SUCCINYLCHOLINE CAUSES PROFOUND HYPERKALEMIA IN HEMORRHAGIC, ACIDOTICRABBITS

Citation
Jf. Antognini et Ga. Gronert, SUCCINYLCHOLINE CAUSES PROFOUND HYPERKALEMIA IN HEMORRHAGIC, ACIDOTICRABBITS, Anesthesia and analgesia, 77(3), 1993, pp. 585-588
Citations number
12
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00032999
Volume
77
Issue
3
Year of publication
1993
Pages
585 - 588
Database
ISI
SICI code
0003-2999(1993)77:3<585:SCPHIH>2.0.ZU;2-I
Abstract
Two recent clinical reports suggested that succinylcholine (SCh) may c ause severe hyperkalemia in hemorrhagic, acidotic humans. To investiga te this, we anesthetized rabbits with halothane and N2O, and inserted venous and arterial catheters. Control rabbits (Group C, n = 4) remain ed anesthetized and undisturbed. Hemorrhage/profound acidosis (HPA) wa s accomplished by withdrawal of 25-30 mL/kg of blood and waiting until pHa almost-equal-to 7.05 (Group HPA, n = 5). Hemorrhage/minimal acido sis (HMA) was accomplished by withdrawal of 25-30 mL/kg of blood, but acidosis was minimized by not waiting for it to occur and by administe ring NaHCO3 0-1.4 mEq/kg (Group HMA, n = 4). In a metabolic acidosis g roup (n = 4), HCI was infused until pHa almost-equal-to 7.05. Respirat ory acidosis (n = 4) was accomplished by partial obstruction of the en dotracheal tube until PaCO2 almost-equal-to 120 mm Hg and pHa almost-e qual-to 7.05. Potassium levels were determined before the above interv entions (baseline), immediately before (pre-SCh), and 1, 3, 5, 7, 10, and 13 min after SCh 1 mg/kg intravenously. In Group C, potassium grad ually increased from 3.5 +/- 0.2 mEq/L to 4.8 +/- 0.2 mEq/L 13 min aft er SCh. In Group HPA, potassium increased from 3.8 +/- 0.3 to 7.0 +/- 1.8 mEq/L after hemorrhage/acidosis and then to 11.4 +/- 1.7 mEq/L at 13 min after SCh. The metabolic acidosis group was significantly diffe rent from Group C at 7, 10, and 13 min after SCh (maximum at 13 min, 6 .8 +/- 1.2 mEq/L). This difference was due to the HCI infusion, inasmu ch as the potassium change after SCh (1.5 +/- 0.7 mEq/L) was nearly th e same as in Group C (1.3 +/- 0.1 mEq/L). The HMA and respiratory acid osis groups were not significantly different from Group-C; however, wh en the maximum post-SCh potassiums in Groups HPA and HMA were compared to the decreases in base excess, there was a significant correlation between maximum potassium and the degree of acidosis. We conclude that Sch causes profound hyperkalemia in hemorrhagic, acidotic rabbits.