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 Mizock BA. Utility of standard base excess in acid-base analysis.[comment]. [Comment. Editorial] Critical Care Medicine. 26(7):1146-7, 1998 Jul.
UI: 9671353

 Link Directly to Fulltext article in Ovid

Schlichtig R. Grogono AW. Severinghaus JW. Human PaCO2 and standard base excess compensation for acid-base imbalance.[comment]. [Journal Article. Meta-Analysis] Critical Care Medicine. 26(7):1173-9, 1998 Jul.
 

<1>

Unique Identifier:9671365

Authors: Schlichtig R. Grogono AW. Severinghaus JW.

Institution: Department of Research and Development, Pittsburgh Veterans Affairs Medical Center, PA, USA.

Title: Human PaCO2 and standard base excess compensation for acid-base imbalance.[comment].

Source: Critical Care Medicine. 26(7):1173-9, 1998 Jul.

Abstract: OBJECTIVES: Renal and respiratory acid-base regulation systems interact with each other, one compensating (partially) for a primary defect of the other. Most investigators striving to typify compensations for abnormal acid-base balance have reported their findings in terms of arterial pH, PaCO2, and/or HCO3-. However, pH and HCO3- are both altered by both respiratory and metabolic changes. We sought to simplify these relations by expressing them in terms of standard base excess (SBE in mM), which quantifies the metabolic balance and is independent of PaCO2. DESIGN: Meta-analysis. SETTING: Historical synthesis developed via the Internet. PATIENTS: Arterial pH, PaCO2, and/or HCO3- data sets were obtained from 21 published reports of patients considered to have purely acute or chronic metabolic or respiratory acid-base problems. INTERVENTIONS: We used the same data to compute the typical compensatory responses to imbalances of SBE and PaCO2. Relations were expressed as difference (delta) from normal values for PaCO2 (40 torr [5.3 kPa]) and SBE (0 mM). MEASUREMENTS AND MAIN RESULTS: The data of patient compensatory changes conformed to the following equations, as well as to the traditional PaCO2 vs. HCO3- or H+ vs. PaCO2 equations: Metabolic change responding to change in PaCO2: Acute deltaSBE = 0 x deltaPaCO2, hence: SBE = 0, Chronic deltaSBE = 0.4 x deltaPaCO2. Respiratory change responding to change in SBE: Acidosis deltaPaCO2 = 1.0 x deltaSBE, Alkalosis deltaPaCO2 = 0.6 x deltaSBE. CONCLUSION: Data reported by many investigators over the past 35 yrs on typical, expected, or "normal" human compensation for acid-base imbalance may be expressed in terms of the independent variables: PaCO2 (respiratory) and SBE (metabolic). CAS Registry/EC Number 0 (Bicarbonates). 124-38-9 (Carbon Dioxide).

<2>

Unique Identifier:9671353

Authors: Mizock BA.

Title: Utility of standard base excess in acid-base analysis.[comment].

Source: Critical Care Medicine. 26(7):1146-7, 1998 Jul.

<3>

Unique Identifier:8599264

Authors: Siggaard-Andersen O. Fogh-Andersen N.

Institution: Department of Clinical Biochemistry, Herlev Hospital, University of Copenhagen, Denmark.

Title: Base excess or buffer base (strong ion difference) as measure of a non-respiratory acid-base disturbance.

Source: Acta Anaesthesiologica Scandinavica. Supplementum. 107:123-8, 1995.

