Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II MHM - Exam 3 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What are non-VW agents used in arrhythmias?

A

Adenosine and digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the Vaughan Williams classification of antiarrhythmics

A 
Class I = Na channel blockers
Class II = Beta blockers
Class III = K channel blockers
Class IV = CCBs
Class V = variable mechanisms (adenosine, digoxin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class IA antiarrhythmics

A

Procainamide
Quinidine
Disopyramide
(Na channel blockers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class IB antiarrhythmics

A 
Lidocaine
Mexilitine
(Na channel blockers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Class IC antiarrhythmics

A 
Flecainide
Propafenone
(Na channel blockers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which Class I antiarrhythmics should NOT be used after IC?

A

IA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Effects of Class IA drugs

A
  • Reduces AP duration and ventricular refractoriness

- Increases repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Effects of Class IB drugs

A

Shortens AP duration, ventricular refractoriness and repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effects of Class IC drugs

A

Markedly slows depolarization without affecting repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Procainamide (class, indications, key features)

A
  • Class IA Na channel blocker
  • Stable monomorphic VT, VT w/accessory pathway, non-VT/VF arrest
  • IV only!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Procainamide ADRs

A
  • Peripheral vasodilation
  • Hypotension
  • Reflex tachy
  • Arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is procainamide metabolized? What is its half life?

A
  • CYP2D6

- 2.5 to 8 hours (NAPA metabolite 5-9 hours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is procainamide dosed in renal and hepatic impairments?

A
  • Lower loading dose in renal

- Cut all doses 50% in hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drugs interact with procainamide?

A
  • Tricyclics
  • SSRIs
  • Opioids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Procainamide serious adverse events

A
  • Heart block, widening QRS, Torsades
  • Hepatotoxicity
  • Drug induced lupus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Disopyramide (class, indications, key features)

A
  • Class IA Na channel blocker
  • Stable monomorphic VT, AF conversion
  • Used as an alternative to procainamide
  • A/w cardiogenic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is disopyramide metabolized? What is its half life?

A
  • CYP3A4, significant 1st pass

- Half life 4-10 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is disopyramide dosed?

A

Weight based

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When is disopyramide adjusted in renal impairment?

A

CrCl less than 40 mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Disopyramide serious adverse events

A
  • Torsades, HF, hypotension
  • Xerostomia
  • Urinary hesitancy
  • Constipation
  • Rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Disopyramide contraindications

A
  • AV block
  • QT prolongation
  • Cardiogenic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Disopyramide has significant ____ effects, so it should be avoided in patients with _____

A
  • Anticholinergic

- Avoid in glaucoma and myasthenia gravis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Quinidine (class, indications, key features)

A
  • Class IA Na channel blocker
  • Maintenance of sinus rhythm when LV function is preserved
  • NOT used for ventricular arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is quinidine metabolized?

A
  • CYP3A4

- Metabolite has antiarrhythmic effects that need to be accounted for

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Quinidine serious adverse events

A
  • Arrhythmias, QT prolonged, Torsades
  • GI issues
  • Dizzy, HA, tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Quinidine contraindications

A
  • WPW
  • AV block
  • Digitalis toxicity
  • Myasthenia gravis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Lidocaine (class, indications, key features)

A
  • Class IB Na channel blocker
  • VT/VF when defib/epi fails and amiodarone unavailable
  • Digoxin induced VT, monomorphic VT
  • Efficacy is reduced over duration of arrest
  • “Safest” of all Na channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the safest of all Na channel blockers?

A

Lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is lidocaine metabolized? What is its half life?

A
  • CYP1A2, hepatic blood flow determines rate (significantly impaired during arrest)
  • 1.8 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lidocaine serious adverse events

A
  • Arrhythmias

- Seizure, tremor, paresthesias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mexiletine (class, indications)

A
  • Class IB Na blocker

- Used for conversion and maintenance when other agents fail

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How is mexiletine metabolized? What is its half life?

A
  • CYP2D6 and 1A2 (higher doses needed in smokers)

- Variable half life (6-17 hrs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Mexiletine adverse events

A
  • GI
  • Dizziness
  • Arrhythmias
  • Tremor, ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mexiletine contraindications

A

AV block, cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Flecainide (class, indications, key features)

A
  • Class IC Na blocker
  • SVT, AF induced VT
  • Pill in pocket conversion to sinus rhythm, paroxysmal AF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is flecainide metabolized? What is its half life?

