Pharmacology - Final - Part 8

davidwurbel7's version from 2016-08-14 07:24


Question Answer
Sodium channel blocker. Subclasses of this action reflect effects on the action potential duration (APD) and the kinetics of sodium channel blockersClass I
A substient action potential that interrupts phase III of the previous action potentialEarly After Action Potential
A substient action potential that interrupts phase IV of the previous action potentialLate After Action Potential
Action is sympatholytic - Beta blockersClass II
Action is manifest by prolongation of the APD (by altering potassium current) Ikr (Inward rectifier K current - K+ channel blockersClass III
Action is block of the cardiac calcium current - Ca+2 channel blockersClass IV
Class 1 that slows phase 0 depolarization and prolongs the action potential durationClass IA
Class 1 that slow phase 3 repolarization and shortens the action potential duration Class IB
Class 1 that markedly slows phase 0 depolarization but has no effect on action potential durationClass IC
Antirhythmic that suppresses phase 4 depolarizationClass II
Antirhythmic that block K+ channels and prolong action potential durationClass III
Antirhythmic that blocks Ca+2 channels and shortens the action potential durationClass IV
Quinidine, Procainamide and Disopyramide belong to this classClass IA
Lidocaine, Phenytoin, Tocainide and Mexiletine belong to this classClass IB
Flecainide and Propafenone belong to this classClass IC
Propranolol, Metoprolol, Nadolol, Atenolol, Acebutolol, Pindolol, Sotalol, and Esmolol belong to this classClass II
Bretylium, Amiodarone, Sotalol, Dofetilide, and Ibutilide belong to this classClass III
Verapamil and Diltiazem belong to this classClass IV
Digoxin, Adenosine and Magnesium belong to this classOther
Act by blocking the voltage sensitive Na channels. Decreased rate of Na entry slows the rate of rise of Phase 0 of AP. Cause decrease in excitability and conduction velocity. Block channels in abnormal tissue more effectively than channels in normal tissue. Use-dependant or state-dependant phenomenaClass I
These drugs block cells that discharge at high frequency without interfering with normal low frequency impulses in heart. MOA: Primary - Blockade of I[Na] and Secondary – Blockade of I[Kr]. Drugs slow the rate of rise of AP > slows conduction > prolongs AP > increases ventricular ERP. Drugs can cause QT prolongation syndrome. Drugs can be used to treat both atrial and ventricular arrhythmiasClass IA
These drugs MOA- Blockade of I[Na]. They decrease duration of AP by shortening repolarizationClass IB
These drugs MOA- Blockade of I[Na]. There is no action on the duration of AP or ventricular ERPClass IC
β-blockers. MOA: diminish phase 4 depolarization. Thus depresses automaticity, prolongs conduction and decreases HR. Useful in Rx of tachyarrhythmias caused by increased sympathetic activity (e.g. hyperthyroidism). Atrial flutter and fibrillation and AV nodal reentry tachycardiaClass II
Act by blocking potassium channels and diminish outward current during repolarization. Prolong duration of AP by blockade of IK potassium channels. They prolong ERPClass III
These are Ca channel blockers. Slows conduction in tissues dependant on Ca current (AV node). The SA node and AV node depolarize in response to the slow inward current of calcium and sodium. All other cardiac cells depolarize in response to the rapid inward current of sodium ions. Greater action on heart than on vasculature. Effective in atrial dysrrhythmias. Reentrant SVT, I.V use in PSVTClass IV


