Editd anti arrhythmic - Presentation Transcript
Editd anti arrhythmic - Presentation Transcript
1. ANTI-ARRHYTHMIC DRUGS Ma. Janetth B. Serrano, M.D.,DPBA
2.
o Cardiac Arrhythmias:
▪ 25% treated with digitalis
▪ 50% anesthetized patients
▪ 80% patients with AMI
o reduced cardiac output
o drugs or nonpharmacologic :
o - pacemaker, cardioversion, catheter ablation, surgery
ANTI – ARRHYTHMIC DRUGS
3. ELECTRO-PHYSIOLOGY OF NORMAL CARDIAC RHYTHM
o SA node
AV node ATRIA His-Purkinje System VENTRICLES ANTI – ARRHYTHMIC DRUGS
4. IONIC BASIS OF MEMBRANE ELECTRICAL ACTIVITY
o Transmembrane potential of cardiac cells is determined by the concentrations of the ff. ions:
▪ Sodium, Potassium, Calcium
o The movement of these ions produces currents that form the basis of the cardiac action potential
ANTI – ARRHYTHMIC DRUGS
5. PHASES OF ACTION POTENTIAL
o Phase 0
o >Rapid depolarization
o >Opening fast Na+
o channels -> Na+ rushes in ->depolarization
Phase 1 >Limited depolarization >Inactivation of fast Na+ 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 >Rapid repolarization >Na+ gates closed >K+ efflux >Inactivation of slow Ca++ channels Phase 4 >Resting Membrane Potential >High K+ efflux >Ca++ influx ANTI – ARRHYTHMIC DRUGS
6. MECHANISMS OF ARRHYTHMIA
o ARRHYTHMIA – absence of rhythm
o DYSRRHYTHMIA – abnormal rhythm
ARRHYTHMIAS result from:
o Disturbance in Impulse Formation
o 2. Disturbance in Impulse Conduction
o Block results from severely depressed conduction
o Re-entry or circus movement / daughter impulse
ANTI – ARRHYTHMIC DRUGS
7. FACTORS PRECIPITATING CARDIAC ARRHYTHMIAS:
o 1. Ischemia
▪ pH & electrolyte abnormalities
▪ 80% – 90% asstd with MI
o 2. Excessive myocardial fiber stretch/ scarred/ diseased cardiac tissue
o 3. Excessive discharge or sensitivity to autonomic transmitters
o 4. Excessive exposure to foreign chemicals & toxic substances
▪ 20% - 50% asstd with General Anesthesia
▪ 10% - 20% asstd with Digitalis toxicity
ANTI – ARRHYTHMIC DRUGS
8.
o Supraventricular:
o - Atrial Tachycardia
o - Paroxysmal Tachycardia
o Multifocal Atrial Tachycardia
o - Atrial Fibrillation
o - Atrial Flutter
o Ventricular:
o Wolff-Parkinson-White (preexcitation syndrome)
o Ventricular Tachycardia
o Ventricular Fibrillation
o Premature Ventricular Contraction
ARRHYTHMIAS: ANTI – ARRHYTHMIC DRUGS
9. CLASS I: Sodium Channel Blocking Drugs
o IA - lengthen AP duration
▪ - Intermediate interaction with Na+ channels
▪ - Quinidine, Procainamide, Disopyramide
o IB - shorten AP duration
o - rapid interaction with Na+ channels
o - Lidocaine, Mexiletene, Tocainide, Phenytoin
o IC - no effect or minimal AP duration
o - slow interaction with Na+ channels
o - Flecainide, Propafenone, Moricizine
ANTI – ARRHYTHMIC DRUGS
10.
o Increase AV nodal conduction
o Increase PR interval
o Prolong AV refractoriness
o Reduce adrenergic activity
o Propranolol, Esmolol, Metoprolol, Sotalol
CLASS II: BETA-BLOCKING AGENTS ANTI – ARRHYTHMIC DRUGS
11.
o Prolong effective refractory period by prolonging Action Potential
▪ Amiodarone - Ibutilide
▪ Bretylium - Dofetilide
▪ Sotalol
CLASS III: POTASSIUM CHANNEL BLOCKERS ANTI – ARRHYTHMIC DRUGS
12. CLASS IV: CALCIUM CHANNEL BLOCKERS
o Blocks cardiac calcium currents
o -> slow conduction
o -> increase refractory period
o *esp. in Ca++ dependent tissues (i.e. AV node)
o Verapamil, Diltiazem, Bepridil
ANTI – ARRHYTHMIC DRUGS
13. Miscellaneous:
o ADENOSINE -> inhibits AV conduction & increases AV refractory period
o DIGITALIS -> Indirectly alters autonomic outflow
o MAGNESIUM -> Na+/K+ ATPase, Na+, K+, Ca++ channels
o POTASSIUM -> normalize K+ gradients
ANTI – ARRHYTHMIC DRUGS
14.
