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Pharm Test 4 :( > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

0
Q

after-depolarization

A

Arrhythmia mechanism

Early- Arises from prolonged action potentials (K channel blockers)
Delayed -arises from baseline conditions of Ca overload

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1
Q

Ectopic pacemaker

A

Arrhythmia mechanism
-Spontaneous generation of action potentials by tissue that does not normally display automaticitiy

Caused by tissue depolarization, following ischemia

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2
Q

Arrhythmias result from:

A

Abnormal initiation of cardiac action

  • ectopic pacemaker
  • after-depolarization

Abnormal conduction pathway (reentry)

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3
Q

Reentry

A

Impulse travels in a loop sending depolarizing impulses to the rest of the heart each time it goes around the loop

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4
Q

How to treat reentry Arrhythmias

A

Lengthen action potential, thus lengthening the refractory period so the action potential is extinguished by entering refractory tissue

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5
Q

Premature ventricular beat

A

Premature beat, often due to delayed after-polarization (lots of Ca)

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6
Q

Atrial/ventricular tachycardia

A

Due to reentry or ectopic pacemakers

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7
Q

Supraventricular tachycardia

A

Tachycardia originating in the SA node, AV node

Types:
AV nodal reentry
Wolff-Parksinson White
Accessory AV node

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8
Q

Paroxysmal tachycardia

A

Rapid abnormal beats

Sudden onset and offset

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9
Q

Flutter

A

Rapid regular contractions
Due to reentry
Can degenerate into fibrillation

Tx: dampen transmission at AV node-give time for ventricles to fill
Ca channel blocker

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10
Q

Fibrillation

A

Self-sustaining, random waves of depolarization which prevent coordinated blood-pumping contractions

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11
Q

Torsade de pointes

A

Rotation of the QRS vector on the EKG

Acquired: due to drug induced early after-depolarization (K channel blockers)

Congenital: long QT syndrome

  • mutation of Na channels that reduces inactivation so channels remain active longer, extending the plateau.
  • mutation of K channels so K can’t exit the cell, prolonging the action potential
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12
Q

Class 1 drugs

A

Na channel blockers

1a: Na and K channel block
1b: block Na in depolarizes tissue
1c: potent and selective Na channel blockers

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13
Q

Class 1a drugs

A

1a: Na and K channel blocker

Na: decreases excitability and conduction velocity
K: prolong action potential by inhibiting repolarization

Quinidine
Procainamide

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14
Q

Class 1b dugs

A

1b: block Na in depolarizes tissue

Lidocaine

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15
Q

Class 1c drugs

A

1c: potent and selective Na channel blockers

Flecamide

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16
Q

Class II drugs

A

Beta blocker
Blocks NE stimulation of CA channels

Propranolol

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17
Q

Class III drugs

A

K channel blockers

Amiodarone, sotalol, dofetilide

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18
Q

Class IV drugs

A

Ca channel blockers

Vermapil, diltiazem

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19
Q

Adenosine

A

K channel activator

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20
Q

Quinidine

A

Class 1a: Na and K blocker

A. Flutter, a fib, supra ventricular Arrhythmias
V. Tachycardia

Not first line due to side effects

Cardio toxicity:
Lengthens QRS interval

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21
Q

Quinidine syncope

A

Lightheadedness and fainting caused by quinidine induced torsade de pointes

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22
Q

Quinidine side effects

A

Cardio toxicity
GI disturbances
Cinchonism (tinnitus, dizziness, blurred vision, HA)
Rare:thrombocytopenia, hepatitis,

23
Q

Procainamide

A

Class 1a: Na and K channel blockers

Metabolized to NAPA in liver- increased K channel blocking effects

Used for atrial and ventricular Arrhythmias, not good for long term use due to Lupus

24
Q

Procainamide side effects

A

Torsades de pointes less common than quinidine
Increases w/ elevated NAPA

Hypotension
Lupus erythematosus

25
Q

Lidocaine

A

Class 1b drug: Na channel blocker in depolarized fast tissue

Blocks open and inactivated Na channels more than closed channels

  • stronger effects on unhealthy, depolarized tissue
  • use after Arrhythmias (ectopic pacemakers) after an MI, w/ ischemia, digitalis toxicity
26
Q

Lidocaine side effects

A

Affects CNS: parenthesis, prickling, drowsiness, tinnitus, blurred vision

27
Q

Prophylaxis of lidocaine with patients thought to have an MI _____survival

A

Decreases

-maybe due to enhanced likelihood of heart block or HF

28
Q

Flecainide

A

Class 1c: potent and selective Na channel blockers

Strong effects on His/Purkinje fiber system
*tx of supraventricular Arrhythmias (ex) A fib

