antiarrhythmics Flashcards
class 1 agents
block Na channels which depresses phase 0, in depolarization of the cardiac AP which results in decreased AP propagation–
decrease in depolarization rate, and slowing of conduction velocity
decreasing upstroke of depolarization
blocks excitation of myocardium (which occurs with tachy)
membrane stabilization drugs
(ex: LA also block Na channels)
3 sub types
class 1a
Intermediate Na channel blockers (intermediate dissociation)
decreased depolarization rate
Phase 0 decreased conduction velocity
Prolonged repolarization
Increased AP duration and refractory period of cells
in addition blocking K channels
class 1a drugs
Quinidine- Class 1a prototype, rarely used
Procainamide: not used bc of SE: hypotension
Disopyramide: PO,
Moricizine: PO
Disopyramide
suppresses atrial and ventricular tachyarrhythmias
membrane stabilizing, decreased excitability of cells
PO
SE: has significant myocardial depressant effects and can precipitate congestive Heart failure and hypotension
Class 1b agents
FAST Na channel blockers (fast dissociation) Phase 0 weak or less powerful bc so quick: fast association and dissociation with Na channels alters the AP by inhibiting Na ion influx via rapidly binding to and blocking Na channels (fast) Produces little effect on max velocity depolarization rate (the rate of the rise of phase 0) leaves many channels blocked by time AP reaches the peak but shortens AP duration and shortens refractory period bc fast has different effect that class 1a, advantage can be use for topic and premature beats
class 1b agents
lidocaine- class 1b prototype, still used for arrhythmia
mexiletine
tocainide: no uses in US
phenytoin: torsades
Lidocaine dose, kinetics
Dose: 1-1.5mg/kg IV
gtt: 1-4mg/min (max 3mg/kg)
there is PO but has extensive 1st pass
50% pb
hepatic metabolism: active metabolite which prolongs e1/2t
metabolism may be impaired by drugs: cimetidine and propanolol. conditions: CHF, acute MI, liver dysfunction GA
metabolism my be INDUCED by barbs, phenytoin or rifampin
10% renal
Lidocaine e1/2t, therapeutic plasma [ ], AE
e1/2t 1.4-8hr
[ ] 1-5mcg/ml
lidocaine use
**acute tx/prevention of vent dysrhythmias immediate post MI–raises vent fib threshold
vent tachy, fibs, PVC,
pulseless VT, and VF
lidocaine AE
CNS effects leading to resp depression leading to cardiac arrest
hypotension, brady, sz, decreased CNS, drowsiness, dizziness, tinnitus, condusion, apnea, myocardial depression, sinus arrest, HB, vent depression, cardiac arrest,
Mexiletine
class 1b
for chronic suppression of ventricular cardiac tachyarrhymias
PO
Class 1C
Slow Na channel blocker (slow dissociation) so does not vary much during cardiac cycle
Very Potent
Phase 0: potent decreased of depolarization rate with increased AP and refractory period
markedly inhibit conduction through His-purkinje system
Flecainide
class 1c prototype
effective in tx of suppressing ventricular PVC, Vtach, Atach, WPW(reentry rhythm)
PO
SE: proarrhythmic
Propafenone
class 1c
suppression of vent and atrial tachy
PO
SE: proarrhythmic
Class II
Beta-adrenergic antagonist
depress spontaneous Phase 4 depolarization
depress pacemaker activity
**push threshold down in nodal tissue
decrease in SA node discharge
antiSNS
drug-induced slowing of heart rate results in decreased myocardial O2 demands–desirable in pts with CAD
Slow speed of conduction of cardiac impulses through atrial tissue and AV node resulting in prolongation of the PR interval on ECG, increased duration of the AP in atrial
decreased automaticity
**Slows HR, Decrease force of contractility
Class II drugs
propanolol-prototype, both
metoprolol,
esmolol
labetolol (alpha and beta)
Propanolol class, use
prototype, class II, b-blocker, B1and 2
in heart and bronchial tone
decrease rate of Phase 4 depolarization, which leads to decreased automaticity
decrease SNS activity of heart,
decrease conduction through AV node,
decreased QT interval
use: prevent reoccurrence of tachyarrh–SVT caused by SNS stimulation aka tachys caused by catacolamines and also atrial tachy, decrease mortality after MI
Proparanolol does onset peak e 1/2t cardiac effects
dose: 1mg/min total dose 3-6mg IV or 10-80mg PO
onset: PO
Peak effect 10-15min duration 3-4hr??
E1/2t 2-4hr
Cardiac effects: decreased HJR, contractility, CO, Increased PVR, coronary vascular resistance, however, O2 demand lowered
Proparanolol kinetics SE
90-95%pb hepatic metabolism, with weak metabolite. therapeutic plasma level 10-30mcg/ml
SE: brachy, hypotension, myocardial depression, fatigue, **worse brochospasm, drug fever, rash,N, worse raynauds, interferance with glucose metabolism, caution with: reactive airway disease, **CHF, AV block
Metoprolol
class II, bblocker, selective b1 dose: 5mg IV over 5min max 15mg, over 20min onset:2.5m E1/2t 3-4hrs hepatic metab can be used in mild CHF
Esmolol
class II bblocker selective B1
dose: 0.5mg/kg bolus over 1min the 50-300mcg/kg/min
duration: <15m
effects HR without decreasing BP significantly in small doses
Rapidly hydrolyzed by plasma esterases
not the same as sux, so NO effect on sux metabolism
Class III
block potassium ion channels, resulting in prolongation of cardiac depolarization (refractory period) which
increasing AP duration
lengthening repolarization
decreased conduction velocity
decrease the proportion of the cardiac cycle during which myocardial cells are excitable and thus susceptible to triggering event
increased QT interval
decrease automaticity
class III use
tx SVT, vent arrhythmias
prophylaxis in cardiac surgery pts r/t high incidence of Afib
preventative therapy in pts who have survived sudden cardiac death who are not candidates for ICD
control rhythm in Afib
**re-entery tachy, effective at control of arrhythmia and rate
Prevent more serious arrhythmias from rate control
Class III drugs
amiodarone - prototype
Dronedarone
Sotalol
