Zusammenfassung
Bereits vor rund 20 Jahren veröffentlichte Peter Stewart seine Abhandlung über eine moderne quantitative Analytik des Säure-Basen-Haushalts [88, 89]. Folgt man seinen Interpretationen, so wird die traditionelle Lehre vom Säure-Basen-Haushalt erheblich in Frage gestellt. Das wichtigste physikochemische Prinzip, das in Körperflüssigkeiten immer erfüllt sein muß, ist das Prinzip der Elektroneutralität.
Es existieren dabei 3 verschiedene Komponenten in biologischen Flüssigkeiten, die diesem Prinzip unterliegen:
- a):
-
Wasser, das nur in geringen Teilen in H+ und OH− dissoziiert vorliegt,
- b):
-
„starke“, d. h. vollständig dissoziierte und damit chemisch nicht mit anderen Substanzen reagierende, Elektrolyte und körpereigene Substanzen, wie Laktat und
- c):
-
„schwache“, d. h. unvollständig dissoziierte, Substanzen.
Peter Stewart unterschied nun strikt zwischen abhängigen und unabhängigen Variablen und beschrieb damit tatsächlich eine neue Ordnung des Säure-Basen-Haushalts. Die 3 abhängigen Variablen (die Bikarbonatkonzentration [Bic−], der pH und damit auch die Wasserstoffionenkonzentration [H+]) sind den unabhängigen Variablen vollständig untergeordnet, können sich also nur verändern, wenn die 3 unabhängigen Variablen dies zulassen. Zu den unabhängigen Variablen zählen:
-
1.
der Kohlendioxidpartialdruck,
-
2.
die Gesamtkonzentration aller schwachen Säuren ([A−] (Stewart nannte diese ATOT) und
-
3.
die Differenz der starken Ionen (SID).
[A−] erschließt sich aus der Albumin (Alb)- und der Phosphatkonzentration (Pi): [A−]=[Alb×(0,123×pH−0,631)]+[Pi×(0,309×pH−0,469)].
Mit Hilfe der messbaren Ionenkonzentrationen lässt sich eine apparente SID (oder „Bedside-SID“) berechnen: SID=[Na+]+[K+]−[Cl−]−Laktat.
Betrachtet man die metabolischen Störungen des Säure-Basen-Haushalts, so sind nach der Terminologie von Stewart Veränderungen von pH, [H+] und [Bic−] nur möglich, wenn sich entweder die SID oder [A−] verändert. Nimmt z. B. die SID ab (etwa im Rahmen einer Hyperchloridämie), so bewirkt dieser Zuwachs an unabhängigen negativen Ladungen eine Abnahme der abhängigen negativen Ladungen in Form von [Bic−] mit dem entsprechenden Resultat einer Acidose (und vice versa). Damit wird aber beispielhaft bei der hyperchlorämen Acidose, die durch den Chloridanstieg bedingte Abnahme der SID als Ursache der Acidose identifiziert. Umgekehrt resultiert z. B. aus einer Abnahme von [A−] (etwa im Rahmen einer Hypoalbuminämie) ein Anstieg von [Bic−] und damit eine Alkalose (ebenfalls vice versa). Mit Hilfe dieser Analytik können also völlig neue Säure-Basen-Störungen, wie etwa die „hyperchloräme Acidose“ oder die „hypoalbuminäme Alkalose“ (die natürlich auch kombiniert vorliegen können), diagnostiziert werden, die der klassischen Säure-Basen-Analytik verschlossen waren. Damit kann diese Analytik zu einem vertieften Verständnis der Mechanismen, denen der Säure-Basen-Haushalt unterliegt, führen.
Abstract
About twenty years ago, Peter Stewart had already published his modern quantitative approach to acid-base chemistry [88, 89]. According to his interpretations, the traditional concepts of the mechanisms behind the changes in acid-base balance are considerably questionable. The main physicochemical principle which must be accomplished in body fluids, is the rule of electroneutrality. There are 3 components in biological fluids which are subject to this principle:
- a):
-
Water, which is only in minor parts dissociated into H+ and OH–,
- b):
-
“strong”, i.e. completely dissociated, electrolytes, which thus do not interact with other substances, and body substances, such as lactate, and
- c):
-
“weak”, i.e. incompletely dissociated, substances.
Peter Stewart strictly distinguished between dependent and independent variables and thus indeed described a new order of acid-base chemistry. The 3 dependent variables (bicarbonate concentration [Bic–], pH, and with this also hydrogen ion concentration [H+]) can only change if the 3 independent variables allow this change. These 3 independent variables are:
-
1.
