Antiarrhythmic Drugs

Front 1

Class I A

Back 1

Blocks fast Na+ channels (activated)--decreases Vmax
Increased APD and ERP block K channels (delayed rectifier current
Quinidine
Procainamide

Front 2

Quinidine

Back 2

Class 1A
Blocks fast Na+ channels--increased threshold for excitability and decreased automaticity.
alpha block and vagal stimulation
Prolongs QT up to 25%
SE: Nausea, diarrhea, vomiting, cinchonism(GI, tinnitus, ocular dysfunction CNS excitation), hypotension, torsades, thrombocytopenia, drug induced SLE, BM depression

Front 3

Quinidine drug interactions

Back 3

potent inhibitor of CYP2D6
e.g. codeine to morphine metabolism inhibited--less analgesia
hyperkalemia enhances effects
displaces digoxin from tissue binding sites & reduces digoxin and digitoxin clearance
may oppose AchE inhibitors in MG
Phenytoin and phenobarbitol induce Quinidine metabolism--higher dose needed

Front 4

Procainamide

Back 4

Class 1A
Blocks fast Na+
less M block than quinidine and no alpha block--more cardiodepressant
Orally effective, metabolized via N-acetyltransferase.
SE: SLE (30%) w/ slow acetylators, hematotoxicity (thrombo & agranulocytosis), CNS-dizziness and hallucinations, CV effects(torsades)

Front 5

Class 1 B

Back 5

Blocks fast Na+ channels--decreases Vmax
less state dependent than class 1A (can block inactivated channels)
Preference for tissues partly depolarized (slow conducting and hyopoxic/ischemic
Lidocaine
Mexiletine
Tocainide-no longer used-BM aplasia & pulmonary fibrosis
Moricizine--increased mortality, limited use

Front 6

Lidocaine

Back 6

Class 1 B anti-arrhytmics
Blocks fast Na+ channels--decreases Vmax & automacity--prefers ischemic or rapidly driven tissues

Acute IV use--ventricular arrhytmias
Post MI, during open heart surgery or due to cardioversion or digitalis induced arrhytmia
SE: Can worsen heart block or CHF--not given routinely anymore
CNS tox--seizures in OD--nystagmus is an early sign of toxicity
Least cardiotoxic of antiarrhytmics

Front 7

Phenytoin

Back 7

Anti-epileptic drug (class 1B anti-arrhytmic like activity as well)
Blocks Na+--inhibits AP's

Blocks fast Na+ channels decreases Vmax

Antiseizure drug, used occasionally in digitalis OD to reverse AV block
SE: Nystagmus, diplopia, ataxia, hirsutism, gingival hyperplasia, Drug induced SLE

Front 8

Mexiletine

Back 8

similar to lidocaine except orally active
Mexiletine is approved for treating ventricular arrhythmias

Front 9

Class 1 C

Back 9

markedly decreased Vmax due to blockage of fast Na+ channels (His-Purkinje tissue)
No effect on APD
No ANS effects

Flecainide
Encainade-no longer available
Propafenone

Front 10

Flecainide

Back 10

Class 1 C
blocks Na+ current and delayed rectifier K+ current

very long recovery from Na+ channel block

approved for the maintenance of sinus rhythm in patients with supraventricular arrhythmias, including atrial fibrillation, in whom structural heart disease is absent

SE: increased mortality in patients convalescing from MI, heart block, arrhytmias, CHF worsens

Front 11

Class 2

Back 11

Beta Blockers
decreases SA/AV activity by removing SANS stimulus
Decreased slope of phase 4 (diastolic currents of AP pacemakers)
Use: Post MI prophylaxis (e.g. Metoprolol), SVT's

Front 12

Class 3

Back 12

K+ channel blockers (delayed rectifier current)
Increased APD and ERP, especially in Purkinje and Ventricular tissues

Front 13

Amiodarone

Back 13

Has activity of all classes (class 1-4)
Blocks inactivated Na+ channels,beta adrenergics, K+ rectifier and Ca2+ channels

increased APD and ERF in all cardiac tissues
T1/2 30-60 days

structural analog of thyroid hormone

SE: (chronic therapy) Pulmonary fibrosis, corneal deposits, smurf skin, phototoxicity,neuropathy, thyroid hyper/hypofunction, torsades, hepatic necrosis and increased LDL

Front 14

Sotolol

Back 14

Class 3 (K+ & Beta1 block)
two enantionmers--both increase APD and ERP due to K+ channel block
one acts as a Beta 1 blocker to decrease HR and AV conduction
SE: Lassitude, impotence, depression, torsades, AV block

Front 15

Class 4

Back 15

Ca2+ channel blockers
decrease SA and AV pacemaker activity
Decreased slope 4 in pacemakers

SE:GI distress, GERD,polyuria/nocturia,gingival enlargement (44% Nifedipine), dizziness, flushing, hypotension, AV block, inhibition of CYP3A4
CHF-don't use together w/ beta blockers

Front 16

Verapamil

Back 16

Class 4
Ca2+ blocker
Cardioselective-but also block vascular Ca2+-hypotension & reflex tachy
Use: Prophylaxis in reentrant nodal and atrial tachy (not for WPW), avoid in VT, interaction w/ Digitalis

Front 17

Diltiazem

Back 17

Class 4 Ca2+ blocker

Front 18

Nifedipine

Back 18

Class 4 Ca2+ blocker
most potent, no AV block

Front 19

Adenosine

Back 19

Class X
Decrease in SA/AV activity and AV nodal refractory period
Activates A receptors--causes Gi coupled decrease in cAMP--K+ efflux causes membrane hyperpolarization
Use: PSVTs and AV nodal arrhytmias (stops AV node ~less than 5 sec to reset)
IV T1/2 less than 30 sec
SE: Flushing, sedation, dyspnea, bronchospasm (rare), a-fib (rare).
Antagonized by Theophylline

Front 20

Treatment of Torsades

Back 20

Correct hypomagnesimia
Discontinue drugs that prolong QT
Try to shorten APD with drugs (e.g. isoproterenol--Beta agaonist) or electrical pacing

Front 21

Drugs that prolong QT

Back 21

Prolonged QT--torsades
(>450 ms in men, >470 ms in women; normal less or equal to 430)
(blockers of K+, also w/ enhanced inward Na+)

Quinidine
Ibultide
Sotolol
Procainamide
Disopyramide
Dofelitide
Ibultilde
Amiodorone (rare)

Non-cardiac drugs
Azole anti-fungals
Cisapride (5-HT4 agonist--IBS)
Haloperidol
Thioridazine
Ziprasidone
Tricyclic Antidepressants