A
  • CYP2D6
  • 7-14 hrs in healthy ppl
  • 19-22 hrs post-MI
  • 27 hrs w/HF and repeated dosing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Flecainide serious adverse events

A
  • AV/BBB, QT prolong
  • Dizzy, HA, fatigue
  • Dyspnea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Flecainide contraindications

A

RBBB, AV block, cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Propafenone (class, indications, key features)

A
  • Class IC Na blocker
  • VT and conversion to sinus rhythm
  • Structure similar to propranol
40
Q

How is propafenone metabolized? What is its half life?

A
  • CYP2D6 (extensive 1st pass)

- 5 to 8 hours

41
Q

Propafenone serious adverse events

A
  • AV block, Torsades, QT prolonged

- Dizzy and CNS issues

42
Q

Propafenone contraindications

A
  • Bradycardia, AV block, sick sinus
  • Electrolyte depletion
  • Decompensated HF, hypotension
43
Q

What is unique about esmolol?

A

Ultra-short acting (effective duration 20-30 mins)

44
Q

What is esmolol used for?

A

Intraoperative and perioperative tachycardias

45
Q

What are the ADRs of esmolol?

A
  • Hypotension (dose related)
  • Diaphoresis
  • Nausea
  • Bradycardia, bronchospasm, seizure
46
Q

Contraindications of esmolol

A
  • Severe sinus bradycardia
  • 2nd or 3rd degree AV block
  • Cardiogenic shock
47
Q

Propranolol and its uses

A
  • Nonselective B blocker
  • Used for acute rate control
  • ER form used for long term rate control
48
Q

How is propranolol metabolized and what is unique about its composition?

A
  • CYP2D6 and 1A2 (extensive 1st pass effect)

- Highly protein bound

49
Q

ADRs of propranolol

A
  • Hypotension and bradycardia
  • Raynaud’s
  • Cognitive effects
  • Dyslipid and dysglycemia
50
Q

When is propranolol contraindicated?

A

Severe pulmonary and liver disease

51
Q

What is nadolol and its uses?

A
  • Nonselective B blocker
  • 3rd or 4th line for rate control
  • Other uses: HTN, CAD, variceal hemorrhage, thyroid storm
52
Q

When is nadolol dosing adjusted?

A

Renal impairment

53
Q

ADRs of nadolol

A

Same as propranolol

  • Hypotension, bradycardia
  • Raynaud’s
  • Cognitive effects
  • Dyslipid and dysglycemia
54
Q

Contraindications for nadolol

A

Severe pulmonary disease

55
Q

What is atenolol and its uses?

A
  • Selective B1 blocker
  • Acute VT and maintenance (unlabeled)
  • Migraine proph, ETOH withdrawal, HTN, angina, hyperthyroid
56
Q

How is atenolol metabolized?

A
  • Limited hepatic metabolism

- Excreted unchanged in urine/feces

57
Q

Half life of atenolol

A

6-7 hrs

58
Q

When is dosing of atenolol adjusted?

A

Renal impairment

59
Q

ADRs of atenolol

A
  • Same as all other selective agents
  • Hypotension, bradycardia
  • Raynaud’s
  • Cognitive effects
  • Dyslipid and dysglycemia
60
Q

What is metoprolol and its uses?

A
  • Selective B1 blocker
  • Acute VT and maintenance (unlabeled)
  • Migraine proph, essential tremor, HTN, angina, cardiomyopathy, hyperthyroid
61
Q

How is metoprolol metabolized?

A

Extensive hepatic (and 1st pass) via CYP2D6

62
Q

ADRs of metoprolol

A
  • Hypotension, bradycardia
  • Raynaud’s
  • Cognitive dysfunction
  • Dyslipid and dysglycemia
63
Q

What is carvedilol and its uses?