Carbon dioxide partial pressure,
-
2.
the total amount of all weak acids ([A–] (Stewart called these ATOT), and
-
3.
strong ion difference (SID).
[A–] can be calculated from the albumin (Alb) and the phosphate concentration (Pi): [A−]=[Alb×(0.123×pH−0.631)]+[Pi×(0.309×pH−0.469)].
An apparent SID (or “bedside” SID) can be calculated using measurable ion concentrations: SID=[Na+]+[K+]–[Cl–]–lactate.
Regarding the metabolic disturbances of acid-base chemistry, according to Stewart‘s terminology, changes in pH, [H+], and [Bic–] are only possible if either SID or [A–] itself changes. If, for example, SID decreases (e.g. in case of hyperchloremia), this increase in independent negative charges leads to a decrease in dependent negative charges in terms of [Bic–] resulting in acidosis (and vice versa). Therefore, according to Stewart, the decrease in SID during hyperchloremic acidosis results from the increase in serum chloride concentration and is the causal mechanism behind this acidosis. Contrary for example, a decrease in [A–] (e. g. during hypoalbuminemia) leads to an increase in [Bic–] and therefore to an alcalosis (and vice versa). Thus, by Stewart‘s approach, completely new acid-base disturbances, like “hyperchloremic acidosis“ or “hypoalbuminemic alcalosis“ (which, of course, can also exist in combination) can be detected, which had been unrecognised by the classic acid-base concepts. Consequently, Stewart‘s analysis can lead to a better understanding of the mechanisms behind the changes in acid-base balance.
Literatur
Alfaro V, Torras R, Ibáñez J, Palacios L (1996) A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease. Can J Physiol Pharmacol 74:1229–1235
Astrup P, Jorgensen K, Siggaard Andersen O (1960) The acid-base metabolism—A new approach. Lancet 1:1035–1039
Azzam FJ, Steinhardt GF, Tracy TF, Gabriel KR (1995) Transient perioperative metabolic acidosis in a patient with ileal bladder augmentation. Anesthesiology 83:198–200
Balasubramanyan N, Havens PL, Hoffman GM (1999): Unmeasured anions identified by the Fencl-Stewart method predict mortality better than base excess, anion gap, and lactate in patients in the pediatric intensive care unit. Crit Care Med 27:1577–1581
Bellomo R, Liskaser F (2001) In reply. Anesthesiology 95:810–811
Bellomo R, Ronco C (1999) New paradigms in acid-base physiology: editorial commentary. Curr Opin Crit Care 5:427–428
Bellomo R, Ronco C (1999) The pathogenesis of lactic acidosis in sepsis. Curr Opin Crit Care 5:452–457
Bellone E (2002) Galileo Galilei. Spektrum der Wissenschaft, Heidelberg
Boyle M, Baldwin I (2002) Introduction to an alternative view on acid/base balance: the strong ion difference or Stewart approach. Aust Crit Care 15:14–20
Carlson GP, Jones JH (1999) Effects of frusemide on electrolyte and acid-base balance during exercise. Equine Vet J Suppl 30:370–374
Cole L, Bellomo R, Baldwin I, Hayhoe M, Ronco C (2003) The impact of lactate-buffered high-volume hemofiltration on acid-base balance. Intensive Care Med 29:1113–1120
Constable PD (1997) A simplified strong ion model for acid-base equilibria: application to horse plasma. J Appl Physiol 83:297–311
Constable PD (2000) Clinical assessment of acid-base status: confusion of the Hendersen-Hasselbalch and strong ion approach. Vet Clin Pathol 29:115–128
Constable PD (2001) Total weak acid concentration and effective dissociation constant of nonvolatile buffers in human plasma. J Appl Physiol 91:1364–1371
Constable PD (2003) Hyperchloremic acidosis: the classic example of strong ion acidosis (editorial). Anesth Analg 96:919–922
Corey HE (2003) Stewart and beyond: new models of acid-base balance. Kidney Int 64:777–787
Cusack RJ, Rhodes A, Lochead P et al. (2002) The strong ion gap does not have prognostic value in critically ill patients in a mixed medical/surgical ICU. Intensive Care Med 28:864–869
Dorje P, Adhikary G, McLaren ID (1997) Dilutional acidosis or altered strong ion difference (letter). Anesthesiology 87:1011–1012
