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Cardiovascular II Exam 3 > Antiarrhythmics - SRS > Flashcards

Antiarrhythmics - SRS Flashcards

1
Q

What are the Class Ia Na+ channel blockers?

A

—Disopyramide (Norpace)
—Quinidine
—Procainamide

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2
Q

What are the class Ib Na+ channel blockers?

A

—Lidocaine (Xylocaine)
—Mexiletine
—Tocainide

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3
Q

Class Ic Na+ channel blockers include what drugs?

A

—Moricizine
—Flecainide (Tambocor)
—Propafenone (Rythmol)

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4
Q

What are the class II antiarrhythmics?

A

β-Adrenergic Receptor Blockers
—Esmolol (Brevibloc)
—Metoprolol (Lopressor, Toprol XL)
—Propranolol (Inderal)

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5
Q

What are the class III antiarrhythmics?

A

K+ Channel Blockers
—Amiodarone (Cordarone)
—Bretylium
—Dofetilide (Tikosyn)
—Ibutilide
—Sotalol (Betapace)

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6
Q

What are the class IV antiarrhythmics?

A

Ca2+ Channel Blockers
—Verapamil (Calan)
—Diltiazem (Cardizem)

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7
Q

What are the “Other” ACLS drugs?

A

—Adenosine
—Atropine
—Anticoagulants
—Digoxin
—MgSO4
—Naloxone (Narcan)
—Vasopressors

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8
Q

Which of the shown channels are blocked by Na+ channel blocking drugs?

A

Middle - Activated

Right - Inactivated

channels are impacted by Na+ channel blockers

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9
Q

What are m gates?

A

The activation gates for sodium channels

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10
Q

What are the inactivation gates for sodium channels?

A

H gates

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11
Q

What two things cause arrhythmias?

A

Abnormal Impulse Generation

Abnormal Impulse conduction

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12
Q

Abnormal impulse generation can arise due to triggered automaticity, what phase does early afterdepolarization disrupt?

Delayed afterdepolarization?

A

EAD: Phase 3

DAD: phase 4

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13
Q

Which of the graphs shows DAD? EAD?

A
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14
Q

Abnormal impulse conduction can arise from what two types of things?

A

Depressed conduction

Reentry

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15
Q

What are examples of arrythmias resulting from depressed conduction?

A

Simple block

  • AVnodal block
  • Bundle Branch block
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16
Q

What does reentry describe? What is required for a reenty derived arrhythmia to occur?

A

Impulse reenters/excites areas of heart more than once
Must be an obstacle – establishes a circuit
Must be unidirectional block
Conduction time must be long enough that retrograde impulse does not encounter refrac

tory tissues

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17
Q

What are the three main things that anti-arrhythmic drugs do?

A

—Induce arrhythmias (weigh benefits vs. risks)

—Depress autonomic properties of abnormal pacemaker cell

—Alter conduction characteristics of reentrant loop

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18
Q

By what means do antiarrhythmic drugs depress autonomic properties of abnormal pacemaker cells?

A

Decrease slope of phase 4
Elevate threshold potential

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19
Q

How do anti-arrhythmic drugs alter the conduction characteristics of reentrant loop?

A 
Facilitate conduction (shorten refractoriness)
Depress conduction (prolong refractoriness)
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20
Q

What drugs have the effects shown in the four graphs?

A

A. B-Blockers

B. Na+ channel blockers and Ca2+ channel blockers

C. Adenosine

D. K+ channel blockers

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21
Q

What is the predominant mechanism of Type IA ACLS?

Describe the dissociation kinetics

A

Na+ channel blocker

Dissociates with intermediate kinetics

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22
Q

What is the predominant mechanism of type IB ALCS drugs?

Describe the dissociation kinetics

A

Na+ channel blocker

Dissociates with rapid kinetics

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23
Q

What is the predominant mechanism for type IC ACLS drugs

Describe the dissociation kinetics

A

Na+ channel blocker

Slow kinetics

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24
Q

What is the predominant mechanism of type II ACLS drugs?

A

B-blocker

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25
Q

What is the predominant mechanism of the type III ACLS drugs?

