Arrhythmias Flashcards

1
Q

What are the 3 conditions for this to occur?

A
  1. An obstacle must be present
  2. there must be unidirectional block
  3. Conduction time around the cicuit must be long enough that the retrograde impulse does not enter refractory tissue
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2
Q

the 4 major pharmacologic mechanisms available to achieve the goals of antiarrhythmic agents

A
  1. Na channel Blockade
  2. blockade of SNS effects in the heart
  3. prolongation of effective refractory period
  4. Ca channel blockade
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3
Q

Example of Condition where Reentry is anatomically determined

A

Wolff-Parkinson-White Syndrome

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4
Q

Mechanisms of Arrhythmia

A
  1. Disturbances in impulse formation
  2. Disturbances in impulse conduction
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5
Q

the time between phase 0 and sufficient and sufficient recovery of Na Channels in Phase 3

A

Refractory Period

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6
Q

Describe the Action Potential Phases

A
  1. Phase 0: Upstroke
  2. Phase 1: Early-fast repolarization
  3. Phase 2: Plateau
  4. Phase 3: Repolarization
  5. Phase 4: Diastole
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7
Q

What are the common causes of Arrhythmia in clinical practice?

A

Digitalis (25%)

Anesthesia (50%)

Acute Myocardial Infarction (80%)

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8
Q

frequency of SA node conduction

A

60-100 bpm

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9
Q

lag time from SA node to AV node is?

this particularly provides what?

A

0.15s

provides time for atrial contraction to propel blood into ventricles

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10
Q

What channels are open during the Phase 3 or Late Repolarization

A

Delayed Ca Rectifying Channels (slow and rapid)

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11
Q

Differentiate the Phase 4 of pacemaker AP and non pacemaker AP

A

Pacemaker AP: (no true RMP) Slow inward Na current and Transient calcium current

Non Pacemaker AP: (RMP) K current

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12
Q

Classification of antiarrhythmic agents and thier main actions

A

Class 1: Sodium Channel Blocker

Class 2: Sympatholytic (Beta Blocker)

Class 3: Prolongation of APD (Action Potential Duration) via blockade of rapid delayed rectifier potassium current

Class 4: Calcium current blocker

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13
Q

Subgroups under class 1 of antiarrhythmic agents

A

Class 1A: prolong APD;dissociate from channel with intermediate kinetics

Class 1B: shorten APD; dissociate from the channel with rapid kinetics

Class 1C: minimal effects on the APD; dissociate for the channel with slow kinetics

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14
Q

what type of drug action is described by “the channels that are being used frequently/in an active state are mosre susceptible to block

A

use dependent / state dependent

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15
Q

mechanisms by which antiarrhythmic agents slow conduction

A
  1. steady-state reduction in the number of available unblocked channels
  2. prolongation of recovery time of channels (increasing effective refractory period)
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16
Q

Drugs that prolong APD (group 1A) (3)

A

Procainamide

Quinidine

Disopyramide

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17
Q

anti arrhythmic drug that has an SLE-like Side Effects

A

Procainamide

18
Q

Side effects include tinnitus /cinchonism

A

Quinidine

19
Q

True/False. Disopyramide is an antiarrhythmic agent indicated for Heart Failure Px

A

False. it is CI for Heart Failure Px

20
Q

blocks activated and inactivated sodium channels with rapid kinetics; has a selective conduction in depolarized cells

A

Lidocaine

21
Q

what acute phase protein binds lidocaine making less free drug available to exert is pharmacologic effect

A

Alpha-1-Acid Glycoprotein

22
Q

the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia

A

Lidocaine

23
Q

an orally active congener of Lidocaine

A

Mexilitine

24
Q

potent inhibitor of sodium and potassium channels with slow unblocking kinetics (does not prolong the AP or QT interval)

A

Flecainide

25
Q

very effective in suppressing premature ventricular contractions

A

Flecainaide

26
Q

A Class 1C antiarrhythmic agent that has similarities with propranolol

A

Propafenone

27
Q

an anti arrhythmic phenothiazine derivative; for ventricular arrhythmias

A

Moricizine

28
Q

Class 2 Anti-arrhythmic agents

A

Propanolol
Esmolol
Sotalol*

29
Q

Action potenial prolongation is least marked at fast rates(where it is desirable) and most marked at slow rates (where it can contribute to the risk of torsades de pointes)

A

“Reverse-use dependence”

30
Q

Class 3 Anti Arrhythmic drugs (7)

A

Amiodarone
Dronedarone
Celivarone
Vernakalant
Sotalol
Dofetilide
Ibutelide

31
Q

What are the cardiac effects of Amiodarone

A
  1. Blockade of Ikr
  2. Blockade of Iks (at chronic admin)
  3. slows HR and AV node conduction
32
Q

A structural analogue of Amiodarone without its toxic effects of the thyroxine metabolism

A

Dronedarone

33
Q

At low doses, what action of sotalol is predominant?

A

Beta blocking action

(high dose: prolonged AP)

34
Q

Action potential prolongation mechanisms of

Ibutilide

Dofetilide

A

Ibutelide: (-) rapid delayed rectifier potassium current and (+) slow inward soudium current

Dofetilide: dose dependent (-) rapid delayed rectifier potassium current

35
Q

the prototype of Class 4 AntiArrhythmic agents

A

Verapamil

36
Q

Calcium channel blockers that do not have antiarrhythmic effects

A

Dihydropyridines (e.g. Nifedipine)

37
Q

Verapamil suppresses Early or Delayed After Depolarization?

A

Both

38
Q

Miscellaneous Antiarrhythmic agents (3)

A

Adenosine
Magnesium
Potassium

39
Q

which drug is renderred less effective by theophylline and caffeine but potentiated by dipyridamole

A

Adenosine

(Theophylline and Caffeine: Adenosine receptor blockers
Dipyridamole: adenosine uptake inhibitors)

40
Q
A