Dorje P, Adhikary G, Tempe DK (2000) Avoiding iatrogenic acidosis—Call for a new crystalloid fluid (letter). Anesthesiology 92:625–626
Fencl V, Leith DE (1993) Stewart’s quantitative acid-base chemistry: applications in biology and medicine. Respir Physiol 91:1–16
Fencl V, Rossing TH (1989) Acid-base disorders in critical care medicine. Annu Rev Med 40:17–29
Fencl V, Jabor A, Kazda A, Figge J (2000) Diagnosis of metabolic acid-base disturbances in critically ill patients. Am J Respir Crit Care Med 162:2246–2251
Feriani M, Dell’Aquila R, Ronco C, La Greca G (1999) The acid- base effects of peritoneal dialysis. Curr Opin Crit Care 5:448–451
Figge J, Rossing TH, Fencl V (1991) The role of serum proteins in acid-base equilibria. J Lab Clin Med 117:453–467
Figge J, Mydosh T, Fencl V (1992) Serum proteins and acid-base equilibria: a follow-up. J Lab Clin Med 120:713–719
Finsterer U, Scheingraber S, Rehm M (2000) In reply. Anesthesiology 92:626
Gan TJ, Bennet-Guerrero E, Phillips-Bute B, Wakeling H, Moskowitz DM, Olufolabi Y, Konstadt N, Bradford C, Glass PSA, Machin SJ, Mythen MG and the Hextend study group (1999) Hextend, a physiologically balanced plasma expander for large volume use in major surgery: a randomized phase III clinical trial. Anesth Analg 88:992–998
Gilfix BM, Bique M, Magder S (1993) A physical chemical approach to the analysis of acid-base balance in the clinical setting. J Crit Care 8:187–197
Goodkin DA, Raja RM, Saven A (1990) Dilutional acidosis. South Med J 83:354–355
Graham-Thiers PM, Kronfeld DS, Kline KA (1999) Dietary protein influences acid-base responses to repeated sprints. Equine Vet J Suppl 30:463–467
Greene HM, Wickler SJ, Anderson TP, Cogger EA, Lewis CC, Wyle A (1999) High-altitude effects on respiratory gases, acid-base balance and pulmonary artery pressures in equids. Equine Vet J Suppl 30:71–76
Hasselbalch KA (1916) Die Berechnung der Wasserstoffzahl des Blutes aus der freien und gebundenen Kohlensäure desselben, und die Sauerstoffbindung des Blutes als Funktion der Wasserstoffzahl. Biochem Z 78:112–144
Hayhoe M, Bellomo R (1999) The pathogenesis of acid-base changes during cardiopulmonary bypass. Curr Opin Crit Care 5:464–467
Hayhoe M, Bellomo R, Lui G, Kellum JA, McNicol L, Buxton B (1999) Role of splanchnic circulation in acid-base balance during cardiopulmonary bypass. Crit Care Med 27:2671–2677
Hayhoe M, Bellomo R, Lui G, McNicol L, Buxton B (1999) The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime. Crit Care Med 25:680–685
Heenan AP, Wolfe LA (2000) Plasma acid-base regulation above and below ventilatory threshold in late gestation. J Appl Physiol 88:149–157
Himpe D, Neels H, Hert S de, Cauwelaert P van (2003) Adding lactate to the prime solution during hypothermic cardiopulmonary bypass: a quantitative acid-base analysis. Br J Anaesth 90:440–445
Jaber BL, Madias NE (1997) Marked dilutional acidosis complicating management of right ventricular myocardial infarction. Am J Kidney Dis 30:561–567
Kaplan LJ, Bailey H, Kellum J (1999) The etiology and significance of metabolic acidosis in trauma patients. Curr Opin Crit Care 5:458–463
Kellum JA (1997) New insights in acid-base physiology applied to critical care. Curr Opin Crit Care 3:414–419
Kellum JA (1999) Acid-base physiology in the post-Copernican era. Curr Opin Crit Care 5:429–435
Kellum JA (2002) Saline-induced hyperchloremic metabolic acidosis (editorial). Crit Care Med 30:259–261
Kellum JA (2002) Fluid resuscitation and hyperchloremic acidosis in experimental sepsis: improved short-term survival and acid-base balance with Hextend compared with saline. Crit Care Med 30:300–305
Kellum JA, Kramer DJ, Pinsky MR (1995) Strong ion gap: a methodology for exploring unexplained anions. J Crit Care 10:51–55
Kellum JA, Bellomo R, Kramer DJ, Pinsky MR (1998) Etiology of metabolic acidosis during saline resuscitation in endotoxemia. Shock 9:364–368
Kohrasani A, Appavu SK (1997) Decrease in the total amount of extracellular bicarbonate is not dilution (letter). Anesthesiology 87:1012–1013
