title: A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study.
abstract: BACKGROUND
  Metabolic acidosis is common in patients with cardiac arrest and is conventionally considered to be essentially due to hyperlactatemia. However, hyperlactatemia alone fails to explain the cause of metabolic acidosis. Recently, the Stewart-Figge methodology has been found to be useful in explaining and quantifying acid-base changes in various clinical situations. This novel quantitative methodology might also provide useful insight into the factors responsible for the acidosis of cardiac arrest. We proposed that hyperlactatemia is not the sole cause of cardiac arrest acidosis and that other factors participate significantly in its development.
  
  
  METHODS
  One hundred and five patients with out-of-hospital cardiac arrest and 28 patients with minor injuries (comparison group) who were admitted to the Emergency Department of a tertiary hospital in Tokyo were prospectively included in this study. Serum sodium, potassium, ionized calcium, magnesium, chloride, lactate, albumin, phosphate and blood gases were measured as soon as feasible upon arrival to the emergency department and were later analyzed using the Stewart-Figge methodology.
  
  
  RESULTS
  Patients with cardiac arrest had a severe metabolic acidosis (standard base excess -19.1 versus -1.5; P < 0.0001) compared with the control patients. They were also hyperkalemic, hypochloremic, hyperlactatemic and hyperphosphatemic. Anion gap and strong ion gap were also higher in cardiac arrest patients. With the comparison group as a reference, lactate was found to be the strongest determinant of acidosis (-11.8 meq/l), followed by strong ion gap (-7.3 meq/l) and phosphate (-2.9 meq/l). This metabolic acidosis was attenuated by the alkalinizing effect of hypochloremia (+4.6 meq/l), hyperkalemia (+3.6 meq/l) and hypoalbuminemia (+3.5 meq/l).
  
  
  CONCLUSIONS
  The cause of metabolic acidosis in patients with out-of-hospital cardiac arrest is complex and is not due to hyperlactatemia alone. Furthermore, compensating changes occur spontaneously, attenuating its severity.
authors.affiliation: Tertiary Emergency Medical Center, Tokyo Metropolitan Bokuto Hospital, Tokyo, Japan. makinet@jt7.so-net.ne.jp
authors.forename: Jun
authors.initials: J
authors.lastname: Makino
authors.forename: Shigehiko
authors.initials: S
authors.lastname: Uchino
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morimatsu
authors.forename: Rinaldo
authors.initials: R
authors.lastname: Bellomo
mesh_terms: D000138:Acidosis / Q000097:blood* / Q000453:epidemiology*; D000328:Adult; D002712:Chlorides / Q000097:blood; D015897:Comorbidity; D005260:Female; D006323:Heart Arrest / Q000097:blood* / Q000453:epidemiology*; D006801:Humans; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008875:Middle Aged; D010710:Phosphates / Q000097:blood; D011188:Potassium / Q000097:blood; D011446:Prospective Studies; D012016:Reference Values; D012709:Serum Albumin / Q000378:metabolism; D014947:Wounds and Injuries / Q000097:blood / Q000453:epidemiology
chemical_list: D002712:Chlorides; D010710:Phosphates; D012709:Serum Albumin; D019344:Lactic Acid; D011188:Potassium