Antiarrhythmic drugs
Antiarrhythmic drugs
OVERVIEW the heart contains specialized cells that exhibit automaticity,that is,they can intrinsically generate rhythmic action potentials in the absence of external stimuli
OVERVIEW ◼ the heart contains specialized cells that exhibit automaticity, that is, they can intrinsically generate rhythmic action potentials in the absence of external stimuli
INTRODUCTION TO THE ARRHYTHMIAS cardiac arrhythmias may cause the heart ■ (1)to beat too slowly (sinus bradycardia); (2)to beat too rapidly (sinus or ventricular tachycardia,atrial or ventricular premature depolarization,atrial flutter); (3)to respond to impulses originating from sites other than the SA node; (4)to respond to impulses traveling along accessory (extra)pathways that lead to deviant depolarizations (A-V reentry)
INTRODUCTION TO THE ARRHYTHMIAS ◼ cardiac arrhythmias may cause the heart ◼ (1) to beat too slowly (sinus bradycardia); ◼ (2) to beat too rapidly (sinus or ventricular tachycardia, atrial or ventricular premature depolarization, atrial flutter); ◼ (3) to respond to impulses originating from sites other than the SA node; ◼ (4) to respond to impulses traveling along accessory (extra) pathways that lead to deviant depolarizations (A-V reentry)
Causes of arrhythmias Abnormal automaticity:The SA node shows the fastest rate of Phase 4 depolarization if cardiac sites other than the SA node show enhanced automaticity,they may generate competing stimuli
Causes of arrhythmias ◼ Abnormal automaticity: The SA node shows the fastest rate of Phase 4 depolarization ◼ if cardiac sites other than the SA node show enhanced automaticity, they may generate competing stimuli
Effect of drugs on automaticity Most of the antiarrhythmic agents suppress automaticity (1)by decreasing the slope of Phase 4 (diastolic)depolarization (2)by raising the threshold of discharge to a less negative voltage
Effect of drugs on automaticity ◼ Most of the antiarrhythmic agents suppress automaticity ◼ (1) by decreasing the slope of Phase 4 (diastolic) depolarization ◼ (2) by raising the threshold of discharge to a less negative voltage
Abnormalities in impulse conduction Impulses from higher pacemaker centers are normally conducted down pathways that bifurcate to activate the entire ventricular surface .A phenomenon called reentry can occur if a unidirectional block caused by myocardial injury or a prolonged refractory period results in an abnormal conduction pathway
Abnormalities in impulse conduction ◼ Impulses from higher pacemaker centers are normally conducted down pathways that bifurcate to activate the entire ventricular surface .A phenomenon called reentry can occur if a unidirectional block caused by myocardial injury or a prolonged refractory period results in an abnormal conduction pathway
Effects of drugs on conduction abnormalities Antiarrhythmic agents prevent reentry by slowing conduction and/or increasing the refractory period required to convert a unidirectional block into a bidirectional block
Effects of drugs on conduction abnormalities ◼ Antiarrhythmic agents prevent reentry by slowing conduction and/or increasing the refractory period required to convert a unidirectional block into a bidirectional block
Antiarrhythmic drugs the antiarrhythmic drugs can modify impulse generation and conduction
Antiarrhythmic drugs ◼ the antiarrhythmic drugs can modify impulse generation and conduction
Classification Mechanism of Action Comment of Drug A Na channel blocker Slows Phase 0 depoiarizatlon B Nachannel blocker Shortens Phase 3 repoiarization IC Natchannei biocker Markediy siows Phase 0 depoiarization B Adrenoreceptor biocker Suppresses Phase 4 depoiarization K*channei blocker Prolongs Phase 3 repolarization IV Ca+channei blocker Shortens action potential
CLASS I ANTIARRHYTHMIC DRUGS Class I antiarrhythmic drugs act by blocking voltage-sensitive sodium channels Class I antiarrhythmic drugs therefore generally cause a decrease in excitability and conduction velocity
CLASS I ANTIARRHYTHMIC DRUGS ◼ Class I antiarrhythmic drugs act by blocking voltage-sensitive sodium channels ◼ Class I antiarrhythmic drugs therefore generally cause a decrease in excitability and conduction velocity