Present therapies for patients having lactic acidosis are controversial. Bicarbonate has often been used in these patients with the aim of improving cardiac function, although conventional therapies including bicarbonate, have not improved the well known high mortality associated with lactic acidosis. Bicarbonate did not improve hemodynamics in critically ill patients having lactic acidosis, during the first prospective randomised trial published recently. Furthermore, in these patients, bicarbonate was associated with hypercapnia and hypocalcemia. In related large animal studies, bicarbonate did not increase left ventricular contractility during endogenous and infused lactic acidosis. Because there are no clinical studies to support a role for bicarbonate therapy in critically ill patients having lactic acidosis and shock, and because important side effects are well described, the usage of bicarbonate in these patients should now be discouraged. Bicarbonate therapy during cardiac arrest is in most cases ineffective, counterproductive, and therefore rarely indicated. Carbicarb and dichloroacetate are therapeutic alternatives to bicarbonate but neither have been shown to improve outcome in any patient group. It is likely that improved outcome for patients having lactic acidosis will depend most importantly upon improved therapies for the underlying conditions which cause lactic acidosis, and on a greater emphasis by clinicians on assessing and improving tissue perfusion during shock.
|Number of pages||8|
|Journal||Applied Cardiopulmonary Pathophysiology|
|Publication status||Published - 1 Dec 1991|