Alkaline buffers for correction of metabolic acidosis during cardiopulmonary resuscitation with focus on Tribonat--a review.

A combined hypercarbic and metabolic acidosis develops during the low flow state of cardiac arrest treated with cardiopulmonary resuscitation. Several negative consequences of the acidosis have been demonstrated, two of the most important being reduced contractility of the ischaemic but still beating myocardium and impaired resuscitability of the arrested heart. Even though interventions to re-establish a spontaneous circulation should be the number one priority during cardiopulmonary resuscitation, attempts to treat the acidosis are often carried out in order to avoid the reported negative inotropic effect. Different alkaline buffers have been used, but it has been demonstrated over the years that such treatment may aggravate the situation due to a variety of deleterious side-effects of the buffers. A mixture of THAM, acetate, sodium bicarbonate and phosphate registered as Tribonat has been suggested as a suitable alternative to conventional buffer substances. The problems preceding the designation of Tribonat as well as studies evaluating its effects are reviewed in this article. Tribonat seems to offer a more well-balanced buffering without any major disadvantages compared with previously used alkaline buffers, even though improved survival has not been reported.