Abstract: Stewart in 1983 (Can J Physiol Pharmacol 1983: 61: 1444) reintroduced plasma buffer base under the name "strong ion difference" (SID). Buffer base was originally introduced by Singer and Hastings in 1948 (Medicine (Baltimore) 1948: 27: 223). Plasma buffer base, which is practically equal to the sum of bicarbonate and albuminate anions, may be increased due to an excess of base or due to an increased albumin concentration. Singer and Hastings did not consider changes in albumin as acid-base disorders and therefore used the base excess, i.e., the actual buffer base minus the buffer base at normal pH and pCO2, as measure of a non-respiratory acid-base disturbance. Stewart and followers, however, consider changes in albumin concentration to be acid-base disturbances: a patient with normal pH, pCO2, and base excess but with increased plasma buffer base due to increased plasma albumin concentration get the diagnoses metabolic (strong ion) alkalosis (because plasma buffer base is increased) combined with metabolic hyperalbuminaemic acidosis. Extrapolating to whole blood, anaemia and polycytaemia should represent types of metabolic alkalosis and acidosis, respectively. This reveals that the Stewart approach is absurd and anachronistic in the sense that an increase or decrease in any anion is interpreted as indicating an excess or deficit of a specific acid. In other words, a return to the archaic definitions of acids and bases as being the same as anions and cations. We conclude that the acid-base status (the hydrogen ion status) of blood and extracellular fluid is described in terms of the arterial pH, the arterial pCO2, and the extracellular base excess. It is measured with a modern pH-blood gas analyser. The electrolyte status of the plasma is a description of the most important electrolytes, usually measured in venous blood with a dedicated electrolyte analyser, i.e., Na+, Cl-, HCO3-, and K+. Albumin anions contribute significantly to the anions, but calculation requires measurement of pH in addition to albumin and is usually irrelevant. The bicarbonate concentration may be used as a screening parameter of a nonrespiratory acid-base disturbance when respiratory disturbances are taken into account. A disturbance in the hydrogen ion status automatically involves a disturbance in the electrolyte status, whereas the opposite need not be the case. CAS Registry/EC Number 0 (Bicarbonates). 0 (Blood Proteins). 0 (Buffers). 0 (Chlorides). 0 (Hemoglobins). 0 (Phosphates). 0 (Serum Albumin). 0 (Serum Globulins). 124-38-9 (Carbon Dioxide). 7440-09-7 (Potassium). 7440-23-5 (Sodium).

<4>

Unique Identifier:8599263

Authors: Jabor A. Kazda A.

Institution: Department of Clinical Biochemistry, Hospital Kladno, Czech Republic.

Title: Modelling of acid-base equilibria.

Source: Acta Anaesthesiologica Scandinavica. Supplementum. 107:119-22, 1995.

Abstract: A quantitative evaluation of metabolic acid-base component is described. The model is based on Stewart's analysis of acid-base chemistry. The metabolic component of acid-base disturbances is divided into four partial metabolic disorders; they can result from abnormal concentrations of chloride, albumin and phosphate disturbances, or from appearance of abnormal unidentified strong anions. The efficiency of the model is sufficient, quantitative partial results are given in the same units as base excess. In complex acid-base disturbances, such as are seen in critically ill patients, a detailed analysis of the specific components of the metabolic acid-base status allows one to plan specific therapeutic interventions. CAS Registry/EC Number 0 (Anions). 0 (Bicarbonates). 0 (Chlorides). 0 (Phosphates). 0 (Serum Albumin). 7439-95-4 (Magnesium). 7440-09-7 (Potassium). 7440-23-5 (Sodium). 7440-70-2 (Calcium).

<5>

Unique Identifier:8393530

Authors: Rama BN. Varghese J. Genova G. Kumar S.

Institution: Creighton Cardiac Center, Omaha, NE 68131-2044.

Title: Severe acute metabolic alkalosis.

Source: Nebraska Medical Journal. 78(6):151-4, 1993 Jun.

Abstract: We have presented the case of a 34 year old male patient who was admitted with severe metabolic alkalosis (MA). Peak serum HCO3 was 96 mg/dl and compensatory PCO2 was 95 which, to our knowledge, has never been reported before in a patient with MA. MA was probably generated by consumption of high amount of NaHCO3 and renal impairment and maintained by impaired renal function due to volume depletion hypokalemia and hyochloremia. The patient was successfully treated with IV administration of saline and KCL. CAS Registry/EC Number 0 (Bicarbonates). 144-55-8 (Sodium Bicarbonate). 7440-23-5 (Sodium).

<6>

Unique Identifier:3439553

Authors: Vaz Carneiro A. Sebastian A. Cogan MG.

Institution: Department of Medicine, University of California, San Francisco.

Title: Reduced glomerular filtration rate can maintain a rise in plasma bicarbonate concentration in humans.

Source: American Journal of Nephrology. 7(6):450-4, 1987.