o Depress pacemaker rate
o Depress conduction & excitability
o Slows repolarization & lengthens AP duration
o -> due to K+ channel blockade with reduction of repolarizing outward current -> reduce maximum reentry frequency -> slows tachycardia
o (+) alpha adrenergic blocking properties -> vasodilatation & reflex ↑ SA node rate
CLASS I: Sodium Channel Blocking Drugs CLASS IA: QUINIDINE ANTI – ARRHYTHMIC DRUGS
15. CLASS I: SODIUM CHANNEL BLOCKERS
o Pharmacokinetics:
▪ Oral -> rapid GI absorption
▪ 80% plasma protein binding
▪ 20% excreted unchanged in the urine -> enhanced by acidity
▪ t½ = 6 hours
▪ Parenteral -> hypotension
o Dosage: 0.2 to 0.6 gm 2-4X a day
CLASS IA: QUINIDINE ANTI – ARRHYTHMIC DRUGS
16. CLASS I: SODIUM CHANNEL BLOCKERS
o Therapeutic Uses:
▪ Atrial flutter & fibrillation
▪ Ventricular tachycardia
▪ IV treatment of malaria
o Drug Interaction:
▪ Increases digoxin plasma levels
CLASS IA: QUINIDINE ANTI – ARRHYTHMIC DRUGS
17. CLASS I: SODIUM CHANNEL BLOCKERS
o Toxicity:
▪ Antimuscarinic actions -> inh. vagal effects
▪ Quinidine syncope (lightheadedness, fainting)
▪ Ppt. arrhythmia or asystole
▪ Depress contractility & ↓ BP
▪ Widening QRS duration
▪ Diarrhea , nausea, vomiting
▪ Cinchonism (HA, dizziness, tinnitus)
▪ Rare: rashes, fever, hepatitis, thrombocytopenia,etc
CLASS IA: QUINIDINE ANTI – ARRHYTHMIC DRUGS
18.
o Less effective in suppressing abnormal ectopic pacemaker activity
o More effective Na+ channel blockers in depolarized cells
o Less prominent antimuscarinic action
o (+) ganglionic blocking properties -> ↓PVR -> hypotension (severe if rapid IV or with severe LV dysfunction)
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: PROCAINAMIDE ANTI – ARRHYTHMIC DRUGS
19.
o PHARMACOKINETICS:
o Oral, IV, IM
o N-acetylprocainamide (NAPA) -> major metabolite
o Metabolism: hepatic
o Elimination: renal
o t½ = 3 to 4 hrs.
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: PROCAINAMIDE ANTI – ARRHYTHMIC DRUGS
20.
o Dosage:
o Loading IV – 12 mg/kg at 0.3 mg/kg/min or less rapidly
o Maintenance – 2 to 5 mg/min
o Therapeutic Use:
o 2 nd DOC in most CCU for the treatment of sustained ventricular arrhythmias asstd. with MI
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: PROCAINAMIDE ANTI – ARRHYTHMIC DRUGS
21.
o Toxicity:
o - ppt. new arrhythmias
o - LE-like syndrome
o - pleuritis, pericarditis, parenchymal pulmonary disease
o - ↑ ANA
o - nausea, DHA, rash, fever, hepatitis, agranulocytosis
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: PROCAINAMIDE ANTI – ARRHYTHMIC DRUGS
22.
o More marked cardiac antimuscarinic effects than quinidine -> slows AV conduction
o Pharmacokinetics:
o - oral administration
o - extensive protein binding
o - t½ = 6 to 8 hrs
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: DISOPYRAMIDE ANTI – ARRHYTHMIC DRUGS
23.
o Dosage : 150 mg TID up to 1 gm/day
o Therapeutic Use : Ventricular arrhythmias
o Toxicity:
o - negative inotropic action (HF without prior myocardial dysfunction)
o - Urinary retention, dry mouth, blurred vision, constipation, worsening glaucoma
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: DISOPYRAMIDE ANTI – ARRHYTHMIC DRUGS
24.
