Abstract P121: Post-resuscitation Ionized Hypocalcemia Revisited
Objective: Hypocalcemia during cardiac arrest has been reported. However, hypotheses for the decrease in ionized calcium (iCa) vary and its importance unknown. The objective of this study was to assess the relationships of iCa, pH, and base excess (BE) in two porcine cardiac arrest models, and to determine the effect of exogenous calcium on postresuscitation hemodynamics.
Methods: Swine were instrumented and VF was induced either electrically (EVF, n=49) or spontaneously, ischemically induced (IVF) with balloon occlusion of the LAD (n=37). Animals were resuscitated after 7 minutes of VF. BE, iCa, and pH, were determined prearrest and at 15, 30, 60 min after ROSC. Arterial lactate was also measured in 10 pigs. In three animals, 1 gm of CaCl2 was infused over 20 min after ROSC.
Results: iCa, BE, and pH declined significantly over the 60 min following ROSC, regardless of VF type (figure⇓). Lactate was strongly correlated with BE (r = −0.83, p<0.0001). In a multivariate generalized linear mixed model, iCa was 0.007 mg/dL higher for every one unit increase in BE (95% CI 0.005– 0.008, p<0.0001), while controlling for type of induced VF. CaCl2 improved post-ROSC hemodynamics when compared to saline infusion (figure⇓).
Conclusions: Ionized hypocalcemia occurs following ROSC. This may be due to binding by lactate as evidenced by its strong association with the decline in base excess. CaCl2 improves post-ROSC hemodynamics suggesting that hypocalcemia may play adial dysfunction.