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Pharm 2 > I. Antiarrhythmics > Flashcards

I. Antiarrhythmics Flashcards

1
Q

Causes of Cardaiac arrhythmias

A
  1. Arterial Hypoxemia
  2. Electrolyte or Acid-Base Abnormality (Alkalosis, Acidosis, Hypokalemia, Hypomagnesemia)
  3. Myocardial Ischemia
  4. Altered Sympathetic Nervous System Activity
  5. Severe Bradycardia
  6. Pharmacological Factors
  7. Idiopathic or Anatomical Variants (RBBB in military, Prior Open Heart Surgery)
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2
Q

Arrhythmia treatment indications:

A
  1. No correction after removal of precipitating cause
  2. Hemodynamic function is compromised
  3. Disturbance predisposes to a more serious cardiac arrhythmia (VF or VT)
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3
Q

Non-pharmacological Antiarrhythmic Treatments

A
  • chronic arrhythmia patients treated with catheter ablation (often performed under GA in EP lab, lengthy 6-8 hours)
  • Pacemaker
  • Cardioversion
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4
Q

What happens if too much of heart conduction pathway gets burned during ablation?

A

Pt will need to be paced

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5
Q

What drug may be used to cardiovert patient ?

A

Adenosine

will stop heart and allow it to reset

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6
Q

How many phases of action potential

A

5

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7
Q

What classification is used to classify drugs based on primary mechanism of antiarrhythmic properties?

A

Vaughn-Williams (5 classes)

  • imperfect
  • drugs classified based on the action that was first described, NOT necessarily the most therapeutically signifiant MMOA
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8
Q

Class 1a

  • description
  • indications
A
  • Blocks Na channels
  • Slowed conduction by prolongation of AP duration
  • Tx if heart is beating too rapidly or in uncoordinated fashion
  • Indications:
    1. SVT
    2. VTach
    3. Symptomatic PVCs
    4. Prevention of Recurrent Afib
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9
Q

Class 1a drugs

A

Quinidine
Procainamide (Pronestyl)
Disopyramide (Norpace)

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10
Q

Quinidine Indicatoin

A

Acute & chronic SVT

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11
Q

Quinidine dose

A

50-75 mg/hr (IV)

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12
Q

Quinidine clinical considerations/effects

A
  1. Displace Digoxin from tissue stores (increase levels)
  2. VD & myocardial depression when rapid push (can get tachy)
  3. Blocks Na & K
  4. Prolong QT. & widened QRS
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13
Q

Procainamide indication

A

VTach & WPW

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14
Q

Procainamide dose

A

IVP: 10-15 mg/kg

Infusion: 2-6 mg/min

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15
Q

Procainamide causes a high incidence of ____

A

Hypotension

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16
Q

Disopyramide Indications

A
  1. Atrial & Ventricular dysrhythmias
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17
Q

Which class 1a antiarrhythmic has mild antichoinergic side effects?

A

Disopyramide (Norpace)

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18
Q

Clinical considerations with Disopyramide (Norpace):

A
  • significant myocardial depression
  • can precipitate CHF & hypotension
  • mild anticholinergic effects
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19
Q

Class 1b

A
  • blocks Na channels
  • decreases duration of action potentials & refractories
  • do NOT affect QRS
  • Tx Ventricular arrhythmias
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20
Q

Class 1b indications

A
  • Vtac
  • Symptomatic PVCs
  • Prevention of Vfib
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21
Q

Class 1b drugs

A
  • Lidocaine (Cardiac Xylocaine PF)
  • Phenytoin (Dilantin)
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22
Q

Lidocaine indication

A

PVCs & Vtac

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23
Q

Lidocaine Dose

A

1-2 mg/kg IVP

1-4 mg/min

100mg common dose to knockout run of PVCs, 3-4+, or Vtac

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24
Q

Lidocain clinical considerations

A
  • Fast on/off
  • Can decrease AV node conduction
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25
Q

Phenytoin (Dilantin) Indications

A
  • Ventricular Dysrhythmias or Digitals Toxicity
  • Mostly used to treat seizures
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26
Q

Phenytoin (Dilantin) dose

A

100 mg (1.5 mg/kg) q. 5 min

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27
Q

Phenytoin (Dilantin) clinical considerations

A
  • CNS S/E
  • Mostly used to treat seizures: Cyt P450 inducer - metabolizes NMB quickly
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28
Q

Class 1c

A
  • most potent sodium channel blocker
  • decrease conductivity of cardiac impulses
  • may have pro-dysrhythmic effects
  • Slow sodium channel binding kinetics
  • Both atrial and ventricular arrhythmias
29
Q

Class 1c indications

A
  • Refractory A-fib
  • Life-threatening Vtac
  • V-fib
30
Q

Class 1c contraindications

A

-LVH
-Prior MI

31
Q

Class 1c common drugs

A
  • Flecainide (Tambocor)
  • Propafenone (Rhythmol)
32
Q

Class II

A
  • Beta adrenergic antagonists
  • Decrease sympathetic activity of the heart & decrease AV node conduction = decreased HR
  • competitively antagonizes effects of catecholamines
33
Q

Class II anti-arrhythmics treat ____

A

Superventricular tachycardia (SVT)

34
Q

Class II common agents

A
  1. Esmolol (Brevibloc)
  2. Propranolol (Inderal)
  3. Metoprolol (Lopressor)

Selective Beta 1 blockers

not Labetalol = more of a BP drug

35
Q

Class III anti-arrhythmics

A
  • prolong repolarization by blocking potassium channels (due to increases build up of sodium? Na/K pump inhibited)
  • Results in prolongation of cardiac depolarization, and increased refractoriness
  • Highly efficacious for both ventricular and atrial arrhythmias
  • Potentially deadly due to QT prolongation leading to Torsades
36
Q

Class III common agents

A
  • Amiodarone (Cordarone)
  • Sotalol (Betapace)
37
Q

Amiodarone (Cordarone) clinical effects:

A
  • beta blocker like effects on SA node
  • Increases refractory period
  • Slow intra-cardiac conduction
38
Q

Amiodarone indications

A
  • refractory V-Fib
  • Refractory V-Tac
  • Acute ischemia
39
Q

Amiodarone dosing

A

Loading: 150 mg over 10 min

0-6 hrs: 360 mg

Next 18 hrs: 540 mg

40
Q

Sotalol indications

A
  • Sustained V-Tac or V-Fib

non-selective beta-blocker

41
Q

Sotalol is not recommended for:

A

Patients with asthma

42
Q

Class IV anti-arrhythmics

A
  • Block Ca channels
  • decreases conduction through the AV node
  • Decreases the force of contraction (inotropy) and rate of contraction (chronotropy)
43
Q

Class IV common agents

A
  • Verapamil (Isoptan)
  • Diltiazem (Cardizem)
44
Q

Verapamil dosing

A

IVP: 5-10 mg

Infusion: 5 mcg/kg/min

45
Q

Verapamil S/E

A

Decreased HR
Vasodilation

46
Q

Verapamil indications

A
  • SVTs
  • AFib/Flutter
47
Q

Diltiazem indications

A
  • angina
  • A-Fib/Flutter
  • SVT
  • HTN
48
Q

Diltiazem dilates ____.

A

Coronary arteries

49
Q

Class V MOA

A

UNK

50
Q

Class V agents

A
  • Adenosine (Adenocard)
  • Digoxin (Lanoxin)
51
Q

Adenosine causes transient heart block at ____

A

AV NODE

52
Q

Adenosine is used to treat ___

A

SVT

53
Q

Digoxin decreases ____

A

AV node conduction

54
Q

Digoxin can be used to treat:

A
  • A-Fib/Flutter
  • CHF (increases LV filling time)
55
Q

Adenosine dose

A

6mg IVP

56
Q

T/F: Adenosine is a potent dilator of coronary arteries.

A

TRUE

*Reduces myocardial oxygen consumption by anti-adrenergic and negative HR actions

57
Q

Adenosine half life

A

0.6 - 1.5 seconds

58
Q

Clinical uses of Adenosine

A
  • Tx: PSVT
  • Dx: tachydysrhythmias
  • VD for pharmacological stress testing
59
Q

Digoxin extracted from:

A

Flowers of Digitalis Ianta

  • “fox glove”
  • “Dead Man’s Bell”
  • “Witches Gloves”
  • Toxic if eaten
  • Cardiac glycoside
60
Q

Digoxin MOA

A
  • Selective & Reversible inhibition of the Na/K pump in cardiac cell membranes (by binding to Na/K ATPase
  • decreased Ca extrusion?
  • Increased intracellular Ca (via Na/Ca exchanger) accounts for positive inotropic effects
    -Digoxin increases parasympathetic activity via the Vagus Nerve
61
Q

Digoxin Cardiovascular effects:

A
  • Increase myocardial contractility (improve EF)
    • Increased SV
    • Decreased heart size
    • Decreased LVEDP
  • Decreased AV Node Conduction rate

Good for CHF patients

62
Q

Digoxin EKG effects

A
  • Prolonged PRI
  • Shortened QT
  • ST depression
  • Diminished amplitude of inversion or T waves
63
Q

Digoxin clinical indications:

A
  • Decrease AV Node conduction
    • A-Fib
    • A-Flutter
    • Paroxysmal Atrial Tachycardia (PAT)
  • Positive Inotropy
    • CHF
64
Q

Digitalis toxicity is caused by ____.

A

Hypokalemia

this worsens digitalis toxicity b/c K is already inhibited from entering the cardiac cell due to blocking Na/K ATPase pumps; so even lower levels exacerbate the problem

Hyperkalemia diminishes the effects of Digoxin

65
Q

Digitalis Toxicity: what type of fluids should be given?

A

Potassium sparing diuretics

66
Q

Digitalis toxicity interferes with phrenic nerve activity and can cause ____.

A

Hyperventilation

Phrenic = diaphragm

67
Q

Tx for Digitalis Toxicity

A
  • Correction of predisposing cause
  • Administration of anti-dysrhythmics
  • Transvenous Pacemaker
  • IV Potassium: 0.025 - 0.05 mEq/kg ”10-20 mEq”
68
Q

Digoxin (Lanoxin) commercial preparation

A

IV: 0.25 mg/mL
PO: 0.25 mg tablets

69
Q

Digoxin Dosing

A

IV: 10 mcg/kg (0.5-1.0 mg) over 30 min

PO: 0.75-1.5 mg

Pharm 2 (6 decks)

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