Antiarrhythmic Drugs- Exam 3 Flashcards
**What is happening at each of the boxes? What type of cell?
blue: Na coming IN
red: Ca coming IN
purple: K leaving
cardiac pacemaker cell
**What phase is happening at each colored box?
blue: phase 4: slow Na coming IN- depolarization
red: phase 0: rapid Ca coming IN- depolarization
purple: phase 3: K leaving and cell repolarization
**What phase number does each colored circle represent?
yellow: 4
red: 0
green: 1
blue: 2
pink: 3
yellow: 4
**What is happening at each number phase 4, 0, 1, 2, 3, 4?
4: K
0: rapid Na IN
1: K and Cl out
2: Ca IN and K out
3: K out
** When Ca is blocked, the electrical conduction is (longer/shorter)
block Ca and the electrical conduction takes LONGER
The aim of therapy of the arrhythmias is to ______ activity and modify conduction or refractoriness in _____ to disable ______
reduce ectopic pacemaker
reentry circuits
circus movement
Antiarrhythmic drugs decrease the _____ of _______ more than that of the _____. They also reduce _______ and ______ and increase the _______ to a greater extent in depolarized tissue than in normally polarized tissue
automaticity
ectopic pacemakers
SA node
conduction
excitability
refractory period
How are AAD classified? What are the different drug classes?
Vaughan-Williams Classification system
Class I-IV
class I: drugs that block fast sodium channels
class II: BB
class III: block potassium channels
class IV: calcium channel blockers
Maybe consider looking at this summary table again??
What drug class?
quinidine, procainamide, disopyramide
Class Ia
what drug class? slow the rate of rise of the action potential and prolong its duration, thus slowing conduction and increasing refractoriness (moderate depression of phase 0 upstroke of the action potential)
class Ia: quinidine, procainamide, disopyramide)
What drug class?
lidocaine, mexiletine
class Ib agents
what drug class? shorten action potential duration; they do not affect conduction or refractoriness (minimal depression of phase 0 upstroke of the action potential)
class Ib agents: lidocaine, mexiletine
What drug class?
flecainide, propafenone
Class Ic agents
What drug class? Dissociates from channel with slow kinetics (no change in action potential duration)
class Ic: (flecainide, propafenone)
How are the class I drugs further subdivided?
Three subclasses are further defined by the effect of the agents on the Purkinje fiber action potential:
What drug class does this represent?
class Ia
What drug class does this represent?
class Ib
What drug class does this represent?
class Ic
______ has potent anticholinergic properties that affect the SA and AV nodes, which can increase the SA nodal discharge rate and AV nodal conduction. What does it lead to?
quinidine
This may lead to increased ventricular rates with afib or aflutter
**What also needs to be prescribed concurrently with quinidine? What drug class?
Addition of a beta blocker, non-dihydropyridine CCB, or digoxin protects against increased ventricular rates with afib or aflutter
Ia
quinidine can also lead to ______ and interacts with ______
torsades
CYP3A4 inducers or inhibitors
_____ is similar to quinidine but without the anticholinergic effects.
procainamide
procainamide also carries a risk of ______ because of ______. What are the SE?
torsades
prolongs the QT interval
SLE like s/s- MC adverse effect
_______ is a potent anticholinergic and negative inotropic effects limits uses clinically. When is it used clinically?
Disopyramide (Norpace)
hypertrophic cardiomyopathy
Disopyramide (Norpace) also increases risk of ______ due to _______. When is it CI?
Prolongs QT, increasing risk of torsades
Contraindicated in patients with reduced LV EF (<40%)
What are the adverse events associated with Disopyramide (Norpace)?
Precipitation of CHF
Anticholinergic effects – dry mouth, urinary retention, constipation, blurred vision
______ is selective to ischemic tissue, and especially to active fast sodium channels in the bundle of HIS, Purkinje fibers, and ventricular myocardium. What drug class?
lidocaine
class Ib
How is lidocaine administered? What is the typical pt?
continuous IV infusion following an MI
need to check levels because it can be toxic especially in pts with liver failure
What are the adverse effects of lidocaine?
CNS effects: dizzy, paresthesia, disorientation, tremor etc etc
_______ is similar to lidocaine but in oral form. What drug class?
Mexiletine
class Ib
_______ can be used in combination with class IA and III drugs for the treatment of refractory ventricular dysrhythmias. NOT as a single agent
mexiletine
What are the SE of mexiletine?
