Drugs For Cardiac Arrhythmias - Dr. Konorev Flashcards

(50 cards)

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
Lidocaine administered how and clinical use
IV only = ventricular tachy during Acute MI = also used for a local anesthetic
26
Lidocaine adverse effects
least toxic | - can cause hypotension , tremor, slurred speech, paresthesias
27
Mexiletine administration and clinical use
oral = V arrhythmia = chronic pain relief (diabetic neuropathy + nerve injury)
28
Mexiletine adverse effects
tremor blurred vision lethargy
29
Class 1C drugs do what
``` block NA (prolong QRS) Block K+ (only same QT and AP length) ```
30
Flecainide clinical use
= supraventricular arrhythmia | = refractory severe V arrhythmia
31
Flecainide adverse reactions
make arrhythmia worse
32
Propafenone clinical use
= supraventricular arrhythmia
33
Propafenone adverse effect
worse arrhythmia
34
Class 2 drugs effect what channels and usually acts on what cells
1. increase cAMP 2. If (funny current) to open slower 3. lower Ca channel = pacemaker cells (lower slope of phase 4
35
BB have what effect on EKG
1. SA = decrease HR (longer RR interval) | 2. AV = decrease AV conductance (longer PR interval)
36
Propanolol clinical use
``` cardiac arrhythmia from : = atrial flutter, atrial fib = stress and thyroid storm = MI = Paroxysmal supraventricular arrhythmia ```
37
Esmolol clinical use and administration
short lived B1 blocker, continuous IV = supraV = thyrotoxicosis
38
Class 3 drugs do what
block K+ (regulate AP length = regulating refractory period)
39
BB and EKG
prolong QT segment | = lower slope of phase 3
40
Amiodarone clinical use
most used = recurrent V tachy = atrial fib (slows HR and AV conduction)
41
Amiodarone adverse effects
= fatal pulmonary fibrosis = hypo or hyperthyroidism = torsades de pointes (since it prolongs QT and AP) ONLY RARE with this drug**
42
Sotalol does what and clinical use
= nonselective B blocker and K+ blocker = severe V arrhythmia = atrial fib to keep sinus rhythm
43
Sotalol adverse effects
1. torsades | 2. depress cardial function
44
Doferilide and Ibutilide clinical use
restore sinus rhythm esp after Atrial fib Doferilide maintains it
45
Class 4 drugs L CA+ channels
also has inactive phase | = Ca+ usually closes the gate (when its high ICM)
46
Class 4 drugs L CA+ channels does what to graph and what cells
1. phase 0 decrease slope | 2. increase threshold potential in SA and AV node
47
Verapamil, Diltiazem clinical use
= termination + prevention of paroxysmal supraventricular tachycardia = V rate during A fib and a flutter controlled
48
adenosine does what MOA
1. activates a Gi 2. increase K+ exit and inhibit Ca+, inhibit If 3. hyperrepolarization, lowering AP
49
adenosine clinical use
sinus rhythm in paroxysmal supraventricular arrhythmia | by IV
50
Adenosine cells it acts on and graph
``` pacemaker cells (AV and SA) = inhibits AV conduction and longer AV refractory period ```