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British Journal of Anaesthesia, 1995, Vol. 74, No. 4 424-429
© 1995 The Board of Management and Trustees of the British Journal of Anaesthesia

research-article

Cardiovascular consequences of severe hypophosphataemia in brain-dead patients{dagger}

B. RIOU, MD*, P. KALFON, MD, M. AROCK, MD, J.-P. GOARIN, MD, M. SAADA, MD and P. VIARS, MD

Department of Anesthesiology, CHU Pitié-Salpêtrière, Paris VI University Paris, France
Department of Biology for Emergencies, CHU Pitié-Salpêtrière, Paris VI University Paris, France

*Address for correspondence: Département d'Anesthésie-Réanimation, Groupe Hospitalier Pitié-Salpêtrière, 47 Boulevard de l'hôpital, 75651 Paris Cedex 13, Paris, France

Hypophosphataemia is known to induce reversible myocardial dysfunction, but the incidence of hypophosphataemia and its effect on myocardial function during brain death are unknown. In 90 consecutive brain-dead patients, we measured plasma concentrations of phosphate and left ventricular ejection fraction area (LVEFa), using transoesophageal echocardiography. In 15 severely hypophosphataemic (<0.40 mmol litre–1), consecutive, brain-dead patients, haemodynamic status, LVEFa, and oxygen delivery and consumption were assessed before and after phosphorus loading (0.30 mmol kg–1). In 10 other brain-dead patients, urine elimination of phosphates was measured. Only 30 (33%) brain-dead patients had normal plasma phosphate concentrations, 22 (24%) had mild hypophosphataemia (0.40–0.80 mmol litre–1) and 38 (42%) had severe hypophosphataemia (<0.40 mmol litre–1). There were no significant differences in LVEFa between these three groups (mean 53 (SD 16), 55 (12) and 51 (17)%, respectively) and no significant correlation between LVEFa and plasma phosphate concen tration (r = 0.04). In 15 severely hypophosphataemic patients, phosphorus loading increased plasma phosphate concentration from 0.30 (0.10) to 1.06 (0.41) mmol litre–1, but did not modify haemodynamic status, LVEFa or oxygen delivery and consumption. In 10 other patients, urine phosphorus elimination was 16.8 (23.3) mmol/ 24 h while plasma phosphate concentration was at its highest level (0.80 (0.37) mmol litre–1), and only one of these patient had a slightly elevated phosphaturia. In conclusion, hypophosphataemia frequently occurs after brain death but has no significant cardiovascular consequences, suggesting that it is related to intracellular transfer and not phosphorus depletion. Consequently, no significant improvement in myocardial function can be expected from phosphorus loading.

{dagger} Presented in part at the Annual Meeting of the American Society of Anesthesiologists, New Orleans, October 1992.


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