Arrhythmias Flashcards
Almost all arrhythmias are ____
acquired= myocardial infarction (MI), ischemia, acidosis, alkalosis, electrolyte abnormalities.
Drug toxicity is a common cause of arrhythmia
when are antiarrhythmic drugs used
1) treating some arrhythmias (e.g., supraventricular
2) used with ICDs- decr arrhythmic episodes, decr discharges
Familial Long QT
cardiac AP is extended
prolonged phase 2 –> too much Ca2+ entry –> afterdepolarizations –> torsades –> v-fib and sudden death
which phase is prolonged in familial long QT
phase 2 –> too much Ca2+ entry
how do mutations in K+ channels lead to long QT
mutations = decr expression of K+ channels so less K+ current to end Phase 2
how do mutations in Na+ channels lead to long QT
prevent Na+ channels from inactivating completely –> continued flow of Na+ –> prolong phase 2
Triggered afterpolarizations are a cause of _____
inappropriate impulse initiation –> abnormally depolarized diastolic membrane potential triggered by an AP
when do Early afterdepolarizations arise
late phase 2 or phase 3
what causes Early afterdepolarizations
1) prolonged phase 2
2) reactivation of Ca2+ channels so more Ca2+ enter into cytoplasm
3) allows 2nd AP to fire releasing more Ca2+ from SR
when do delayed afterpolarizations arise
phase 4
what causes delayed afterpolarizations
NCX exchanger working fast enough to trigger depol
1) elevated cytoplasmic Ca2+
2) causes NCX to pump out Ca2+
3) but NCX leads to net positive charge inward
4) depolarization
Criteria for re-entry arrhythmia
1) unidirectional conduction block in a functional circuit
2) conduction time around circuit is longer than refractory period
what triggers re-entry arrhythmia
triggered by afterpolarizations
what happens in re-entry arrhythmia
block in normal conduction –> prevents current from flowing in norma pathway
current cirumvents block and excites damaged area on other side of block not in refractory (due to incr conduction time)
what does use-dependent block mean for class 1
channel must be open before it is blocked by drug
drug enters pore –> binds, and blocks ions from crossing
more a channel open, more chance drug has to bind
what do class 1 drugs preferentially target with use dependent block
abnormally high firing rates or abnormally depolarized membranes
2 effects of class 1 antiarrhythmics
increase Na+ channel refractory period by (2)
1) use dependent mechanism
2) prolonged phase 2
class 1 use dependent mechanisms
class 1 have high affinity for inactive state of channel –> stabilizes in inactive state and prolong refractory period
class 1 prolonged phase 2 duration
during phase 2, more Na+ channels inactivated –> prolongs refractory period
ONLY CLASS 1A AND 1C (CLASS 3 EFFECT BY BLOCKING K+ CHANNELS)
which class 1 prolong phase 2
CLASS 1A AND 1C
how do beta blockers help suppress arrhythmias?
reducing If, ICa-L and IKs
decreasing
1) diastolic depolarization
2) upstroke rate
3) refractory rate
–> decr HR and prolong refractory period in SA and AV cells
which cells are beta blockers effective against
AV node
used to treat arrhythmias with AV nodal re-entry
control ventricular rate during a-fib
how do class 3 drugs increase refractory period
increasing fast response phase 2
inactivation of more Na+ channels and extended refractory period
how do class 4 reduce re-entry ?
decreasing conduction velocity
prolonging refractory period (especially AV node)
