Anti-arrhythmic Drugs Flashcards Preview

Cardiology 2 > Anti-arrhythmic Drugs > Flashcards

Flashcards in Anti-arrhythmic Drugs Deck (22)
Loading flashcards...
1

Digoxin
aka
Used for

aka
-digitalis glycoside

Used for
-antiarrhytimic effects on the AV node
-ventricular rate control for a fib/flutter
-positive ionotrope in CHF

2

How does Digoxin work on the AV node?

Digoxin slows the electrical conduction through the AV node by stimulating the parasympathetic nervous system and increases vagal tone; also prolongs the AV nodal refractory period, increasing PR interval, downward sloping ST segment depression, shortened QT.

3

How does Digoxin work during Atrial Fibrillation/ Flutter?

Digoxin slows ventricular rates.

*does NOT convert rhythms to sinus and does not work well for slowing ventricular rates during exercise.

4

Digoxin
time to onset
do you need a loading dose period?
time to steady state
therapeutic range

time to onset
-slow onset

do you need a loading dose period?
-yes

time to steady state
-may take a week to achieve steady state

therapeutic range
-0.8- 2.0 ng/mL

5

Digoxin
toxicity can be caused by
sx and signs of toxicity

toxicity can be caused by
-declining renal function
-electrolyte distrubances (hypokalemia, hypomagnesemia, hypercalcemia can predispose the myocardium to the toxic effects of digoxin)
-drug interactions

sx and signs of toxicity
-heart block
-AV junctional tachycardia
-ventricular arrhythmias
-visual disturbances (blurred vision, yellow/green halos)
-dizziness
-weakness
-n/v/d/anorexia

6

Adenosine
Use
mechanism
half life
CI

Use
-to convert PSVT to SR

Mechanism
-activates potassium channels by increasing the outward potassium current, hyperpolarizing the membrane potential which decreases spontaneous SA node depolarization. Inhibits automaticity and conduction in the SA and AV nodes

Half life
-10 seconds! thats quick!

CI
-2nd or 3rd degree heart block or sick sinus syndrome in the absence of a pacemaker

7

Atropine
Use
Mechanism
May induce...
CI

Use
-parasympatholytic drug
-to treat symptomatic bradycardia

Mechanism
-enhances sinus nodal automaticity and AV nodal conduction through direct vagolytic action
-block acetylcholine and parasympathetic neuroeffector sites

May induce...
-tachycardia

CI
-angle closure glaucoma
-obstructive uropathy
-tachycardia
-bowel obstruction or altered bowel transit time

8

Class I - Sodium channel blockers
Class Ia
Class Ib
Class Ic

-time to onset/offset
-examples of each class

Class Ia
-intermediate onset/offset
-Disopyramide (Norpace)
-Procainimide (Pronestyl)
-Quinidine (Quinidex)

Class Ib
-fast onset/offset
-Lidocaine
-Mexiletine (Mexitil)
-Phenytoin (Dilantin)

Class Ic
-slow onset/offset
-Flecainide (Tambocor)
-Propafenone (Rythmol)

9

Class Ia Sodium channel blockers
Use
Examples

Use
-proarrhythmic
-treat atrial and ventricular rhythms
-Disopyramide (Norpace) and Quinidine (Quinidex) have anticholenergic effects that can lead to increased automaticity of the SA and AV nodes (need to have beta blocker or CCB on board to prevent tachyarrhythmias in afib/flutter)
-torsades

Examples
-Disopyramide (Norpace)
-Procainimide (Pronestyl) (IV only)
-Quinidine (Quinidex)

10

Class Ib Sodium channel blockers
Use
toxicity
examples

Use
-ventricular arrhythmias (VT, VF)
-exerts most of its effects on ischemic or infarcted tissue of the ventricles
-give in emergent situations (fast onset/offset)

Toxicity
-lidocaine toxicity: seizures and respiratory arrest

Examples
-Lidocaine (IV only)
-Mexiletine (Mexitil) (oral analog of lidocaine)
-Phenytoin (Dilantin)

11

Class Ic Sodium Channel Blockers
Use
examples
CI

Use
-rhythm control in afib/flutter (nothing works better for a fib/flutter than amiodarone so these aren't first line)

Examples
-Flecainide (Tambocor)
-Propafenone (Rythmol)

CI
-Flecainide (Tambocor): if hx of structural heart disease (CAD, LVSD, valvular disorders, LVH) otherwise proarrhythmic
-Propafenone (Rythmol): if hx of structural heart disease

