Normokalemia and hyperglycemia in subarachnoid hemorrhage patients resuscitated from prehospital cardiopulmonary arrest

Severe metabolic acidosis develops following prolonged periods of cardiopulmonary arrest (CPA), and excessive hydrogen ions derived from lactate and other noxious acids cause marked hyperkalemia in most CPA patients. This study investigated whether the serum electrolyte imbalance in resuscitated CPA patients is affected by the etiology of the CPA. Between 1999 and 2000, return of spontaneous circulation (ROSC) was achieved and serum electrolyte concentration measurements and blood gas analysis (BGA) were performed in 65 of 270 CPA patients treated. Of the 65 patients, subarachnoid hemorrhage (SAH) was the cause of the CPA in ten, cardiac attack was the cause in 16 and asphyxia was the cause in nine patients. The clinical and laboratory data of these 35 patients were retrospectively compared among the three groups. The SAH group had significantly lower serum potassium concentrations than the other two groups and significantly higher glucose concentrations than the asphyxia group. Massive amounts of catecholamines are released into the systemic circulation of SAH patients and our results may indicate that the amount of catecholamines released in resuscitated SAH patients is greater than in heart attack or asphyxia patients, resulting in a lower serum potassium concentration despite the presence of severe metabolic acidosis. It should be clarified in a prospective study whether the presence of normokalemia and hyperglycemia in resuscitated CPA patients reliably predicts the presence of SAH.