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D1 Spring > Pharmacology - Anti-Arrhythmic Drugs > Flashcards

Pharmacology - Anti-Arrhythmic Drugs Flashcards

1
Q

Resting HR is ___________ correlated to life expectancy

A

inversely

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2
Q

Why is having a fast heartbeat bad?

A
  1. Heart works harder (higher O2 demand)
  2. Diastole gets shorter (less O2 supply)
  3. Risk of ischemia (higher O2 demand + less O2 supply)
  4. Prone to arrhythmias
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3
Q

Irregular heartbeat

A

Arrhythmia

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4
Q

Your heart beats too fast, too slow, or with an irregular pattern

A

Arrhythmia

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5
Q

> 100 bpm (too fast)

A

Tachycardia

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6
Q

<60 bpm (too slow)

A

Bradycardia

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7
Q

Which is the more frequent issue: tachycardia or bradycardia

A

Tachycardia

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8
Q

What three things can cause arrhythmia?

A

Ischemia
Muscle death
Heart failure

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9
Q

Which drugs are specific to arrhymthia?

A

Na+ blockers
K+ blockers

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10
Q

Difference in electrical potential between inferior and exterior of a cell

A

Membrane potential

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11
Q

Which part of the cell is more negative?

A

Inside

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12
Q

Rapid rise and fall of membrane potential upon stimulus; occurs in excitable cells like neurons and muscle cells

A

Action potential

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13
Q

Resting membrane potential

A

-90 mV

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14
Q

Negative membrane potential starts becoming more positive

A

Depolarization

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15
Q

Positive membrane potential starts becoming more negative again

A

Repolarization

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16
Q

Which lead in EKG is most commonly used?

A

Lead II

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17
Q

What is “P” on an EKG?

A

Atrial depolarization

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18
Q

What is “R” on an EKG?

A

Ventricular depolarization

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19
Q

What is “T” on an EKG?

A

Ventricular repolarization

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20
Q

Where is atrial repolarization on an EKG?

A

Hidden between “P” and “R” in the PR segment

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21
Q

Explain the electrochemical gradient

A

Outside membrane: positive, more Na+, less K+, more Ca2+

Inside membrane: negative, less Na+, more K+, less Ca2+

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22
Q

Voltage gated channels are also called what?

A

Ion channels

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23
Q

What are voltage gated channels NOT activated by?

A

Ligands

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24
Q

What are voltage gated channels activated by?

A

Changes in membrane potential

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25
Q

T/F voltage gated ion channels are transmembrane

A

True

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26
Q

What are the 2 types of action potentials?

A
  1. Nodal
  2. Non-nodal
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27
Q

What is nodal action potential made by?

A

Pacemaker cells
SA/AV nodes

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28
Q

What is non-nodal action potential made by?

A

Myocytes

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29
Q

What 3 things regulate HR?

A
  1. Automaticity
  2. Refractoriness
  3. Conduction velocity
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30
Q

Spontaneous impulse generation

A

Automaticity

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31
Q

What controls automaticity?

A

SA node
AV node

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32
Q

Increased automaticity causes what?

A

Increased rate of impulse generation
Increased HR

33
Q

What 2 things can change automaticity?

A
  1. Rate of leakiness
  2. Magnitude of threshold potential (under neurohormonal control)
34
Q

Which action potential has a leaky Na+ current?

A

Pacemaker action potential

35
Q

T/F the ventricular action potential has a leaky Na+ current

A

FALSE

36
Q

How long is the effective refractory period in non-nodal/ventricular action potential?

A

~0.2 seconds

37
Q

Period during which no AP can be fired again

A

Effective refractory period (ERP)

38
Q

Speed of impulse conduction (travel) in cardiac fibers?

A

Conduction velocity

39
Q

Influenced by rate (slope) of depolarization and resting membrane potential

A

Conduction velocity

40
Q

What causes cardiac arrhythmias?

A

Abnormal impulse generation and conduction

41
Q

What are impulse generation and conduction determined by? (3)

A
  1. Automaticity
  2. Refractoriness
  3. Conduction speed
42
Q

What are the etiologies of cardiac arrhythmias? (5)

A
  1. Ischemia/hypoxemia
  2. Fibrosis/scar tissue
  3. Electrolyte imbalance (Na+, K+, Ca2+)
  4. Drug toxicities
  5. Congenital defects
43
Q

What are the 2 types of cardiac arrhythmias?

A
  1. Supraventricular tachycardia (SVT)
  2. Ventricular tachycardia (V-tach)
44
Q

What are the 4 types of supraventricular tachycardia (SVT)?

