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J Thorac Cardiovasc Surg 1994;107:941-942
© 1994 Mosby, Inc.
LETTERS TO THE EDITOR |
UCLA Medical Center
Department of Surgery
B2-375 CHS
Los Angeles, CA 90024-1741
To the Editor:
A recent survey of more than 1400 cardiac surgeons
1 showed that 72% use blood cardioplegia and approximately 40% use formulations developed through our experimental studies and used clinically for many years
2
We continue to use intermittent cold blood cardioplegia, with warm reperfusion regularly and warm induction in high-risk patients. The target concentrations after mixture 4:1 with blood are unchanged, whereby the final calcium concentrations for cold solutions (0.5 to 0.6 mmol/L) and warm solutions (0.15 to 0.25 mmol/L) are achieved after mixing with normocalcemic systemic blood from the extracorporeal circuit. These original concentrations were achieved after the circuit was primed with Ringer's lactate solution (containing calcium 1.5 mmol/L) and normocalcemic blood (1.0 to 1.2 mmol/L), but we, like others, now routinely use hemodilution primes and add albumin for onconicity. Blood cardioplegic calcium concentrations below these target levels are associated with decreased recovery under experimental conditions
3 and are sometimes observed clinically to transiently delay return of synchronized atrioventricular conduction and increase the likelihood of ventricular fibrillation immediately after aortic unclamping. No long-term effects were noted, and these changes were avoided by delivering the cardioplegic solution with the target calcium concentrations in the original formulation. This is achieved by supplementing the priming fluid in the extracorporeal circuit with CaCl2.
Initially, we added CaCl2, 200 mg/L, to any acalcemic priming fluid (Plasma-Lyte-A, Isolyte, or Normosol) to furnish the same CaCl2 in the crystalloid component as present in Ringer's lactate solution. This addition, in general, avoided systemic hypocalcemia because (1) the 2 L prime is mixed with 5 L of normocalcemic blood (the patient's blood volume) and (2) body calcium stores are mobilized promptly. Occasionally, however, borderline calcium levels (0.9 mmol/L) were observed in smaller patients(<50 kg) with less blood volume.
Our recent analysis suggests that the 2000 ml acalcemic prime used in adult patients, which contains 1800 ml acalcemic crystalloid (i.e., Plasma-Lyte) and 200 ml 25% albumin, should be supplemented with 300 mg CaCl2 per liter of prime: (1) Plasma-Lyte solution contains gluconate, which binds ionized calcium; (2)there is further binding of calcium by albumin. The increase in CaCl2 from 200 mg/L to 300 mg/L compensates for this and ensures a normal ionized calcium in the asanguineous component. We tested also asanguineous priming fluids containing Ringer's lactate and albumin and found that normal calcium concentrations are achieved by adding 100 mg CaCl2 per liter of prime. The calcium binding by albumin caused the mild lowering of calcium levels.
Fig. 1, A andB shows in vitro data generated with simulation of the standard pump prime (9:1, reflecting 1800 ml Plasma-Lyte and 200 ml 25% albumin) and with Ringer's lactate and albumin, as well as when the crystalloid component is reduced (ratios < 9:1). The potential for iatrogenic systemic hypocalcemia and subsequent inadvertent excessive lowering of ionized calcium concentrations in the cardioplegic solution would, of course, be increased if (1) a standard prime were used in patients with a smaller blood volume (i.e., <50 kg patient) or in children, in whom proportionately more albumin is used. The minor modification of adding CaCl2 to the priming fluid will leave nothing to chance and will ensure delivery of the target concentrations in the induction, maintenance, and reperfusate solutions. Periodic measurement of ionized calcium in blood from the extracorporeal circuit will allow detection and correction of inadvertent hypocalcemia.
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