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)
how do class 4 decrease conduction velocity
blocking of L-type Ca2+ channels in upstroke (phase 0) of slow AP
therefore, slower and less likely to cross cardiac tissue in re-entry
how do class 4 increase refractory period
use-dependent block of calcium channels (stabilize inactive state) –> refractive cells can’t conduct AP
how does increasing refractory period help decrease re-entry arrhythmias
refractory tissue can’t generate AP
AP that reaches refractory tissue is extinguished.
why is decreasing cardiac automaticity good for treating arrhythmia?
rogue cardiomyocytes generating AP independent of AP node (ectopic foci)
which antiarrhythmic drugs treat arrhythmias by decr cardiac automaticity?
class 2, 3, 4, and adenosine
