antiarrhythmic drugs Flashcards
1
Q
What is digoxin? What is digoxin used for?
A
- digitalis glycoside
- antiarrhythmic effect on AV node
- used for ventricular rate control in afib and flutter
- used for its positive inortope effect in CHF
- IT DOESNT convert rhythms to sinus
- doesn’t work well for slowing ventricular rates during exercise
2
Q
MOA of digoxin?
A
- slows the electrical conduction through the AV node
- stimulates the parasympathetic nervous system and increases vagal tone
- slows av conduction and prolongs AV nodal refractory period:
increases PR interval, downward sloping ST seg depression, and shortened QT interval
** wont work in exercise: SNS will override PNS effect of digoxin
3
Q
Dosing of digoxin?
A
- slow onset
- need a loading dose period
- may take a week fo 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 (higher levels in pts with LVSD(CHF) = higher mortality)
4
Q
How can digoxin reach toxic levels in the body?
A
- declining renal fxn: renal excretion
- electrolyte disturbances: hypokalemia, hypomagnesemia, and hypercalcemia can predispose the myocardium to toxic effects of digoxin
- drug interactions: may meds may increase serum digoxin levels: amiodarone, and verapamil
5
Q
Signs and sxs of digoxin toxicity?
A
- heart block
- AV junctional tachycardia
- ventricular arrhythmias
- visual disturbances: blurred vision, yellow/green halos
- dizziness
- weakness
- GI: N/V/D and anorexia
6
Q
What is adenosine? MOA?
A
- used to convert PSVT to SR
- activates K channels by increasing the outward K current
- hyperpolarizes the membrane potential and decreases spontaneous SA node depolarization
- inhibits automaticity and conduction in SA and AV nodes
- half life is only 10 seconds
7
Q
CIs to adenosine?
A
- 2nd or 3rd heart block or sick sinus syndrome in absence of pacemaker
8
Q
MOA and use of atropine?
A
- parapsympathetic drug
- enhances sinus nodal automaticity and AV nodal conduction through direct vagolytic action
- blocks acetylcholine and parasympathetic neuroeffector sites
- used for sx bradycardia!!!!!
- may induce tachycardia
9
Q
Atropine CIs?
A
- angle closure glaucoma
- obstructive uropathy (BPH)
- tachycardia
- bowel obstruction or altered bowel transit time
10
Q
Class 1: sodium channel blockers?
A
- class 1a (intermediate onset/offset) - disopyramide, procainimide, and quinidine
- class 1b (fast onset/offset)- lidocaine, mexiletine, and phenytoin
- class 1c (slow onset/offset): flecainide, propafenone
- subdivided by rate of Na channel dissociation
- variable rates of binding and dissociating from Na channel receptor
11
Q
Class 1a drugs? MOA
A
- proarrhythmic (stay away from these)
- used to tx atrial and ventricular rhythms
- ex: quinidine and disopyramide have anticholinergic effects that can lead to increase automaticity of SA and AV nodes.
- need to have BB or CCB to prevent tachyarrhythmias in afib/flutter pts
- used in torsades
- Procainimide IV only
12
Q
Class 1B drugs? MOA?
A
- lidocaine: used for VT and vF
- exerts most of it’s effects on ischemic or infarcted tissue of the ventricles
- particularly usefuly for VT/VF assoc with AMI
- IV only
- toxicity: seizures and respiratory arrest
- mexiletine: oral analog of lidocaine used for ventricular arrhythmias
13
Q
Class 1c: Flecainide (Tambocor)
A
- mainly used for rhyhthm control in afib/flutter
- FDA approved for vent arrhythmias but isn’t very effective (adverse effects)
- can’t be used if any hx of structural heart disease (CAD, LVSD, valvular disorders, LVH). otherwise proarrhythmic
- not first line in afib/flutter
14
Q
Class 1c: propafenone (rhythmol)
A
- used for atrial arrhythmias such as afib/flutter
- can’t be used if hx of structural heart disease
15
Q
Class II BBs list?
A
- atenolol
- esmolol
- metoprolol
- propranolol
16
Q
MOA of BBs and use?
