Drugs For Cardiac Arrhythmias - Dr. Konorev Flashcards

1
Q
antiarrhymia drugs :
class 1
class 2
class 3
class 4
A
  1. Na channel Blockers class, ABC
  2. Beta blockers
  3. K+ Channel Blockers
  4. Cardioactive CCB
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2
Q

class 1A drugs 3

A

= Na channel Blockers class

  1. Quinidine
  2. Procainamide
  3. Disopyramide
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3
Q

class 1B drugs 2

A

= Na channel Blockers class

  1. Lidocane
  2. Mexiletine
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4
Q

class 1C drugs 2

A

= Na channel Blockers class

  1. Flecainide
  2. Propafenone
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5
Q

Class 2 drugs 2

A

= BB

  1. Esmolol
  2. Propanolol
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6
Q

Class 3 Drugs 4

A

= K+ Channel Blocker

  1. Amiodarone
  2. Sotalol
  3. Dofetilide
  4. Ibutilide
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7
Q

Class 4 drugs 2

A

= Cardioactive CCB

  1. Dilitiazem
  2. Verapamil
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8
Q

Fast AP where

A
  1. Ventricular contractile cells
  2. Atrial cells
  3. Purkinje fibers
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9
Q

Slow AP where

A
  1. SA node

2. AV node

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10
Q

Fast AP phases

A

0 : fast Na+ open , Na+ enters cell
1 : K+ exit cell, Na+fast close (some repolarization)
2. plateau phase, K+ exit, Ca+ enter slow voltageC
3. Ca+2 slow close, K+ exits faster
(fast repolarization)
4. resting membrane potential (Na/K+, and Na/Ca)

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11
Q

phase 4 has what channels pacemaker (slow AP)

A
  1. If (funny current) : Na+ channel, K+ channels
  2. slow Ca+
    = slanted up line until threshold
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12
Q

phase 0 has what channels pacemaker (slow AP)

A
  1. slow L type (long lasting Ca+ influx)
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13
Q

phase 3 has what channels pacemaker (slow AP)

A
  1. K+ exits, repolarization

2. Ca+ close

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14
Q

no class antiarrhythmic drug

A

adenosine

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15
Q

refractory period

A

Na+ inactive stage

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16
Q

class 1 drug Na blockers MOA

A

Block Na = prolong phase 0

Block K+ = prolong AP duration

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17
Q

class 1 drug Na blockers EKG changes

A
  1. prolong QRS (NA+ block)
  2. prolong QT interval (K+
    block)
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18
Q

Procainamide clinical use

A
  1. not as much due to lupus related side effects

2. sustained V Tachy, or MI arrhythmia

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19
Q

Procainamide adverse effects

A
  1. prolong QT
  2. torsade de pointes **
  3. syncope
  4. Lupus erythemaatosus syndrome ** + arthritis, pleuritis, pulm D, fever, hep
  5. hypotension
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20
Q

Quinidine is from what and clinical use

A

Cinchona bark

  1. rare
  2. may enhance AV conductance
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21
Q

Quinidine adverse effects

A

QT interval prolongation
torsade de pointes **
GI issues
CNS probs

22
Q

Disopyramide MOA beside Na block

clinical use

A

anti-muscarinic effect

= recurrent V arrythmias

23
Q

Disopyramide adverse effects

A
  1. QT prolongation **
  2. torsades de pointes **
    • iontrophic effect can cause HF
  3. atropine -like sx : tachy, dry, blurred vision, C, urinary retention
24
Q

class 1B drugs do what

A

block NA by binding to inactivated NA (long QRS)

DONT block K+ (QT and AP length normal)

25
Q

Lidocaine administered how and clinical use

A

IV only
= ventricular tachy during Acute MI
= also used for a local anesthetic

26
Q

Lidocaine adverse effects

A

least toxic

- can cause hypotension , tremor, slurred speech, paresthesias

27
Q

Mexiletine administration and clinical use

A

oral
= V arrhythmia
= chronic pain relief (diabetic neuropathy + nerve injury)

28
Q

Mexiletine adverse effects

A

tremor
blurred vision
lethargy

29
Q

Class 1C drugs do what

A
block NA (prolong QRS)
Block K+ (only same QT and AP length)
30
Q

Flecainide clinical use

A

= supraventricular arrhythmia

= refractory severe V arrhythmia

31
Q

Flecainide adverse reactions

A

make arrhythmia worse

32
Q

Propafenone clinical use

A

= supraventricular arrhythmia

33
Q

Propafenone adverse effect

A

worse arrhythmia

34
Q

Class 2 drugs effect what channels and usually acts on what cells

A
  1. increase cAMP
  2. If (funny current) to open slower
  3. lower Ca channel
    = pacemaker cells (lower slope of phase 4
35
Q

BB have what effect on EKG

A
  1. SA = decrease HR (longer RR interval)

2. AV = decrease AV conductance (longer PR interval)

36
Q

Propanolol clinical use

A
cardiac arrhythmia from :
= atrial flutter, atrial fib
= stress and thyroid storm 
= MI 
= Paroxysmal supraventricular arrhythmia
37
Q

Esmolol clinical use and administration

A

short lived B1 blocker, continuous IV
= supraV
= thyrotoxicosis

38
Q

Class 3 drugs do what

A

block K+ (regulate AP length = regulating refractory period)

39
Q

BB and EKG

A

prolong QT segment

= lower slope of phase 3

40
Q

Amiodarone clinical use

A

most used
= recurrent V tachy
= atrial fib
(slows HR and AV conduction)

41
Q

Amiodarone adverse effects

A

= fatal pulmonary fibrosis
= hypo or hyperthyroidism
= torsades de pointes (since it prolongs QT and AP) ONLY RARE with this drug**

42
Q

Sotalol does what and clinical use

A

= nonselective B blocker and K+ blocker
= severe V arrhythmia
= atrial fib to keep sinus rhythm

43
Q

Sotalol adverse effects

A
  1. torsades

2. depress cardial function

44
Q

Doferilide and Ibutilide clinical use

A

restore sinus rhythm
esp after Atrial fib
Doferilide maintains it

45
Q

Class 4 drugs L CA+ channels

A

also has inactive phase

= Ca+ usually closes the gate (when its high ICM)

46
Q

Class 4 drugs L CA+ channels does what to graph and what cells

A
  1. phase 0 decrease slope

2. increase threshold potential in SA and AV node

47
Q

Verapamil, Diltiazem clinical use

A

= termination + prevention of paroxysmal supraventricular tachycardia
= V rate during A fib and a flutter controlled

48
Q

adenosine does what MOA

A
  1. activates a Gi
  2. increase K+ exit and inhibit Ca+, inhibit If
  3. hyperrepolarization, lowering AP
49
Q

adenosine clinical use

A

sinus rhythm in paroxysmal supraventricular arrhythmia

by IV

50
Q

Adenosine cells it acts on and graph

A
pacemaker cells (AV and SA)
= inhibits AV conduction and longer AV refractory period