anti arrhythmic
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ANTIANTI- -ARRHYTHMICARRHYTHMICDRUGSDRUGS
Ma. Janetth B. Serrano, M.D.,DPBA
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ANTI ± ARRHYTHMIC DRUGS
Cardiac Arrhythmias:
- 25% treated with digitalis
- 50% anesthetized patients
- 80% patients with AMI
reduced cardiac output
drugs or nonpharmacologic :
- pacemaker, cardioversion, catheter
ablation, surgery
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ELECTRO- PHYSIOLOGY
OF
N ORMAL
CARDIAC
RHYTHM
SA node
ANTI ± ARRHYTHMIC DRUGS
AV node
ATRIA
His-Purkinje System
VENTRICLES
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IO N IC B ASIS OF MEM BRA N E ELECTRICAL ACTIVITY
T ransmembrane potential of cardiac cellsis determined by the concentrations of the ff. ions: ±
Sodium, Potassium, CalciumT he movement of these ions producescurrents that form the basis of the cardiacaction potential
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PHASES OF ACTIO N POTE N TIAL
Phase 0>R apid depolarization>O pening fast Na+channels Na+ rushes
in depolarization
ANTI ± ARRHYTHMIC DRUGS
Phase 1
>Limited depolarization>Inactivation of fastNa+ channels Na+ion conc equalizes> K+ efflux & Cl- influx
Phase 2
>Plateau Stage>Cell less permeable to Na+>Ca++ influx through slow
Ca++ channels>K+ begins to leave cell
Phase 3>R apid repolarization>Na+ gates closed>K+ efflux>Inactivation of slow
Ca++ channels
Phase 4>R esting Membrane Potential>High K+ efflux>Ca++ influx
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FACTORS PRECIPITATI N G CARDIAC ARRHYTHMIAS :
1. Ischemiap H & electrolyte abnormalities80% ± 9 0% asstd with MI
2. Excessive myocardial fiber stretch/ scarred/diseased cardiac tissue
3. Excessive discharge or sensitivity to autonomictransmitters4. Excessive exposure to foreign chemicals & toxic
substances20% - 50% asstd with General Anesthesia10% - 20% asstd with Digitalis toxicity
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Supraventricular:- Atrial T achycardia- Paroxysmal
T achycardia
- Multifocal AtrialT achycardia- Atrial Fibrillation- Atrial Flutter
V entricular:- W olff-Parkinson-
W hite (preexcitationsyndrome)
- Ventricular T achycardia
- Ventricular Fibrillation- Premature Ventricular
Contraction
ANTI ± ARHYTHMIC DRUGS
ARRHYTHMIAS :
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CLASS I: Sodium Channel Blocking Drugs
IA - lengthen AP duration- Intermediate interaction with Na+ channels- Q uinidine, P rocainamide, D isopyramide
IB - shorten AP duration- rapid interaction with Na+ channels- L idocaine, M exiletene, T ocainide, P henytoin
IC - no effect or minimal AP duration- slow interaction with Na+ channels- F lecainide, P ropafenone, M oricizine
ANTI ± ARRHYTHMIC DRUGS
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Increase AV nodal conductionIncrease P R intervalProlong AV refractorinessReduce adrenergic activityP ropranolol, E smolol, M etoprolol,S otalol
CLASS II: BE T A-B LO CKING AGEN T S
ANTI ± ARRHYTHMIC DRUGS
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Prolong effective refractory period byprolonging Action Potential ± A miodarone - Ib utilide
± Bretylium - D ofetilide ± S otalol
ANTI ± ARRHYTHMIC DRUGS
CLASS III: P OT ASSIUM C HANNE L BLO CKERS
ANTI ± ARRHYTHMIC DRUGS
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Miscellaneous:ADE N OSI N E inhibits AV conduction &
increases AV refractory period
MAG N ESIUM Na+/ K+ A T Pase, Na+, K+,Ca++ channels
POTASSIUM normalize K+ gradients
ANTI ± ARRHYTHMIC DRUGS
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Depress pacemaker rateDepress conduction & excitabilitySlows repolarization & lengthens AP duration
due to K+ channel blockade with reduction of
repolarizing outward current reduce maximumreentry frequency slows tachycardia(+) alpha adrenergic blocking properties vasodilatation & reflex SA node rate
ANTI ± ARRHYTHMIC DRUGS ANTI ± ARRHYTHMIC DRUGS
CLASS I: Sodium Channel Blocking Drugs
CLASS IA : Q UI N IDI N E
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CLASS I: S ODIUM C HANNE L BLO CKERS
P harmacokinetics: ± Oral rapid GI absorption
± 80% plasma protein binding ± 20% excreted unchanged in the urine
enhanced by acidity ± t½ = 6 hours ± Parenteral hypotension
D osage: 0.2 to 0.6 gm 2-4X a day
ANTI ± ARRHYTHMIC DRUGS
CLASS IA : Q UI N IDI N E
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CLASS I: S ODIUM C HANNE L BLO CKERS
T herapeutic U ses: ± Atrial flutter & fibrillation ± Ventricular tachycardia ± IV treatment of malaria
D rug I nteraction: ± Increases digoxin plasma levels
ANTI ± ARRHYTHMIC DRUGS
CLASS IA : Q UI N IDI N E
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CLASS I: S ODIUM C HANNE L BLO CKERS
