Diagnosis of Metabolic Acid–Base Disturbances in Critically Ill Patients
VLADIMIR FENCL, ANTONÍN JABOR, ANTONÍN KAZDA, and JAMES FIGGE
Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, and Departments of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts; Departments of Clinical Biochemistry, Hospital Kladno and PostgraduateMedical School, Prague, Czech Republic; Departments of Medicine, St. Peter’s Hospital, and Biomedical Sciences, State University of New York, Albany, New York
We compare two commonly used diagnostic approaches, one relying on plasma bicarbonate concentration and “anion gap,” the other on “base excess,” with a third method based on physicochemical principles, for their value in detecting complexmetabolic acid–base disturbances. We analyzed arterial blood samples from 152 patients and nine normal subjects for pH, PCO2, and concentrations of plasma electrolytes and proteins. Ninety-six percent of the patients had serum albumin concentration 3 SD below the mean of the control subjects. In about one-sixth of the patients, base excess and plasma bicarbonate were normal. In a great majority ofthese apparently normal samples, the third method detected simultaneous presence of acidifying and alkalinizing disturbances, many of them grave. The almost ubiquitous hypoalbuminemia confounded the interpretation of acid–base data when the customary approaches were applied. Base excess missed serious acid–base abnormalities in about one-sixth of the patients; this method fails when the plasmaconcentrations of the nonbicarbonate buffers (mainly albumin) are abnormal. Anion gap detected a hidden “gap acidosis” in only 31% of those samples with normal plasma bicarbonate in which such acidosis was diagnosed by the third method; when adjusted for hypoalbuminemia, it reliably detected the hidden abnormal anions. The proposed third method identifies and quantifies individual components ofcomplex acid–base abnormalities and provides insights in their pathogenesis.
Two diagnostic systems are commonly used for interpreting acid–base data. One centers on plasma bicarbonate concentration ([HCO3 ]) (1) and “anion gap” (AG) (2), and the other on “base excess/deficit” (BE) (3). These two systems do not ascribe an explicit role to abnormal concentrations of plasma nonbicarbonate buffers inthe pathogenesis of nonrespiratory (metabolic) acid–base abnormalities. We posit that, owing to this omission, important metabolic acid–base abnormalities can be missed in the complex disturbances seen in critically ill patients. The main “nonbicarbonate buffers” in blood plasma are the plasma proteins (4); another (minor) component of this buffer system is inorganic phosphate (Pi) (5). Among theplasma proteins it is the serum albumin that participates in the chemical equilibria that determine the acid–base status of plasma, by carrying a variable net negative charge at pH values compatible with life (6, 7). Because this negative charge figures in the electroneutrality of plasma, the amphiprotic molecule of albumin can be viewed to act as a nonvolatile weak
(Received in original formApril 26, 1999 and in revised form July 28, 2000) Supported by Research Grant 0702-3 from the Ministry of Health, Czech Republic (A.K. and A.J.) and by Lucille P. Markey Charitable Trust (J.F.). Correspondence and requests for reprints should be addressed to Dr. V. Fencl, Division of Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115-6110. E-mail:email@example.com This article has an online data supplement, which is accessible from the table of contents online at www.atsjournals.org. Am J Respir Crit Care Med Vol 162. pp 2246–2251, 2000 Internet address: www.atsjournals.org
acid in plasma’s chemical equilibria. Normal serum globulins do not carry a significant net electric charge at pH values prevailing in plasma (6, 7)....
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