Module: EASY FATIGABILITY (ANTIARRHYTHMIC DRUGS)

DRUGS MOA INDICATION DOSE

PROCAINAMIDE suppresses both atrial & ventricular arrhythmias  AF & atrial flutter (Class IIa)  20 mg/min infusion until
 Preexcited atrial arrhythmias (Class llb) arrhythmia is suppressed,
 Wide complex tachycardia that cannot be hypotension developed, or > 50%
distinguished as being supraventricular or prolongation of the QRS,or a total
ventricular in origin (Class IIb) of 17mg/kg.
LIDOCAINE MOA: not specified  VF/ pulseless VT that persist after  Initial bolus of 1 – 1.5 mg/ kg IV.
 Delicate toxic-to-therapeutic balance defibrillation and administration of Additional bolus of 0.5 to 0.75mg/
 Routine use in AMI is not recommended epinephrine kg can be given over 3 – 5 minutes
 No proven short-term or long-term efficacy in  Hemodynamically stable VT for refractory VT/ VF.
cardiac arrest  Alternative if Amiodarone unavailable
 CNS Toxicity: muscle twitching, slurred speech,
respiratoty arrest, altered consciousness,
seizures
FLECAINIDE Potent sodium channel blocker with significant  atrial flutter and AF,  2 mg/ kg body weight at 10 mg/ min
*** Not approved for conduction slowing effects  ectopic atrial tachycardia, infusion
use in the US  AV nodal reentrant tachycardia and
 SVTs associated with accessory pathway
(WPW)
PROPAFENONE Significant conduction slowing & negative inotropic  Avoided in patients with impaired LV function  1 to 2 mg/kg body weight at 10
***Vaughn Williams effects mg/min (relatively slow infusion for
Class IC Antiarrhythmic Nonselective B-blocking properties emergency situations)
B-ADRENERGIC Beta blockage  Class I in acute coronary syndromes
BLOCKERS Contraindications:  To convert to sinus or to slow ventricular
 Hemodynamic instability response or both (AF/ flutter, MAT, re-entry
 2o and 3o AV block SVT)
 Asthma Second line after adenosine
 Cocaine-induced ACS ***Labetalol recommended for emergency anti-
hypertensive therapy for hemorrhagic and acute
ischemic stroke
AMIODARONE  Affects Na, K and Ca channels as well as alpha  After defibrillation and epinephrine in cardiac  VT with pulse – 150mg IV over
***Class III anti- and beta adrenergic blocking properties arrest 10mins followed by1mg/kg/min
arrhythmic  Prolongs action potential duration and  Ventricular rate control of rapid atrial infusion for 6 hours, then
refractory period arrhythmias 0.5mg/kg/min
 decreases AV node conduction and sinus node  Adjunct to electrical cardioversion  Pulseless VT/VF – 300mg IV push
function Side effects are hypotension and bradycardia then 150mg IV - 2nd dose if needed
after another cycle of CPR
SOTALOL  Prolongs action potential duration & increases  1 to 1.5 mg/ kg body weight at 10
***Vaughn Williams cardiac tissue refractoriness mg/min (relatively slow infusion for
Class III Antiarrhythmic  Nonselective B-blocking properties emergency situations)
CALCIUM CHANNEL Slow conduction & increase refractoriness in the AV node VERAPAMIL  2.5 – 5 mg IV given in 2 minutes.
BLOCKERS  May also control ventricular response rate in  Effective in stable narrow complex PSVT  Administered every 15 – 30 mins to
patients with AF, AFlutter, or MAT  Alternative drug after Adenosine a max of 20 mg
 Systemic vasodilation ***Should not be given in patients with impaired
 Negative Inotropic effect ventricular function or heart failure
Should not be given if hypotensive
ADENOSINE  Depresses AV node & sinus node activity
 Half-life is < 5 seconds (degraded in the blood &
periphery)
MAGNESIUM
ATROPINE Parasympatholytic action:
- accelerates rate of sinus node discharge
- improves AV conduction
Reverses cholinergic-mediated decreases in heart rate,
systemic vascular resistance, & blood pressure
EPINEPHRINE  Increases SVR, BP, HR, Contractility,
automaticity-
 Increases blood flow to heart & brain, AV
conduction velocity
 Alpha-adrenergic effects can increase coronary
& cerebral perfusion pressure during CPR
ISOPROTERENOL  Pure B-adrenergic agonist with potent inotropic
and chronotropic effects
Limited evidence of use
DIGOXIN  enhances central and peripheral vagal tone
 slows SA node discharge rate
 shortens atrial refractoriness
 prolongs AV nodal refractoriness through ANS
effect
 Should be used if SVT is suspected
 Effectively terminates torsades de pointes
Not effective in irregular/ polymorphic VT in patients
with normal QT
Not recommended in cardiac arrest except when
arrhythmias are suspected to be caused by magnesium
deficiency
 Symptomatic sinus bradycardia (Class I)-
 AV block Nodal level
 use with caution in AMI
***Should not be relied fully in Mobitz type II block
 Temporizing measure for torsades de
pointes before pacing & in significant
bradycardia when atropine and dobutamine
has failed and pacing is not available
 Not indicated in patients with cardiac arrest
or hypotension
 supraventricular arrhythmias (AF/flutter)
Less effective than adenosine, verapamil, or beta
blockers.
 Peak effect - after 1.5 - 3 hours
 6 mg rapid IV push in 2-3 seconds,
followed by 20ml saline flush.
 If no response may give 2nd dose:
12 mg after 1-2 minutes
 May give a 3rd dose: 12 mg if still
no response
 1 – 2 gm (8-16meqs) mixed in 50 –
100 ml D5W given over 5 to 60
mins.
 Followed by 0.5 to 1gm IV infusion
(1 to 2 gm diluted in 100 ml D5W
administered over 1 – 2 mins in emergency
situations)
 0.5 mg every 3 – 5 mins
 A total dose of 3 mg (0.04 mg/kg)
results in full vagal blockade in
humans
If atropine is not effective, may give
epinephrine infusion for symptomatic
bradycardia as an alternative to pacing
 2-10 mcg/min (1mg in 500cc of D5
W or normal saline by continuous
infusion)
 Dose: 2 – 10 mcg/ min titrated
according to the heart rate and
rhythm response
 Acute loading dose 0.5 to 1.0 mg IV
or PO 0.004 to 0.006mg/kg initially
over 5 min.
 Then 0.002 to 0.003mg/kg at 4-8hr
interval.
 Total of 0.008 to 0.012mg/kg
divided to 8 to 16hrs