TY  - CHAP
M1  - Book, Section
TI  - Chapter 12. Cholinesterase Inhibitors & Other Pharmacologic Antagonists to Neuromuscular Blocking Agents
A1  - Butterworth, John F.
A1  - Mackey, David C.
A1  - Wasnick, John D.
PY  - 2013
T2  - Morgan & Mikhail's Clinical Anesthesiology, 5e
AB  - The  primary  clinical  use  of  cholinesterase  inhibitors,  also  called  anticholinesterases,  is  to  reverse  nondepolarizing  muscle  blockade.  Acetylcholine  is  the  neurotransmitter  for  the  entire  parasympathetic  nervous  system  (parasympathetic  ganglions  and  effector  cells),  parts  of  the  sympathetic  nervous  system  (sympathetic  ganglions,  adrenal  medulla,  and  sweat  glands),  some  neurons  in  the  central  nervous  system,  and  somatic  nerves  innervating  skeletal  muscle.  Neuromuscular  transmission  is  blocked  when  nondepolarizing  muscle  relaxants  compete  with  acetylcholine  to  bind  to  nicotinic  cholinergic  receptors.  The  cholinesterase  inhibitors  indirectly  increase  the  amount  of  acetylcholine  available  to  compete  with  the  nondepolarizing  agent,  thereby  reestablishing  neuromuscular  transmission.  In  excessive  doses,  acetylcholinesterase  inhibitors  can  paradoxically  potentiate  a  nondepolarizing  neuromuscular  blockade.  In  addition,  these  drugs  prolong  the  depolarization  blockade  of  succinylcholine.  Any  prolongation  of  action  of  a  nondepolarizing  muscle  relaxant  from  renal  or  hepatic  insufficiency  will  probably  be  accompanied  by  a  corresponding  increase  in  the  duration  of  action  of  a  cholinesterase  inhibitor.  The  time  required  to  fully  reverse  a  nondepolarizing  block  depends  on  several  factors,  including  the  choice  and  dose  of  cholinesterase  inhibitor  administered,  the  muscle  relaxant  being  antagonized,  and  the  extent  of  the  blockade  before  reversal.  A  reversal  agent  should  be  routinely  given  to  patients  who  have  received  nondepolarizing  muscle  relaxants  unless  full  reversal  can  be  demonstrated  or  the  postoperative  plan  includes  continued  intubation  and  ventilation.  In  monitoring  a  patient’s  recovery  from  neuromuscular  blockade,  the  suggested  end  points  are  sustained  tetanus  for  5  sec  in  response  to  a  100-Hz  stimulus  in  anesthetized  patients  or  sustained  head  lift  in  awake  patients.  If  neither  of  these  end  points  is  achieved,  the  patient  should  remain  intubated  and  ventilation  should  be  continued.  Sugammadex  exerts  its  effects  by  forming  tight  complexes  in  a  1:1  ratio  with  steroidal  neuromuscular  blocking  agents.  Cysteine  causes  inactivation  of  gantacurium  via  metabolic  degradation  and  adduct  formation.  
SN  - 
PB  - The McGraw-Hill Companies
CY  - New York, NY
Y2  - 2021/09/22
UR  - accessanesthesiology.mhmedical.com/content.aspx?aid=57231778
ER  -