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Pharmacology > Dysrhythmia > Flashcards

Dysrhythmia Flashcards

0
Q

Which site in the heart is known as the pacemaker?

A

Sinoatrial node

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1
Q

Which classes of drugs are frontline agents for dysrhythmia?

A

Calcium channel blockers
Sodium channel blockers
Potassium channel blockers
Some Beta-blockers

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2
Q

In an ECG, what does the P-wave represent?

A

Atrial depolarization

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3
Q

In an ECG, what does the QRS complex represent?

A

Ventricle depolarization

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4
Q

In an ECG, what does the T wave represent?

A

Ventricle repolarization

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5
Q

In an ECG, what does the QT interval represent?

A

Duration of time between depolarization and repolarization of the ventricles.

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6
Q

What does Sotalol do to QT interval?

A

Lengthens it

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7
Q

How does Sinoatrial cardiac tissue spontaneously depolarize?

A

Positive slope during phase 4- tissue eventually gets to threshold potential for depolarization on its own.
The AV node also has a positive slope during phase 4, just not as positive as SA node, so SA node reaches threshold first.

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8
Q

What determines conduction velocity in cardiac tissues?

A

The number of functional sodium channels.

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9
Q

25% of patients taking ________ ____________ experience dysrhythmia (tachycardia).

A

Cardiac glycosides

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10
Q

In a cardiac action potential, what happens at phase 0?

A

Sodium ion channels open- rapid depolarization

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11
Q

In a cardiac action potential, what happens at phase 1?

A

Sodium ion channels close and Potassium ion channels open then close soon after.

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12
Q

In a cardiac action potential, what happens during phase 2?

A

Opening and closing of the Calcium channel. Some potassium leakage. “Plateau phase”.

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13
Q

In a cardiac action potential, what happens during phase 3?

A

Opening and closing of the Potassium channel. “Repolarization phase”.

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14
Q

In a cardiac action potential, what happens during phase 4?

A

Leakage that leads to spontaneous depolarization.

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15
Q

What are the three general ways in which dysrhythmias are discouraged?

A
  • Alter automaticity
  • Alter conduction velocity
  • Alter the refractory period
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16
Q

In what ways can automaticity be altered?

A
  • Decrease slope of phase 4 depolarization
  • Increase the threshold for action potentials
  • Decrease the resting membrane potential
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17
Q

In what ways can conduction velocity be decreased?

A
  • Decrease phase 0 slope
  • Decrease phase 4 slope
  • Decrease resting membrane potential and responsiveness
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18
Q

In what ways can refractory period be altered?

A
  • Prolong phase 2 plateau
  • Prolong phase 3 repolarization
  • Increase action potential duration
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19
Q

Drugs of Vaughan-Williams Class IA have what effect?

A

Moderate Na channel block, lowers conduction velocity by decreasing phase 0 slope.

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20
Q

Drugs of Vaughan-Williams class IB have what effect?

A

Minimal block of Na channels. Phase 0 slope decreased, conduction velocity slowed some. Phase 3 repolarization shortened. Net effect decrease in action potential duration.

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21
Q

Drugs of Vaughan-Williams class IC have what effect?

A

Marked blockage of Na channels, slow conduction velocity, though there is no change in action potential duration or repolarization (QT interval).

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22
Q

What are the IA prototypes?

A
  • Quinidine

- Procainamide

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23
Q

What are the class IB prototypes?

A
  • Lidocaine

- Phenytoin

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24
Q

What is the class IC prototype agent?

A

Flecainide

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25
Q

Drugs of Vaughan-Williams class II have what effect?

A

As beta blockers, they suppress sympathetic input. Phase 4 slope is decreased and conduction velocity is decreased. There is no effect on action potential duration.

26
Q

Drugs of Vaughan-Williams class III have what effect?

A

These potassium channel blockers prolong the phase 3 repolarization. This lengthens QT interval.

27
Q

What are the prototype class III agents?

A

Amiodarone

Ibutilide

28
Q

Drugs of Vaughan-Williams Class IV have what effect?

A

Calcium Channel Blockers
Decrease conduction velocity, increase effective refractory period, increase action potential duration.
They have the greatest effect in tissues that are more calcium sensitive, like the SA and AV nodes.

29
Q

What are the Class IV prototype drugs?

A

Verapamil

Diltiazem

30
Q

Vaughan-Williams Classification is based on the action of drugs in ___________ tissue.

A

normal, healthy

31
Q

Although Amiodarone is a Class III drug, it exhibits actions of all other V-W classes of drugs. Which additional actions does it exhibit?

A
  • Sodium Channel blockade
  • Noncompetetive alpha & beta adrenergic inhibition
  • Calcium Channel blockade
32
Q

Beta blockers and Calcium channel blockers are used for ______________ and not for _____________.

A
  • supraventricular tachycardias

- ventricular tachycardias

33
Q

Ca channel blockers are selective for ______ and __________ where Ca AP’s predominate.