T oxicity: ± Antimuscarinic actions inh. vagal effects ± Quinidine syncope (lightheadedness, fainting) ± Ppt. arrhythmia or asystole ± Depress contractility & BP ± W idening Q RS duration ± Diarrhea , nausea, vomiting ± Cinchonism ( HA, dizziness, tinnitus) ± Rare: rashes, fever, hepatitis, thrombocytopenia,etc
ANTI ± ARRHYTHMIC DRUGS
CLASS IA : Q UI N IDI N E
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Less effective in suppressing abnormal ectopicpacemaker activity
More effective Na+ channel blockers indepolarized cells
Less prominent antimuscarinic action
(+) ganglionic blocking properties PV Rhypotension (severe if rapid IV or with severe LVdysfunction)
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : PROCAI N AMIDE
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PHARMACOKI N ETICS :
Oral, IV, IMN-acetylprocainamide (NAPA) major
metaboliteMetabolism: hepaticElimination: renalt½ = 3 to 4 hrs.
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : PROCAI N AMIDE
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D osage:Loading IV ± 1 2 mg/kg at 0.3 mg/kg/min or lessrapidlyMaintenance ± 2 to 5 mg/min
T herapeutic U se:2nd DOC in most CCU for the treatment of sustained ventricular arrhythmias asstd. with MI
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : PROCAI N AMIDE
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T oxicity:- ppt. new arrhythmias- LE-like syndrome
- pleuritis, pericarditis, parenchymalpulmonary disease- ANA- nausea, D HA, rash, fever, hepatitis,
agranulocytosis
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : PROCAI N AMIDE
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More marked cardiac antimuscarinic effectsthan quinidine slows AV conduction
P harmacokinetics:- oral administration- extensive protein binding- t½ = 6 to 8 hrs
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : DISOPYRAMIDE
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D osage : 1 50 mg T ID up to 1 gm/dayT herapeutic U se : Ventricular arrhythmiasT oxicity:
- negative inotropic action ( HF withoutprior myocardial dysfunction)- Urinary retention, dry mouth, blurredvision, constipation, worsening glaucoma
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : DISOPYRAMIDE
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Approved only in serious ventricular arrhythmiasBroad spectrum of action on theVery effective Na+ channel blocker but low affinityfor activated channelsMarkedly lengthens AP by blocking also K+channelsW eak Ca++ channel blocker Noncompetetive inhibitor of beta adrenoceptorsPowerful inhibitor of abnormal automaticity
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : AMIODARO N E
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Slows sinus rate & AV conductionMarkedly prolongs the Q T intervalProlongs Q RS duration
atrial, AV nodal & ventricular refractoryperiods
Antianginal effects ± due to noncompetetive & blocking property and block Ca++influx in vascular sm.m.
Perivascular dilatation - blocking propertyand Ca++ channel-inhibiting effects
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : AMIODARO N E
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P harmacokinetics:> t½ = 13 to 1 03 days> effective plasma conc: 1- 2 g/ml
D osage: - Loading ± 0.8 to 1. 2 g daily
- Maintenance ± 200 to 4 00 mg dailyD rug I nteraction: reduce clearance of warfarin,theophylline, quinidine, procainamide, flecainideT herapeutic U se: Supraventricular & Ventricular
arrhythmias
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : AMIODARO N E
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T oxicity:
- fatal pulmonary fibrosis- yellowish-brown microcrystals corneal deposits- photodermatitis- grayish blue discoloration
- paresthesias, tremor, ataxia & headaches- hypo - / hyperthyroidism- Symptomatic bradycardia or heart block- Ppt. heart failure- Constipation, hepatocellular necrosis, inflam¶n, fibrosis,
hypotension
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IA : AMIODARO N E
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Intravenous route onlyArrhythmias asstd with MIPotent abnormal cardiac activity suppressor Rapidly act exclusively on Na+ channels
Shorten AP, prolonged diastole extends timeavailable for recoverySuppresses electrical activity of DEP OL ARIZED,ARRHY T HMOGENIC tissues only
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS I B: LIDOCAI N E
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Pharmacokinetics:- Extensive first-pass hepatic metabolism- t½ = 1 to 2 hrs
Dosages: loading- 1 50 to 200 mgmaintenance- 2-4 mg
Drug Interaction:propranolol, cimetidine ± reduce clearance
T herapeutic Use:DOC for suppression of recurrences of ventricular tachycardia & fibrillation in the firstfew days after AMI.