A
- used for suppression of ventricular and supraventricular arrhythmias (PVCs, a fib, CHF) - rate control
- slow av nodal conduction and SA nodal rates
- neg inotropic agents
- decrease myocardial O2 consumption
17
Q
SEs of BBs?
A
- bronchospasm
- fatigue
- depression
- nighmares
- ED
- hypotension
- bradycardia
- worsening CHF (end stage or acute decompensated state)
18
Q
Class III - K channel blockers
A
- prolong the AP
- amiodarone (cordorone): rhythm control of afib and flutter, ventricular arrhythmias ( DOC for afib/flutter)
- sotalol (betapace): VT and afib
- ibutilide (covert): rhythm control of afib and flutter
- dofetilide (tikosyn)
19
Q
What should you watch for on EKG with K channel blockers?
A
- may induce ventricular arrhythmias and ectopy
- may change intervals: PR, QRS, and QT (prolong AP)
- don’t use with other drugs that prolong QT interval
20
Q
Use of Amiodarone?
A
- most widely used med for rhyhtm control for afib and VT
- all 4 antiarrhythmic drug class characteristics
- given IV for acute tx
21
Q
Amiodarone toxicities?
A
- poor bioavailability
- large volume of distribution
- highly lipophilic
- lead to build up of drugs in various organs:
lungs, thyroid, eyes, heart, liver, skin, GI tract, CND - pulm toxicity acutely can be life threatening, chronically leads to interstitial lung disease
-derm: photosensitivity, blue gray skin discoloration - neuro: ataxia, periph neuropathy, fatigue, and insomnia
22
Q
What tests should be done with pt on amiodarone?
A
- baseline PFTs and CXR and yearly (DLCO)
- eye exam at baseline and yearly: optic neuritis, optic neuropathy, corneal and lens opacities, halos, blurred vision, photophobia
- TSH, CBC, LFTs q 6 months
23
Q
SEs of amiodarone and drug interactions
A
- GI disturbance common on higher doses: N/V, anorexia, abd pain, constipation
- drug interactions:
substrate of CYP3A4 isoenzyme - sig interactions with dig and warfarin
- potentiates effects of warfarin
- can double serum dose of digoxin
- interacts with simvastatin (zocor) so max dose of zocor is 20 mg
24
Q
MOA and use of sotalol (betapace), SEs
A
- VT and afib/flutter
- has some beta blocking properties and prolongs QT
- during initiation of drug: hosp for 3 days to monitor QT interval due to risk for torsades
- SE sim to BBs: fatigue, dyspnea, bradycardia, neg inotropic efefcts so don’t use in LVSD
- renal clearance
- risk for tornadoes
25
Q
Dofetilide (tikosyn) MOA and use?
A
- used for afib/flutter
- QT prolong
- risk of torsades when increased serum concentrations
- SE include HA and dizziness
- many drug interactions including:
TMP-SMX, macrolide abx, verapamil, antifungals, SSRIs, diltiazem, grapefruit juice, caution with metformin
26
Q
Ibutilide (covert) use?
A
- IV only for acute conversion of afib/flutter to sinus rhythm, major adverse effect is torsades
27
Q
Class IV - CCBs
A
nondihydropyridines CCBs: diltiazem (cardizem) and verapamil
- decrease automaticity in SA and AV node
- decrease conduction through AV node
- used for tx of supraventricular arrhythmias: PSVT, afib, aflutter
28
Q
MOA of NDHP CCBs?
A
- vascular relaxation
- neg inotropic effect (don’t use in LVSD): verapamil has more neg inotropic effect than diltiazem
- neg chronotropic effect
- don’t use in WPW or an accessory pathway b/c tey can shorten refractory period of accessory pathway and increase ventricular rate and lead to VF
29
Q
SE of NDHP CCBs?
A
- verapamil IV: given slowly otherwise can cause severe hypotension
- bradycardia, heart block, HA, flushing, dizziness, peripheral edema
- constipation with verapamil
- many drug-drug interactions: CYP 3a4 isoenzyme
