Date of Award


Document Type

Open Access Thesis

Degree Name

Medical Doctor (MD)

First Advisor

Dr. Howard Levitin


[From the Introduction] In chronic renal insufficiency one of the products of metabolism which accumulates in the body is the hydrogen ion. The phosphoric, sulfuric, and organic acids usually eliminated in the urine accumulate. The respiratory system can and does decrease the hydrogen ion content of the body by decreasing the amount of carbonic acid present. The accumulating hydrogen ions also react with various bases throughout the body. The net result of metabolic production, respiratory elimination, and body buffering is reflected in the blood as chronic, partially compensated, metabolic acidosis. As expected the carbonic acid and block buffer concentrations are decreased while the concentration of the accumulating anions and hydrogen ion are increased. The adaptive logic of respiratory compensation and body buffering are obvious. Given amounts of unexcretable acids produce lesser increases in hydrogen ion concentration and the organism is protected from the potentially fatal effects of increased hydrogen ion concentration. Respiratory compensation and buffering have been extensively studies in the past two decades in an attempt to quantitatively describe the phenomena and define the mechanisms involved Patients receiving periodic hemodialysis for chronic renal insufficiency have may characteristics which make them particularly suited for studying the reactions to changes in acid-base status. Their kidneys no longer excrete significant amounts of acid. They are repeatedly subjected to a changing acid-base status during therapy and can serve as their own controls. Painless sampling of arterial blood is available. In addition the data obtained might be useful to the clinicians responsible for the care of the patients studied. For these reasons it was decided to measure the acid-base parameters of the patients treated by the Hemodialysis Unit of the Yale-New Haven Hospital and the respiratory response to the changes in those parameters reflected by the carbon dioxide tension in the arterial blood (pCO2).