test 2 Flashcards
what is an arrhythmia
▪ Abnormalities in the electrical impulse generation
or conduction through the heart
▪ Abnormal automaticity
▪ Too fast
▪ Too slow
▪ Irregular
▪ Abnormal impulse conduction
▪ Reentry
▪ The most common cause of arrhythmias!!why is knowing about arrhythmias important to us?
- > 50% of anesthetized patients have arrhythmias!
- 80% of MI patients have arrhythmias!
- Nearly 100% of patients on CPB will be affected with arrhythmias
Goals of antiarrhythmic Therapy
▪ Restore normal heart function
▪ Alleviate symptoms
▪ Prevent sudden cardiac death
how do virtually all antiarrhythmics work?
▪ Virtually all antiarrythmics work by altering the ionic
transmembrane balance or the sympathetic tone to the heart
▪ THINK: Na+, Ca++, & K+
▪ Suppress automaticity and change the shape of the cardiac action potential graph
Overview of how the Class I sodium channel blockers work
- exert their effects through blocking voltage-gated Na+ channels
- preferentially bind to the open Na+ channels
- block conduction to the tissues that are depolorizing more frequently (overexcited cells) => USE-DEPENDENCE BLOCKADE
Class 1A
- slows phase 0 depolarization in ventricular muscle fibers
- widen action potential and affects QRS complexes
- slows phase 0 => shifts AP to the RIGHT
- (known as membrane stabilizers) - inhibits K+ channels
- long QT interval
Chinconism
▪ Toxic side effect of quinidine (class 1A) ▪ Tinnitus (ringing in the ear) ▪ Blurred vision ▪ Impaired hearing ▪ Confusion ▪ Headache ▪ Vertigo and dizziness ▪ Nausea and vomiting
Torsades de Pointes
▪ Toxic side effect of quinidine (class 1A)
▪ Polymorphic ventricular tachycardia
▪ Usually resolves spontaneously
▪ May develop into V-fib
- anytime you lengthen the action potential you have a risk of this because you are lengthening the QT interval
Class 1B
- shorten phas 3 repolarization in ventriclular muscle fibers
- shorten action potential WITHOUT affecting QRS complexes
- shifts in AP to the LEFT
- greatest affect on heart cells with long AP like purkinje fibers and ventricular myocytes
Class 1C
- markedly slows phase 0 depolarization in ventricular muscle fibers
- do not shorten action potential
- triggers all tissues (even normal tissues)
- does not shift AP
- very strong effect
- some are very dangerous so used less often
Class II Beta blockers
- inhibits phase 4 depolarization in SA and AV nodes
- decreases slope of phase 4 depolarization (block of adrenergic tone which takes longer to get to threshold)
- work by diminishing phase 4 depolarization
- decreases automaticity
- prolonged AV conduction
- negative chronotrope and ionotrope
Class II Beta blockers used for
- Atrial tachyarrhythmias
- including AV nodal re-entrant tachyarrhythmias (the most common type, particularly in women)
- Also extensively used post-MI for ventricular arrhythmias
Class III Potassium Channel Blockers
- prolongs phase 3 repolarization in ventricular muscle fibers
- blocks K+ channels with little effect on Na+ channels
- block outward flow of K+ during depolarization
- prolonged AP without affecting phase 0 (depolarization) - increase refractory period
- blocks reentry arrhythmias
- reverse use-dependence blockade
- contributes to arrhythmias by preferentially affecting normal tissues - more prone than other classes in causing arrhythmias (especially tosades de points)
- extends QT interaval
- more effect when rates are slow
Class IV Calcium Channel Blockers
- inhibits AP in SA and AV nodes
- decrease rate of phase 4 spontaneous depolarization in SA and AV node
- preferentially slow the rate of conduction in tissues dependent on Ca2+ currents for depolarization
