RT Book, Section
A1 Jackson, Sam
A2 Olson, Kent R.
A2 Anderson, Ilene B.
A2 Benowitz, Neal L.
A2 Blanc, Paul D.
A2 Clark, Richard F.
A2 Kearney, Thomas E.
A2 Kim-Katz, Susan Y.
A2 Wu, Alan H. B.
SR Print(0)
ID 1179993011
T1 NEUROMUSCULAR BLOCKERS
T2 Poisoning & Drug Overdose, 7e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9780071839792
LK accessmedicine.mhmedical.com/content.aspx?aid=1179993011
RD 2024/04/23
AB PharmacologyNeuromuscular  blocking  agents  produce  skeletal  muscle  paralysis  by  inhibiting  the  action  of  acetylcholine  at  the  neuromuscular  junction  (NMJ).  Depolarizing  agents  (succinylcholine;  Table  III–12)  depolarize  the  motor  end  plate  and  block  recovery;  transient  muscle  fasciculations  occur  with  the  initial  depolarization.  Nondepolarizing  agents  (atracurium,  pancuronium,  and  others;  see  Table  III–12)  competitively  block  the  action  of  acetylcholine  at  the  motor  end  plate,  preventing  depolarization.  Therefore,  with  nondepolarizing  agents,  no  initial  muscle  fasciculations  occur  and  a  flaccid  paralysis  is  produced.The  neuromuscular  blockers  produce  complete  muscle  paralysis  with  no  depression  of  CNS  function  (they  are  positively  charged  and  water-soluble  compounds  that  do  not  cross  the  brain-blood  barrier  rapidly).  Thus,  patients  who  are  conscious  will  remain  awake  but  be  unable  to  move,  and  patients  with  status  epilepticus  may  continue  to  have  seizure  activity  despite  paralysis.  Furthermore,  the  neuromuscular  blockers  do  not  relieve  pain  or  anxiety  and  have  no  sedative  or  amnestic  effects.Succinylcholine  produces  the  most  rapid  onset  of  neuromuscular  blockade.  After  intravenous  administration,  total  paralysis  ensues  within  30-60  seconds  and  lasts  10-20  minutes.  It  is  hydrolyzed  rapidly  by  pseudocholinesterase,  an  enzyme  present  in  the  vascular  compartment  but  not  at  the  NMJ.  Therefore,  a  relatively  small  fraction  of  the  administered  dose  reaches  the  site  of  action,  and  diffusion  from  the  NMJ  back  into  the  intravascular  space  determines  metabolism.  Larger  (1.5  mg/kg  IV  based  on  total  body  weight  in  adults)  rather  than  smaller  doses  should  be  used  to  achieve  optimal  paralysis  during  rapid-sequence  intubation  (RSI).Rocuronium,  a  nondepolarizing  agent,  also  has  a  rapid  onset  of  effect  when  used  at  an  RSI  dose  of  1  mg/kg  IV  (based  on  ideal  body  weight)  in  adults.  However,  the  duration  of  the  blockade  (20-90  minutes)  is  considerably  longer  than  that  of  succinylcholine.  Sugammadex,  a  specific  and  rapid  reversal  agent  for  rocuronium  and  vecuronium,  has  recently  received  FDA  approval  for  use  in  adult  patients  undergoing  surgery.  The  utility  of  this  agent  in  the  patient  who  requires  emergent  intubation  is  not  clear.The  onset  and  duration  of  several  other  neuromuscular  blockers  are  described  in  Table  III–12.IndicationsNeuromuscular  blockers  are  used  to  abolish  excessive  muscular  activity,  rigidity,  or  peripheral  seizure  activity  when  continued  muscle  activity  may  produce  or  aggravate  rhabdomyolysis,  mechanical  injury,  or  hyperthermia.  Their  primary  indication  is  to  improve  the  view  of  the  larynx  and  other  relevant  anatomy  during  endotracheal  intubation  (see  II.  B,  below).  They  are  also  employed  when  excessive  muscular  movement  may  place  the  patient  (or  others)  at  risk  for  injury.Drug  overdoses  involving  stimulants  (eg,  amphetamines,  cocaine,  phencyclidine,  monoamine  oxidase  inhibitors)  or  strychnine.Tetanus.  Nondepolarizing  agents  should  be  chosen  because  infection  with  Clostridium  species  can  predispose  patients  to  pathologic  hyperkalemia  induced  by  the  use  of  succinylcholine.Hyperthermia  associated  with  muscle  rigidity  or  hyperactivity  (eg,  status  epilepticus,  neuroleptic  malignant  syndrome,  or  serotonin  syndrome).  Note:  In  susceptible  patients,  malignant  hyperthermia  can  be  triggered  by  succinylcholine  (see  discussion  under  "adverse  effects").In  intubated  patients,  partial  or  complete  neuromuscular  blockade  may  facilitate  improved  patient-ventilator  synchrony  and  enhanced  gas  exchange  and  lower  the  risk  for  barotrauma.Suspected  or  verified  cervical  spine  injury,  or  any  setting  in  which  there  is  increased  intracranial  pressure  (eg,  intracranial  hemorrhage,  hepatic  ...