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS I B: LIDOCAI N E
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T oxicity: ± Ppt. SA nodal standstill or worsen impaired
conduction ± Exacerbates ventricular arrhythmias
± Hypotension in HF ± Neurologic: paresthesias, tremor, nausea,
lightheadedness, hearing disturbances,slurred speech, convulsions
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS I B: LIDOCAI N E
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Congeners of lidocaineOral route - resistant to first-pass hepaticmetabolismT ptic use: ventricular arrhythmiasElimination t½ = 8 to 20 hrs
Dosage: Mexiletene ± 6 00 to 1 200 mg/dayT ocainide ± 8 00 to 2400 mg/day
S/E: tremors, blurred vision, lethargy, nausea,rash, fever, agranulocytosis
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS I B: TOCAI N IDE & MEXILETE N E
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Anti-convulsant with anti-arrhythmic propertiesSuppresses ectopic pacemaker activityUseful in digitalis-induced arrhythmiaExtensive, saturable first-pass hepatic metabolismHighly protein boundT oxicity: ataxia, nystagmus, mental confusion,
serious dermatological & BM reactions,hypotension, gingival hyperplasia
D/I: Quinidine, Mexiletene, Digitoxin, Estrogen,T heophyllin, Vitamin D
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS I B: PHE N YTOI N
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Potent blocker of Na+ & K+ channelsNo antimuscarinic effectsUsed in patients with supraventricular arrhythmiasEffective in PVC¶sHepatic metabolism & renal eliminationDosage: 1 00 to 200 mg bid
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IC : FLECAI N IDE
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(+) weak -blocking activityPotency § flecainideAverage elim. t½ = 5 to 7 hrs.Dosage: 4 50 ± 9 00 mg T IDT ptic use: supraventricular arrhythmiasAdv. effects: metallic taste, constipation,arrhythmia exacerbation
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IC : PROPAFE N O N E
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Antiarrhythmic phenothiazine derivativeUsed in ventricular arrhythmiasPotent Na+ channel blocker
Donot prolong AP durationDosage: 200 to 3 00 mg orally tidAdv. effects: dizziness, nausea
ANTI ± ARHYTHMIC DRUGS
CLASS I: S ODIUM C HANNE L BLO CKERS
CLASS IC : MORICIZI N E
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AV nodal conduction time ( P R interval)
Prolong AV nodal refractoriness ± Useful in terminating reentrant arrhythmias that
involve the AV node & in controlling ventricular response in AF & A.fib.
Depresses phase 4 slows recovery of cells, slows
conduction & decrease automaticityReduces HR , decrease IC Ca 2+ overload & inhibit after depolarization automaticityPrevent recurrent infarction & sudden death inpatients recovering from AMI
ANTI ± ARHYTHMIC DRUGS
CLASS II: BE TA AD REN OCEP T OR BLO CKERS
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³ membrane stabilizing effect´Exert Na+ channel blocking effect at high dosesAcebutolol, metoprolol, propranolol, labetalol,pindolol
³ intrinsic sympathetic activity´
Less antiarrhythmic effectAcebutolol, celiprolol, carteolol, labetalol, pindolol
T herapeutic indications:Supraventricular & ventricular arrhythmias
hypertension
ANTI ± ARHYTHMIC DRUGS
CLASS II: BE TA AD REN OCEP T OR BLO CKERS
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P ropranolol ± (+) MSAA ce b utolol ± as effective as quinidine in
suppressing ventricular ectopicbeats
E smolol - short acting hence usedprimarily for intra-operative &other acute arrhythmias
S otalol ± has K+ channel blockingactions (class III)
ANTI ± ARHYTHMIC DRUGS
CLASS II: BE TA AD REN OCEP T OR BLO CKERS
Specific agents:
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Antihypertensive
Interferes with neuronal release of catecholaminesW ith direct antiarrhythmic propertiesLengthens ventricular AP duration & effective
refractory periodMarkedly strength of electrical stimulationneeded to induce V.fib. & delays onset of fibrillation after acute coronary ligation
(+) inotropic action
ANTI ± ARHYTHMIC DRUGS
CLASS III: P OTASSIUM C HANNE L BLO CKERS
BRETYLIUM
