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Pharm II MHM - Exam 3 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

1
Q

What are non-VW agents used in arrhythmias?

A

Adenosine and digoxin

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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)
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3
Q

Class IA antiarrhythmics

A

Procainamide
Quinidine
Disopyramide
(Na channel blockers)

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4
Q

Class IB antiarrhythmics

A 
Lidocaine
Mexilitine
(Na channel blockers)
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5
Q

Class IC antiarrhythmics

A 
Flecainide
Propafenone
(Na channel blockers)
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6
Q

Which Class I antiarrhythmics should NOT be used after IC?

A

IA

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7
Q

Effects of Class IA drugs

A
  • Reduces AP duration and ventricular refractoriness

- Increases repolarization

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8
Q

Effects of Class IB drugs

A

Shortens AP duration, ventricular refractoriness and repolarization

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9
Q

Effects of Class IC drugs

A

Markedly slows depolarization without affecting repolarization

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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!
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11
Q

Procainamide ADRs

A
  • Peripheral vasodilation
  • Hypotension
  • Reflex tachy
  • Arrest
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12
Q

How is procainamide metabolized? What is its half life?

A
  • CYP2D6

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

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13
Q

How is procainamide dosed in renal and hepatic impairments?

A
  • Lower loading dose in renal

- Cut all doses 50% in hepatic

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14
Q

What drugs interact with procainamide?

A
  • Tricyclics
  • SSRIs
  • Opioids
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15
Q

Procainamide serious adverse events

A
  • Heart block, widening QRS, Torsades
  • Hepatotoxicity
  • Drug induced lupus
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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
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17
Q

How is disopyramide metabolized? What is its half life?

A
  • CYP3A4, significant 1st pass

- Half life 4-10 hours

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18
Q

How is disopyramide dosed?

A

Weight based

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19
Q

When is disopyramide adjusted in renal impairment?

A

CrCl less than 40 mL/min

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20
Q

Disopyramide serious adverse events

A
  • Torsades, HF, hypotension
  • Xerostomia
  • Urinary hesitancy
  • Constipation
  • Rash
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21
Q

Disopyramide contraindications

A
  • AV block
  • QT prolongation
  • Cardiogenic shock
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22
Q

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

A
  • Anticholinergic

- Avoid in glaucoma and myasthenia gravis

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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
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24
Q

How is quinidine metabolized?