12

Class II- Beta Blockers
Examples
Use
Mechanisms
SE

Examples
-Atenolol (Tenormin)
-Esmolol (Brevibloc)
-Metoprolol (Lopressor) (Toprol XL)
-Propranolol (Inderal)

Use
-for suppression of ventricular and supraventricular arrhythmias

Mechanisms
-slow AV nodal conductions and SA nodal rates
-negative ionotrpic
-decrease myocardial O2 consumption

SE
-bronchospasm
-fatigue, depression, nightmares
-ED
-hypotension, brasycardia

13

Class III- Potassium channel blockers
Examples (and use for each)
Mechanism
Monitor EKG changes...
Do Not use with

Examples
-Amiodarone (Cordarone): rhythm control of a fib/flutter, ventricular arrhythmias
-Dofetilide (Tikosyn):rhythm control of a fib/flutter
-Ibutilide (Corvert): rhythm control of a fib/flutter
-Sotalol (Betapace): VT and atrial fibrillation

Mechanism
-prolong the action potential

Monitor EKG changes
-may induce ventricular arrhythmias and ectopy
-may change PR, QRS, QT intervals

Do Not use with
-other drugs that prolong the QT

14

What is the best of all the drugs to treat atrial fib/flutter?

AMIODARONE

15

Why is amiodarone unique?

it has characteristic of all 4 antiarrhythmic drug classes

16

Amiodarone
Good or bad bioavailability
large or small volume of distribution
lipophilic/phobic
what do these characteristic lead to

poor bioavailability (bioavailability (BA) is a subcategory of absorption and is the fraction of an administered dose of unchanged drug that reaches the systemic circulation)

large volume of distribution

highly lipophilic

-These characteristics may lead to build up of the drug in organs (lungs, thyroid, eyes, heart, liver, skin, GI, CNS)
-the pulmonary toxicity acutely can be life threatening and chronically leads to interstitial lung disease
-can stay in the system for 6 months after treatment

17

Amiodarone Toxicity manifestations
dermatologic
neurologic

dermatologic
-photosensitivity
-blue/grey skin discoloration

neurologic
-ataxia
-peripheral neuropathy
-fatigue
-insomnia

18

Amiodarone
class
Monitoring tests
SE

Class
-Class III- Potassium channel blockers

Monitoring tests
-baseline PFTs and CXR and yearly (with DLCO)
-eye exam baseline and yearly (optic neuritis, optic neuropathy, corneal and lens opacities, halos, blurred vision, photophobia)
-TSH, CBC, LFTs q 6 months

SE
-GI disturbance (in higher doses)
-Drug interactions
--substrate of the CYP3A4 isoenzyme
-significant interactions with Digoxin and Warfarin and Zocor
-potentiates effects of warfarin
-can double serum dose of digoxin

19

Sotalol (Betaspace)
class
use
SE

Class
-Class III- Potassium channel blockers
-has some beta blocking properties and prolongs the QT
-during initiation of the drug-hospitalize for 3 days to monitor QT interval d/t risk of torsades

Use
-VT and afib/flutter

SE
-similar to beta blockers (fatigue, dyspnea, bradycardia)
-negative inotropic effects so dont use in LVSD
-risk of torsades

20

Dofetilide (Tikosyn)
class
use
SE

class
-Class III- Potassium channel blockers

Use
-a fib/flutter

SE
-risk of torsades when increased serum concentrations
-HA, dizziness
-many drug interactions

21

Ibutilide (Corvert)
class
use
AE

class
-Class III- Potassium channel blockers

Use
-a fib/flutter, IV only

AE
-torsades

22

Class IV- Calcium Channel Blockers
examples
Use
Mechanism
Cardiac effects
SE

Examples
-Diltiazem (Carizem)
-Verapamil (Calan)

Use
-tx of supreaventricular arrhythmias (PSVT, atrial fib/ flutter)

Mechanism
-decrease automaticity in the SA and AV node
-Decrease conduction through the AV node

Cardiac effects
-vascular relaxation
-negative inotropic and chronotropic effects
-DO NOT use in WPW or and accessory pathway because they can shorten the refractory period of the accessory pathway and increase the vent rate and lead to VF

SE
-Verapamil IV should be given slowly, could cause severe hypotension
-bradycardia, heart block, HA, flushing, dizziness, peripheral edema
-constipation with verapamil
-many drug interactions: CYP3A4 isoenzyme