title: Ionized hypocalcemia during prolonged cardiac arrest and closed-chest CPR in a canine model.
abstract: BACKGROUND
  Free or ionized calcium (Ca+2) is known to play a critical role in normal cardiovascular function, and Ca+2 administration in the setting of ionized hypocalcemia has been shown to improve indexes of cardiac function. The value of Ca+2 administration in the setting of cardiac arrest and resuscitation is unproven and controversial, in large part because ionized Ca+2 levels during cardiac arrest and resuscitation have not been adequately studied and exogenous calcium therapy may worsen ischemic cellular injury.
  
  
  OBJECTIVE
  To measure free calcium during prolonged cardiac arrest and CPR in a canine model.
  
  
  METHODS
  Central arterial and venous catheters were positioned in nine dogs, and ventricular fibrillation (VF) was induced electrically. After seven and one-half minutes of VF, countershocks were administered, and CPR was initiated and performed in accordance with current recommendations for 20 minutes. At five-minute intervals during resuscitation efforts, arterial pH, ionized Ca+2, and lactate as well as aortic pressure were measured.
  
  
  RESULTS
  During resuscitation, average systolic arterial pressure was 50 mm Hg. Within five minutes of instituting CPR, ionized Ca+2 significantly decreased from control values (5.1 +/- 0.1 at control to 4.0 +/- 0.1 mg/dL); after 20 minutes of attempted resuscitation, it averaged 3.2 +/- 0.2 mg/dL (P less than .05 vs control). There was no change in total Ca+2 during the arrest period (9.2 +/- 0.5 at control to 8.6 +/- 0.8 mg/dL at 27.5 minutes). Arterial lactate significantly increased throughout the arrest and resuscitation period (1.9 +/- 0.2 at control to 7.5 +/- 0.4 mM/L at 27.5 minutes). A significant correlation was demonstrated between ionized Ca+2 and lactate concentrations (r = -.72, P less than .001) but not between ionized calcium and pH (r = -.22, P greater than .20).
  
  
  CONCLUSIONS
  Ionized hypocalcemia occurs during prolonged cardiac arrest and resuscitation, and ionized hypocalcemia during prolonged arrest and resuscitation may be due to binding by lactate, as has been demonstrated in vitro.
authors.affiliation: UCLA School of Medicine.
authors.forename: C B
authors.initials: CB
authors.lastname: Cairns
authors.forename: J T
authors.initials: JT
authors.lastname: Niemann
authors.forename: P C
authors.initials: PC
authors.lastname: Pelikan
authors.forename: J
authors.initials: J
authors.lastname: Sharma
mesh_terms: D000818:Animals; D001158:Arteries / Q000502:physiology; D001794:Blood Pressure; D002118:Calcium / Q000097:blood*; D002245:Carbon Dioxide / Q000097:blood; D016887:Cardiopulmonary Resuscitation; D004285:Dogs; D005260:Female; D006323:Heart Arrest / Q000097:blood* / Q000150:complications; D006863:Hydrogen-Ion Concentration; D006996:Hypocalcemia / Q000097:blood* / Q000209:etiology; D007477:Ions; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D008297:Male; D013997:Time Factors
chemical_list: D007477:Ions; D007773:Lactates; D002245:Carbon Dioxide; D019344:Lactic Acid; D002118:Calcium