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
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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
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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)
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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
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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
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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
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7
Q

CIs to adenosine?

A
  • 2nd or 3rd heart block or sick sinus syndrome in absence of pacemaker
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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
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9
Q

Atropine CIs?

A
  • angle closure glaucoma
  • obstructive uropathy (BPH)
  • tachycardia
  • bowel obstruction or altered bowel transit time
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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
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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
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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
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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
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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

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15
Q

Class II BBs list?

A
  • atenolol
  • esmolol
  • metoprolol
  • propranolol
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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