Should calcium be used in cardiac arrest?

Hughes, William; Ruedy, John

doi:10.1016/0002-9343(86)90265-2

Cited by 19 publications

(5 citation statements)

References 54 publications

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“…In 1985, calcium chloride was no longer recommended in these cardiac arrest settings, largely due to the lack of demonstrated benefit and the concern that high levels of calcium following intravenous bolus administration might be detrimental. (14,32,33) The findings of our study suggest that calcium infusion therapy, acting as an inotrope and vasopressor, may be beneficial after resuscitation.…”

Section: Discussionmentioning

confidence: 64%

Hypocalcemia following resuscitation from cardiac arrest revisited

et al. 2010

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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 postresuscitation 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 minutes 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 gm 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). Postresuscitation CaCl2 infusion improved post-ROSC hemodynamics when compared to saline infusion (LV stroke work control 8 ± 5 gm-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.

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Section: Discussionmentioning

confidence: 64%

Hypocalcemia following resuscitation from cardiac arrest revisited

et al. 2010

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“…Clinically, the therapeutic use of calcium infusions in horses is justified in cases of hypocalcemia, hyperkaliemia and after an overdose of calcium blockers (OLSON, 1980;PASCOE, 1987). Although the use of calcium as a bolus during cardiac arrest is a discussable issue (HUGHES and RUEDY, 1986;MEURET et al, 1984) calcium can be used in emergency medicine in horses (GOLDSTEIN et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular Effects of Low Dose Calcium Chloride Infusions During Halothane Anaesthesia in Dorsally Recumbent Ventilated Ponies

Gasthuys

Moor

Parmentier

1991

Journal of Veterinary Medicine Series A

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Summary The effects of calcium chloride administered at low infusion rates on the cardiovascular depression and the blood calcium balance were studied during a constant halothane anaesthesia in dorsally recumbent ventilated ponies. A pronounced cardiopulmonary depression characterized by decreases of all cardiac parameters and lowering of the mean arterial blood pressure was observed after the initial anaesthetic stabilization period of 30 minutes in the ponies. A significant decrease in the total calcium plasma concentration together with a constant ionized and complexed calcium fraction was present after the stabilization period.

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“…Up to 50 mL of 10% gluconate and up to 30 mL of 10% chloride solution has been recommended. 16–18 It is worth reiterating that the two formulations of calcium have distinct properties. 19 First, the amount of elemental calcium (Ca 2+ ) is approximately 27.2 mg Ca 2+ /mL as 10% calcium chloride and 8.9 mg Ca 2+ /mL as 10% calcium gluconate.…”

Section: Discussionmentioning

confidence: 99%

Slow‐release potassium overdose: Is there a role for magnesium?

Davey

Kuhn

1999

Emergency Medicine

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Slow‐release potassium overdose is rare and often fatal. Recommended treatment is derived from that of other, more common, causes of hyperkalaemia and from the general principles of overdose management. We present a patient who survived after a massive slow‐release potassium (Slow‐K®) ingestion resulting in a peak potassium concentration of 12 mmol/L, the highest yet reported. A review of previously reported cases of potassium overdose and a summary of recommended therapies for the treatment of hyperkalaemia are presented. Laboratory and current clinical evidence support the addition of magnesium to standard therapy for potassium overdose, particularly where there is concern about increasing doses of calcium; this suggestion requires further clinical research.

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Should calcium be used in cardiac arrest?

Cited by 19 publications

References 54 publications

Hypocalcemia following resuscitation from cardiac arrest revisited

Hypocalcemia following resuscitation from cardiac arrest revisited

Cardiovascular Effects of Low Dose Calcium Chloride Infusions During Halothane Anaesthesia in Dorsally Recumbent Ventilated Ponies

Slow‐release potassium overdose: Is there a role for magnesium?

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