Abstract
The effect of sodium citrate infusion on the cardiovascular system was studied in six mongrel dogs. Serum ionized calcium concentration ([Ca++]) was monitored continuously using a Radiometer calcium selective electrode (Selectrode) in an extracorporeal blood shunt. Twelve, 24 and 48 mg- kg-1 of sodium citrate were infused into each animal. These concentrations correspond to the maximum amount of citrate that would be received by a 70 kg man given 0.5, 1.0 and 2.0 units of CPD treated blood. Each of the solutions were infused over a 5-minute period to duplicate a fairly rapid rate of blood transfusion in man. The decrease in [Ca++] along with blood pH and cardiovascular parameters were measured to determine the relationship between [Ca++] and cardiovascular dynamics. The following parameters were analyzed: mean arterial pressure (MAP), heart rate (HR), stroke volume (SV), peripheral vascular resistance (PVR), cardiac output (CO), pulmonary arterial pressure (PAP), pulmonary wedge pressure (PWP), [Ca++], total calcium (Ca) and pH. Statistically significant decreases occurred in SV, MAP and CO. Decreases in serum [Ca++] of 7.7± 1.0 per cent, 15.4 ± 1.9 per cent and 33.6± 3.6 per cent were observed for the 12, 24 and 48 mg kg-1 sodium citrate solution infusions, respectively. The recovery time for the [Ca++] to reach pre-infusion levels was 7.3 ±0.4 minutes, 14.3 ± 1.6 minutes and 21.3 ± 1.4 minutes,respectively,for the three solutions.
Our data show that significant degrees of hypocalcaemia and myocardial depression may accompany the infustion of citrate solutions. The degree of myocardial depression that we observed in healthy, unstressed animals was not a threat to life with the quantities of citrate we infused. However, in cases requiring larger blood transfusions, such as haemorrhagic shock or RH incompatibility, the cardiovascular system will be compromised considerably at the outset and further myocardial depression secondary to hypocalcaemia may result. The extracorporeal blood shunt proved to be a very simple, efficient and illustrative way of monitoring the level of [Ca++] continuously in the circulatory system during citrate infusion.
Résumé
Six chiens de sang mêlé ont servi à I’étude du réténtissement de la perfusion de citrate de soude sur le système cardiovasculaire. La concentration sérique du calcium ionisé (Ca++) a été monitorée de façon continue avec une électrode sélective au calcium fabriquée par Radiométér (Selectrode) placée dans un shunt extracorporel. Du citrate de soude aux doses de 12,24 et 48 mg . kg-1 a été perfusé à chaque animal. Ces concentrations équivalent à la quantité maximale de citrate que reçoit un homme de 70 kg lorsqu’il est transfusé avec 0.5, 1.0 et 2.0 unités de sang. Chacune des solutions a été injectée sur une période de cinq minutes de façon ç imiter une transfusion rapide de sang chez I’humain. La baisse de Ca++ ainsi que les paramètres acidobasiques et cardiovasculaires ont été mesurés pour déterminer la relation entre Ca++ et la dynamique cardiovasculaire. Les paramètres suivants ont été analysés: la pression artérielle moyenne, la fréquence cardiaque, le volume d’éjection, la résistance vasculaire périphérique, le débit cardiaque, la pression artérielle pulmonaire, la pression capillaire pulmonaire, le Ca++, le calcium total (Ca) et le pH. Des baisses significatives sont survenues pour le volume d’éjection, la pression arterielle moyenne et le débit cardiaque. Des diminutions dans le Ca++sérique de 7.7 ± 1.0pourcent, 15.4 ± 1.9 pour cent et de 33.6± 36 pour cent ont été observés lors de la perfusion de 12, 24 et 40 mg’ kg-1 respectivement. Le temps nécessité pour le retour du Ca++ au niveau antérieur à la perfusion a été de 7.3 ± 0.4 minutes, 14.3± 1.6 minuteset21.3± 1.4 minutes respectivement pour les trois solutions.
