Pharmacology- Antiarrythmics

Front 1

Procainamide
(Pronestyl)

Back 1

DC: Class IA antiarrhythmic (half-life 2 to 3 hrs)
Route: Oral
MOA: Blocks Na+ channel, slows phase 0, Increases action potential duration, Increases effective refractory period
USES: All Types of atrial and ventricular arrythmias
CI: Long QT syndrome
SE:Lupus like syndromes, hypotension, depression, hallucinations, potential for new arrythmias
Note: Active metabolite, cleared renally

Front 2

Quinidine
(Quinidex)

Back 2

DC: Class IA Na+ channel blocker (5-12 hr half-life)
Route: Oral or IV
MOA: Blocks Na+ channel, slows phase 0, Increases action potential duration, Increases Effective Refractory Period
USES: All Types of atrial and ventricular arrythmias
CI: Long QT syndrome
SE: Nausea, Syncope, Cinchonism (deafness, tinnitus, blurred vision, flushing, and tremor), thrombocytic purpura
Note: Derived from cinchona bark,Metabolized in liver, REDUCES CLEARANCE OF DIGOXIN

Front 3

Disopyramide
(Norpace)

Back 3

DC: Class IA Na+ channel blocker
Route:
MOA:Block Na+ channel, slows phase 0, Increases action potential duration, Increases Effective Refractory Period
USES: Treatment of ventricular arrythmias that are refractory to quinidine or procainamide
CI: Long QT syndrome
SE: Pronounced antimuscarinic effects (dry mouth, blurred vision, constipation, urine retention, glaucoma, can worsen heart block & adversely effect sinus node activity

Front 4

Lidocaine
(Xylocaine)

Back 4

DC: Class IB fast Na+ channel blocker (2 hr half life)
Route: IV only
MOA: Blocks voltage gated Na+ channels, rate of dissociation from channel is normal so it doesn't affect normal conduction, Reduce action potential duration, No effect on ERP, Shorten phase 3
Uses: First line treatment of V-Tach during acute MI
CI:
SE: CNS are common
Note: Rapidly metabolized by liver

Front 5

Mexilitine
(Mexitil)

Back 5

DC: Class IB fast Na+ channel blocker
Route: Orally active
MOA: Blocks voltage gated Na+ channels, rate of dissociation from channel is normal so it doesn't affect normal conduction, Reduce action potential duration, No effect on ERP, Shorten phase 3
USES:Chronic treatment of ventricular arrythmias associated with previous MI
CI:
SE: CNS most common
Note: Combination of Mex with B-Blockers is more effective

Front 6

Flecainide
(Tambocor)

Back 6

DC: Class IC slow Na+ channel blocker (16-20 hr half-life)
Route: Oral
MOA: Potent Na+ channel blocker, Slow phase 0, Slows conduction thru ventricle, Slow dissociation of drug from the channel, Increases QRS duration in the EKG
Uses: Effective in both atrial and ventricular arrythmias, Approved only for refractory V-Tach
CI: Negative inotropic effect can aggravate CHF
SE: Proarrythmic, Dizziness, blurred vision, headache, nausea

Front 7

Esmolol

Back 7

DC: Class II B-blocker
Route: IV
MOA: Blockade of B adrenoceptors and reduction in cAMP leading to reduction in both Na+ and Ca++ currents, Suppression of abnormal pacemakers at the nodes, Slows conduction through AV node
Uses: Control ventricular rate in atrial fib, flutter and during excess sympathetic activation
CI: Asthma
SE: Bradycardia, Bronchospasm, Depression, Fatigue
Note: Used exclusively in acute arrythmias

Front 8

Propranolol

Back 8

DC: Class II B-blocker
Route:
MOA: Blockade of B adrenoceptors and reduction in cAMP leading to reductionin both Na+ and Ca++ currents, Suppression of abnormal pacemakers at the nodes, Slows conduction through AV node
Uses: Control ventricular rate in atrial fib, flutter and during excess sympathetic activation
CI: Asthma
SE: Bradycardia, Bronchospasm, Depression, Fatigue
Note: First choice to reduce mortality in patients who have had a previous myocardial infarction

Front 9

Metaprolol

Back 9

DC: Class II B-blocker
Route:
MOA: Blockade of B adrenoceptors and reduction in cAMP leading to reductionin both Na+ and Ca++ currents, Suppression of abnormal pacemakers at the nodes, Slows conduction through AV node
Uses: Control ventricular rate in atrial fib, flutter and during excess sympathetic activation
CI: Asthma
SE: Bradycardia, Bronchospasm, Depression, Fatigue
Note: First choice to reduce mortality in patients who have had a previous myocardial infarction

