Anti-arrhythmic Drugs Flashcards
(22 cards)
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
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.
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.
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
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
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
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
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)
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)
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)
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
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
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
What is the best of all the drugs to treat atrial fib/flutter?
AMIODARONE
Why is amiodarone unique?
it has characteristic of all 4 antiarrhythmic drug classes
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
Amiodarone Toxicity manifestations
dermatologic
neurologic
dermatologic
- photosensitivity
- blue/grey skin discoloration
neurologic
- ataxia
- peripheral neuropathy
- fatigue
- insomnia
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
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
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
Ibutilide (Corvert)
class
use
AE
class
-Class III- Potassium channel blockers
Use
-a fib/flutter, IV only
AE
-torsades
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