Ces données montrent qu’un degré significatif d’hypocalcémie et de dépression myocardique peut accompagner la perfusion de solutions citratées. Le degré de dépression myocardique observé chez les animaux en santé et non soumis au stress n’a jamais causé de menace à la vie lors de l’injection des quantités de citrate mentionnées. Cependant, lorsque plusieurs transfusions sont requises, comme dans le choc hémorragique ou l’incompatibilité RH et que le système cardiovasculaire peut être sérieusement compromis au départ, une dépression myocardique secondaire à l’hypocalcémie peut se surajouter. Le shunt sanguin extracorporel s’est avéré un moyen simple, efficace et démonstratif de monitorer les niveau de Ca++ du système circulatoire pendant la perfusion de citrate.
Article PDF
Similar content being viewed by others
References
Tepperman, J. Metabolic and endocrine physiology, 3rd edition. Chicago: Yearbook Medical Publishers, Inc. (1973).
Ganong, W.F. Review of medical physiology, 8th edition. Los Altos, California: Lange Medical Publishers (1977).
OLinger, G., Hottenrott, C., Mulder, D.G.,et al. Acute clinical hypocalcemic myocardial depression during rapid blood transfusion and postoperative hemodialysis. J. Thorac. Cardiovas. Surg.72:503(1976).
Rumancik, W.M., BenLInger, K.J., Nahrwold, M.L.,et al. The QT interval and serum ionized calcium. J. A.M. A.240: 366(1978).
Hinkle, J.E. &Cooperman, L.H. Serum ionized calcium changes following citrated blood transfusion in anaesthetized man. Br. J. Anaesth.43: 1108 (1971).
Eyzaguirre, C. &Fidone, S.J. Physiology of the nervous system, 2nd edition. Chicago: Yearbook Medical Publishers, Inc. (1975).
Langer, G.A. Heart: excitation-contraction coupling. Ann. Rev. Physiol.55: 55 (1973).
Paschkis, K.E., Rakoff, A.E., Cantarow, A.,et al. Clinical Endocrinology, 3rd edition. New York: Harper and Row (1967).
Perkins, H.A., Snyder, M., Thatcher, C.,etal. Calcium ion activity during rapid exchange transfusion with citrated blood. Transfusion11: 204 (1971).
Gershanik, J.J., Levkoff, A.H. &Duncan, R. Serum ionized calcium values in relation to exchange transfusion. J. Ped.82: 847(1973).
Schaer, H. &Bachman, U. Ionized calcium in acidosis: differential effect of hypercapnia and lactic acidosis. Br. J. Anaesth.48: 842 (1974).
Denlinger, J.K., Nahrwold, M.L., Gibbs, P.S.,et al. Hypocalcaemia during rapid blood transfusion in anaesthetized man. Br. J. Anaesth.45: 995(1976).
Szymanski, J.O. Ionized calcium during plateletheresis. Transfusion18: 701 (1978).
Ladenson, J.H., Muller, W.V. &Sherman, L.A. Relationship of physical symptoms, ECG, free calcium and other blood chemistries in reinfusion with citrated blood. Transfusion18: 670 (1978).
Kahn, R.C., Jascott, D., Carlson, G.C.,et al. Massive blood replacement: correlation of ionized calcium, citrate and hydrogen ion concentration. Anesth. Analg.55: 274(1979).
McConnell, D. Shock: rapid transfusion, calcium levels, pH and body temperature. General Surgery - Epitomes129: 130(1978).
Maisels, J.M., Li, T.K., Piechocki, J.T.,et al. The effects of exchange transfusion on serum ionized calcium. Pediatrics53: 683 (1974).
Estes, E.H. Electrocardiology and vectorcardiology. In The Heart, by J.W. Hurst and R.B. Logue, eds. New York: McGraw-Hill Book Company Inc. (1970).
Author information
Authors and Affiliations
Additional information
Supported by a grant from The Utah Heart Association.
Additional research is being done in co-operation with the Department of Bioengineering at the University of Utah using intravascular miniature ChemFET (chemical field effect transistor) electrodes to monitor ionized calcium, potassium and hydrogen ion activity continuously.
Rights and permissions
About this article
Cite this article
Hayes, J.K., Bremer, R.A., Wong, K.C. et al. Continuous monitoring of serum ionized calcium in the dog during sodium citrate infusion using an extracorporeal blood shunt. Canad. Anaesth. Soc. J. 27, 458–463 (1980). https://doi.org/10.1007/BF03007044
Issue Date:
DOI: https://doi.org/10.1007/BF03007044