A

K+ channel blocker

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26
Q

What is the predominant mechanism of the type IV ACLS drugs?

A

Ca2+ channel blocker

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27
Q

What impact do Type IA drugs have on…

Conduction velocity

Refractoriness

Autonomic properties

?

A

Conduction velocity - Decrease

Refractoriness - Increase

Autonomic properties - Decrease

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28
Q

What effect do Type IB drugs have on…

Velocity

Refractoriness

A

No effect on velocity

May decrease refractoriness

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29
Q

What effect do type IC drugs have on conduction velocity?

Refractoriness?

A

Decrease conduction velocity

No effect on refractoriness

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30
Q

What effect do Type II drugs have on conduction velocity?

Refractoriness?

Autonomic properties?

A

Decrease conduction velocity

Increase refractoriness

Decrease autonomic properties

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31
Q

What effect do Type III drugs have on refractoriness?

Action potential duration?

A

Increase refractoriness

Increase action potential duration

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32
Q

What impact do type IV drugs have on conduction velocity?

Refractoriness?

Autonomic properties?

A

Decreases conduction velocity

Increase refractoriness

Decrease autonomic properties

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33
Q

What phase of depolarization do class IA drugs slow?

A

Phase 0 depolarization

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34
Q

What are the cardiac effects of Procainamide? (4)

Extracardiac?

A
  1. —Slows upstroke of action potential,
  2. slows conduction,
  3. prolongs QRS,
  4. prolongs action potential duration.

Ganglion-Blocking

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35
Q

Procainamide is metabolized to N-acetylprocainamide (NAPA), what class of activity does this metabolite have?

A

Class III

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36
Q

What are the therapeutic uses of procainamide?

A

Atrial and ventricular arrhythmias

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37
Q

Name three ADR’s for procainamide?

A
  1. Excessive APD prolongation,
  2. QT prolongation,
  3. reversible lupus erythematosus (~33%)
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38
Q

What are the common SLE type ADR’s seen in procainamide ADR’s?

A

Arthritis, Arthralgia and rarely renal effects

39
Q

What type of atrial arrhythmias are class IB drugs used for?

A

NONE.

40
Q

Ok, so what are the arrhythmias that class IB drugs are used for?

A

Ventricular only

41
Q

What phase of the depolarization/repolarization cycle do class IB drugs impact?

A

Shorten phase 3 repolarization

42
Q

What are the effects of lidocaine?

A

Decreases action potential duration

Shortens phase 3 repolarization

43
Q

What is lidocaine the DOC for?

A

Termination of VT and prevention of VF after cardioversion in the the setting of acute ischemia

44
Q

Lidocaine has relatively low cardiotoxicity, but what ADR’s should we keep in mind?

In what patients are these effects more common? At what dose do they tend to manifest?

A

Neurologic effects… more common in the elderly, and tend to manifest at doses greater than 9 ug/mL

  • paresthesias
  • tremor
  • nausea
  • lightheadedness
45
Q

How is lidocaine administered?

A

IV only. If you want oral, you can use mexiletine

46
Q

Class IC drugs have a high incidence of drug induced arrhythmias. In what situation are these drugs absolutely contraindicated?

A

Cannot be used in structural heart disease, this significantly increases mortality

47
Q

What phase of the myocyte depolarization/repolarization cycle do type IC drugs work on?

A

Phase 0

48
Q

Flecainide blocks both Na+ and K+ channels but does not…

A

prolong action potential or QT interval

49
Q

What is the therapeutic use of Flecainide?

A

Supraventricular arrhythmias

50
Q

What is the major ADR of flecainide?

A

Severe exacerbation of arrhythmia

51
Q

Propafenone is similar to flecainide except in that it…

A

Also has B-blocking activity

52
Q

What are the four major effects of the Class II drugs?

A

—Decrease automaticity
—Prolong AV conduction
—Decrease heart rate and contractility
—Decrease O2 demand

53
Q

Riddle me seven therapeutic uses for B-blockers!

A
  1. —Tachyarrhythmias
  2. —Atrial flutter
  3. —Atrial fibrillation
  4. —AV nodal re-entrant tachycardia
  5. —Hypertension
  6. —Heart failure
  7. —Ischemic heart disease
54
Q

What are some ADR’s associated with B-blockers?

