A quantitative analysis of the acidosis of cardiac arrest: a prospective observational study

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.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).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.Metabolic acidosis is common in patients with cardiac arrest and is conventionally considered to be due essentially to hyperlactatemia [1-6]. However, hyperlactatemia alone fails to explain the cause of metabolic acidosis in some patients [3]. Traditional measures using the anion gap, standard bicarbonate and standard base excess might help to understand this acidosis [7,8]. However, they give little information about the mechanisms involved and the quantitative contribution of each variable [9-12], especially in the presence of major changes in serum electrolytes and albumin concentration.Recently, the Stewart–Figge methodology [13,14] has been