Evidence obtained in animal and man in shock indicates that the initial acid-base disturbance in hemorrhagic shock is metabolic acidosis.1 This acidosis results from the production of acid metabolites by cells forced into anaerobic metabolism by hypoxia. The hypoxia may be due to failure of the perfusion pump (heart), increased vascular resistance, loss of the perfusate (blood), or a failure to oxygenate the perfusate. In hemorrhagic shock without pulmonary injury, the first three are the most important. The opportunity to study previously healthy humans with severe hemorrhagic traumatic shock before treatment might cast light on the nature of the acid-base disturbance of shock in man.
The following study was designed to answer the following questions: (1) What is the initial acid-base profile in humans, in shock, from trauma and blood loss. (2) Can the degree of acid-base derangement be predicted from the magnitude of injury and blood loss, or