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Cardiovascular II > Anti-arrhythmia drugs > Flashcards

Anti-arrhythmia drugs Flashcards

1
Q

What is occurring during phase 0 of action potential in cardiac electrical system fast response fibers?

A

Activate NA channels open and Na moves into the cell

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2
Q

What is occurring during phase 1 of action potential in cardiac electrical system fast response fibers?

A

Na channels inactivated and K moves outward

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3
Q

What is occurring during phase 2 of action potential in cardiac electrical system fast response fibers?

A

Ca inward balanced by K outward - plateau

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4
Q

What is occurring during phase 3 of action potential in cardiac electrical system fast response fibers?

A

Inactivation of Ca channels
Repolarization –> K outward

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5
Q

What is occurring during phase 4 of action potential in cardiac electrical system fast response fibers?

A

Resting membrane potential by Na/K ATPase pump

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6
Q

What is occurring during phase 0 of action potential in cardiac electrical system slow response fibers?

A

Activation of L-type Ca channels –> Ca inward

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7
Q

What is occurring during phase 3 of action potential in cardiac electrical system slow response fibers?

A

K outward –> repolarization

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8
Q

What is occurring during phase 4 of action potential in cardiac electrical system slow response fibers?

A

Na and Ca inward –> K outward
Pacemaker current

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9
Q

4 properties of the electrophysiology of the heart

A

Responsiveness
Conductance
Automaticity
Refractoriness

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10
Q

Equation that illustrates measure of refractoriness of the heart electrical system

A

ERP/APD
ERP = effective refractory period
APD = action potential duration

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11
Q

Result of increase SyNS activity in SA node

A

Tachycardia

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12
Q

Result of increase PsNS activity in the SA node

A

Bradycardia

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13
Q

General mechanism of Vaughn Williams class I antiarrhythmic drugs

A

Na channel blockers

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14
Q

Mechanism of Vaughn Williams class Ia antiarrhythmic drugs

A

Block activated Na channel to decrease Vmax and prolong ADP

Anticholinergics

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15
Q

Anticholinergic effect on the heart

A

Increase HR and conduction

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16
Q

Adverse effects of quinidine

A

Cinchonism
Increase QT interval –> Torsades de pointes
Displace digoxin –> decrease VD
Antacids increase absorption

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17
Q

Symptoms of cinchonism

A

Tinnitus
Hearing loss
GI upset
Diplopia

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18
Q

Adverse effects of procainamide

A

Agranulocytosis
SLE like syndrome –> slow acetylators

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19
Q

Drugs included in Vaughn Williams class Ia antiarrhythmic drugs

A

Quinidine - also an alpha blocker
Procainamide - least anticholinergic
Disopyramide - most anticholinergic

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20
Q

Mechanism of Vaughn Williams class Ib antiarrhythmic drugs

A

Decrease APD and no effect on Vmax
Increase threshold of V fib
Slow conduction in hypoxic and ischemic tissue
Preference for ischemic tissue

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21
Q

Drugs included in Vaughn Williams class Ib antiarrhythmic drugs

A

Lidocaine –> least cardiotoxic
Tocainide
Mexiletine

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22
Q

Cardiovascular uses of lidocaine

A

V tach after MI
Digitalis toxicity

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23
Q

Adverse effects of lidocaine

A

Drowsiness
Paresthesia
Convulsions –> toxic doses

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24
Q

Mechanism of Vaughn Williams class Ic antiarrhythmic drugs

A

Both Na channels to markedly decrease Vmax with no effect on APD

25
Q

Drugs included in Vaughn Williams class Ic antiarrhythmic drugs

A

Flecainide
Propafenone
Moricizine

26
Q

Clinical uses of Vaughn Williams class Ic antiarrhythmic drugs

A

Life threatening V tach or V fib
Refractory SVTs

27
Q

Adverse effects of Vaughn Williams class Ic antiarrhythmic drugs

A

Pro-arrhythmic effect
Increase risk for sudden death and cardiac arrest by decreasing LV function after MI

