THE presence of acidemia in conditions of ventilatory insufficiency, such as asphyxia neonatorum, circulatory insufficiency, and in prematurely born infants with respiratory distress, has been well documented. Rudolph and his associates have reasoned that when pulmonary blood flow is reduced, physiologic compensation for the acidemia is impaired and a vicious circle leading to uncontrolled metabolic acidemia and possible death may result. Attempts to interrupt this process have been presented by Usher for respiratory distress syndrome and by Rudolph and Danilowicz in congenital heart disease.
The approach of the use of infusions of alkali to correct the "metabolic component" of an acidemia that has an underlying basis in failure of ventilation has achieved widespread acceptance. The purpose of this paper is to call attention to an important possible risk of such therapy—hyperosmolality.
In particular, the recent interest in instant repair of neonatal acidemia and the now common practice in patients of all ages of rapid repair of acidemia by NaHCO3 infusions in the management of patients undergoing cardiac surgery and of those being resuscitated have rekindled interest in the limits of tolerance for the infusion of hyperosmolal solutions.
The current use of concentrated contrast materials for angiography, the intravenous use of 50% glucose solutions for neonates, and the increased use of concentrated mannitol and other hyperosmolal solutions for treatment of shock and cerebral edema constitute other clinical situations calling for a review of the underlying physiologic changes attending such therapy and emphasizing when and where serious danger exists in inducing changes in body fluid osmolality.
THE TREATMENT OF VENTILATORY INSUFFICIENCY AFTER PULMONARY RESECTION WITH TRACHEOSTOMY AND PROLONGED ARTIFICIAL VENTILATION