GI and neuro SE
________ slows conduction velocity in the Purkinje fibers and the AV node. May lengthen PR interval and QRS duration. What drug class? When is it commonly used?
Flecainide (Tambacor)
class Ic
afib/flutter
What kind of pt is Flecainide (Tambacor) and Propafenone (Rythmol) good for? Why?
MUST have a structurally normal heart!! no hypertrophy, valvular dz or ischemia
high risk of vent tachy in pts without normal hearts
Blurred vision, dizziness, headache, tremor, N/V
What are the SE of Flecainide (Tambacor)?
_______ slows conduction velocity in the Purkinje fibers and the AV node; also has a mild nonselective beta blocking effect
May lengthen PR interval and QRS duration, leading to conduction disturbances such as bradycardia and heart block. What drug class?
Propafenone (Rythmol)
class Ic
Propafenone (Rythmol) may _____ PR interval and ____ duration, leading to ______ disturbances such as ______ and heart block. When is it commonly used?
lengthen
QRS
conduction
bradycardia
afib/flutter
Blurred vision, dizziness, headache, N/V, bronchospasm, and taste disturbances METALLIC TASTE
What are the SE of Propafenone (Rythmol)?
______ decrease automaticity, prolong AV conduction, and prolong refractoriness.
Negative chronotropic and inotropic effects. What drug class?
Beta Blockers
class II
What BB is used MC in arrhythmias? how? ______ can be used as a continuous IV infusion for rapid afib/flutter
Metoprolol
given in IV bolusus NOT continuous drip
Esmolol
_____ are useful in suppressing ventricular dysrhythmias, as well as supraventricular dysrhythmias. Especially helpful when used in COMBO with other AAD
Beta blockers
_______ block POTASSIUM channels and _____ repolarization, widening the QRS and prolonging the QT interval.
Decrease automaticity and conduction and prolong refractoriness
class III
prolong
Avoid concomitant use of _____ with other drugs that can ______ to minimize the risk of torsades
class III AADs
prolong the QT interval
NEVER use class III AAD with ______ due to _____
class Ia : quinidine, procainamide, disopyramide)
risk of torsades
What are the 4 class characteristics that amiodarone processes?
Primarily a potassium channel blocker, but also blocks sodium channels, has non-selective beta blocking activity, and has weak calcium channel blocking properties
Works on all cardiac cells (SA node, AV node, atria, ventricles and Purkinjes)
amiodarone has minimal to no _____ effects and can safely be used in patients with ______
no negative inotropic effects
LV dysfunction
What is the generic dosing for amiodarone? What kind of heart pt is amiodarone good for?
start amiodarone dosing at HIGH levels then go down
good for structurally weak hearts
_______ is an uncommon, but possibly life-threatening adverse event of amiodarone. What is the screening?
Pulmonary toxicity
annual chest xrays, if fibrosis is seen on xray need to stop amiodarone immediately
_____ is also a common SE of amiodarone. why? what is the monitoring?
thyroid problems:
hypo give synthroid
hyper-> need to stop immediately
because amiodarone is 38% iodine by weight
obtain baseline TSH and repeat q6 months while the pt is taking it
amiodarone can also build up in the eyes causing ____ and _____. What is the screening?
corneal and lens opacities
annual eye exams
What derm reactions are possible with amiodarone?
blue/gray skin and photosensitivity
What are the monitoring requirements for a pt on amiodarone?
pulm toxicity -> annual chest xray
TSH at baseline and Q6 months
yearly eye exam
GI: liver toxicity -> screening LFTs every 6 months
neuro: tremor, ataxia, fatigue, insomnia
derm: photosensitivity and blue/gray skin discoloration, need to wear sunscreen
amiodarone is also a potent inhibitor of _______. Potentiates the effects of ______ and can double serum ______ concentrations
CYP3A4 enzymes
warfarin
digoxin
______ A class III AAD that also has nonselective beta-adrenergic blocking properties. May decrease cardiac contractility and therefore should be avoided in patients with LV dysfunction
Sotalol (Betapace)
QT prolongation is common with _______ and should be monitored for closely.
Discontinue if QT interval _______.
Avoid combining with other QT prolonging drugs
Sotalol (Betapace) is a potassium channel blocker
greater 550 ms
_______ is a potassium channel blocker that does NOT have any BP lower effects and must be given at the same time everyday. What are the SE?