A
  1. Heart Block
  2. bradycardia
  3. worsening of reactive airway disease
  4. cold extremities
  5. fatigue
  6. cardiac decompensation if heart relies on sympathetic drive
55
Q

The ADR’s of metoprolol are similar to other B-blockers except they have reduced risk of?

A

Bronchospasm and diabetes exacerbation

56
Q

Esmolol, also known as Brevibloc is used when?

A

During surgery to control heart rate

57
Q

What phase of the action potential do Class III drugs work on?

A

Phase 3 repolarization

58
Q

How do class III drugs work?

A

K+ channel blockade leads to diminished outward K+ flow during repolarization, increasing the duration of the action potential and prolonging refractory period

59
Q

Amiodarone has multiple MOA, what are they?

A
  1. K+ channel blockade -> prolonged action potential duration and QT interval
  2. Significantly blocks Na+ channels
  3. Weak adrenergic blockade
  4. Weak calcium channel blockade
60
Q

The pharmacokinetics of amiodarone are unique.

In what way?

How long are the effects maintained after withdrawal?

A

Half life biphasic…

Rapid component (50%) is 3-10 days

Slower component is several weeks

Effects persisty 1-3 months after discontinuation of the drug

61
Q

Why is it important to know about the wierdness of amiodarones biphasic half life?

A

It significantly increases the drug levels of statins, Digoxin and warfarin.

For instance, warfarin Digoxin and Statin doses must be decreased by 33-50% if a patient is also on amiodarone. Then, when amiodarone is discontinued you will need to monitor and increase the dosing.

62
Q

What are the notable ADR’s associated with amiodarone?

A
  1. Symptomatic Bradycardia
  2. Heart block (in those with preexisting AV node disease)
  3. Accumulation in Heart, Lungs, Liver and Skin
  4. Pulmonary toxicity with fatal pulmonary fibrosis
  5. Abnormal LFTs
  6. Skin deposits and gray-blue discoloration due to iodine
63
Q

What effect does cimetidine have on amiodarone levels?

A

Cimetidine is a CYP3A4 inhibitor, and leads to increased levels of amiodarone

64
Q

What impact does rifampin have on amiodarone levels?

A

Since it is an inducer of CYP3A4, it decreases the amiodarone levels

65
Q

What phase of the action potential do class IV drugs work on?

A

slows the phase 4 spontaneous depolarization

66
Q

What ion current do class IV drugs work on?

A

Decrease inward Ca2+ current

67
Q

Verapamil slows the SA node by direct action, and suppresses both early and delayed afterdepolarizations. What type of channels does it block?

A

Activated and inactivated L-type Ca++ channels

68
Q

What is the extracardiac effect of verapamil?

A

Peripheral vasodilation

69
Q

What are the 5 therapeutic uses of Verapamil?

A
  1. pSVT
  2. Drop ventricular rate in Atrial fibrillation
  3. Drop rate in Atrial Flutter
  4. Angina
  5. HTN
70
Q

You walk into your fourth year cardiology rotation and the first thing you see is an attending physician tearing apart an R1. Apparently they gave a patient Verapamil after misreading the EKG. What did the R1 think the EKG indicated?

What was the actual rhytm and what likely happened to the patient?

A

R1 thought the patient has pSVT, for which Verapamil would be perfectly fine for.

However they misdiagnosed, and the patient actually had ventricular tachycardia.

If you give verapamil to a patient with VT, they can decompensate into ventricular fibrillation and become hypotensive.

71
Q

Apart from the bit about confusing pSVT and VT, what are the other ADR’s of verapamil?

A
  1. can induce AV block
  2. constipation
  3. lassitude
  4. nervousness
  5. peripheral edema
72
Q

Adenosine is a nucleoside, what does it do?

A

Activates the inward rectifier K+ current and inhibits Ca++ current. Resulting in marker hyperpolarization and increased refractory period.

73
Q

What is the therapeutic use for adenosine?

A

DOC for conversion of paroxysmal SVT

74
Q

What are the ADRS for Adenosine?

