Anti-arrhythmics Flashcards
what is the purpose of Na/K pump (;
K+ into cell, Na+ out of cell
Class I MOA (generally)
modulates/blocks Na+ channels
Class II MOA (generally)
inhibits sympathetic activity
Class III MOA (generally)
Blocks K+ channels
Class IV MOA (generally)
block Ca+ channels
what are the Class IA drugs
quinidine, procainamide, disopyramide
what are the class IB drugs
lidocaine, mexiletine
what are the class IC drugs
flecainide, propafenone
how does class IA affect conduction velocity and ADP (action potential duration)
increases conduction velocity, prolongs ADP
how do class IB affect conduction velocity and ADP (action potential duration)
no effect on conduction velocity, may shorten ADP
how do class IC affect conduction velocity and ADP (action potential duration)
increases conduction velocity, prolong ADP
how do class III affect conduction velocity and ADP?
no effect on conduction velocity, prolongs ADP
what are the class II drugs
B-blockers
what are class III drugs
sotalol, ibutilide, dofetilide, amiodarone, dronedarone
what are the class IV drugs
non-dhp CCBs - verapamil, diltiazem
what is a major ADR of all anti-arrhythmics
can be proarrhythmic (cause arrhythmias) –> may be fatal
TdP is more common with…
hypokalemia, hypmagnesemia, bradycardia
TdP results from what
QT prolongation, usually d/t blockade of the IKr potassium current
class interactions of anti-arrhythmics
QTc prolongers, rate slowers
CYP3A4, 2D6 enzymes b/c most are metabolized by these cyps
drugs that cause hypokalemia/hypomagnesemia
class ADRs of anti-arrhythmics
QTC prolongation/proarrhythmic potential
careful in pts with bradycardia/heart blocks
ADRs of quinidine
quinidine syncope - recurrent lightheadedness & fainting 2* to self-terminating Tdp
cinchonism - dry as bone, red as beet, blind as bat, etc…
ADRs of procainamide
reversible lupus-like syndrome
severe bone marrow suppression
ADRs of disopyramide
anticholinergic SE (urinary retention»_space;)
ADRs of mexiletine and lidocaine
CNS toxicity (dizziness, lightheadedness, unsteady gait, tremor, seizures)
ADR of flecainide
mostly proarrhythmic
monitoring of flecainide
make sure K+ is normal
echo to make sure pt has structurally normal heart
monitoring of propafenone
echo to make sure pt has structurally normal heart
propafenone ADRs
dysgeusia (altered taste)
lupus-like rxn
Sotalol interactions
avoid concurrent B-blockers, CCBs
ibutilide ADR
proarrhythmic
dofetilide ADR
dysrhythmia - death possible
amiodarone pharm characteristics
highly lipid soluble (stored in high levels in muscle, fat , liver, lungs, skin) = long 1/2 life
iodine-containing (like thyroxine)
FDA indications for amiodarone
life-threatening VF or hemodynamically unstable VT
common clinical use for amiodarone
AF pharmacologic cardioversion
AF prophylaxis following open heart surgery
recurrent AF
interactions of amiodarone
substrate of 2C9, 3A4; inhibits multiple isoezymes
additive QTc drugs
additive AV block/bradycardia
drugs that induce increase K or Mg
what effect can amiodarone have on digoxin
can increase digoxin for up to 3 months
ADRs of amiodarone (generally)
ocular effects, hypothyroidism», pulmonary toxicity, cardiac effects, dermatologic, CNS
how does pulmonary toxicity with amiodarone present
IPF (idiopathic pulmonary fibrosis) –> ARDS
interstitial infiltrates on imaging
how to treat amiodarone pulmonary toxicity
d/c drug, corticosteroids, supportive
amiodarone ocular toxicity
corneal microdeposits, optic neuropathy / optic neuritis
may –> blindness
derm effects of amiodarone
photosensitivity, blueish skin discoloration
CNS effects of amiodarone
abnormal gait, ataxia, dizziness memory impairment, involuntary body movements, peripheral neuropathy
cardiac effects of amiodarone
bradycardia, AV nodal block
dronedarone indications
AF/ atrial flutter
monitoring for dronedarone
K+, Mg+, SCr, LFTs, ECG q3 months
contraindications of dronedarone
NYHA class IV HF Class II-III HF with recent decompensation pts with 2nd/3rd degree AV blocks pts with SSS (sick sinus syndrome) pts with bradycardia <50bpm
dronedarone interactions
CYP3A4 substrate
pgp inhibitor (remember digoxin)
QTc prolonger
INR elevations with warfarin?
dronedarone ADRs
N/V/D, photosensitivity?
MOA of digoxin for HF
inhibits Na/K pump = increase intracellular Na= Ca influx = increase intracellular Ca= increase contractility
MOA of digoxin for SV arrhythmias
increases vagal tone = decrease conduction through SA and AV nodes
clinical use of digoxin
- advanced systolic HF - only AFTER they have been optimized w ACE, ARB, b-blocker, diuretic, aldosterone antagonist
- 2nd line for AF in HF pts - only if b-blocker of non-dhp ccb isn’t enough/isn’t tolerated
monitoring of digoxin
ECG
K+, Mg+, Ca2+
serum SCr
serum trough [digoxin] measured prior to next dose
optimal [digoxin] for HF
0.5-0.9 ng/mL
optimal [digoxin] for AF
= 2 ng/mL
when should you monitor [digoxin] routinely
elderly, on interacting med (amiodarone, verapamil)
digoxin interactions
monitor if there is a toxicity risk with other drugs
oral steroids, diuretics (increases toxicity because digoxin has more of a distribution to heart and muscles with low K or Mg)
bile acid sequestrants (give other meds 1 hr before or 4-6 hrs after bile acid sequestrants)
acute digoxin toxicity
Cardiac - PVC, AV nodal blockade
GI- n/v, abd pain, anorexia
neuro - confusion, weakness
chronic digoxin toxicity
cardiac - rhythm disturbances
neuro - lethargy, delirium, weakness
visual - chromatopsia (yellow-green), scotomas, blindness
workup for digoxin toxicity
- [digoxin]
- serum [k]
- BUN/SCr
- baseline ECG
treatment for digoxin toxicity
- assess/stabilize ABCs
- continuous tele, pOx
- place IV
- blood sugar
- digoxin immune Fab
can digoxin be stopped
yeth
