an abnormality of impulse initiation, impulse conduction or both
Normal automaticity
arrhythmias associated with normal automatic pacemakers
abnormal automaticity
arrhythmias associated with non pacemaker cells that develop automaticity
triggered activity
oscillations in membrane potential that trigger an action potential
Normal SAN pacemaker
60-100 bpm
Atrial conduction fibers
60-80 bpm
AV junction
40-60
Ventricular Purkinje
20-40
True normal pacemaker
SA node
What makes the latent pacemakers emerge?
High parasympathetic tone
High catecholamine concentration
hypoxemia
ischemia
electrolyte distrbances
drug toxicities
Abnormal automaticity
tissue that is not normally automatic becomes automatic; often cannot be overdrive suppressed
Triggered activity
early afterdepolarizations
delayed afterdepolarizations
EAD
occur before full phase 3 repolarization
DAD
occur after phase 3 repolarizations
Digoxin
Blocks Na/K pump. Dig toxicity will lead to DADs and has increase in intracellular Na+ which will inhibit Na/Ca pump leading to increased Ca in the SR.
1st degree block
every pulse conducts
2nd degree block
some, not all pulses conduct
3rd degree block
no pulses conduct
2nd degree type I
Wenkebach; progressive prolongation thru the av node with an eventual dropped beat
2nd degree type II
Mobitz II; dropped beats without the prolongation of the PR interval
2:1 Morbitz block
dropping every other beat. Every other P wave has a QRS
3:1 Morbitz
3 P's for every QRS
What are some of the mechanisms that could contribute to block in the AV node?