o Approved only in serious ventricular arrhythmias
o Broad spectrum of action on the
o Very effective Na+ channel blocker but low affinity for activated channels
o Markedly lengthens AP by blocking also K+ channels
o Weak Ca++ channel blocker
o Noncompetetive inhibitor of beta adrenoceptors
o Powerful inhibitor of abnormal automaticity
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: AMIODARONE ANTI – ARRHYTHMIC DRUGS
25.
o Slows sinus rate & AV conduction
o Markedly prolongs the QT interval
o Prolongs QRS duration
o ↑ atrial, AV nodal & ventricular refractory periods
o Antianginal effects – due to noncompetetive α & β blocking property and block Ca++ influx in vascular sm.m.
o Perivascular dilatation - α blocking property and Ca++ channel-inhibiting effects
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: AMIODARONE ANTI – ARRHYTHMIC DRUGS
26.
o Pharmacokinetics:
o > t ½ = 13 to 103 days
o > effective plasma conc: 1-2 μ g/ml
o Dosage: - Loading – 0.8 to 1.2 g daily
o - Maintenance – 200 to 400 mg daily
o Drug Interaction: reduce clearance of warfarin, theophylline, quinidine, procainamide, flecainide
o Therapeutic Use: Supraventricular & Ventricular arrhythmias
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: AMIODARONE ANTI – ARRHYTHMIC DRUGS
27.
o Toxicity:
o - fatal pulmonary fibrosis
o - yellowish-brown microcrystals corneal deposits
o - photodermatitis
o - grayish blue discoloration
o - paresthesias, tremor, ataxia & headaches
o - hypo - / hyperthyroidism
o - Symptomatic bradycardia or heart block
o - Ppt. heart failure
o - Constipation, hepatocellular necrosis, inflam’n, fibrosis, hypotension
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IA: AMIODARONE ANTI – ARRHYTHMIC DRUGS
28.
o Intravenous route only
o Arrhythmias asstd with MI
o Potent abnormal cardiac activity suppressor
o Rapidly act exclusively on Na+ channels
o Shorten AP, prolonged diastole -> extends time available for recovery
o Suppresses electrical activity of DEPOLARIZED, ARRHYTHMOGENIC tissues only
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IB: LIDOCAINE ANTI – ARRHYTHMIC DRUGS
29.
o Pharmacokinetics:
o - Extensive first-pass hepatic metabolism
▪ - t ½ = 1 to 2 hrs
o Dosages: loading- 150 to 200 mg
o maintenance- 2-4 mg
o Drug Interaction:
o propranolol, cimetidine – reduce clearance
o Therapeutic Use:
o DOC for suppression of recurrences of ventricular tachycardia & fibrillation in the first few days after AMI.
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IB: LIDOCAINE ANTI – ARRHYTHMIC DRUGS
30.
o Toxicity:
▪ Ppt. SA nodal standstill or worsen impaired conduction
▪ Exacerbates ventricular arrhythmias
▪ Hypotension in HF
▪ Neurologic: paresthesias, tremor, nausea, lightheadedness, hearing disturbances, slurred speech, convulsions
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IB: LIDOCAINE ANTI – ARRHYTHMIC DRUGS
31.
o Congeners of lidocaine
o Oral route - resistant to first-pass hepatic metabolism
o Tptic use: ventricular arrhythmias
o Elimination t ½ = 8 to 20 hrs
o Dosage: Mexiletene – 600 to 1200 mg/day
o Tocainide – 800 to 2400 mg/day
o S/E: tremors, blurred vision, lethargy, nausea, rash, fever, agranulocytosis
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IB: TOCAINIDE & MEXILETENE ANTI – ARRHYTHMIC DRUGS
32.
o Anti-convulsant with anti-arrhythmic properties
o Suppresses ectopic pacemaker activity
o Useful in digitalis-induced arrhythmia
o Extensive, saturable first-pass hepatic metabolism
o Highly protein bound
o Toxicity: ataxia, nystagmus, mental confusion, serious dermatological & BM reactions, hypotension, gingival hyperplasia
o D/I: Quinidine, Mexiletene, Digitoxin, Estrogen, Theophyllin, Vitamin D
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IB: PHENYTOIN ANTI – ARRHYTHMIC DRUGS
33.
o Potent blocker of Na+ & K+ channels
o No antimuscarinic effects
o Used in patients with supraventricular arrhythmias
o Effective in PVC’s
o Hepatic metabolism & renal elimination
o Dosage: 100 to 200 mg bid
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IC: FLECAINIDE ANTI – ARRHYTHMIC DRUGS
34.