A
  • Mixed alpha and beta blocker
  • Labeled uses: HTN, angina, post MI LVD and HF
  • Unlabeled: maintenance in some AF pts (post MI, stable LVD and HF)
64
Q

Metabolism of carvedilol

A
  • CYP2C9, 2D6, 2C19, 3A4
  • Extensive 1st pass hepatic
  • Metabolite is 13x more potent
65
Q

ADRs of carvedilol

A
  • Hypotension, bradycardia
  • Dizzy, fatigue, weak
  • Endocrine and metabolic
  • Peripheral edema
66
Q

What is sotalol and its uses?

A
  • Nonselective B blocker and K blocker
  • Conversion of sustained VT
  • Maintenance after AF converted to NSR
  • Maintenance in AF w/HCM (unlabeled)
67
Q

Metabolism of sotalol

A
  • None, excreted unchanged
  • 90-100% bioavailable
  • Decreased absorption w/food (take on empty stomach)
68
Q

Half life of sotalol

A

12 hours

69
Q

When must sotalol dosing be adjusted?

A

Renal impairment

70
Q

ADRs of sotalol

A
  • Bradycardia, CP, palpitations

- Fatigue, dizzy, weak

71
Q

What is ibutilide and how is it used?

A
  • K channel blocker

- Used acutely for AF conversion to NSR

72
Q

How is ibutilide metabolized?

A

Extensive hepatic

73
Q

ADRs of ibutilide

A
  • Post op (Torsades)

- LV dysfunction

74
Q

Ibutilide contraindications

A
  • Long QT
  • Low K
  • Symptoms more than 48 hrs
75
Q

What is dofetilide and its use?

A
  • K channel blocker

- Acute conversion of AF to NSR (later for maintenance too)

76
Q

What are some caveats of dofetilide?

A
  • Less effective at higher ventricular rates

- Requires corrected QT and electrolytes prior to dosing

77
Q

How does amiodarone work?

A
  • K channel blocker

- ALSO Na, Ca channels and alpha/beta receptors

78
Q

What is amiodarone used for?

A
  • Maintain SR during AF
  • Breakthrough VT/VF
  • Pulseless VT/VF
79
Q

ADRs of amiodarone

A
  • Pulm toxicity
  • Hypotension, HF, cardiogenic shock
  • SJS
80
Q

When does K channel blocking effects occur with sotalol?

A

Doses 160+ mg/day

81
Q

Uses of Verapamil

A
  • AVNRT, SVT, rate control in AF, HTN

- Unlabeled: migraine proph, bipolar, HCM

82
Q

How is verapamil metabolized?

A

Extensive hepatic

83
Q

ADRs of verapamil

A
  • Gingival hyperplasia
  • HA, constipation
  • Fatigue, dizzy
84
Q

When does verapamil dosing need to be adjusted?

A

End stage liver disease

85
Q

Uses of diltiazem?

A
  • PSVT and AF

- Unlabeled: stable narrow complex tachy after adenosine/vagal maneuvers

86
Q

How is diltiazem metabolized?

A

Extensive 1st pass hepatic

87
Q

ADRs of diltiazem

A
  • Edema, AV block, brady

- HA, dizzy, SOB

88
Q

How is diltiazem dose adjusted?

A

It is NOT adjusted with renal or hepatic disease

89
Q

What is adenosine?

A
  • Non-VW agent

- Degradation product of ATP

90
Q

Uses of adenosine

A
  • Induces rapid, reversible AV block
  • Terminates SVT from AVNRT
  • Allows diagnosis of pre-excitation from accessory pathways
91
Q

Half life of adenosine

A

Less than 10 seconds

92
Q

ADRs of adenosine

A
  • Severe AV block, brady

- Bronchospasm

93
Q

Contraindications of adenosine

A
  • Symptomatic bradycardia
  • 2nd/3rd AV block
  • WPW
94
Q

How does digoxin increase inotropy?

A
  • Inhibits Na/K ATPase pump
  • Increases Na entry, K efflux
  • Increases Na/Ca exchange to increase contractility
95
Q

Digoxin and maintenance of sinus rhythm

A
  • Inconsistent
  • May induce toxicity
  • B blockers are safer
  • BUT careful use reduces hospitalization
96
Q

Metabolism of digoxin

A
  • Minor hepatic NOT CYP dependent
  • Sugar hydrolysis in stomach
  • Gut bacteria
  • REDUCED rate in HF
97
Q

Half life of digoxin

A

38 hours

Pharm II MHM - Exam 3 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions