Antiarrhythmic Drugs Flashcards

1
Q

Digoxin

  1. Antiarrhythmic effect is on the what?
  2. Used for what?
  3. Used for it’s effect on?
A
  1. AV node
  2. ventricular rate control in atrial fibrillation and flutter
  3. positive inotrope effect in CHF
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2
Q
  1. Digoxin_____ the electrical conduction through the AV node
  2. Stimulates the ____________ nervous system and increases ______ ______
A
  1. slows
  2. parasymathetic
    vagal tone
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3
Q

Slows AV conduction and prolongs the AV nodal refractory period. What does this cause on the EKG? 3

A
  1. Increased PR interval
  2. Downward sloping ST segment depression
  3. Shortened QT interval
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4
Q

Dig is used to slow ventricular rates in Afib and A flutter. What is the downside to this? 2

A

Slows rates (for rate control)!!!

  1. Does NOT convert rhythms (afib/flutter) to sinus!
  2. Does not work well for slowing ventricular rates during exercise!
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5
Q

Digoxin:

  1. Onset?
  2. Administration/dosing?
  3. Steady State?
  4. Theuropeutic range?
A
  1. Slow onset
  2. Need a loading dose period
  3. May take a week to achieve steady state
  4. Monitor serum blood levels periodically
    Therapeutic range 0.8 – 2 ng/mL
    AF and concomitant LVSD is 0.5-1 ng/mL
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6
Q

Who has increased mortality on Dig?

A

Higher levels in pts with LVSD = higher mortality

AF and concomitant LVSD is 0.5-1 ng/mL

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7
Q

Digoxin toxicity can be caused by

3

A
  1. Declining renal function
    Renal excretion
  2. Electrolyte disturbances
  3. Drug interactions
    Many meds may increase serum digoxin concentrations
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8
Q

What electrolyte disturbances can cause dig toxicity? 3

What drug interactions may increase serum dig concentrations? 2

A
  1. Hypokalemia,
  2. hypomagnesemia and
  3. hypercalcemia

can predispose the myocardium to the toxic effects of digoxin

  1. amiodarone,
  2. verapamil
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9
Q

Signs and symptoms of digoxin toxicity

8

A
  1. Heart block
  2. AV junctional tachycardia
  3. Ventricular arrhythmias
  4. Visual disturbances
  5. Blurred vision, yellow/green halos
  6. Dizziness
  7. Weakness
  8. GI: N/V/D and anorexia
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10
Q

Why is adenosine used?

A

Used to convert PSVT to SR

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11
Q
  1. Activates _______ channels by increasing the outward ________ current
  2. __________ the membrane potential and __________ spontaneous SA node depolarization
  3. _______ automaticity and conduction in the SA and AV nodes
  4. Half life?
A
    • potassium
    • potassium
    • Hyperpolarizes
    • decreases
  1. Inhibits
  2. 10 seconds
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12
Q

Adenosine contraindications

2

A
  1. 2nd or 3rd degree heart block

2. sick sinus syndrome in the absence of a pacemaker

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13
Q
  1. What kind of drug is atropine?

2, What does it enhance and how? 2

  1. What does it block? 2
  2. Used for the treatment of what?
  3. May induce what?
A
  1. Parasympatholytic drug
  2. Enhances
    - -sinus nodal automaticity and
    - -AV nodal conduction through direct vagolytic action
  3. Block
    - -acetylcholine and
    - -parasympathetic neuroeffector sites
  4. Used for the treatment of symptomatic bradycardia
  5. May induce tachycardia
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14
Q

Atropine contraindications

4

A
  1. Angle closure glaucoma
  2. Obstructive uropathy (think BPH)
  3. Tachycardia
  4. Bowel obstruction or altered bowel transit time
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15
Q

Class 1 blocks what?

What are the sub classes?
3

A

sodium channel blockers

  1. Class Ia (intermediate onset/offset)
  2. Class Ib (fast onset/offset)
  3. Class Ic (slow onset/offset)
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16
Q

Class Ia (intermediate onset/offset)
are which drugs?
3

A
  1. Disopyramide (Norpace)
  2. Procainimide (Pronestyl)
  3. Quinidine (Quinidex)
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17
Q
Class Ib (fast onset/offset) are which drugs?
3
A
  1. Lidocaine
  2. Mexiletine (Mexitil)
  3. Phenytoin (Dilantin)
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18
Q

Class Ic (slow onset/offset) are which drugs? 2

A
  1. Flecainide (Tambocor)

2. Propafenone (Rythmol)

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19
Q

3 classes of sodium channel blockers are categorized how? 2

A
  1. Subdivided by the rate of sodium channel dissociation

2. Variable rates of binding and dissociating from the sodium channel receptor

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20
Q
  1. What kind of drugs are Class Ia?
  2. What are they used to treat? 2
  3. They have anticholinergic effects that can lead to?
  4. WHat do you need to prescribe with this?
  5. Major complication?
  6. Which drug is IV only?
A
  1. These drugs are proarrhythmic

Used to treat atrial and ventricular rhythms

  1. Ex: Quinidine and Disopyramide increase automaticity of the SA and AV nodes
  2. Need to have a Beta blocker or Calcium channel blocker on board to prevent tachyarrhythmias in afib/flutter pts
  3. Torsades
  4. Procainimide IV only
21
Q

What are the drugs for Class Ib?

2

A

Lidocaine

Mexiletine

22
Q
  1. What is lidocaine used for?
  2. Exerts most of it’s effects on what?
  3. Particularily useful for what?
  4. Administered how?
  5. Toxicity causes? 2
A
  1. Used for ventricular arrhythmias (VT, VF)
  2. ischemic or infarcted tissue of the ventricles
  3. VT/VF associated with AMI
  4. IV only
  5. Toxicity: seizures and respiratory arrest
23
Q

What is mexiletine?

A

Oral analog of Lidocaine used for ventricular arrhythmias

24
Q

What are the Class Ic drugs? 2

A

Flecainide (Tambocor)

Propafenone (Rhythmol)

25
Q
  1. Flecainide (Tambocor) mainly used for what?

2. When can we not use it? 4

A
  1. Mainly used for rhythm control in afib/flutter
    - –FDA approved to use for ventricular arrhythmias but is not very effective for these and has a high incidence of adverse effects

Cannot use if any hx of structural heart disease

  1. CAD,
  2. LVSD,
  3. valvular disorders,
  4. LVH

otherwise proarrhythmic

26
Q

Propafenone (Rhythmol) is used for what?

Cannot be used in what situations?

A

Used for atrial arrhythmias such as afib/flutter

Cannot be used if hx of structural heart disease

27
Q

Beta blockers are used for?

4

A
  1. Used for suppression of ventricular and supraventricular arrhythmias
  2. Slow AV nodal conduction and SA nodal rates
  3. Negative inotropic agents
  4. Decrease myocardial oxygen consumption
28
Q

Review of beta blocker SE

8

A
  1. Bronchospasm
  2. Fatigue
  3. Depression
  4. Nightmares
  5. Erectile dysfunction
  6. Hypotension
  7. Bradycardia
  8. Worsening CHF (in some patients…end stage or in acute decompensated state)
29
Q

What are Class III drugs?

what does it block and what are the drugs 4?

A

POTASSIUM CHANNEL BLOCKERS

  1. Amiodarone (Cordarone)
  2. Dofetilide (Tikosyn)
  3. Ibutilide (Corvert)
  4. Sotalol (Betapace)
30
Q

Class III Antiarrhythmics

work how?

A

Prolong the action potential

31
Q

Amiodarone (Cordorone) is used for what? 2

A
  1. Rhythm control of atrial fibrillation and flutter

2. Ventricular arrhythmias

32
Q

Sotalol (Betapace) used for what? 2

Ibutilide (Tikosyn) used for what?

A

VT and atrial fibrillation

Rhythm control of atrial fibrillation and flutter

33
Q

Monitor for EKG changes
2

Which drugs should we not use it with?

A
  1. May induce ventricular arrhythmias and ectopy
  2. May change intervals
    PR, QRS, QT

Don’t use with other drugs that prolong the QT interval

34
Q

Why is Amiodarone unique?

How is it administered?

A

Probably the most widely used medication for rhythm control for atrial fibrillation and VT

Unique in that it has characteristics of all 4 antiarrhythmic drug classes
Given IV for acute treatment

35
Q

Amiodarone PK/PD

  1. Bioavialbility?
  2. Volume of distribution?
  3. lipophilic or hydrophilic?
  4. These characteristics may lead to what?
A
  1. Poor bioavailability
  2. Large volume of distribution
  3. Highly lipophilic
  4. These characteristics may lead to build up of the drug in various organs
36
Q

What organs might amiodarone build up in? 8

Amiodarone toxicities can cause?
9

(what is the most life threatening?)

A
  1. Lungs,
  2. thyroid,
  3. eyes,
  4. heart,
  5. liver,
  6. skin,
  7. GI tract,
  8. CNS
  9. Dermatologic
  10. Photosensitivity
  11. Blue-gray skin discoloration
  12. Neurologic
  13. Ataxia
  14. Peripheral neuropathy
  15. Fatigue
  16. insomnia
  17. The pulmonary toxicity acutely can be life threatening, chronically leads to interstitial lung disease
37
Q

Amiodarone monitoring
What labs should be looked at every 6 months to monitor amiodarone? 3

Baseline and Yearly? 3

A
  1. TSH,
  2. CBC,
  3. LFTs
  4. PFTs (DLCO)
  5. CXR
  6. Eye Exam
38
Q

Amiodarone visual complications?

6

A
  1. Optic neuritis,
  2. optic neuropathy,
  3. corneal and lens opacities,
  4. halos,
  5. blurred vision,
  6. photophobia
39
Q

SE of amiodarone

A
  1. GI disturbance common on higher doses

2. Drug interactions

40
Q

Amiodarone:
GI disturbance common on higher doses are? 4

Drug interactions?
5
(what are the two to remember?)

A
  1. N/V,
  2. anorexia,
  3. abd pain,
  4. constipation
  5. Substrate of the CYP3A4 isoenzyme
  6. Significant interactions with digoxin!!!!! and warfarin!!!!
  7. Potentiates the effects of warfarin
  8. Can double the serum dose of digoxin
  9. Interacts with simvastatin (Zocor) so max dose of Zocor is 20 mg
41
Q
  1. Sotalol (Betapace)
    used for? 2
  2. Has what kind of properies? (which causes what kind of EKG SE?)
  3. During initiation of the drug what do we need to do and why?
  4. Side effects?
  5. Who should we not use in and why?
  6. Cleared by what?
  7. Risk for what?
A
  1. VT and afib/flutter
  2. Has some beta blocking properties and prolongs the QT
  3. During initiation of the drug: hospitalize for 3 days to monitor
    QT interval due to risk for TdP
  4. SE similar to B-blockers: fatigue, dyspnea, bradycardia.
  5. Negative inotropic effects so usually don’t use in LVSD
  6. Renal clearance
  7. Risk for torsades
42
Q
  1. Dofetilide (Tikosyn) used for what?
  2. Can cause what on the EKG?
  3. Risk of what with increased serum concentrations?
  4. SE? 2
A
  1. Used for afib/flutter
  2. QT prolongation
  3. Risk of torsades when increased serum concentrations
  4. SE include HA and dizziness
43
Q

Dofetilide (Tikosyn)
Many drug interactions including what?
8

A
  1. TMP-SMX,
  2. macrolide abx,
  3. verapamil,
  4. antifungals,
  5. SSRIs,
  6. Diltiazem,
  7. Grapefruit juice,
  8. caution with metformin
44
Q

Ibutilide (Corvert) is used for what?
Administered how?

Major adverse effect?

A

IV only for acute conversion of afib/flutter to sinus rhythm

Major adverse effect is torsades

45
Q

CLASS IV block what?

Which kind do we use?

A

CALCIUM CHANNEL BLOCKERS

Nondihyros

46
Q

Nondihydropyridine calcium channel blockers:

  1. Decrease automaticity where?
  2. Decrease conduction where?
  3. Treatment for? 4

What do we need to remember about this drug???

A
  1. Decrease automaticity in the SA and AV node
  2. Decrease conduction through the AV node
  3. Used for treatment of
    - -supraventricular arrhythmias
    - -PSVT,
    - -atrial fibrillation,
    - -atrial flutter

ONLY WORK ON ATRIA (if you have someone with PVCs you need to give them a beta blocker instead)

47
Q

Cardiac effects of NDHP CCBs:

  1. Relaxes what?
  2. Dont use in which pts and why?
  3. which is the best?
  4. What kind of chronotropic effect?
A
  1. Vascular relaxation
  2. Negative intropic effect (don’t use in LVSD)
  3. Verapamil > Diltiazem
  4. Negative chronotropic effect
48
Q

NDHP CCBs should not be used in which pts and why?

A

Do not use in WPW or an accessory pathway because they can shorten the refractory period of the accessory pathway and increase the ventricular rate and lead to VF

49
Q

SE of NDHP CCBs:
1. Why do we need to give verapamil slowly?

  1. Other side effects? 8
A
  1. Verapamil IV should be given slowly otherwise can cause severe hypotension
  2. Bradycardia,
  3. heart block,
  4. headache,
  5. flushing,
  6. dizziness,
  7. peripheral edema
  8. Constipation with verapamil
  9. Many drug-drug interactions: CYP3A4 isoenzyme