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Intravenous administrationDosage: 5 mg/kgT ptic Use: ventricular fibrillationIn emergency setting, during attemptedresuscitation from ventricular fibrillation whenlidocaine & cardioversion have failedS/E: postural hypotension***
ppt. ventricular arrhythmianausea & vomiting
ANTI ± ARHYTHMIC DRUGS
CLASS III: P OTASSIUM C HANNE L BLO CKERS
BRETYLIUM
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Nonselective beta-blocker that also slowsrepolarization & prolongs AP durationEffective antiarrhythmic agentUsed in supraventricular & ventricular arrhythmias in pediatric age groupRenal excretionDosage: 8 0 ± 3 20 mg bidT oxicity: torsades de pointes
beta-blockade symptoms
ANTI ± ARHYTHMIC DRUGS
CLASS III: P OTASSIUM C HANNE L BLO CKERS
SOTALOL
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Slows repolarizationProlong cardiac action potentialsMOA: > enhance inward Na+ current
> by blocking I kr-
> bothroutes: Oral, IV (1 mg over 1 0min)Clin. Uses: atrial flutter, atrial fibrillationT oxicity: T orsades de pointes
ANTI ± ARHYTHMIC DRUGS
CLASS III: P OTASSIUM C HANNE L BLO CKERS
I BUTILIDE
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A potential I kr- blocker Dosage: 250 -500 ug bidClin. Uses: Atrial flutter & fibrillation
Renal excretionT oxicity: T orsade de pointes
ANTI ± ARHYTHMIC DRUGS
CLASS III: P OTASSIUM C HANNE L BLO CKERS
DOFETILIDE
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Oral administration 20% bioavailabilityt½ = 7 hrsLiver metabolismDosage:IV: 5-10 mg every 4-6 hrs or infusion of 0.4 ug/kg/min
Oral: 1 20 -64 0 mg daily, divided in 3-4 dosesT ptic use: SV T , AF, atrial fib, ventricular arrhythmiasT oxicity: AV block, can ppt. sinus arrest
constipation, lassitude, nervousness,peripheral edema
ANTI ± ARHYTHMIC DRUGS
CLASS IV: CA LCIUM C HANNE L BLO CKERS
VERAPAMIL
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Similar efficacy to verapamil insupraventricular arrhythmias & ratecontrol in atrial fibrillationBepridil
AP & Q T prolonging action ventricular arrhythmias but may ppt. torsade de pointesRarely used primarily to control refractoryangina
ANTI ± ARHYTHMIC DRUGS
CLASS IV: CA LCIUM C HANNE L BLO CKERS
DILTIAZEM & B EPRIDIL
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Indirectly alters autonomic outflow byincreasing parasympathetic tone &decreasing sympathetic tone
Results in decreased conduction time &increased refractory period in the AVnode
ANTI ± ARHYTHMIC DRUGS
MISCE LLANE OUS AN T IARRHY T HMIC AGEN T S:
DIGITALIS
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A nucleoside that occurs naturally in the bodyt½ § 1 0 secondsMOA: enhances K+ conductance & inhibitscAMP-induced Ca++ influx results in marked
hyperpolarization & suppression of Ca++-dependent APIV bolus: directly inhibits AV nodal conduction &
AV nodal refractory period
ANTI ± ARHYTHMIC DRUGS
MISCE LLANE OUS AN T IARRHY T HMIC AGEN T S:
ADE N OSI N E
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DOC for prompt conversion of paroxysmal SV T to sinus rhythm due to its high efficacy & veryshort duration of actionDosage: 6-1 2 mg IV bolusD/I:
theophylline, caffeine ± adenosine receptor blockersDipyridamole ± adenosine uptake inhibitor
T oxicity: flushing, S OB or chest burning, atrialfibrillation, headache, hypotension, nausea,paresthesia
ANTI ± ARHYTHMIC DRUGS
MISCE LLANE OUS AN T IARRHY T HMIC AGEN T S:
ADE N OSI N E
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Effective in patients with recurrentepisodes of torsades de pointes (MgS O 4 1to 2 g IV) & in digitalis-induced arrhythmiaMOA: unknown influence Na+/ K+
AT Pase, Na+ channels, certain K+ andCa++ channels
ANTI ± ARHYTHMIC DRUGS
MISCE LLANE OUS AN T IARRHY T HMIC AGEN T S:
MAG N ESIUM
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T herapy directed toward normalizing K+ gradients &pools in the bodyEffects of increasing serum K+:1. resting potential depolarizing action2. membrane potential stabilizing action
Hypokalemia:
risk of early & delayed afterdepolarizationectopic pacemaker activity esp if (+) digitalis
Hyperkalemia:Depression of ectopic pacemakersSlowing of conduction
ANTI ± ARHYTHMIC DRUGS
MISCE LLANE OUS AN T IARRHY T HMIC AGEN T S:
POTASSIUM