o (+) weak β -blocking activity
o Potency ≈ flecainide
o Average elim. t½ = 5 to 7 hrs.
o Dosage: 450 – 900 mg TID
o Tptic use: supraventricular arrhythmias
o Adv. effects: metallic taste, constipation, arrhythmia exacerbation
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IC: PROPAFENONE ANTI – ARRHYTHMIC DRUGS
35.
o Antiarrhythmic phenothiazine derivative
o Used in ventricular arrhythmias
o Potent Na+ channel blocker
o Donot prolong AP duration
o Dosage: 200 to 300 mg orally tid
o Adv. effects: dizziness, nausea
CLASS I: SODIUM CHANNEL BLOCKERS CLASS IC: MORICIZINE ANTI – ARRHYTHMIC DRUGS
36.
o ↑ AV nodal conduction time (↑ PR interval)
o Prolong AV nodal refractoriness
▪ Useful in terminating reentrant arrhythmias that involve the AV node & in controlling ventricular response in AF & A.fib.
o Depresses phase 4 -> slows recovery of cells, slows conduction & decrease automaticity
o Reduces HR, decrease IC Ca 2+ overload & inhibit after depolarization automaticity
o Prevent recurrent infarction & sudden death in patients recovering from AMI
CLASS II: BETA ADRENOCEPTOR BLOCKERS ANTI – ARRHYTHMIC DRUGS
37.
o “ membrane stabilizing effect”
▪ Exert Na+ channel blocking effect at high doses
▪ Acebutolol, metoprolol, propranolol, labetalol, pindolol
o “ intrinsic sympathetic activity”
▪ Less antiarrhythmic effect
▪ Acebutolol, celiprolol, carteolol, labetalol, pindolol
o Therapeutic indications:
▪ Supraventricular & ventricular arrhythmias
▪ hypertension
CLASS II: BETA ADRENOCEPTOR BLOCKERS ANTI – ARRHYTHMIC DRUGS
38.
o Propranolol – (+) MSA
o Acebutolol – as effective as quinidine in suppressing ventricular ectopic beats
o Esmolol - short acting hence used primarily for intra-operative & other acute arrhythmias
o Sotalol – has K+ channel blocking actions (class III)
CLASS II: BETA ADRENOCEPTOR BLOCKERS Specific agents: ANTI – ARRHYTHMIC DRUGS
39.
o Drugs that prolong effective refractory period by prolonging action potential
o Prolong AP by blocking K+ channels in cardiac muscle ( ↑ inward current through Na+ & Ca++ channels)
o Quinidine & Amiodarone -> prolong AP duration
o Bretylium & Sotalol -> prolong AP duration & refractory period
o Ibutilide & Dofetilide -> “pure” class III agents
o Reverse use-dependence
CLASS III: POTASSIUM CHANNEL BLOCKERS ANTI – ARRHYTHMIC DRUGS
40.
o Antihypertensive
o Interferes with neuronal release of catecholamines
o With direct antiarrhythmic properties
o Lengthens ventricular AP duration & effective refractory period
o Markedly ↑ strength of electrical stimulation needed to induce V.fib. & delays onset of fibrillation after acute coronary ligation
o (+) inotropic action
CLASS III: POTASSIUM CHANNEL BLOCKERS BRETYLIUM ANTI – ARRHYTHMIC DRUGS
41.
o Intravenous administration
o Dosage: 5 mg/kg
o Tptic Use: ventricular fibrillation
o In emergency setting, during attempted resuscitation from ventricular fibrillation when lidocaine & cardioversion have failed
o S/E: postural hypotension***
o ppt. ventricular arrhythmia
o nausea & vomiting
CLASS III: POTASSIUM CHANNEL BLOCKERS BRETYLIUM ANTI – ARRHYTHMIC DRUGS
42.
o Nonselective beta-blocker that also slows repolarization & prolongs AP duration
o Effective antiarrhythmic agent
o Used in supraventricular & ventricular arrhythmias in pediatric age group
o Renal excretion
o Dosage: 80 – 320 mg bid
o Toxicity: torsades de pointes
o beta-blockade symptoms
CLASS III: POTASSIUM CHANNEL BLOCKERS SOTALOL ANTI – ARRHYTHMIC DRUGS
43.