Abstract: In humans, deficiency of chloride and potassium were found to perpetuate the hyperbicarbonatemia that attends metabolic alkalosis induced by gastric aspiration partly by increasing renal bicarbonate reabsorption, commensurate with the attendant increase in filtered bicarbonate load, and partly by decreasing glomerular filtration rate (GFR), which minimizes the degree of which the filtered bicarbonate load increases and thereby minimizes the requisite increase in bicarbonate reabsorption. The relative contribution of stimulated renal bicarbonate reabsorption might increase, however, if the supply of extrarenal bicarbonate is increased, in which case a greater degree of hyperbicarbonatemia would be sustained. To investigate that possibility, we reexamined the mechanism of perpetuation of gastric alkalosis in normal subjects eating a low NaCl diet supplemented with bicarbonate salts. Prior to gastric aspiration, plasma bicarbonate concentration ([HCO3]p) and pH were higher than in similarly studied subjects not receiving bicarbonate: 29.9 +/- 0.6 vs. 25.3 +/- 0.1 and 7.43 +/- 0.008 vs. 7.41 +/- 0.002 mEq/l, respectively. With continued bicarbonate supplementation, gastric aspiration induced a further significant increase (p less than 0.05) in [HCO3]p of 10.8%, to values not significantly different from those in nonbicarbonate-loaded subjects with gastric alkalosis: 33.2 +/- 1.2 mEq/l. GFR decreased significantly by 8.4% (from 98 +/- 4 to 90 +/- 3 ml/min, p less than 0.025), offsetting nearly commensurately the increase in [HCO3]p so that total bicarbonate reabsorption was not significantly increased (2.90 +/- 0.12 vs. 2.97 +/- 0.19 mEq/min, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS) CAS Registry/EC Number 0 (Bicarbonates). 0 (Sodium, Dietary). 7440-09-7 (Potassium).

<7>

Unique Identifier:3122108

Authors: Lameire N. Matthys E. Vanholder R. De Keyser K. Pauwels W. Nachtergaele H. Lambrecht L. Ringoir S.

Institution: University Hospital, Renal Division, Gent, Belgium.

Title: Causes and prognosis of acute renal failure in elderly patients.

Source: Nephrology Dialysis Transplantation. 2(5):316-22, 1987.

Abstract: In this retrospective study, 287 patients with acute renal failure observed between 1980 and 1985 were divided into 2 groups, according to age: group 1 of 65 years or more (n = 100) and group 2 between 17 and 64 years (n = 187). In both age groups the whole spectrum of causes of acute renal failure was found, but within that spectrum a higher incidence of post-renal failure, acute renal vascular disease and of hypovolaemic acute renal failure was noted in group 1 versus group 2. On the other hand, pigment-induced acute renal failure was lower in group 1 (4%) versus group 2 (13%). The overall survival was 54% in the elderly versus 56% in the younger patients (NS). A close relationship between survival and the number of postadmission complications was found in both groups. Interestingly, the presence of severe hypokalaemia (less than 3.5 mmol/l) and metabolic alkalosis (plasma HCO3 greater than 30 mmol/l) was associated with a very high mortality of 73% and 86% respectively in the elderly patients. Complete or incomplete recovery of renal function was the same in both age groups. It is concluded that age alone should not be used as a discriminating factor in therapeutic decisions concerning acute renal failure in an older patient.

<8>

Unique Identifier:3116894

Authors: Javaheri S. Kazemi H.

Institution: Pulmonary Division, Veterans Administration Medical Center, Cincinnati, OH 45220.

Title: Metabolic alkalosis and hypoventilation in humans. [Review] [62 refs]

Source: American Review of Respiratory Disease. 136(4):1011-6, 1987 Oct.

<9>

Unique Identifier:2983518

Authors: Kassirer JP.

Title: Life-threatening acid-base disorders.

Source: Advances in Nephrology From the Necker Hospital. 14:67-85, 1985.

<10>

Unique Identifier:3917878

Authors: Walmsley RN. White GH.

Title: Mixed acid-base disorders.

Source: Clinical Chemistry. 31(2):321-5, 1985 Feb.

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. CAS Registry/EC Number 0 (Bicarbonates). 124-38-9 (Carbon Dioxide).

<11>

Unique Identifier:6410135

Authors: Cogan MG. Liu FY. Berger BE. Sebastian A. Rector FC Jr.

Title: Metabolic alkalosis. [Review] [63 refs]

Source: Medical Clinics of North America. 67(4):903-14, 1983 Jul.

<12>

Unique Identifier:6818032

Authors: Oberleithner H. Greger R. Lang F.

Title: The effect of respiratory and metabolic acid-base changes on ionized calcium concentration: in vivo and in vitro experiments in man and rat.

