolonged QT syndromes leading to other arrhythmias

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17
Q

what is the MOA of atrial flutters

A

atrial firing rates of 280-300 bpm, but not conducted through AV node during refractory peiod

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18
Q

What are the 4 Vaughan Williams Classes general types of drugs

A

Class 1 = sodium channel blockers
Class 2 = beta blockers
Class 3 = prolongation of AP/ repolarization blockers
Class IV = Calcium channel blockers

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19
Q

What are the 4 main MOA of antiarrhythmic agents

A
  1. rate of phase 4 depolarization
  2. threshold potential
  3. max diastolic potential in pacemaker
  4. AP duration
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20
Q

what type of arrhythmia is considered transient

A

atrial flutter (normally goes away)

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21
Q

What are the two major MOAs of class 1 antiarrhythmics?

A
  1. decreases SA nodal cells automaticity by shifting threshold to a more positive potential
  2. prevents re-entry by ventricular myocytes
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22
Q

What are the 4 MOAs of class 1A antiarrhythmics?

A
  1. moderate block of Na channels in both SA and ventricles
  2. blocks K channels
  3. binds to open Na channels
  4. disassociate with intermediate kinetics
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23
Q

What are the effects of class IA drugs on K channels

A

reduce outward K current
prolongs repolarization
increases effective refractory period

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24
Q

What is saying to remember Class 1 antiarrhythmics

A

Double Quarter Pounder = Class 1A
Lettuce and Mayo = Class 1B
Fries Please = Class 1C