o Slows repolarization
o Prolong cardiac action potentials
o MOA: > enhance inward Na+ current
o > by blocking I kr-
o > both
o routes: Oral, IV (1 mg over 10min)
o Clin. Uses: atrial flutter, atrial fibrillation
o Toxicity: Torsades de pointes
CLASS III: POTASSIUM CHANNEL BLOCKERS IBUTILIDE ANTI – ARRHYTHMIC DRUGS
44.
o A potential I kr- blocker
o Dosage: 250-500 ug bid
o Clin. Uses: Atrial flutter & fibrillation
o Renal excretion
o Toxicity: Torsade de pointes
CLASS III: POTASSIUM CHANNEL BLOCKERS DOFETILIDE ANTI – ARRHYTHMIC DRUGS
45.
o Blocks both activated & inactivated calcium channels
o Prolongs AV nodal conduction & effective refractory period
o Suppress both early & delayed afterdepolarizations
o May antagonize slow responses in severely depolarized tissues
o Peripheral vasodilatation -> HPN & vasospastic disorders
CLASS IV: CALCIUM CHANNEL BLOCKERS VERAPAMIL ANTI – ARRHYTHMIC DRUGS
46.
o Oral administration -> 20% bioavailability
o t ½ = 7 hrs
o Liver metabolism
o Dosage:
o IV: 5-10 mg every 4-6 hrs or infusion of 0.4 ug/kg/min
o Oral: 120-640 mg daily, divided in 3-4 doses
o Tptic use: SVT, AF, atrial fib, ventricular arrhythmias
o Toxicity: AV block, can ppt. sinus arrest
o constipation, lassitude, nervousness, peripheral edema
CLASS IV: CALCIUM CHANNEL BLOCKERS VERAPAMIL ANTI – ARRHYTHMIC DRUGS
47.
o Similar efficacy to verapamil in supraventricular arrhythmias & rate control in atrial fibrillation
o Bepridil
▪ AP & QT prolonging action-> ventricular arrhythmias but may ppt. torsade de pointes
▪ Rarely used -> primarily to control refractory angina
CLASS IV: CALCIUM CHANNEL BLOCKERS DILTIAZEM & BEPRIDIL ANTI – ARRHYTHMIC DRUGS
48.
o Indirectly alters autonomic outflow by increasing parasympathetic tone & decreasing sympathetic tone
o Results in decreased conduction time & increased refractory period in the AV node
MISCELLANEOUS ANTIARRHYTHMIC AGENTS: DIGITALIS ANTI – ARRHYTHMIC DRUGS
49.
o A nucleoside that occurs naturally in the body
o t ½ ≈ 10 seconds
o MOA: enhances K+ conductance & inhibits cAMP-induced Ca++ influx -> results in marked hyperpolarization & suppression of Ca++-dependent AP
o IV bolus: directly inhibits AV nodal conduction & ↑ AV nodal refractory period
MISCELLANEOUS ANTIARRHYTHMIC AGENTS: ADENOSINE ANTI – ARRHYTHMIC DRUGS
50.
o DOC for prompt conversion of paroxysmal SVT to sinus rhythm due to its high efficacy & very short duration of action
o Dosage: 6-12 mg IV bolus
o D/I:
▪ theophylline, caffeine – adenosine receptor blockers
▪ Dipyridamole – adenosine uptake inhibitor
o Toxicity: flushing, SOB or chest burning, atrial fibrillation, headache, hypotension, nausea, paresthesia
MISCELLANEOUS ANTIARRHYTHMIC AGENTS: ADENOSINE ANTI – ARRHYTHMIC DRUGS
51.
o Effective in patients with recurrent episodes of torsades de pointes (MgSO 4 1 to 2 g IV) & in digitalis-induced arrhythmia
o MOA: unknown -> influence Na+/K+ ATPase, Na+ channels, certain K+ and Ca++ channels
MISCELLANEOUS ANTIARRHYTHMIC AGENTS: MAGNESIUM ANTI – ARRHYTHMIC DRUGS
52.
o Therapy directed toward normalizing K+ gradients & pools in the body
o Effects of increasing serum K+:
▪ 1. resting potential depolarizing action
▪ 2. membrane potential stabilizing action
o Hypokalemia:
▪ ↑ risk of early & delayed afterdepolarization
▪ ↑ ectopic pacemaker activity esp if (+) digitalis
o Hyperkalemia:
▪ Depression of ectopic pacemakers
▪ Slowing of conduction
ANTI – ARRHYTHMIC DRUGS MISCELLANEOUS ANTIARRHYTHMIC AGENTS: POTASSIUM
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