Hypocalcemia following resuscitation from cardiac arrest revisited

Objective

Hypocalcemia associated with cardiac arrest has been reported. However, mechanistic 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, base excess (BE), and lactate in two porcine cardiac arrest models, and to determine the effect of exogenous calcium administration on post-resuscitation hemodynamics.

Methods

Swine were instrumented and VF was induced either electrically (EVF, n = 65) or spontaneously, ischemically induced (IVF) with balloon occlusion of the LAD (n = 37). Animals were resuscitated after 7 min of VF. BE, iCa, and pH, were determined prearrest and at 15, 30, 60, 90, 120 min after ROSC. Lactate was also measured in 26 animals in the EVF group. Twelve EVF animals were randomized to receive 1 g of CaCl₂ infused over 20 min after ROSC or normal saline.

Results

iCa, BE, and pH declined significantly over the 60 min following ROSC, regardless of VF type, with the lowest levels observed at the nadir of left ventricular stroke work post-resuscitation. Lactate was strongly correlated with BE (r = −0.89, p < 0.0001) and iCa (r = −0.40, p < 0.0001). In a multivariate generalized linear mixed model, iCa was 0.005 mg/dL higher for every one unit increase in BE (95% CI 0.003-0.007, p < 0.0001), while controlling for type of induced VF. While there was a univariate correlation between iCa and BE, when BE was included in the regression analysis with lactate, only lactate showed a statistically significant relationship with iCa (p = 0.02). Post-resuscitation CaCl₂ infusion improved post-ROSC hemodynamics when compared to saline infusion (LV stroke work control 8 ± 5 g m vs 23 ± 4, p = 0.014, at 30 min) with no significant difference in tau between groups.

Conclusions

Ionized hypocalcemia occurs following ROSC. CaCl₂ improves post-ROSC hemodynamics suggesting that hypocalcemia may play a role in early post-resuscitation myocardial dysfunction.