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25
list the Class 1A drugs
disopyramide quinidine procainamide
26
what is the active metabolite that can cause torsades via increased AP duration
NAPA
27
what are 3 effects all class 1A antiarrhythmics have?
1. decrease upstroke 2 increase refractory period 3. decrease automaticity
28
Quinidine is primarily to treat what?
``` Atrial arrhythmias: atrial flutter atrial fibrillation paroxysmal supraventricular contraction paroxysmal AV atrial tach AND vent. tachycardia ```
29
procainamide treats what arrhythmias?
1. symptomatic premature ventricular contractions 2. life threatening v-tach 3. sinus rhythm maint. after atrial flutter 4. malignant hyperthermia
30
cinchonism refers to what? | what drug causes this?
cinchonism= deafness/ ringin | quinidine
31
what is considered last resort 1A antiarrhythmic, for folks who can't tolerate the others?
disopyramide
32
quinidine has what side effects?
1. Torsades 2. v-tach 3. acute asthma 4. resp arrest 5. D, N and V
33
what drug can cause lupus like syndrome with prolonged use? | is it reversible?
procainamide | yes will go away
34
what 1A antiarrhythmic has the least amunt of anticholinergic effects?
procainamide
35
what 1A antiarrhythmic is contraindicated in heart failure
Disopyramide
36
all 1A antiarrythmis are contraindicated for what
1. history of torsades 2. concurrent use of drug that can prolong QT interval 3. conduction defects 4. myasthenia gravis
37
what should be given in conjunctin with quinidine
a beta blocker or Ca-blocker to overcome tachycardia
38
what class 1A antiarrhythmic has few GI effects but profound anticholinergic effects
disopyramide
39
quinidine causes the vagolytic effect. what is that?
blocking K channels that are opened upon vagal stimulation in AV node
40
``` What are the class 1B antiarrhythmic drugs? which is IV which is PO ```
``` lidocaine = iv mexiletine = po ```
41
what is the MOA of class 1B antiarrhythmics
use dependent block of Na channels in ventricular myocytes (decreasing phase 0 upstroke velocity
42
what subclass of class 1 antiarrhythmics causes no change or decreases relative refractory period (ERP)
class IB
43
what is the indication of class IB antiarrhythmics?
ventricular arrhythmias
44
what are some side effects of class IB's
seizures restlessness hypotension nausea
45
dosing of clas IB antiarrhythmics should be adjusted when administered with what
p450 inducers or inhitors
46
what class has the most potent Na channel blockers
class IC
47
Class IC Na blockers have little effect on what?
AP duration
48
what type of effects do class IC antiarrhythmics exert on cardiac function
depressive effects on cardiac function
49
what is the major difference in clas IB and IC antiarrhythmics
IB are use dependent; don't effect normal cells, diseased only IC blocks Na Channels in ventricular myocytes, healthy or diseased
50
what do class IC's treat?name the IC antiarrhythmics
flecainide | propafenone
51
why are class IC considered last resort drugs
can cause cardiac arrest and heart failure
52
what are 3 common side effects of class IC's
1. metallic taste 2. constipation 3. dizziness
53
what patients should not be given class IC antiarrhythmics
Post MI patients (aggrevates heart failure) | pt.s with preexisting v-tach's
54
what node is most sensitive to beta blockers? SA or AV
AV node
55
``` what specific receptors are blocked by class II Antiarrhythmics? What MOA does blocking this receptor have ```
B-1 receptors in heart | inhibits sympathetic input into pacing reions of the heart
56
what effect do B-blockers have at SA node
blocking b-1 decreases rate of phase 4 depolarization decreasing automaticity and myocardial oxygen demand
57
what effect do B-blockers have at AV node
1. prolong repolarization 2. increase refractory period 3. decreases incidence of re-entry
58
What are 3 clinical applications of class II antiarrhythmics
1. supraventricular arrhythmias 2. ventricular arrhythmias 3. reduce mortality after myocardial infarction
59
what are 3 main mechanisms of adverse effects of B-blockers?
1. smooth muscle spasm 2. exaggeration of therapeutic effects 3. penetration into CNS
60
list 4 drugs that are B-1 selective at low doses
1. atenolol 2. metoprolol 3. acebutolol 4. bisoprolol
61
what B-blocker is nonselective and treats tachyarrythmias due to catecholamine stimulation
propanolol
62
what B-blocker is very short acting and used for arrhythmias during surgery
esmolol
63
what drug looks like a beta blocker but is actually a potassium blocker
sotalol
64
what B-blocker is a partial agonist at B-2 receptors
pindolol
65
what B-blocker stimulates nitric oxide production
Bebivolol
66
what B-blockers also block a-1 receptors and cause vasodilation
labetalol | carvedilol
67
beta-blockers can exaggerate therapeutic effects. this can cause what 3 problems
1. negative inotropic effects 2. heart block 3. bradycardia
68
all class III's do what?
prolong QT interval by blocking K channels
69
Class III drugs blockade of K channels causes what 3 antiarrhythmic effects
1. lengthen plateau and prolong repolarization 2. increase refractory period 3. decrease incidence of re=entry
70
Class III's having reverse use dependency is dangerous why?
action is most pronounced at slow rates. arrhythmias are at fast rate increases risk of torsades
71
what is the one class III with no reverse use dependancy
amiodarone
72
what phase is not effected by class III's
phase 0
73
Name the class III drugs (SAD ID)
1. sotalol 2. Amiodarone 3. Dronedarone 4. Ibutilide 5. Dofetilide
74
what K blocker converts atrial fivrillations or flutters to normal sinus rhythm
Ibutilide
75
``` what class III is only available IV? what precaution must be taken with it? ```
Ibutilide | EKG thru infusion (risk of torsades)
76
who is contraindicated for ibutilide
pt's with preexisting long QT syndrome
77
who is contraindicated for dofetilide
CrCl less than 20ml/min
78
what oral class III has a special dispensing program
dofetilide | program is called TIPS
79
what class III contains iodine
amiodarone
80
Amiodorone pt's must be tested for what?
``` Thyroid Eyes Liver Lungs Skin ```
81
what is used frequently in pt's that can't tolerate amiodorone
Sotalol
82
what class III is good for pt's with a recent MI or heart failure
Sotalol
83
what isomer of Sotalol is best as an antiarrhythmic
L=isomer
84
what is similar to amiodarone minus the iodine
dronedarone
85
what class III is good for A and V arrhythmias and fits into every antiarrhythmic class
amiodarone
86
what drug is contraindicated in pt's with hepatic impairment or pregnant pt's
dronedarone
87
what drug should be used with caution in patients with impaired renal function or diabetes
sotalol
88
what drug gives CrCl level that makes kidneys appear to be damaged when they actually work fine
dronedarone
89
what class III must be taken with food
dronedarone
90
name the class IV drugs
verapamil and diltiazem (Ca blockers)
91
where do verapamil and diltiazem work
mainly the AV node
92
what effect does Ca channel blockade cause
slow action potential upstroke and slow conduction velocity
93
Are the class IV's use dependent
yes
94
what do class IV's treat?
treats re-entrant paroxysmal supraventricular tachycardias
95
what side effect is associated with diltiazem and verapamil
negative inotropic effect; so can't be used in pt's with heart failure
96
hypokalemia can cause what type of arrhythmias
1. early afterdepolarizations 2. delayed afterdepolarizations 3. ectopic beats (esp w digoxin)
97
hyperkalemia can cause arrhythmias due to what
slowed conduction velocity
98
what nucleoside can be used as an antiarrhythmic agent
adenosine
99
what type of arrhythmia is adenosine a first line agent for
narrow complex PSVT (90% effective)
100
what is adenosines MOA
1. inhibits conduction by opening K channels | 2. suppresses Ca dependent APs
101
what are the two main indications of magnesium for arrhythmias
1. digitalis induced arrhythmias with hypomagnesemia | 2. Torsades with normal Mg levels
102
what is Digoxin's MOA
1. decereases AV automaticity by prolonging refractory period and slowing conduction velocity thru AV node
103
what are Digoxin's chronotropic and inotropic effects
negative chronotropic | positive inotropic
104
digoxin toxicity can produce what
ectopic ventricular beats
105
what is digoxin's main use
in pt's with heart failure
106
what can be used for rapid ventricular response rates
digoxin
107
list 3 nonpharmacologic treatments for arrhythmias and define them
1. ICD 2. DCC 3. Ablation via radiofrequency or cryoablation

Pharmacology II (4 decks)

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