TY  - CHAP
M1  - Book, Section
TI  - BICARBONATE, SODIUM
A1  - Kearney, Thomas E.
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.
PY  - 2018
T2  - Poisoning & Drug Overdose, 7e
AB  - PharmacologySodium  bicarbonate  is  a  buffering  agent  that  reacts  with  hydrogen  ions  to  correct  acidemia  and  produce  alkalemia.  Urinary  alkalinization  from  renally  excreted  bicarbonate  ions  enhances  the  renal  elimination  of  certain  acidic  drugs.It  also  may  help  prevent  renal  tubular  damage  from  deposition  of  myoglobin  in  patients  with  rhabdomyolysis;  precipitation  (by  enhancing  solubility)  of  methotrexate;  and  dissociation  of  BAL-metal  complex;  and  it  may  prevent  contrast-induced  nephropathy  (by  slowing  free  radical  production).  In  addition,  maintenance  of  a  normal  or  high  serum  pH  may  prevent  intracellular  distribution  of  weak  acids  such  as  salicylate.The  sodium  ion  load  and  alkalemia  produced  by  hypertonic  sodium  bicarbonate  reverse  the  sodium  channel-dependent  membrane-depressant  ("quinidinelike")  effects  of  several  drugs  (eg,  tricyclic  antidepressants,  type  Ia  and  type  Ic  antiarrhythmic  agents,  propranolol,  propoxyphene,  cocaine,  diphenhydramine).Alkalinization  causes  an  intracellular  shift  of  potassium  and  is  used  for  the  acute  treatment  of  hyperkalemia.Sodium  bicarbonate  given  orally  or  by  gastric  lavage  forms  an  insoluble  salt  with  iron  and  theoretically  may  help  prevent  absorption  of  ingested  iron  tablets  (unproven).Neutralization  of  acidic  substances  to  prevent  caustic  injury  usually  is  not  recommended  because  of  the  potential  for  an  exothermic  reaction,  generation  of  gas,  and  lack  of  evidence  that  tissue  injury  is  minimized.  Nebulized  sodium  bicarbonate  has  been  used  to  neutralize  the  hydrochloric  acid  formed  on  mucosal  surfaces  from  chlorine  gas  exposures  (efficacy  uncertain).Early  animal  studies  and  human  case  series  of  organophosphate  (OP)  poisonings  in  regions  lacking  sufficient  access  to  traditional  antidotes  (oximes,  atropine)  have  suggested  beneficial  outcomes  from  high-dose  IV  bicarbonate  therapy  (5  mEq/kg  over  60  minutes,  then  5–6  mEq/kg/d).  The  authors  of  those  studies  theorize  that  alkalinization  may  enhance  degradation  or  elimination  of  OPs,  improve  tissue  perfusion  with  volume  expansion,  and  enhance  the  efficacy  of  2-PAM.  Systematic  reviews  of  human  trials  have  failed  to  show  differences  in  mortality  but  have  demonstrated  a  trend  toward  improved  outcomes  (lower  atropine  requirements  and  shorter  length  of  hospital  stay).IndicationsSevere  metabolic  acidosis  resulting  from  intoxication  by  methanol,  ethylene  glycol,  or  salicylates  or  from  excessive  lactic  acid  production  (eg,  resulting  from  status  epilepticus  or  shock,  mitochondrial  toxins  or  chemical  asphyxiants,  cyanide,  carbon  monoxide,  metformin).To  produce  urinary  alkalinization,  enhance  elimination  of  certain  acidic  drugs  (salicylate,  phenobarbital,  chlorpropamide,  chlorophenoxy  herbicide  2,4-D  [dichlorophenoxyacetic  acid]).  Note:  Although  enhanced  elimination  may  be  achieved,  it  is  uncertain  whether  clinical  outcomes  are  improved  with  this  therapy.To  prevent  nephrotoxicity  resulting  from  the  renal  deposition  of  myoglobin  after  severe  rhabdomyolysis;  the  precipitation  of  methotrexate;  dissociation  of  BAL-metal  complex;  and  to  prevent  contrast-induced  nephropathy.Also  recommended  for  internal  contamination  of  uranium  from  radiation  emergencies  to  prevent  acute  tubular  necrosis  (see  "Radiation").Cardiotoxicity  with  impaired  ventricular  depolarization  (as  evidenced  by  a  prolonged  QRS  interval)  caused  by  tricyclic  antidepressants,  type  Ia  or  type  Ic  antiarrhythmics,  and  other  membrane-depressant  drugs.  Note:  Not  effective  for  dysrhythmias  associated  with  abnormal  repolarization  (prolonged  QT  interval  and  torsade  de  pointes).  Wide-complex  dysrhythmias  associated  with  yew  berries  (Taxus  spp)  and  bupropion  intoxications  may  not  be  responsive  to  sodium  bicarbonate  (mechanism  of  toxicity  may  not  be  related  to  sodium  channel  blockade).Contraindications.  The  following  contraindications  are  relative:Significant  metabolic  or  respiratory  alkalemia  or  hypernatremia.Severe  pulmonary  edema  associated  with  volume  ...
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/19
UR  - accessmedicine.mhmedical.com/content.aspx?aid=1174607369
ER  -