Antiarrhythmic Drugs Flashcards
Digoxin
- Antiarrhythmic effect is on the what?
- Used for what?
- Used for it’s effect on?
- AV node
- ventricular rate control in atrial fibrillation and flutter
- positive inotrope effect in CHF
- Digoxin_____ the electrical conduction through the AV node
- Stimulates the ____________ nervous system and increases ______ ______
- slows
- parasymathetic
vagal tone
Slows AV conduction and prolongs the AV nodal refractory period. What does this cause on the EKG? 3
- Increased PR interval
- Downward sloping ST segment depression
- Shortened QT interval
Dig is used to slow ventricular rates in Afib and A flutter. What is the downside to this? 2
Slows rates (for rate control)!!!
- Does NOT convert rhythms (afib/flutter) to sinus!
- Does not work well for slowing ventricular rates during exercise!
Digoxin:
- Onset?
- Administration/dosing?
- Steady State?
- Theuropeutic range?
- Slow onset
- Need a loading dose period
- May take a week to achieve steady state
- Monitor serum blood levels periodically
Therapeutic range 0.8 – 2 ng/mL
AF and concomitant LVSD is 0.5-1 ng/mL
Who has increased mortality on Dig?
Higher levels in pts with LVSD = higher mortality
AF and concomitant LVSD is 0.5-1 ng/mL
Digoxin toxicity can be caused by
3
- Declining renal function
Renal excretion - Electrolyte disturbances
- Drug interactions
Many meds may increase serum digoxin concentrations
What electrolyte disturbances can cause dig toxicity? 3
What drug interactions may increase serum dig concentrations? 2
- Hypokalemia,
- hypomagnesemia and
- hypercalcemia
can predispose the myocardium to the toxic effects of digoxin
- amiodarone,
- verapamil
Signs and symptoms of digoxin toxicity
8
- Heart block
- AV junctional tachycardia
- Ventricular arrhythmias
- Visual disturbances
- Blurred vision, yellow/green halos
- Dizziness
- Weakness
- GI: N/V/D and anorexia
Why is adenosine used?
Used to convert PSVT to SR
- Activates _______ channels by increasing the outward ________ current
- __________ the membrane potential and __________ spontaneous SA node depolarization
- _______ automaticity and conduction in the SA and AV nodes
- Half life?
- potassium
- potassium
- Hyperpolarizes
- decreases
- Inhibits
- 10 seconds
Adenosine contraindications
2
- 2nd or 3rd degree heart block
2. sick sinus syndrome in the absence of a pacemaker
- What kind of drug is atropine?
2, What does it enhance and how? 2
- What does it block? 2
- Used for the treatment of what?
- May induce what?
- Parasympatholytic drug
- Enhances
- -sinus nodal automaticity and
- -AV nodal conduction through direct vagolytic action - Block
- -acetylcholine and
- -parasympathetic neuroeffector sites - Used for the treatment of symptomatic bradycardia
- May induce tachycardia
Atropine contraindications
4
- Angle closure glaucoma
- Obstructive uropathy (think BPH)
- Tachycardia
- Bowel obstruction or altered bowel transit time
Class 1 blocks what?
What are the sub classes?
3
sodium channel blockers
- Class Ia (intermediate onset/offset)
- Class Ib (fast onset/offset)
- Class Ic (slow onset/offset)
Class Ia (intermediate onset/offset)
are which drugs?
3
- Disopyramide (Norpace)
- Procainimide (Pronestyl)
- Quinidine (Quinidex)
Class Ib (fast onset/offset) are which drugs? 3
- Lidocaine
- Mexiletine (Mexitil)
- Phenytoin (Dilantin)
Class Ic (slow onset/offset) are which drugs? 2
- Flecainide (Tambocor)
2. Propafenone (Rythmol)
3 classes of sodium channel blockers are categorized how? 2
- Subdivided by the rate of sodium channel dissociation
2. Variable rates of binding and dissociating from the sodium channel receptor