Anti-arrhythmics Flashcards
use of anti-arrhythmics
restricted to dangerous/symptomatic arrhythmias –> Vtach, rapid afib
Class I/II MOA
block Na, K channel
myocyte AP
Class II/IV
slow sinus and AV node conduction
pacemaker AP
Class I MOA
- some block Na –> prolong QRS
- some block K –> prolong Qt
- use dependence (effective @ fast HR)
use dependence
- Class I (IC*)
- bind best in open/inactivated state
- (depress tissue that is freq depolarized –> tachycardia)
Class Ia drugs
quinidine
procanimide
disopyramide
Class Ia MOA
- block Na (phase 0) (inc QRS)
- some block K (inc QT)
Class Ia AE
TDP (prolong QT)
quinidine
- Ia
- oral
- dec recurrence rate of afib
AE: inc mortality, Cinchonism
procanimide
- Ia
- IV
- slow conduction in accessory path (WPW), arrhythmias (bypass tracts)
AE: drug-induced lupus
Class Ib drugs
lidocaine
mexiletine
Class Ib MOA
- least effect on AP of CI
- slight dec AP
- RAPID unbind (effective in tachy)
- bind depolarized tissue (ischemia) (B=Best post MI)
AE: CNS stim (tremor, agitation)
lidocaine
- Ib
- terminates arrhythmias by turning unidirectional block –> bidirectional block
mexiletine
- Ib
- oral version of lidocaine
Class Ic drugs
flecainide
propafenone
Class Ic MOA
- block open Na, very SLOW unbinding (PROLONGED QRS!!!!!!!!!)
- use in struc NORM heart
- dec afib recurrence
AE: proarrhythmic, cardiac arrest, cox at high HR
structurally normal heart
IC
use post-MI
IB
B=Best post-MI
Class III drugs
amiodarone
ibutilide
dofetilide
sotalol
AIDS
Class III MOA
- block K+ –> delay repolarization, prolong QT/AP/ERP in cardiomyocytes
use: afib, a flutter, vtach
AE: torsades
most adverse effects of any of the anti-arrhythmics
amiodarone
amiodarone MOA
-CIII, but I/II/IV effects
-blocks K+, Qt
(lowest torsades incidence)
-use: afib, Vtach
-LIPOPHILIC and LONG half life…
AE: liver/lung accumulation, hypER/hypOthyroidism,
inc LFTs, skin sensitivity to sun, blue/gray man, normal deposits, DEATH BY PULMONARY FIBROSIS
monitor these labs when rx amiodarone
CXR
PFTs
TFTs
LFTs
sotalol
CIII
dofetilide
CIII
sotalol
dofetilide
- block K+ (inc QT)
- REVERSE use-dependence
AE: torsades, tox @ slow HR
REVERSE use-dependence
- bind best at resting state
- tox @ slow HR
- CIII
Ibutilide
- CIII
- IV
- use: chemical cardioversion
AE: torsades
class II antiarrhymics MOA
beta blockers
main effects @ pacemaker cells of SA/AV node
- dec slope of phase 4 (funny current, Na) –> slows HR
- prolong phase 3 (repolariz) –> slows conduction in AV node
- -> prolonged PR
AE: type I AV block, wenkebach (mobitz I)
use: afib, prevent SCD in systolic HF (dec EF pts) –> DEC MORTALITY
Class II drugs
metoprolol propanolol esmolol atenolol timolol carvedilol
Class IV drugs
verapamil
diltiazem
(non-dihydropyridine CCBs)
class II AE
AE: type I AV block, wenkebach (mobitz I)
- impotence
- COPD exacerbation and asthma
- CVS effects (bradycardia, AV block, HF)
- Mask signs of hypOglycemia
Class IV MOA
- block phase 0 of pacemaker AP
- slow HR
- slow AV conduction
use: afib (control ventric. rate) (SVTs)
AE: type I AV block, wenkebach (mobitz I)
adenosine
“breaks AVNRT”
-inc K out (HYPERpolarize)
-dec Ca out
^dec AV node conduction
- short half life
use: dx/terminate certain forms of SVT
AE: flushing/hypotension (vasodilator) CP dyspnea doom bronchospasm
Mg
- blocks Ca influx (avoids early after depolarizations)
use: acute management of torsades AND digoxin toxicity
atropine
- muscarinic r. antagonist
- parasympathetic block
use: bradycardia (*esp via AV block)
ivabradine
- selective inhibit of funny Na chan, prolong phase 4, dec SA node firing
- negative chronotropic effect w/o isotropy
- reduces cardiac O2 req
use: chronic stable angina in pt who can’t take beta blockers, chronic HF w/ reduced EF
AE: luminous phenomena/visual brightness, HTN, bradycardia
metoprolol
B1 selective
propranolol
B1 and 2 (non-selective)
carvedilol
B1 and 2 (non-selective)