16. Cardiac Arrhythmia Drugs Flashcards
What causes arrhythmias?
Disturbance in pacemaker impuse formation, contraction impulse conduction, or a combination of the two.
What is the result of cardiac arrhythmias?
Timing and/or rate of contraction is insufficient to maintain normal cardiac output.
Describe the fast cardiac action potential in terms of ion movement and membrane potential.
Starts at -90mV, influx of Na+ causes depolarisation to +55mV, slight hyperpolarisation due to K+ efflux but stopped by Ca2+ influx, K+ efflux continues and Ca2+ influx stops causing hyperpolarisation back to resting -90mV.
What is the effect of drugs blocking Na+ channels on fast cardiac action potentials?
Slowing conduction in tissue, depolarisation happens more slowly and to lesser extent, action potential duration is slightly shortened.
What is the effect of beta-blockers on fast cardiac action potentials?
Phase 4 depolarisation is slowed so the duration of AP is prolonged.
What is the effect of drugs blocking K+ channels on fast cardiac action potentials?
The action potential duration is increased as slower hyperpolarisation so longer refractory period.
What is the effect of drugs blocking Ca2+ channels on fast cardiac action potentials?
Decreased inwards Ca2+ currents so decreased phase 4 spontaneous depolarisation.
Describe the slow cardiac action potential in terms of ion movement and membrane potential.
Funny channels allow Na+ and K+ influx causing slow depolarisation, Ca2+ influx causes quick depolarisation, K+ efflux then causes hyperpolarisation back to resting potential.
What is the effect of Ca2+ channel blockers on slow cardiac action potentials?
The slope of depolarisation is slower so conduction velocity reduced, the refractory period is later.
Which drugs affect automaticity of slow cardiac action potentials?
B agonists, muscarinic agonists, adenosine.
Which tissues of the heart have fast action potentials and which have slow?
Fast - cardiac tissue.
Slow - SAN or AVN.
What are the two broad mechanisms of arrhythmogenesis?
Abnormal impulse generation, abnormal conduction.
What are the causes of abnormal impulse generation in arrhythmias?
Automatic rhythms, triggered rhythms.
What are the automatic rhythms in arrhythmogenesis?
Enhanced normal automaticity from increased AP from SAN or ectopic focus from AP arising from other sites than SAN.
What are the triggered rhythms in arrhythmogenesis?
Delayed afterdepolarisation, early afterdepolarisation.
What are the causes of abnormal conduction in arrhythmias?
Conduction block and reentry.
What is conduction block?
Impulse is not conducted from the atria to the ventricles.
What are the two types of reentry loops?
Circus movement and reflection.
How does a reentry loop happen?
Pathway is blocked so impulse from one pathway travels backwards so cells are reexcited by the loop.
What are the four classes of action of drugs on arrhythmias?
Abnormal generation: decrease phase 4 slope or raise threshold. Abnormal conduction: decrease conduction velocity, increased effective refractory period.
What is the goal of pharmacology in arrhythmias?
Restore normal sinus rhythm and conduction to prevent more serious/lethal arrhythmias from occuring.
What are the general actions of antiarrhythmic drugs?
Decrease conduction velocty, change duration of ERP, suppress abnormal automaticity.
What is the action of a class Ia antiarrhythmic drug and give an example?
Moderate phase 0 - quinidine, procainamide.
What is the action of a class Ib antiarrhythmic drug and give an example?
No change in phase 0 - lidocaine.
What is the action of a class Ic antiarrhythmic drug and give an example?
Marked phase 0 - flecainide.
What is the action of a class II antiarrhythmic drug and give an example?
Beta-adrenergic blockers - propranolol, bisoprolol, esmolol.
What is the action of a class III antiarrhythmic drug and give an example?
Prolong repolarisation - amiodarone, sotalol, dofetalide, ibutilide.
What is the action of a class IV antiarrhythmic drug and give an example?
Calcium channel lockers - verapmil, diltiazem.
What are the effects of class Ia antiarrythmics on cardiac activity?
Decreased conduction, increased refractory period, decreased automaticity, increased threshold.