A
  1. Flushing
  2. Shortness of breath
  3. Chest burning
  4. High grade AV block
  5. Atrial fibrillation
  6. headache
  7. hypotension
  8. nausea
  9. paresthesias
75
Q

If you give a patient who is not sedated adenosine, what must you warn them of?

A

They may experience a crushing heart attack like pain. Not sure why we would do this but I guess it is sometimes necessary.

76
Q

Atropine blocks actions of acetylcholine at parasympathetic sites and increases CO! What are the therapeutic uses of atropine?

A

The ABC’s of atropine!

Anesthesia - neuromuscular blockade reversal

Bradycardia

Cholinergic poisoning

77
Q

What are five ADR’s associated with atropine?

A

Arrhytmia

tachycardia

dizziness

constipation

urinary retention

78
Q

What is the mechanism of action of digoxin?

A

Inhibits Na+/K+ atpase, resulting in positive inotropy. Increased intracellular Na+, decreased Ca++ expulsion, increased free Ca++.

79
Q

What impact does digoxin have on:

Heart rate

Refractory period

Conduction velocity

A

Digoxin decreases heart rate,

Increases refractory period

Decreases conduction velocity

80
Q

What are the therapeutic uses of Digoxin?

A
  1. Atrial fibrillation
  2. SVT
  3. Heart failure
81
Q

What are the ADR’s for digoxin?

A
  1. Nausea
  2. Vomiting
  3. Diarrhea
  4. Disorientation
  5. visual disturbances
  6. Aberration of color perception
  7. delayed afterdepolarization
82
Q

What are the types of supraventricular arrhythmias? 7

A

Originate above the bundle of HIS, characterised by normal QRS complexes

  1. —Sinus bradycardia
  2. —Sinus tachycardia
  3. —Paroxysmal supraventricular tachycardia
  4. —Atrial flutter
  5. —Atrial fibrillation
  6. —Wolff-Parkinson-White
  7. —Premature atrial contractions
83
Q

What are the ventricular arrhythmias? 3

A

Originate below bundle of HIS

—Premature ventricular contractions
—Ventricular tachycardia
—Ventricular fibrillation

84
Q

What are the types of blocks?

A

—Supraventricular: 1st, 2nd, or 3rd degree AV block
—Ventricular: right or left bundle branch block

85
Q

What drugs would be good for an acute episode of this rhythm?

A

Atrial Fibrillation - IV CCB, Beta-blocker or Digoxin

86
Q

What What would be good drugs for a patient with this rhythm as a chronic condition?

A

Atrial Fibrillation

Oral Beta-blocker and CCB

Digoxin if intolerable side effects from BB and CCB

87
Q

In treating A-fib, what is the long term strategy focus we should prioritize?

A
  1. Rate control more-so than rhythm control.
  2. Also may need to use anticoagulation to prevent dislodgment of thrombus and consequent embolus/stroke
88
Q

What type of cardioversion is best for A-fib?

What are the chemical options?

A

—Direct current cardioversion most effective
—Chemical options: ibutilide IV, propafenone PO, flecainide PO, amiodarone PO/IV, dofetilide PO

89
Q

What would the acute treatment of the shown rhythm involve? 3 main options and two alternatives

A

pSVT

IV adenosine

Verapamil

diltiazem

Or BB or digoxin if the other three fail.

90
Q

If a patient had this rhythm as a chronic problem, what would be the treatment protocol?

A

pSVT

radiofrequency catheter ablation potentially curative
—Drugs – verapamil, diltiazem, BB, or digoxin

91
Q

What drugs would you want to use on a patient with the shown strip? Which ones would you not use?

A

If patient is within 24 hours after MI then use B-blockers if no contraindications

If asymptomatic DO NOT USE CLASS IC AGENTS - leads to increased mortality (CAST trials)

92
Q

What would you use for a stable patient with this strip? 3 options

A

stable VT

  1. procainamide
  2. sotalol
  3. amiodarone
93
Q

For a hemodynamically stable patient with this strip, what would you use?

A

MgSO4 or, alternatively class Ib agents

Cardiovascular II Exam 3 (15 decks)

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