Acid-Base Physiology
References for Chapter 9 - Assessment of Acid-Base Disorders
   
Bernards WC. Interpretation of Clinical Acid-Base Data. Regional Refresher Courses in Anesthesiology. 1973; Vol 1, Chapter 2
Brackett NC et al. Carbon Dioxide Titration Curve of Normal Man. New Engl J Med. 1965; 272: 6-12
Brackett NC et al. Acid Base Response to Chronic Hypercapnia in Man. New Engl J Med. 1969; 280: 124-130.
Bunker J. The Great Trans-Atlantic Acid-Base Debate. Anesthesiology 1965; 25: 591-4.

Ehlers SM et al. Ventilatory Response in Lactic Acidosis and Diabetic Ketoacidosis. Mineral Elect Metab 1980; 3: 200-206.

Lu HC et al. Phenformin-associated Lactic Acidosis due to Imported Phenformin. Diabetes Care. 1996; 19: 1449-
1450.

Narins RG & Emmett M. Simple and Mixed Acid-Base Disorders: A Practical Approach. Medicine. 1980; 59:
161-187.
Abstract: Metabolic and respiratory acid-base disorders occur as single and mixed entities. When induced perturbations in PCO2, HCO3(-), pH, and serum electrolytes are interpreted in the light of sound physiologic principles, even the most complicated mixed disorders may be easily diagnosed. The pathophysiology underlying the simple disturbances is defined and used as a framework for discussion of the mixed metabolic, respiratory acid-base derangements. Formulae are presented which allow one to predict what the appropriate degree of metabolic compensation should be for any primary respiratory disorder, or what the PCO2 should be for any given degree of primary metabolic acidosis or alkalosis. The various clinical settings in which mixed acid-base disorders occur most commonly are discussed.

Perez GO, Oster JR & Rogers A. Acid-Base Disturbances in Gastrointestinal Disease. DigestiveDiseases & Sciences. 1987; 32: 1033-1043.

Saladino R & Shannon M. Accidental and Intentional Poisonings with Ethylene Glycol in Infancy: Diagnostic Clues and Management. Pediatric Emergency Care. 1991; 7: 93-96.
Abstract: Ethylene glycol has long been recognized as a potentially lethal poison and remains available today as automotive antifreeze and windshield deicer fluids. Ethylene glycol is rapidly absorbed from the gastrointestinal tract, with peak levels measured one to four hours after ingestion. Metabolism of the parent compound and the production of several organic acids are responsible for the metabolic acidosis observed in ethylene glycol poisoning. Target organ cellular damage is seen in the kidney, brain, myocardium, pancreas, and blood vessel walls. Renal tubular deposition of calcium oxalate crystals is felt to be responsible for the development of the severe renal injury which may accompany ethylene glycol ingestion. The clinical course is quite varied and includes inebriation, hematuria, cardiorespiratory compromise, and neurologic effects. Prompt diagnosis and initiation of treatment, including ethanol therapy and hemodialysis, is necessary to ameliorate the effects of ethylene glycol ingestion. Two cases of ethylene glycol poisoning, one accidental & one intentional, are reviewed.

Schorn TF et al. Barium Carbonate Intoxication. Intensive Care Medicine. 1991; 17: 60-62.

Schwartz WB & Relman AS. A Critique of the Parameters used in the Evaluation of Acid-Base Disorders. N Engl J Med. 1963; 268: 1382-8.

Severinghaus JW. Acid-Base Balance Nomogram - A Boston-Copenhagen Detente. Anesthesiology. 1976; 45: 539-541.
Abstract: Quantitation of actual and expected complete compensation for chronic hypercapnia in man is facilitated by addition of data of Brackett et al. in the form of an arc to the Siggaard-Andersen alignment nomogram. Percentage of compensation is defined as 100 times the ratio of observed to predicted (fully compensated) base excess at the patient's pCO
2. Extracellular fluid base excess, defined as BE3, is estimated from a 3-g hemoglobin line added to the nomogram.
Severinghaus JW. Siggaard-Andersen and the great Trans-Atlantic Acid-Base Debate. Scand J Clin Lab Invest 1993; 53 Suppl 214: 99-104
Abstract: In the late 1950's, while working with Poul Astrup's equilibration method of blood gas analysis, Siggaard-Andersen introduced a new parameter called base excess (BE) to quantify the non-respiratory acid-base imbalance. "The Great-Transatlantic Acid-Base Debate" arose when the "Boston" school, whose bicarbonate based analysis had been developed during pre-1950 Van Slyke days, (initially) argued that BE was not independent of pCO
2 in vivo. Although Siggaard-Andersen and others then introduced a standard BE independent of PCO2, the Boston and Copenhagen schools are "unreconciled". While SBE is now used by most physicians, teaching and interpretation of acid-base chemistry remains confusing, "Boston" school laboratories refusing to report SBE, their students being asked to learn the 6 bicarbonate equations and rules, an old concept being reintroduced as "strong ion difference", or SID, and some wanting to discard pH in favor of nanomoles of H+, and end the era of "Arrhenius, Severinghaus and Henderson-Hasselbalch".
Walmsley RN & White GH. Normal Anion Gap (Hyperchloremic) Acidosis. Clin Chem 1985;31: 309-313.
Abstract: Hyperchloremic metabolic acidosis in which the anion gap is within normal limits is a common condition in the hospital population, and often presents a difficult diagnostic
problem. We describe nine typical cases of this disorder and suggest a logical approach to its evaluation.
Walmsley RN & White GH. Mixed Acid-Base Disorders. Clin Chem. 1985; 31: 321-325.
Abstract:
Mixed acid-base disorders, the occurrence of two or more primary acid-base disturbances in the same patient, are common in the hospital population, but are usually misdiagnosed because of lack of knowledge of the consequences of the primary disturbances. This paper describes seven examples of these disorders recently seen in the authors' hospital, and provides a logical approach to their diagnosis.
 

 

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