Source: European Journal of Clinical Investigation. 12(6):451-5, 1982 Dec.

Abstract: Correlation of ionized calcium concentration, [Ca2+] and blood pH has long been recognized. So far no distinction of the acid-base changes, i.e. respiratory changes or metabolic changes seemed necessary. The present study, with the use of a recently developed system for in vivo analysis of [Ca2+], and with in vitro experiments reinvestigates this question. In a first series respiratory and metabolic changes were induced in rats. Changes of [Ca2+] (delta [Ca2+]) and of plasma pH (delta pH) were recorded continuously in vivo, plasma bicarbonate, [HCO-3] was measured in vitro. In a second series respiratory and metabolic changes were induced in sixteen volunteers and, separately, in vitro in plasma and modified Ringer solution, and the same parameters were determined. In all experiments delta [Ca2+] correlates negatively with delta pH. However, the correlation in respiratory changes was significantly less as compared to that in metabolic changes. As expected, delta [HCO-3] correlates positively with pH in metabolic and negatively in respiratory changes. We conclude from these experiments that in metabolic changes the effects of calcium-albumin interaction and calcium complexation with bicarbonate are additive, whereas both effects oppose each other in respiratory changes. This might explain the blunted effect of pH changes on [Ca2+] in respiratory changes. CAS Registry/EC Number 0 (Bicarbonates). 0 (Cations, Divalent). 7440-70-2 (Calcium).

<13>

Unique Identifier:6794744

Authors: Javaheri S. Nardell EA.

Title: Severe metabolic alkalosis: a case report.

Source: British Medical Journal Clinical Research Ed.. 283(6298):1016-7, 1981 Oct 17.

Abstract: A 45-year-old man who was admitted with nausea, vomiting, and abdominal pain was found to have severe metabolic alkalosis, with a PaCO2 of 11.4kPa (85.5 mm Hg), PaO2 of 5.8 kPa (43.5 mm Hg), pH of 7.61, and plasma bicarbonate concentration of 82.0 mmol/l. He was treated with oxygen, intravenous physiological saline, and phenytoin and improved within 48 hours. Radiographs showed gastric outlet obstruction secondary to peptic ulcer, which was treated by surgery. Though sever, the rise in carbon dioxide concentration in this patient was probably lifesaving. The PaCO2 was therefore allowed to fall gradually as the alkalosis was treated. The return of both PaCO2 and plasma bicarbonate values to normal in parallel suggests that hypoventilation compensated for the metabolic alkalosis and emphasises the importance of conservative treatment in cases of metabolic alkalosis. CAS Registry/EC Number 0 (Bicarbonates). 124-38-9 (Carbon Dioxide).

<14>

Unique Identifier:6774200

Authors: Narins RG. Emmett M.

Title: Simple and mixed acid-base disorders: a practical approach.

Source: Medicine. 59(3):161-87, 1980 May.

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. CAS Registry/EC Number 0 (Electrolytes). 124-38-9 (Carbon Dioxide).

<15>

Unique Identifier:7355681

Authors: Milhorn HT Jr.

Title: Understanding arterial blood gases.

Source: American Family Physician. 21(3):112-20, 1980 Mar.

Abstract: Arterial blood gases are useful in establishing acid-base status, determining the degree of impairment of the lungs as a gas exchanger, diagnosing such important phenomena as pulmonary emboli and implementing or adjusting oxygen therapy. The balance among H+, HCO3- and CO2 is represented by the equation H+ + HCO3- in equilibrium CO2 + H2O. Primary alterations of either component of the left-hand side of the equation result in metabolic acid-base balance disturbances; primary alterations of CO2 result in respiratory acid-base balance disturbances. CAS Registry/EC Number 0 (Bicarbonates). 124-38-9 (Carbon Dioxide). 7782-44-7 (Oxygen).

<16>

Unique Identifier:578849

Authors: Coe FL.

Title: Metabolic alkalosis.

Source: JAMA. 238(21):2288-90, 1977 Nov 21.

<17>

Unique Identifier:17497

Authors: Martinez-Maldonado M. Sanchez-Montserrat R.

Title: Respiratory acidosis and alkalosis.

Source: Clinical Nephrology. 7(5):191-200, 1977 May.

