Measurement of acid–base resuscitation endpoints: lactate, base deficit, bicarbonate or what?

Abstract

Inadequate oxygen delivery to the tissues frequently results in significant metabolic acidosis. The resultant cellular and organ dysfunction can increase morbidity, mortality and hospital stay. Early diagnosis of shock can lead to early resuscitation efforts that can prevent ongoing tissue injury. This review focuses on the metabolic, hemodynamic and regional perfusion endpoints utilized in the diagnosis of metabolic acidosis resulting from shock. Resuscitation strategies aimed at supranormal oxygen delivery will be discussed. Serum pH, lactate, base deficit and bicarbonate have all been extensively studied as clinical markers of metabolic acidosis in shock. While their trend helps guide resuscitation, no single marker or specific value can be utilized to guide resuscitation for all patients. Hemodynamic parameters and regional tissue endpoints are designed to identify compensated shock before it progresses to uncompensated shock. Resuscitation strategies initiated in the early phases of shock can reduce complications and death. Efforts to resuscitate patients to supranormal oxygen delivery endpoints have demonstrated mixed success, with several notable complications. Despite the large number of endpoints available to the clinician, none are universally applicable and none have independently demonstrated improved survival when guiding resuscitation. Patients who respond well to initial resuscitation efforts demonstrate a survival advantage over nonresponders.