TY  - CHAP
M1  - Book, Section
TI  - Neuromuscular Blocking Agents
A1  - Butterworth IV, John F.
A1  - Mackey, David C.
A1  - Wasnick, John D.
Y1  - 2018
N1  - 
T2  - Morgan & Mikhail's Clinical Anesthesiology, 6e
AB  - KEY  CONCEPTS  It  is  important  to  realize  that  muscle  relaxation  does  not  ensure  unconsciousness,  amnesia,  or  analgesia.  Depolarizing  muscle  relaxants  act  as  acetylcholine  (ACh)  receptor  agonists,  whereas  nondepolarizing  muscle  relaxants  function  as  competitive  antagonists.  Because  depolarizing  muscle  relaxants  are  not  metabolized  by  acetylcholinesterase,  they  diffuse  away  from  the  neuromuscular  junction  and  are  hydrolyzed  in  the  plasma  and  liver  by  another  enzyme,  pseudocholinesterase  (nonspecific  cholinesterase,  plasma  cholinesterase,  or  butyrylcholinesterase).  Muscle  relaxants  owe  their  paralytic  properties  to  mimicry  of  ACh.  For  example,  succinylcholine  consists  of  two  joined  ACh  molecules.  In  contrast  to  patients  with  low  enzyme  levels  or  heterozygous  atypical  enzyme  in  whom  blockade  duration  is  doubled  or  tripled,  patients  with  homozygous  atypical  enzyme  will  have  a  very  long  blockade  (eg,  4–8  h)  following  succinylcholine  administration.  Succinylcholine  is  considered  relatively  contraindicated  in  the  routine  management  of  children  and  adolescents  because  of  the  risk  of  hyperkalemia,  rhabdomyolysis,  and  cardiac  arrest  in  children  with  undiagnosed  myopathies.  Normal  muscle  releases  enough  potassium  during  succinylcholine-induced  depolarization  to  raise  serum  potassium  by  0.5  mEq/L.  Although  this  is  usually  insignificant  in  patients  with  normal  baseline  potassium  levels,  a  life-threatening  potassium  elevation  is  possible  in  patients  with  burn  injury,  massive  trauma,  neurological  disorders,  and  several  other  conditions.  Pancuronium  and  vecuronium  are  partially  excreted  by  the  kidneys,  and  their  action  is  prolonged  in  patients  with  kidney  failure.  Cirrhotic  liver  disease  and  chronic  kidney  failure  often  result  in  an  increased  volume  of  distribution  and  a  lower  plasma  concentration  for  a  given  dose  of  water-soluble  drugs,  such  as  muscle  relaxants.  On  the  other  hand,  drugs  dependent  on  hepatic  or  renal  excretion  may  demonstrate  prolonged  clearance.  Thus,  depending  on  the  drug,  a  greater  initial  dose—but  smaller  maintenance  doses—might  be  required  in  these  diseases.  Atracurium  and  cisatracurium  undergo  degradation  in  plasma  at  physiological  pH  and  temperature  by  organ-independent  Hofmann  elimination.  The  resulting  metabolites  (a  monoquaternary  acrylate  and  laudanosine)  have  no  intrinsic  neuromuscular  blocking  effects.  Hypertension  and  tachycardia  may  occur  in  patients  given  pancuronium.  These  cardiovascular  effects  are  caused  by  the  combination  of  vagal  blockade  and  catecholamine  release  from  adrenergic  nerve  endings.  After  long-term  administration  of  vecuronium  to  patients  in  intensive  care  units,  prolonged  neuromuscular  blockade  (up  to  several  days),  may  be  present  after  drug  discontinuation,  possibly  from  accumulation  of  its  active  3-hydroxy  metabolite,  changing  drug  clearance,  or  the  development  of  a  polyneuropathy.  Rocuronium  (0.9–1.2  mg/kg)  has  an  onset  of  action  that  approaches  succinylcholine  (60–90  s),  making  it  a  suitable  alternative  for  rapid-sequence  inductions,  but  at  the  cost  of  a  much  longer  duration  of  action.  The  new  reversal  agent,  sugammadex,  permits  rapid  reversal  of  rocuronium-induced  neuromuscular  blockade.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - accessanesthesiology.mhmedical.com/content.aspx?aid=1161426824
ER  -