Kowalchuk JM, Scheuermann BW (1994) Acid-base regulation: a comparison of quantitative methods. Can J Physiol Pharmacol 72:818–826
Kronfeld DS, Ferrante PL, Taylor LE, Tiegs W (1999) Partition of plasma hydrogen ion concentration changes during repeated sprints. Equine Vet J Suppl 30:380–383
Leblanc M (1999) The acid-base effects of acute hemodialysis. Curr Opin Crit Care 5:468–478
Levraut J, Grimaud D (2003) Treatment of metabolic acidosis. Curr Opin Crit Care 9:260–265
Lindinger MI, Franklin TW, Lands LC, Pedersen PK, Welsh DG, Heigenhauser GJF (1999) Role of skeletal muscle in plasma ion and acid-base regulation after NaHCO3 and KHCO3 loading in humans. Am J Physiol 276:R32–43
Liskaser FJ, Story DA (1999) The acid-base physiology of colloid solutions. Curr Opin Crit Care 5:440–442
Liskaser FJ, Bellomo R, Hayhoe M et al. (2000) The role of pump prime in the etiology and pathogenesis of cardiopulmonary bypass-associated acidosis. Anesthesiology 93:1170–1173
Madias NE, Cohen JJ (1982) Acid-base,1st edn. Little Brown, Boston, pp 3–25
Maloney DG, Appadurai IR, Vaughan RS (2002) Anions and the anaesthesist. Anaesthesia 57:140–154
Mathes DD, Morell RC, Rohr MS (1997) Dilutional acidosis: is it a real clinical entity? Anesthesiology 86:501–503
McAuliffe JJ, Lind LJ, Leith DE, Fencl V (1986) Hypoproteinemic alkalosis. Am J Med 81:86–90
McCullough SM, Constable PD (2003) Calculation of the total plasma concentration of nonvolatile weak acids and the effective dissociation constant of nonvolatile buffers in plasma for use in the strong ion approach to acid-base balance in cats. Am J Vet Res 64:1047–1051
Miller LR, Waters LH, Provost C (1996) Mechanism of hyperchloremic metabolic acidosis (letter). Anesthesiology 84:482–483
Morgan TJ, Balasubramanian V, Hall J (2002) Crystalloid strong ion difference determines metabolic acid-base change during in vitro hemodilution. Crit Care Med 30:157–160
Morimatsu H, Rocktaschel J, Bellomo R, Ucino S, Goldsmith D, Gutteridge G (2003) Comparison of point-of-care versus central laboratory measurement of electrolyte concentrations on calculations of the anion gap and the strong ion difference. Anesthesiology 98:1077–1084
Moviat M, Haren F van, Hoeven H van der (2003) Conventional or physicochemical approach in intensive care unit patients with metabolic acidosis. Crit Care 7:R41–45
Nahas GG (1962) The pharmacology of Tris (hydroxymethyl)aminomethane (THAM). Pharmacol Rev 14:447–472
Nahas GG, Sutin KM, Fermon C et al. (1998) Guidelines for the treatment of acidemia with THAM. Drugs 55:191–224
O’Connor MF, Roizen MF (2001) Lactate versus chloride: which is better? (editorial). Anesth Analg 93:809–810
Oh MS, Caroll HJ (1977). Current concepts: the anion gap. N Engl J Med 297:814–817
Peters J, Slyke DD van (1946) Quantitative clinical chemistry: interpretations, vol 1, 1st edn. Williams & Wilkins, Baltimore
Preston RJ, Heenan A, Wolfe LA (2001) Physicochemical analysis of phasic menstrual cycle effects on acid-base balance. Am J Physiol 280:R481–487
Prough DS (1999) Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline (editorial). Anesthesiology 90:1247–1249
Prough DS (2000) Acidosis associated with perioperative saline administration: dilution or delusion? (editorial). Anesthesiology 93:1167–1169
Rehm M, Finsterer U (2001) In reply. Anesthesiology 95:811
Rehm M, Finsterer U (2003) Treating intraoperative hyperchloremic acidosis with sodium bicarbonate or tris-hydroxymethyl aminomethane (THAM); a randomized prospective study. Anesth Analg 96:1201–1208
Rehm M, Orth V, Scheingraber S, Kreimeier U, Brechtelsbauer H, Finsterer U (2000) Acid-base changes caused by 5% albumin versus 6% hydroxyethylstarch solution in patients undergoing acute normovolemic hemodilution. Anesthesiology 93:1174–1183
Rocktaschel J, Morimatsu H, Uchino S, Ronco C, Bellomo R (2003) Impact of continuous veno-venous hemofiltration on acid-base balance. Int J Artif Organs 26:19–25