Front 10

Sotolol
(Betapace)

Back 10

DC: Class III K+ channel blocker
Route:
MOA: Block K+ channels & slow phase 3 repolarization, Prolong action potential duration, Prolong ERP
Uses:
CI:
SE: Ability to cause Torsades, Dyspnea, Dizziness
Note: Also is a B-blocker

Front 11

Ibutilide
(Corvert)

Back 11

DC: Class III K+ channel blocker
Route: IV infusion
MOA: Block K+ channels & slow phase 3 repolarization, Prolong action potential duration, Prolong ERP, Pure K+ channel blocker, Also blocks slow inward Na+ pacemaker currents
Uses: Rapid conversion of A- Fib or Flutter to normal sinus rhythm
CI:
SE:
Note:

Front 12

Dofetilide
(Tikosyn)

Back 12

DC: Class III K+ channel blocker
Route:
MOA: Block K+ channels & slow phase 3 repolarization, Prolong action potential duration, Prolong ERP, Potent inhibitor of delayed rectifier K+ channels
Uses: Approved for conversion and maintenance of normal sinus rhythm in atrial flutter and fib
CI:
SE: Serious arrythmias, Conduction abnormalities
Note:

Front 13

Bretylium

Back 13

DC: Class III K+ channel blocker
Route:
MOA: Block K+ channels & slow phase 3 repolarization, Prolong action potential duration, Prolong ERP, Inhibits neuronal release of catecholamines
Uses: Treating life threatening ventricular arrythmias
CI:
SE:
Note: Older drug, not used much

Front 14

Amiodarone
(Cardarone)

Back 14

DC: Class III K+ channel blocker (10- 100 day half life)
Route: IV
MOA: Block K+ channels & slow phase 3 repolarization, Prolong action potential duration, Prolong ERP, Has I, II, and IV actions
Uses: Severe refractory supraventricular tachycardias
CI:
SE: Thyroid abnormailities, photosensitivity, SMURFISM, pulmonary fibrosis, Hepatitis, Corneal deposits
Note: Antianginal, contains iodine, effects last for weeks

Front 15

Verapamil

Back 15

DC: Class IV Ca++ channel blocker
Route: Orally or IV
MOA: AV nodal conduction is slowed, Slows phase 4 depolarization, PR interval increased, decreases contractility
Uses: Long term control of supraventricular tachycardia
CI: Ischemic hearts
SE: AV block (high doses), Peripheral vasodilation and reflex tachycardia (high doses)
Note: Do NOT take with beta blockers

Front 16

Adenosine

Back 16

DC: Miscellaneous Antiarrythmic (seconds half-life)
Route: IV bolus
MOA: Antagonist at A1 adenosine receptors in the SA, AV nodes, Opening of K+ channels and hyperpolarization, Reduces L-type currents
Uses: Drug of choice in acute supraventricular tachycardia
CI:
SE: Flushing, Hypotension, Chest Pain, Dyspnea
Note:

Front 17

Digoxin

Back 17

DC: Miscellaneous Antiarrythmic (36-48 hrs half-life)
Route:
MOA: Positive inotropic effect, Inhibits Na+/K+ ATPase, Increases intracellular Na+, Increases cardiac contractility, Decreases sympathetic activation, Decreases renin, angiotensin, aldosterone activation
Uses: Persistent symptomatic patients (late stage 3 and 4), Atrial fibrillation, Reduce ventricle size, Slow AV conduction
CI: Renal failure
SE: Antiarrythmic increase plasma levels by displacing Digoxin from binding sites, Decrease renal function predisposes patients to toxicity, Anorexia, Nausea, Vomiting, Headache, Delirium, V-Tach
Note: Also is a B-blocker

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Arrythmia
(Treatment Goals)

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Acute:
Restore cardiac rhythm to normal
Reduce risk of progression to a more severe arrythmia
Chronic:
Prevent recurrence
Reduce hemodynamic consequences of arrythmias

Front 19

Drug Classes

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Class I: Sodium channel blockers
Class II: BETA-blockers
Class III: Potassium channel blockers
Class IV: Calcium channel blockers
Miscellaneous: Drugs that do not fall under an above category