A
  • CYP3A4

- Metabolite has antiarrhythmic effects that need to be accounted for

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25
Quinidine serious adverse events
- Arrhythmias, QT prolonged, Torsades - GI issues - Dizzy, HA, tremor
26
Quinidine contraindications
- WPW - AV block - Digitalis toxicity - Myasthenia gravis
27
Lidocaine (class, indications, key features)
- 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
28
What is the safest of all Na channel blockers?
Lidocaine
29
How is lidocaine metabolized? What is its half life?
- CYP1A2, hepatic blood flow determines rate (significantly impaired during arrest) - 1.8 hours
30
Lidocaine serious adverse events
- Arrhythmias | - Seizure, tremor, paresthesias
31
Mexiletine (class, indications)
- Class IB Na blocker | - Used for conversion and maintenance when other agents fail
32
How is mexiletine metabolized? What is its half life?
- CYP2D6 and 1A2 (higher doses needed in smokers) | - Variable half life (6-17 hrs)
33
Mexiletine adverse events
- GI - Dizziness - Arrhythmias - Tremor, ataxia
34
Mexiletine contraindications
AV block, cardiogenic shock
35
Flecainide (class, indications, key features)
- Class IC Na blocker - SVT, AF induced VT - Pill in pocket conversion to sinus rhythm, paroxysmal AF
36
How is flecainide metabolized? What is its half life?
- CYP2D6 - 7-14 hrs in healthy ppl - 19-22 hrs post-MI - 27 hrs w/HF and repeated dosing
37
Flecainide serious adverse events
- AV/BBB, QT prolong - Dizzy, HA, fatigue - Dyspnea
38
Flecainide contraindications
RBBB, AV block, cardiogenic shock
39
Propafenone (class, indications, key features)
- Class IC Na blocker - VT and conversion to sinus rhythm - Structure similar to propranol
40
How is propafenone metabolized? What is its half life?
- CYP2D6 (extensive 1st pass) | - 5 to 8 hours
41
Propafenone serious adverse events
- AV block, Torsades, QT prolonged | - Dizzy and CNS issues
42
Propafenone contraindications
- Bradycardia, AV block, sick sinus - Electrolyte depletion - Decompensated HF, hypotension
43
What is unique about esmolol?
Ultra-short acting (effective duration 20-30 mins)
44
What is esmolol used for?
Intraoperative and perioperative tachycardias
45
What are the ADRs of esmolol?
- Hypotension (dose related) - Diaphoresis - Nausea - Bradycardia, bronchospasm, seizure
46
Contraindications of esmolol
- Severe sinus bradycardia - 2nd or 3rd degree AV block - Cardiogenic shock
47
Propranolol and its uses
- Nonselective B blocker - Used for acute rate control - ER form used for long term rate control
48
How is propranolol metabolized and what is unique about its composition?
- CYP2D6 and 1A2 (extensive 1st pass effect) | - Highly protein bound
49
ADRs of propranolol
- Hypotension and bradycardia - Raynaud's - Cognitive effects - Dyslipid and dysglycemia
50
When is propranolol contraindicated?
Severe pulmonary and liver disease
51
What is nadolol and its uses?
- Nonselective B blocker - 3rd or 4th line for rate control - Other uses: HTN, CAD, variceal hemorrhage, thyroid storm
52
When is nadolol dosing adjusted?
Renal impairment
53
ADRs of nadolol
Same as propranolol - Hypotension, bradycardia - Raynaud's - Cognitive effects - Dyslipid and dysglycemia
54
Contraindications for nadolol
Severe pulmonary disease
55
What is atenolol and its uses?
- Selective B1 blocker - Acute VT and maintenance (unlabeled) - Migraine proph, ETOH withdrawal, HTN, angina, hyperthyroid
56
How is atenolol metabolized?
- Limited hepatic metabolism | - Excreted unchanged in urine/feces
57
Half life of atenolol
6-7 hrs
58
When is dosing of atenolol adjusted?
Renal impairment
59
ADRs of atenolol
* Same as all other selective agents - Hypotension, bradycardia - Raynaud's - Cognitive effects - Dyslipid and dysglycemia
60
What is metoprolol and its uses?
- Selective B1 blocker - Acute VT and maintenance (unlabeled) - Migraine proph, essential tremor, HTN, angina, cardiomyopathy, hyperthyroid
61
How is metoprolol metabolized?
Extensive hepatic (and 1st pass) via CYP2D6
62
ADRs of metoprolol
- Hypotension, bradycardia - Raynaud’s - Cognitive dysfunction - Dyslipid and dysglycemia
63
What is carvedilol and its uses?
- 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
Metabolism of carvedilol
- CYP2C9, 2D6, 2C19, 3A4 - Extensive 1st pass hepatic - Metabolite is 13x more potent
65
ADRs of carvedilol
- Hypotension, bradycardia - Dizzy, fatigue, weak - Endocrine and metabolic - Peripheral edema
66
What is sotalol and its uses?
- Nonselective B blocker and K blocker - Conversion of sustained VT - Maintenance after AF converted to NSR - Maintenance in AF w/HCM (unlabeled)
67
Metabolism of sotalol
- None, excreted unchanged - 90-100% bioavailable - Decreased absorption w/food (take on empty stomach)
68
Half life of sotalol
12 hours
69
When must sotalol dosing be adjusted?
Renal impairment
70
ADRs of sotalol
- Bradycardia, CP, palpitations | - Fatigue, dizzy, weak
71
What is ibutilide and how is it used?
- K channel blocker | - Used acutely for AF conversion to NSR
72
How is ibutilide metabolized?
Extensive hepatic
73
ADRs of ibutilide
- Post op (Torsades) | - LV dysfunction
74
Ibutilide contraindications
- Long QT - Low K - Symptoms more than 48 hrs
75
What is dofetilide and its use?
- K channel blocker | - Acute conversion of AF to NSR (later for maintenance too)
76
What are some caveats of dofetilide?
- Less effective at higher ventricular rates | - Requires corrected QT and electrolytes prior to dosing
77
How does amiodarone work?
- K channel blocker | - ALSO Na, Ca channels and alpha/beta receptors
78
What is amiodarone used for?
- Maintain SR during AF - Breakthrough VT/VF - Pulseless VT/VF
79
ADRs of amiodarone
- Pulm toxicity - Hypotension, HF, cardiogenic shock - SJS
80
When does K channel blocking effects occur with sotalol?
Doses 160+ mg/day
81
Uses of Verapamil
- AVNRT, SVT, rate control in AF, HTN | - Unlabeled: migraine proph, bipolar, HCM
82
How is verapamil metabolized?
Extensive hepatic
83
ADRs of verapamil
- Gingival hyperplasia - HA, constipation - Fatigue, dizzy
84
When does verapamil dosing need to be adjusted?
End stage liver disease
85
Uses of diltiazem?
- PSVT and AF | - Unlabeled: stable narrow complex tachy after adenosine/vagal maneuvers
86
How is diltiazem metabolized?
Extensive 1st pass hepatic
87
ADRs of diltiazem
- Edema, AV block, brady | - HA, dizzy, SOB
88
How is diltiazem dose adjusted?
It is NOT adjusted with renal or hepatic disease
89
What is adenosine?
- Non-VW agent | - Degradation product of ATP
90
Uses of adenosine
- Induces rapid, reversible AV block - Terminates SVT from AVNRT - Allows diagnosis of pre-excitation from accessory pathways
91
Half life of adenosine
Less than 10 seconds
92
ADRs of adenosine
- Severe AV block, brady | - Bronchospasm
93
Contraindications of adenosine
- Symptomatic bradycardia - 2nd/3rd AV block - WPW
94
How does digoxin increase inotropy?
- Inhibits Na/K ATPase pump - Increases Na entry, K efflux - Increases Na/Ca exchange to increase contractility
95
Digoxin and maintenance of sinus rhythm
- Inconsistent - May induce toxicity - B blockers are safer - BUT careful use reduces hospitalization
96
Metabolism of digoxin
- Minor hepatic NOT CYP dependent - Sugar hydrolysis in stomach - Gut bacteria - REDUCED rate in HF
97
Half life of digoxin
38 hours

Pharm II MHM - Exam 3 (5 decks)

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