CARDIOVASCULAR CONSEQUENCES OF SEVERE HYPOPHOSPHATEMIA IN BRAIN-DEAD PATIENTS

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 concentration (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, suggest ing that it is related to intracellular transfer and not phosphorus depletion. Consequently, no significant improvement in myocardial function can be expected from phosphorus loading.