RT Book, Section
A1 Knollmann, Bjorn C.
A1 Roden, Dan M.
A1 Murray, Katherine T.
A2 Brunton, Laurence L.
A2 Knollmann, Björn C.
SR Print(0)
ID 1193233286
T1 Antiarrhythmic Drugs
T2 Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 14th Edition
YR 2023
FD 2023
PB McGraw-Hill Education
PP New York, NY
SN 9781264258079
LK accessanesthesiology.mhmedical.com/content.aspx?aid=1193233286
RD 2024/04/17
AB Cardiac  cells  undergo  depolarization  and  repolarization  about  60  times  per  minute  to  form  and  propagate  cardiac  action  potentials.  The  shape  and  duration  of  each  action  potential  are  determined  by  the  activity  of  ion  channel  protein  complexes  in  the  membranes  of  individual  cells,  and  the  genes  encoding  most  of  these  proteins  and  their  regulators  have  now  been  identified.  Action  potentials  in  turn  provide  the  primary  signals  to  release  Ca2+  from  intracellular  stores  (sarcoplasmic  reticulum)  and  to  thereby  initiate  contraction.  Thus,  each  normal  heartbeat  results  from  the  highly  integrated  electrophysiological  behavior  of  multiple  proteins  on  the  surface  and  within  multiple  cardiac  cells.  Disordered  cardiac  rhythm  can  arise  from  influences  such  as  inherited  variation  in  ion  channels  or  other  genes,  ischemia,  sympathetic  stimulation,  or  myocardial  scarring.  Available  antiarrhythmic  drugs  suppress  arrhythmias  by  modulating  flow  through  specific  ion  channels  or  by  altering  autonomic  function.  An  increasingly  sophisticated  understanding  of  the  molecular  basis  of  normal  and  abnormal  cardiac  rhythm  may  lead  to  identification  of  new  targets  for  antiarrhythmic  drugs  and  perhaps  improved  therapies  (Al-Khatib  et  al.,  2018).