A

SA and AV nodes

34
Q

What are the cardiac actions of Quinidine?

A

Decreased conduction velocity. Moderate Na channel block. Prolonged refractory period. Increased APD. Some K+ channel block- leads to prolonged repolarization. EFFECTS MORE PRONOUNCED IN DEPOLARIZED, DAMAGED TISSUE

35
Q

What are the potential extracardiac effects of Quinidone?

A
  • alpha adrenoreceptor blockage -> vasodilation
  • anti-muscarinic action -> accelerates heart
  • at certain concentrations, QT interval too lengthened. “Torsades de Pointes” arrhythmia
  • GI irritation
  • Headaches, dizziness, tinnitus
36
Q

For which forms of arrhythmia is Quinidine effective?

A

Effective for both ventricular and supraventricular

37
Q

What are the cardiac effects of Procainamide?

A

Class IA
Decreased conduction velocity. Moderate Na channel block. Prolonged refractory period. Increased APD. Some K+ channel block- leads to prolonged repolarization. EFFECTS MORE PRONOUNCED IN DEPOLARIZED, DAMAGED TISSUE

38
Q

What toxicity does procainamide have?

A

Cardiac: some cardiac depression

Non-cardiac: Syndrome that resembles lupus erythematosus

39
Q

What is procainamide predominately used for?

A

Acute ventricular tachycardia

40
Q

What is N-acetylprocainamide (NAPA)?

A

A liver metabolite of Procainamide that has some Class III activity

41
Q

What are the cardiac effects of Lidocaine?

A

Class IB

Mild Na channel blocker. Shortens refractory period. Decreases action potential duration.

42
Q

What kind of dysrhythmia is Lidocaine used to treat?

A

Acute Ventricular Tachycardia

43
Q

What are the cardiac effects of Phenytoin?

A

Class IB

Shortens action potential duration

44
Q

How is Phenytoin best used?

A

Taken orally, for chronic supraventricular and ventricular tachycardia.

45
Q

What are some common extracardiac effects/uses of Phenytoin?

A

Anti-convulsant against epilepsy

Causes gingival hyperplasia

46
Q

What are the cardiac effects of Flecainide?

A

Class IC
Decreases slope of phase 0
Decreases conduction velocity
No major change in APD

47
Q

Which beta blockers have membrane stabilizing propterties, and what does that mean?

A

metoprolol, propranolol
In addition to Class II properties, they function as Na+ channel blockers, decrease slope of phase 0, thereby further reducing conduction velocity.

48
Q

Which beta blockers are commonly used to treat arrhythmias?

A

Esmolol, Metoprolol, Propranolol, Sotalol

Esmolol used only for arrhythmias. Sotalol also has Class III action

49
Q

What is the half-life of esmolol, and what does that suit it for?

A

10 minutes

This makes it suitable for use during surgery when there is risk for arrhythmia.

50
Q

Potential adverse effects of Amiodarone:

A 
Torsades de Pointes
Thyroid dysfunction
Pulmonary fibrosis
Photosensitivity
Corneal microdeposits
51
Q

Donedarone

A

Similar in action to Amiodarone, but with shorter (~24 hr) half-life.
Does not have thyroid or pulmonary fibrosis issues like Amiodarone.

52
Q

This intravenous Class III compound simply prolongs action potentials, has the lowest risk of causing Torsades de Pointes, and treats flutter better than fibrillation.

A

Ibutilide

53
Q

Calcium channel blockers commonly used to treat Arrhythmias

A

Verapamil

Diltiazem

54
Q

Which “Other” dysrhythmic is very short acting (15 seconds) and used for acute supraventricular tachycardias?
What side effects does it have?

A

Adenosine

Flushing, hypotension

55
Q

This cardiac glycoside decreases conduction in the AV node by stimulating the vagus nerve. Used mostly in chronic atrial fibrillation.

A

Digoxin

56
Q

Which Vaughan-Williams class of drug would shorten action potential duration and have minimal effect on the Na+ channel?

A

Class IB

57
Q

What is the half-life of Esmolol?

A

about 9 minutes

58
Q

What is the half-life of Amiodarone?

A

25 to 100 days

59
Q

What kinds of drugs would be suitable for treating ACUTE SUPRAVENTRICULAR tachycardias?

A

Adenosine
Digoxin
Calcium Channel Blockers

60
Q

What kinds of drugs would be suitable for treating CHRONIC SUPRAVENTRICULAR tachycardias?

A

Beta Blockers

Calcium Channel Blockers

61
Q

What drugs would be top choices for treating ACUTE VENTRICULAR tachycardias?

A 
Amiodarone
Procainamide
Sotalol
Bretylium
Lidocaine
62
Q

What drugs would be top choices for treating CHRONIC VENTRICULAR tachycardias?

A

Amiodarone
Sotalol
Flecainide

Pharmacology (4 decks)

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