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Antiarrythmitic Drugs- Garrett

Terms in this set (86)

steps of cardiac electric pathways
1. SA node--> atrial gap jxns
2. AV node (slow potential)
3. AV node--> bundle of His
4. bundle of His--> R and L bundle branches
5. apex of heart--> purkinje fibers--> depolarization of ventricle
fast response AP's found?
in atrial and ventricular myocytes and fast conducting Purkinje fibers
rate of rise of phase 0 consequences
conduction rate of AP's is dependent on the rate of rise in depolarization of phase 0 (common drug target)
phase 1
activation of transient K+ channels (notch)
phase 2
L-type Ca2_ channels to delay rectifier potassium channels... long lasting Ca2+ current (plateau)
if you block K+ channels in phase 3, what happens?
extends phase 3
repolarization of AP is produced by activation of which 2 channels?
1. rapidly activating IKr (HERG) channel
2. slow activating IKs channel
when does IKr (HERG) channel activate
approx -45 mV--> rapid repolarization of membrane potential followed by subsequent depolarization by IKs
during the time of repolarization, what happens to Na+ channels
they make transition from inactivate state to closed state
phase 4
Na+ and Ca2+ removed from cytoplasm and K+ goes through leak channels to maintain resting membrane potential of -90- -80 mV
slow response action potentials located where
SA node and AV node
which phases are in slow response AP's
4, 0, 3
phase 4 depolarization of slow response AP
inward Na+ via If (funny) channels, then T-type Ca2+ channels open to further depolarizaiton
phase 0 upstroke of slow response AP
L-type Ca2+ channel opens--> depolarization
phase 3 repolarization AP due to?
inactivation of L-type Ca2+ channels and outward K+ current through delayed rectifier K+ channels
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