Pharm - Antiarrhythmics Flashcards
(13 cards)
Class I Overview
Mechanism
Drugs bind to activated channels (open m and h gates - at rest m closed, h open) - USE DEPENDENT block - good for tachycardias where heart muscle used more
Na Channel Blockers
Class Ia Drugs
Types, Effect, Side Effects
E: Medium effect on Na Channel/Phase 0 upstroke; LENGTHENS QT
Procainamide - Drug-Induced Lupus (arthralgia, pleuritis, pericarditis), TdP due to extra K-blocking activity
Quinidine - extra vagolytic effects (urinary retention, constipation, blurred vision, dry mouth), cinchonism (cns toxicity - tinnitus, psychosis), TdP (K blocking activity - LQT)
Disopyramide - Stronger vagolytic effects, negative inotropic effects, anti-muscarinic (urinary retention, constipation, blurred vision, dry mouth), TdP (K Blocking - LQT)
Class Ib Drugs
Effect, Use, Types, Side Effects
E: Low effect on Na+ Channel/Phase 0 upstroke; SHORTENS QT
U: used in ischemia - ischemic tissue more depolarized = more activated Na Channels = preferential binding to ischemic tissue
T: Lidocaine (IV) + Mexelitine (PO)
SE: CNS Toxicity (confusion, delirium, Grand Mal Seizures)
Class Ic Drugs
Effect, Types, Side Effects, Contraindications
E: High Effect on Na Channel/Phase 0 Upstroke, No Change to QT
T: Flecainide + Propafenone
SE: Potent negative inotropy (lower contraciton), propafenone has extra b-blocking effects, slows condution due to potent Na blocking even in AV node
CI: LV systolic dysfunction + heart block
Class II Drugs
Types, Mechanism, Side Effects
T: B-Blockers (Esmolol - IV, Metoprolol - PO)
M: Block adrenergic tone - prolong phase IV - slow pacemaking in SAN/AVN
SE: hypotension, bradycardia, depression, bronchospasm, cognitive impairment, sexual dysfunction
Class III Drugs
Type, Mechanism, Side Effects
T: K Channel Blockers
M: block phase 3 repolarization, prolong APD
Amiodarone: Very Effective + Toxic - has Class I, II, IV effects too (Thyroid dysfunction, pulm fibrosis, hepatotoxicity, blue skin discoloration) SE: bradycardia, heart block
Sotalol: B-blocking effects too, PO, avoid in renal failure, CAUSE TDP
Dofetilide: PO, CAUSES TDP
Ibutilide: IV, CAUSES TDP
Class IV Drugs
Types, Mechanism, Side Effects, Contraindications
T: CCBs, Diltiazem, Verapamil
M: prolongs phase IV in AVN/SAN & Increases APD
SE: Constipation, Peripheral Edema, Proarrhythmic (Sinus Bradycardia, Heart Block)
CI: Advanced HF, Heart Block
Adenosine
Mechanism
Binds adenosine receptor = K+ channel activation = hyperpolarize membrane = transient effective heart block
Digoxin
Mechanisms, Therapeutic window, toxicity, toxicity tx
M: Major: Vagomimetic effect - slows sinus rate and prolongs AV Node refractoriness
Minor: Direct membrane effects - increases contractility (only affects conduction at toxic levels)
NARROW THERAPEUTIC WINDOW
Tox: nausea, diarrhea, yellow vision, proarrhythmic for lots
tx of tox: anti-digoxin Fab fragments
Tx for reentrant SVTs (AVNRT, AVRT) - acute, chronic
Acute: Adenosine - rapidly acting, disrupts AVN
Chronic: B-blockers/CCBs (II/IV) - slow conduction through AVN
Tx for Afib/Aflutter/ATach
- Rate Control: Slow AVN to control ventricular rate and leave atria dysfunctional (B-blockers, CCBs, Digoxin [II/IV/-] to slow conduction through AVN)
- Rhythm Control: Modify atrial electrical properties to restore sinus rhythm (Class Ic Agents - slows conduction to interfere with reentry; Class III - prolongs repolarization to interfere with reentry)
Tx to Suppress VT & Symptomatic PVCs
What disease is treated well with these meds? Which single drug best treats this disease?
- Class II Agents/B-Blockers: slow conduction through sick tissue
- Class III agents/K channel blockers: interferes with reentry by prolonging repolarization
- Class Ib Agents: interferes with reentry by slowing conduction
USE ALL THREE TO TREAT MI (AMIODARONE MOST USEFUL)
Tx for TdP
Mg, Phenytoin, Isoproterenol, Overdrive Therapy, SHOCK (best Tx)