29
Q

Flecainide side effects

A

Significantly pro arrhythmic - greater increase of death with prolonged use

30
Q

Propranolol and beta blockers

A

Blocks beta receptor stimulation of Ca channels

*ventricular Arrhythmias due to exercise and emotion after MI to prevent infarction
(Decrease AV nodal conduction, thereby decreasing ventricular rate)

Slows upstroke of action potential in slow tissue (SA/AV nodes)
Decreases excitability and slows conduction velocity
-negative ionotrophic and chronotrophic effects (less contraction, and slower rate)

31
Q

Beta blockers ______ long term survival

A

Increase

32
Q

Metapropalol and other beta blockers also improve mortality in patients with mild to moderate_______

A

Heart failure

33
Q

Amiodarone

A

Blocks K channels -> prolonged action potential duration

Highly effective for supraventricular and ventricular tachyarrhythmias

Many side effects, but still widely used, doesn’t increase mortality

34
Q

Amiodarone side effects

A

Extensively tissue bound -long half life:
Concentration in tissues
Skin deposits leading to photosensitivity
GI, neurological, cardiovascular, hepatotoxic, thyroid

Increases plasma level of other antiarrhymic drugs

35
Q

Sotalol

A

Racemic mix of D- and L- isomers

D: blocks K channels ( prolonging action potential)
L: beta blocker (decreased AV transmission)

Used to tx atrial flutter and fibrillation (rate reducing)

36
Q

Sotalol side effects

A

Torsades de pointes

Same effects as other beta blockers

37
Q

Beta blocker side effects

A

SA and AV block
Sudden withdrawal may worsen angina and Arrhythmias
Dyspnea

38
Q

Dofetilide

A

Selective blocker of delayed rectifier K channels in heart
Few extra cardiac effects

High risk of Torsades de pointes
Clinics must have training on how to monitor

39
Q

Verapamil and Diltiazem

A

Class IV drugs: Ca channel antagonists
Blocking Ca channels suppresses upstroke of phase 0 in slow tissue
-slows excitability and conduction velocity

Direct action on SA node generally slows HR

First choice (w/adenosine) for supraventricular tachycardia due to AV nodal reentry 
( reduce ventricular rate in atrial flutter)
40
Q

Verapamil and diltiazem side effects

A

Cardiac
V. Fibrillation and hypotension if ventricular tachycardia is mid diagnosed as supraventricular tachycardia

Constipation
AV block, negative ionotrophic effects

41
Q

Adenosine

A

Adenosine receptor agonist leads to opening of K channels which hyperpolarizes AV nodal tissue

Terminates paroxysmal supraventricular tachycardia

Short time of action

42
Q

Digoxin

A

Cardiac glycoside

Used to treat CHF 
Positive ionotrophic effects 
-inhibits Na/K ATPase 
     Increases intracellular Ca -> increased force of contraction -> Increased CO
Not first line tx

Reduces ventricular rate in presence of a. A. Tachy, a. Flutter, a. Fib
Acts like a beta blocker

43
Q

One problem with digoxin and bacteria

A

Intestinal bacteria in 10% of patients degrade digoxin, so antibiotic tx can lead to a sudden increase in digoxin availability and toxicity

44
Q

Digitalis toxicity

A

Low toxic dose
Toxicity due to K+ depletion (diuretics)

  1. V tachycardia and v. Fib
  2. AV block
  3. AV junctional rhythm
  4. GI effects
  5. Neurological effects
45
Q

Diuretics

A

Reduce salt and water retention thereby reducing ventricular after load and preload

-loss of K

46
Q

ACE inhibitors

A

Block conversion of angiotensin I to angiotensin II

Reduce salt and water retention and reduce preload and after load

47
Q

Angiotensin receptor agonist

A

Block the actions of angiowtrnsin II on AT1 receptors

Reserved for pts that don’t tolerate ACE inhibitors well

48
Q

Beta blockers

A

Improve mortality by reducing ventricular

49
Q

Vasodilators

A

Reduce after load

*hydralazine

50
Q

K channel blockers mechanism

A

Lengthen action potential which lengthens refractory period and can interrupt re-entry Arrhythmias

  • Torsade de pointes

Quinidine
Procainamide (NAPA)
Sotalol
Dofetilide

51
Q

Ca channel inhibition mechanism

A

Reduces excitability of slow AV nodal and SA nodal tissue
-used for reducing ventricular rate during atrial tachyarrhythmias

  • SA and AV nodal block -too much dampening
  • negative ionotrophic effect
52
Q

Na channel inhibition mechanism

A

Inhibits excitability in fast tissue
-used for ventricular supraventircular arrythimias

Lengthened QRS intervals

Potent Na channel blockers are pro arrythmic

53
Q

Used for re-entry arrythimias

A

K channel blockers

54
Q

Used for reducing ventricular rate during atrial tachyarrhythmias

A

Ca channel blockers

55
Q

Used for ventricular or supraventricular arrythimias involving fast tissue

A

Na channel blockers

Pharm Test 4 :( (6 decks)

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