Calcium flux in continuous venovenous haemodiafiltration with heparin and citrate anticoagulation.
Study Goal
The researchers aimed to quantify calcium loss and improve understanding of calcium homeostasis during continuous venovenous haemodiafiltration (CVVHD-F) with citrate anticoagulation compared to heparin.
Results Summary
Citrate anticoagulation resulted in a net calcium deficit (mean loss of 1.12 mmol/h) despite supplementation, while heparinised circuits showed a slight calcium gain. Calcium loss was significantly higher in citrate circuits (4.01 mmol/h) compared to heparin circuits (0.24 mmol/h).
Population
Intensive care patients requiring CVVHD-F (13 patients, 26 heparinised circuits, 22 citrated circuits).
Effective Dosage
Predilution Prismocitrate 10/2 flows of 1660 mL/h (delivering 2.42 mmol citrate per litre of blood) for citrate; Hemosol B0 predilution flows of 2058 mL/h for heparin.
Duration
Not specified in the abstract.
Interactions
None mentioned.
| Intervention | Direction | Endpoint | Population | Dosage | Impact | Claim # |
|---|---|---|---|---|---|---|
Calcium chelation with citrate | neutral | anticoagulation of the extracorporeal circuit during continuous venovenous haemodiafiltration (CVVHD-F) | - | - | is an effective alternative to heparin | #1 |
citrate anticoagulation | decrease | calcium balance | intensive care patients requiring CVVHD-F | - | results in a net calcium deficit | #2 |
citrate anticoagulation | decrease | calcium flux | intensive care patients requiring CVVHD-F | 4.01 mmol/h | mean calcium loss was | #3 |
heparin anticoagulation | increase | calcium flux | intensive care patients requiring CVVHD-F | 0.24 mmol/h | mean calcium loss was versus a gain of | #4 |
citrate anticoagulation with calcium replacement | decrease | calcium balance | intensive care patients requiring CVVHD-F | 1.12 mmol/h | patients experienced a mean calcium loss of | #5 |
BACKGROUND: Calcium chelation with citrate is an effective alternative to heparin for anticoagulation of the extracorporeal circuit during continuous venovenous haemodiafiltration (CVVHD-F). Calcium release occurs upon citrate metabolism; however, ultrafiltration of citrate-bound and free ions also occurs. OBJECTIVE: To quantify calcium loss and improve understanding of calcium homeostasis in CVVHD-F. METHODS: Calcium loss was prospectively quantified from heparinised and citrated circuits in consecutive intensive care patients requiring CVVHD-F. CVVHD-F prescription and anticoagulation choice was by the treating intensivist using commercial solutions (Gambro, Lundia, Sweden). Sample sets comprising arterial, prefilter and postfilter blood and an effluent sample were analysed for ionised total calcium (iCa(2+)) and magnesium levels. Flow rates were then used to calculate calcium flux. Citrate dose (predilution rate) and calcium replacement followed unit protocols to maintain a circuit iCa(2+) concentration of 0.3-0.5 mmol/L and an arterial iCa(2+) concentration of 0.8-1.1 mmol/L. RESULTS: 26 heparinised circuits and 22 citrated circuits in 13 patients were included; 334 sample sets were tested. For target extracorporeal blood flows of 200 mL/min, mean predilution Prismocitrate 10/2 flows were 1660 mL/h, delivering 2.42 mmol citrate per litre of blood. For heparin, mean predilution flows of Hemosol B0 were 2058mL/h. Mean calcium loss was 4.01 mmol/h from citrate anticoagulated circuits versus a gain of 0.24mmol/h from heparinised circuits (P < 0.001). Despite calcium replacement, citrate patients experienced a mean calcium loss of 1.12 mmol/h (SD, 0.70; 95% CI 1.0-1.22mmol/h; P < 0.001). Calculated effective diffusion volume (Q(E)) for calcium was closer to total blood water volume in heparin circuits and closer to plasma water volume in citrate circuits. CONCLUSIONS: Despite supplementation to maintain arterial iCa(2+) levels, citrate anticoagulation results in a net calcium deficit. An equation for estimating required citrate dose may allow revision of citrate dosing protocols.