PLASMA IONIZED CALCIUM IN BRAIN-DEAD PATIENTS

Background: The mechanism of brain death-induced myocardial dysfunctio n remains debatable. Hypocalcemia is known to induce reversible myocar dial dysfunction. However, the incidence of hypocalcemia and its effec t on myocardial function during brain death is unknown. Methods: In 54 consecutive brain-dead patients, we measured plasma total and ionized calcium concentrations, QT and corrected QT intervals, and left ventr icular ejection fraction area (LVEFa), using transesophageal echocardi ography. Results: 49 (91%) of brain-dead patients had a decrease in to tal plasma total calcium concentration but only 19 (35%) had a decreas e in plasma ionized calcium. Corrected total plasma calcium failed to predict ionized calcium concentration and QT intervals were not signif icantly different in normo and hypocalcemic patients. The LVEFa was no t significantly different between normo and hypocalcemic patients (53 +/- 13 versus 50 +/- 20%), and no correlation was found between LVEFa and ionized calcium (R = 0.02, NS). Hypocalcemic patients required gre ater doses of dopamine (8.2 +/- 5.2 versus 5.0 +/- 3.4 mu g . kg(-). m in(-1), p < 0.02) to maintain arterial pressure. Hypocalcemia was asso ciated with a higher volume loading and a lower plasma protide concent ration which reflected hemodilution. Conclusion: A decrease in plasma ionized calcium is not frequent, rarely severe, and probably not the m ain mechanism of myocardial dysfunction in brain-dead patients. Hypoca lcemic patients required higher doses of dopamine, suggesting a decrea se in systemic resistance. Only direct measurement of ionized calcium can assess plasma calcium ion status in brain-dead patients.