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Flashcards in arrhythmia mechanism 2 Deck (21)
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antiarrhythmic drugs should be selected based on the

specific molecular basis of long QT syndrome.


For patients with the LQT3 mutations, use:

drugs that block Na+ channels


for patients with LQT1 or LQT2 mutations, use:

drugs that open K+ channels ought to be used


effects of Ina

incomplete Ina inactiation


effects of Ica-L

incomplete Ica inactivation
autism (timothy syndrome)


effects of Ikr

decrease in K+ current


effects of Iks

decrease in K+ current


effects of Ik1

decrease in K+ current (during diastole)


Brugada syndrome

1. congenital arrythmia
2. ventricular fibrillation results in a survival rate of only 40% by 5 years of age.


finnish familial arrhythmia mechanism

1, The protein yotiao binds protein kinase A, cardiac Ca2+ channels and K+ channels Yotiao thus anchors this kinase to cardiac Ca2+ and IKS channels
2. A mutation in IKS channels prevents yotiao binding to this channel
3. The mutant K+ is not properly upregulated by β receptor activity


In finnish familial arrythmia, yotiao mutation leads to

1. during ↑ sympathetic activity (exercise, emotion),
2. not enough repolarizing K+ current to match the increased depolarizing Ca2+ current.
3. Phase 2 is prolonged, cytosolic Ca2+ levels rise, triggering afterdepolarizations and arrhythmia.


two types of problems in arrhythmia:

(1) inappropriate impulse initiation in SA node or elsewhere (ectopic focus), and
(2) disturbed impulse conduction in nodes, conduction cells (Purkinje cells) or myocytes.


Inappropriate impulse initiation - identified by

abnormally depolarized diastolic membrane potential


Inappropriate impulse initiation - caused by

1. ectopic foci
2. triggered afterdepolarizations


ectopic foci:

because normal SA nodal pacemaker is abnormally slow, or ectopic focus is abnormally fast infarct - causes membrane to depolarize

(decrease in [K+]i occurs as Na/K-ATPase fails)


early afterdepolarizations (EADs):

1. appear during late phase 2 and phase 3
2. largely dependent upon re-activation of Ca2+ channels in response to elevated [Ca2+]in prolongation of phase 2 (long QT) contributes to elevated [Ca2+]in


delayed afterdepolarizations (DADs):

1. during early phase 4
2. initiated by elevated [Ca2+]in and, consequently, elevated Na+/Ca2+ exchange
3. the Na+/Ca2+ exchanger is electrogenic: 3 Na+ move in for 1 Ca2+ moved out
4. net increase in positive charge inside myocytes corresponds to depolarization this exchanger is called NCX, and the current it generates is INCX


Prolonged phase 2
INCX will cause

excess Ca2+ entry, which triggers excess Ca2+ release from SR.
Elevated [Ca2+]in drives increased Na/Ca exchange via the NCX exchanger.


Prolongation of QT interval leads to

early afterdepolarizations and arrhythmia.


Disturbed impulse conduction: Will cause:

1. conduction block
2. re-entry


Re-entry underlies:

1. atrial flutter and fibrillation,
2. torsades de pointes and
3. ventricular fibrillation.