Abstract: The physiology of respiratory control of acid-base balance is reviewed. The pathophysiological mechanisms during hypercapnia and hypocapnia are discussed in the light of the causes and clinical manifestations of these disturbances. In addition to the role of the kidney in the compensatory processes of these disturbances, renal functional changes during acute and chronic pulmonary acid-base derangement is discussed. Some of the difficulties encountered in the patient with chronic renal disease in whom respiratory abnormalities may be present are also discussed. CAS Registry/EC Number 0 (Bicarbonates). 0 (Electrolytes).

<18>

Unique Identifier:14092

Authors: Haskins SC.

Title: An overview of acid-base physiology. [Review] [70 refs]

Source: Journal of the American Veterinary Medical Association. 110(4):423-8, 1977 Feb 15.

<19>

Unique Identifier:401925

Authors: Emmett M. Narins RG.

Title: Clinical use of the anion gap.

Source: Medicine. 56(1):38-54, 1977 Jan.

Abstract: The concepts underlying the clinical use of the anion gap (AG) and those disorders associated with its alteration are reviewed. A substantial increase in the AG usually indicates the presence of a metabolic acidosis, unless large doses of certain antibiotics or sodium salts of organic acids are being used. The etiology, pathogenesis and diagnosis of high AG metabolic acidoses are discussed. Stress is placed upon the utility of the AG in defining the cause of the acidosis, and as a guide to therapy in certain organic acidoses. A decrease in the normal AG occurs in dilutional states, hypoalbuminemia, hypercalcemia, hypermagnesemia, hypernatremia, diseases associated with hyperviscosity, bromide intoxication, and in certain paraproteinemias. The important clue provided by a low or negative AG in the diagnosis of certain of these life-threatening disorders is emphasized. CAS Registry/EC Number 0 (Bicarbonates). 0 (Electrolytes). 0 (Ethylene Glycols). 0 (Lactates). 123-63-7 (Paraldehyde). 4697-36-3 (Carbenicillin). 50-78-2 (Aspirin). 67-56-1 (Methanol). 7440-23-5 (Sodium).

<20>

Unique Identifier:4414

Authors: Keyes JL.

Title: Blood-gas analysis and the assessment of acid-base status.

Source: Heart & Lung: Journal of Acute & Critical Care. 5(2):247-55, 1976 Mar-Apr.

Abstract: In this article the more common kinds of acid-base disorders have been discussed. To accurately assess the kind of acid-base disturbance found in a patient, the clinician must know the arterial pH, PaCO2, and the [HCO-3] in arterial blood. Acid-base disturbances are associated with fluid and electrolyte disturbances. Potassium balance is often upset in acid-base disturbances. Accurate determination of K+ balance requires serial or repeated determinations of plasma K+ concentration as well as careful clinical monitoring. CAS Registry/EC Number 0 (Bicarbonates). 124-38-9 (Carbon Dioxide). 7440-09-7 (Potassium).

<21>

Unique Identifier:536

Authors: Garella S. Chang BS. Kahn SI.

Title: Dilution acidosis and contraction alkalosis: review of a concept.

Source: Kidney International. 8(5):279-83, 1975 Nov.

<22>

Unique Identifier:4138707

Authors: Anonymous.

Title: Editorial: Acids, bases, and nomograms.

Source: Lancet. 2(7884):814-6, 1974 Oct 5.

<23>

Unique Identifier:4472489

Authors: Boning D.

Title: The "in vivo" and "in vitro" CO2-equilibration curves of blood during acute hypercapnia and hypocapnia. II. Theoretical considerations.

Source: Pflugers Archiv - European Journal of Physiology. 350(3):213-22, 1974.

<24>

Unique Identifier:4472488

Authors: Boning D. Schweigart U. Nutz V. Stegemann J.

Title: The "in vivo" and "in vitro" CO2-equilibration curves of blood during acute hypercapnia and hypocapnia. I. Experimental investigations.

Source: Pflugers Archiv - European Journal of Physiology. 350(3):201-12, 1974.

<25>

Unique Identifier:4606269

Authors: Heinemann HO. Goldring RM.

Title: Bicarbonate and the regulation of ventilation. [Review] [108 refs]

Source: American Journal of Medicine. 57(3):361-70, 1974 Sep.

<26>

Unique Identifier:4733578

Authors: Golden GT. Litwiller RW. Heironimus TW 3rd.

Title: The interpretation of arterial blood gases: a concise guide for clinicians.

Source: Southern Medical Journal. 66(9):1051-6, 1973 Sep.

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