A
  1. Atrial fibrillation (A-fib)
  2. Atrial flutter
  3. Multifocal atrial tachycardia (MAT)
  4. Atrioventricular reentrant tachycardia (AVRT)
45
Q

What are the 4 types of ventricular tachycardia (V-tach)?

A
  1. Focal V-tach
  2. Reentrant V-tach
  3. Torsades de pointes
  4. Ventricular fibrillation (V-fib, deadly)
46
Q

T/F atrial fibrillation (A-fib) has multiple foci of automaticity (not just SA node and AV node)

A

True

47
Q

In atrial fibrillation (A-fib), you have no prominent _____ waves due to absence of synchronous ____________ depolarization

A

P; atrial

48
Q

In atrial fibrillation (A-fib), you have irregular _________ depolarization

A

ventricular

49
Q

What is atrial fibrillation (A-fib) also called?

A

“Irregularly irregular” rhythm

50
Q

What are the 2 pathways of conduction in the heart?

A
  1. AV conduction (normal)
  2. Accessory (abnormal)
51
Q

Which pathway of conduction is present in people with atrioventricular reentrant tachycardia (AVRT)?

A

Accessory (abnormal)

52
Q

T/F the accessory (abnormal) node can fire in 2 directions: up and down

A

True

53
Q

What happens in someone who has Wolff-Parkinson-White syndrome? (3)

A
  1. SA node fires to accessory pathway
  2. No pause
  3. Causes premature ventricular depolarization
54
Q

Wolff-Parkinson-White syndrome falls under what kind of SVT?

A

Atrioventricular reentrant tachycardia (AVRT)

55
Q

Wolff-Parkinson-White syndrome has a short _______ interval

A

PR

56
Q

What kind of wave is seen in Wolff-Parkinson-White syndrome?

A

Delta wave (caused by short PR interval)

57
Q

What can atrioventricular reentrant tachycardia (AVRT) be caused by?

A

Unidirectional block (due to scar tissue)

58
Q

What are the 4 causes of conduction blocks?

A
  1. Ischemia
  2. Fibrosis
  3. Inflammation
  4. Drugs
59
Q

What are the 4 non-pharmacologic interventions?

A
  1. Electrical cardioversion
  2. Automatic implantable cardioversion/defib device
  3. Ablation therapy
  4. Pacemaker
60
Q

What are the 4 anti-arrhythmic drugs in order?

A

“Some block potassium channels”

Na+ blockers
B blockers
K+ blockers
CCBs

61
Q

Majority of arrhythmias are associated with __________

A

tachycardia

62
Q

What is the mechanism of anti-arrhythmic drugs?

A

Decrease automaticity, conduction velocity, HR
Increase refractoriness

63
Q

What are the classes of anti-arrhythmic drugs?

A

Class I - Na+ blockers
Class II - B blockers
Class III - K+ blockers
Class IV - CCBs
Misc. - Adenosine

64
Q

Which drugs are used to treat supraventricular tachycardias (SVTs) such as atrial fibrillation and Wolff-Parkinson-White syndrome?

A

Na+ blockers
K+ blockers
CCBs

65
Q

What drug is used to treat supraventricular tachycardias (SVTs) such as atrial fibrillation and Wolff-Parkinson-White syndrome, as well as ventricular tachycardias (V-tachs)?

A

B blockers

66
Q

What is the problem with K+ blockers?

A

Longer QT interval

67
Q

What is a longer QT interval diagnosed as?

A

Torsade de pointes
Ventricular fibrillation

(V-tach conditions)

68
Q

T/F anti-arrhythmic drugs can cause arrhythmias

A

True, they are arrhythmogenic

69
Q

Which drug is a class III drug?

A

Amiodarone

70
Q

What does Amiodarone block?

A

Na+ channel
K+ channel
Ca2+ channel
B receptor

71
Q

What does Amiodarone resemble?

A

Thyroid hormone

72
Q

Amiodarone is ________ (more/less) arrhythmogenic

A

less

73
Q

What are 2 adverse effects of long term use of Amiodarone?

A

Pulmonary fibrosis
Pneumonitis

74
Q

Which drug is a miscellaneous drug?

A

Adenosine

75
Q

What does Adenosine cause?

A

Hyperpolarization

76
Q

Margin of safety of anti-arrhythmic drugs is ___________

A

narrow

77
Q

Drugs that slow AV conduction like B blockers and Amiodarone can cause what 2 things?

A

Bradycardia
Heart block

78
Q

Drugs with negative ionotropic effects (decreased contractility) like B blockers can precipitate what?

A

Heart failure

D1 Spring (47 decks)

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