28
Q

Mechanism of Vaughn Williams class 2 antiarrhythmic drugs

A

Beta-blocker that decrease SA and AV node conduction –> decrease slope of phase 4 depolarization

29
Q

Clinical uses of Vaughn Williams class 2 antiarrhythmic drugs

A

Prophylaxis for ventricular arrhythmias post MI
SVTs

30
Q

Adverse effects of Vaughn Williams class 2 antiarrhythmic drugs

A

Proarrhythmic
Can cause AV block

31
Q

Mechanism of Vaughn Williams class 3 antiarrhythmic drugs

A

K channel blockers that increase ADP and ERP. Prolong repolarization and lengthen phase 2.

32
Q

Drugs included in Vaughn Williams class 3 antiarrhythmic drugs

A

Amiodarone
Dofetilide
Ibutilide
Sotalol
Dronedarone

33
Q

Mechanism of amiodarone

A

Binds to and inactivates Na channel
Blocks K and Ca channels
Non-competitive inhibition of beta receptors

34
Q

Half-life of amiodarone

A

25-60 days

35
Q

Clinical uses of amiodarone

A

A fib
V tach

Use with anticoagulant

36
Q

Adverse effects of amiodarone

A

Pulmonary fibrosis
Hepatotoxicity
Bluish discoloration of skin
Hypothyroidism in 5%
Hyperthyroidism in 25%
Torsades de pointes

37
Q

Mechanism of dofetilide and ibutilide

A

Selectively block outward K channel (delayed rectifier K channel). Results in prolonged ventricular repolarization and increase QT interval.

38
Q

Uses of dofetilide and ibutilide

A

Pharmacological cardioversion –> A fib and A flutter

39
Q

Mechanism of sotalol

A

Beta blocker and K channel blocker - Decrease HR and AV conduction
- Prolongs APD and ERP

40
Q

Antiarrhythmic uses of sotalol

A

A fib
Life threatening ventricular arrhythmias

41
Q

Adverse effects of sotalol

A

Torsades de pointes
HA
Depression
Impotence

42
Q

Contraindication of sotalol

A

Asthma

43
Q

Ca channel blockers used for arrhythmias

A

Diltiazem
Verapamil

44
Q

Mechanism of Ca channel blockers in arrhythmia

A

Decrease SA and AV nodal conduction
Decrease slope of phase 4

45
Q

Anti-arrhythmic use of Ca channel blockers

A

PSVT due to AV nodal reentry

46
Q

Adverse effects of Ca channel blockers

A

Orthostatic hypotension
Reduce CO
Lower extremity edema
Constipation

47
Q

Drug interactions of verapamil

A

Displaces digoxin, increasing its toxicity

48
Q

Drug interaction of Ca channel blockers

A

Pro-arrhythmic AV block is used with beta blockers

49
Q

Condition in which Ca channel blockers should be used with caution

A

A tach due to WPW

50
Q

Rapid acting AV nodal blocker with a half-life of 30 seconds

A

Adenosine

51
Q

Adenosine receptors and their effect

A

A1 –> Gi coupled –> decrease SA and AV nodal rate

A2a –> Gs coupled –> vasodilate

A2b –> Gq coupled –> bronchoconstrict

52
Q

Clinical use of adenosine

A

Drug of choice for PSVT

53
Q

Antagonist of adenosine

A

Theophylline

54
Q

Adverse effects of adenosine

A

Flushing
SOB
Burning sensation in chest

55
Q

Anti-arrhythmic uses of digoxin

A

Control ventricular rates in A fib and A flutter

56
Q

Arrythmias caused by drugs that prolong QT intervals

A

Torsades de pointes

57
Q

Treatment for Torsades de pointes

A

Discontinue causative agent
Magnesium sulfate and potassium

58
Q

Some drugs that can cause torsades de pointes

A

Amiodarone
Quinidine
Sotalol
Thioridazine
TCAs

Cardiovascular II (29 decks)

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