Question Answer
Class IA drug. In high concentrations can precipitate arrhythmias (fatal VF). MOA: binds to inactivated Na channels and prevents Na influx. Used in Rx of atrial, AV junctional, and ventricular tachyarrhythmias. Used to maintain sinus rhythm after cardioversion of atrial flutter or fibrillation. Drug Interactions: Can increase steady state concentration of digoxinQuinidine
Toxicity symptoms of large doses may induce cinchonism (blurred vision, tinnitus, headache, disorientation and psychosis) Syncope, prolonged QTc & torsades de pointesQuinidine
Class IA drug. Metabolism by acetylation to N-acetylprocainamide (NAPA), which prolongs duration of AP (has properties of class III drugs). Derivative of LA procaine. Given orally (Not IV?????)Procainamide
Toxicity symptoms include reversible lupus erythematosus like syndrome. In the CVS, effects-toxic concentrations cause asystole or ventricular arrhythmias. In the CNS, effects: depression, hallucination, psychosis (high doses)Procainamide
Class IA drug. Has negative inotropic effects (decrease in myocardial contractility). Used in Rx of ventricular arrhythmiasDisopyramide
Toxicity symptoms include anticholinergic effects (anti-DUMBELLS)Disopyramide
Class IB drug. Particularly useful in the Rx of ventricular arrhythmias. MOA: shortens phase 3 repolarization and decreases duration of AP. Abolishes ventricular reentry. Given I.V. Eliminated by liver by dealkylation. Dosage adjustment needed in liver damage. Uses: ventricular arrhythmia following MILidocaine
Toxicity symptoms include CNS effects: circum-oral numbness, drowsiness, slurred speech, paresthesia, agitation, confusion. Seizures and convulsions may occur. May precipitate arrhythmiasLidocaine
These drugs are only approved only for Rx of refractory ventricular arrhythmias. Huge safety concerns. MOA: suppresses phase 0 upstroke of AP. Very minimal effect on duration of AP. Has a significant negative inotropic effect and aggravates CHFFlecainide and Propafenone
The adverse effects of these drugs include dizziness, blurred vision, headache and nausea. Can aggravate preexisting arrhythmias. Can induce VT, which is resistant to RxFlecainide and Propafenone
Class III drug. Contains iodine and structurally related to thyroxine. Has class IA, II, III and some class IV actions. Dominant effect is prolongation of AP duration and ERP. Has antianginal activity. Completely absorbed after oral administration. Has a prolonged half life of several weeks. Full clinical effects achieved only after 6 weeks of initiation of Rx. Useful in Rx of refractory SVT and VTAmiodarone
The adverse effects of this drug include on long term use nearly ½ of the pts have to discontinue its use because of ADR. Thyroid dysfunction, Interstitial pulmonary fibrosis (CXR at regular intervals). Corneal microdeposits. GI intolerance, tremors, ataxia, dizziness, hyper or hypothyroidism (monitor). Neuropathy, blue skin discoloration (because of iodine accumulation)Amiodarone
Class III drug with potent β-blocking activity. MOA: blocks rapid outward potassium current. This prolongs both repolarization and duration of AP, lengthens ERP. Used for long term therapy to decrease the rate of sudden death following MI. Have strong antifibrillary effects in ischemic myocardiumSotalol
Slows conduction in tissues dependant on Ca current (AV node). The SA node and AV node depolarize in response to the slow inward current of calcium and sodium. Greater action on heart than on vasculature. Effective in atrial dysrrhythmias. Reentrant SVT, I.V use in PSVTCalcium Channel Blockers
This drug prolongs ERP. Useful to control atrial fibrillation and flutter. Remember ADR (ectopic ventricular beats). In emergencies used IVDigoxin
This drug is a naturally occurring nucleoside. In high doses decreases conduction velocity. Prolongs refractory period. Decreases SA and AV nodal activity. Acts by stimulating Adenosine receptors (A-receptors). Drug of choice in PSVT and AV nodal arrhythmiasAdenosine
The adverse effects of this drug include flushing, sedation, dyspneaAdenosine
Drug used to treat acute narrow-complex SVTAdenosine
Drug used to treat chronic and for maintenance of narrow-complex SVTBeta Blockers
This drug is used in torsades (QT prolongation syndrome). Interferes with Na/K ATPase, Na, K and Ca channels. Given IV (slow). Used with extreme cautionMagnesium


Question Answer
Chronic AV/PSVT/SVTBeta Blocker
For rate control by AV nodal conduction in A. Flutter/ A-fibDigoxin
For rate control of the ventricle in A. Flutter/ A-fibBeta Blocker and Calcium Channel Blocker
For rhythm control in A. Flutter/ A-fibAmiodarone
Used to treat CHF and Atrial fibulationDigoxin
Used to treat stable, narrow complex SVT and regular monomorphic wide-complex tachycardiaAdenosine
Used to treat polymorphic wide-complex tachycardia (Torsades de Pointes)Magnesium

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