Sotalol (Betapace)
tired, sluggish
_______ results in a prolonged action potential and an increased QT interval.
Affects the ____ more than the ______
No negative inotropic effects, therefore is safe to use in patients with LV dysfunction
Dofetilide (Tikosyn)
atria
ventricles
What is the main concern for pts taking Dofetilide (Tikosyn)? What is the monitoring?
torsades de pointes
Patients should be in the hospital, on telemetry with Q12 hour EKG’s for first 3 days of loading Tikosyn to monitor QT interval and adjust dose
What 6 medications are CI with concurrent use of Dofetilide (Tikosyn)?
cimetidine
ketoconazole
megestrol
prochlorperazine
Bactrim
verapamil
Need to avoid Dofetilide (Tikosyn) and ________ and cleared ______ so do not use in patients _______
inhibitors of the CYP3A4 isoenzyme
renally
so do not use in patients with CrCl < 20 mL/min
_____ is considered it the “safe cousin of amiodarone”; but not nearly as effective, and side effects and toxicities are still common. What drug class?
Dronedarone (Multaq)
class III
dronedarone has very simliar SE profile to amiodarone except _______
dronedarone has NO effect on the thyroid
still cannot use it in HF pts and those with bad livers
_______ is structurally similar to sotalol, but no beta-blocking activity. What drug class?
Ibutilide (Corvert)
** _____ is available only in IV form, and indicated only for afib/flutter cardioversion in the acute setting only. What is the major adverse effect? When should you NOT use it?
Ibutilide (Corvert)
torsades
Should be avoided in patients with LV dysfunction and electrolyte abnormalities (especially hypokalemia and hypomagnesemia)
______ and ______ are the only CCB used in arrhythmias. What drug class?
Verapamil and Diltiazem
class IV
______ and _______ decrease automaticity and AV conduction and have potent negative inotrophic effects. Should be avoided in pts with LV dysfunction
verapamil and diltiazem
class IV
______ predominant AA effect is on the AV node. Inhibits Calcium currents in the AV node and activates acetylcholine-mediated K+ currents in the atrium
Digoxin
______ is mainly used for slowing the ventricular rate in afib/flutter, as well as terminating reentrant arrhythmias involving the AV node
digoxin
What are the changes seen on EKG when a pt is on digoxin?
PR prolongation and ST segment depression
What are 2 important things to note about digoxin?
intestinal microflora may metabolize digoxin so if pt is taking abx, pt is at risk for toxicity because of the lack of intestinal microflora metabolizing digoxin
digoxin has a slow distribution to effector sites so need a higher IV loading dose to begin
What should you do if your pt is taking digoxin and is renally impaired? What is the half life?
Renal elimination accounts for 80%, therefore doses should be reduced or dosing interval increased with renal insufficiency
half life is 36 hours
Amiodarone, quinidine, verapamil, diltiazem, itraconazole, propafenone, and flecainide (increase/decrease) digoxin clearance. so the dose need to be (increased/decreased) if combining with any of these drugs
decrease digoxin clearance
so dose needs to be decreased if combined with any of these drugs
Visual disturbances, dizziness, weakness, N/V/D, anorexia
What am I?
What should you do next?
digoxin toxicity
IV hydration, electrolyte correction AND
Digoxin immune Fab (digoxin reversal agent)
What are some factors that can contribute to a digoxin toxicity?
declining/poor renal function
electrolyte abnormalities
hypoxia
drug interactions
_______ ACTIVATES potassium channels and by increasing the outward potassium current hyperpolarizes the membrane potential, decreasing spontaneous SA nodal depolarization. When is it commonly used?
adensosine
Used for converting SVT to sinus rhythm; essentially causing sinus arrest
What is the 1/2 life of adenosine? What are some SE?
VERY SHORT so the sinus arrest does NOT last long
Chest discomfort, dyspnea, flushing, and headache
______ A parasympatholytic drug that enhances both sinus nodal automaticity and AV nodal conduction through direct vagolytic action. Blocks acetylcholine at parasympathetic neuroeffector sites
atropine
When is atropine used? What may it induce? What type of patient should you use it cautiously in?
emergent setting of SYMPTOMATIC bradycardia
May induce tachycardia,
which may result in poor outcomes in patients with MI, so use cautiously
atropine has been reported to cause a paradoxical slowing of the heart rate when used in patients with _____ and ______. So monitor patient closely if using atropine in this setting
Mobitz type II AVB
third degree AVB