Rocktaschel J, Morimatsu H, Uchino S, Ronco C, Bellomo R (2003) Unmeasured anions in critically ill patients: can they predict mortality? Crit Care Med 31:2131–2136
Rocktaschel J, Morimatsu H, Uchino S et al. (2003) Acid-base status of critically ill patients with acute renal failure: analysis based on Stewart-Figge methodology. Crit Care 7:R60–66
Rossing TH, Maffeo N, Fencl V (1986) Acid-base effects of altering plasma protein concentration in human blood in vitro. J Appl Physiol 61:2260–2265
Russo MA (1997) Dilutional acidosis: a nonentity? (letter). Anesthesiology 87:1010–1011
Roth VR (2001) What is the clinical relevance of dilutional acidosis? (letter). Anesthesiology 95:810
Scheingraber S, Rehm M, Sehmisch C, Finsterer U (1999) Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology 90:1265–1270
Scheingraber S, Heitmann L, Weber W, Finsterer U (2000) Are there acid base changes during transurethral resection of the prostate (TURP)? Anest Analg 90:946–950
Shea W (2003) Nikolaus Kopernikus. Spektrum der Wissenschaft, Heidelberg
Shires GT, Holman J (1948) Dilution acidosis. Annu Int Med 28:557–559
Siggaard-Andersen O (1976) The acid-base status of the blood, 4th edn. Munksgaard, Copenhagen
Siggaard-Andersen O, Fogh-Anderson N (1995) Base excess or buffer base (strong ion difference) as a measure of non-respiratory acid-base disturbance. Acta Anaesth Scand 39 [Suppl 107]:123–128
Sirker AA, Rhodes A, Grounds RM, Bennett ED (2002) Acid-base physiology: the „traditional“ and the „modern“ approaches. Anaesthesia 57:348–356
Slyke DD van, Hastings AB, Hiller A, Sendroy J (1928) Studies of gas and electrolyte equilibria in blood. XIV. Amount of alkali bound by serum albumin and globulin. J Biol Chem 79:769–808
Stewart PA (1981) How to understand acid-base: a quantitative acid-base primer for biology and medicine. Elsevier, North Holland, New York
Stewart PA (1983) Modern quantitative acid-base chemistry. Can J Physiol Pharmacol 61:1444–1461
Staempfli HR, Constable PD (2003) Experimental determination of net protein charge and A(tot) and K(a) of nonvolatile buffers in human plasma. J Appl Physiol 95:620–630
Stephens R, Mythen M (2003) Optimizing intraoperative fluid therapy. Curr Opin Anaesthesiol 16:385–392
Story DA, Bellomo R (1999) The acid-base physiology of crystalloid solutions. Curr Opin Crit Care 5:436–439
Story DA, Poustie S, Bellomo R (2001) Quantitative physical chemistry analysis of acid-base disorders in critically ill patients. Anaesthesia 56:530–533
Story DA, Poustie S, Bellomo R (2001) Estimating unmeasured anions in critically ill patients: anion gap, base-deficit, and strong ion gap. Anaesthesia 57:1102–1133
Story DA, Morimatsu H, Bellomo R (2004) Strong ions and base excess: a simplified Fencl-Stewart approach to clinical acid-base disorders. Br J Anaesth 92:54–60
Takil A, Zeynep E, Irmak P, Yilmaz Gogus F (2002) Early postoperative acidosis after large intravascular volume infusion of lactated Ringer’s solution during major spine surgery. Anesth Analg 95:294–298
Tan HK, Bellomo R (1999) The effect of continuous hemofiltration on acid-base physiology. Curr Opin Crit Care 5:443–447
Waters JH (2001) In reply. Anesthesiology 95:812
Waters JH, Bernstein CA (2000) Dilutional acidosis following hetastarch or albumin in healthy volunteers. Anesthesiology 93:1184–1187
Waters JH, Scanlon TS, Howard RS, Leivers D (1995) Role of minor electrolytes when applied to Stewart’s acid-base approach in an acidotic rabbit model. Anesth Analg 81:1043–1051
Waters JH, Gottlieb A, Schoenwald P, Popovic MJ, Sprung J, Nelson DR (2001) Normal saline versus lactated Ringer’s solution for intraoperative fluid management in patients undergoing abdominal aortic aneurysm repair: an outcome study. Anesth Analg 93:817–822
Watson PD (1999) Modelling the effects of protein on pH in plasma. J Appl Physiol 86:1421–1427
Weinstein Y, Magazanik A, Grodjinovsky A, Inbar O, Dlin RA, Stewart PA (1991) Reexamination of Stewart’s quantitative analysis of acid-base status. Med Sci Sports Exerc 23:1270–1275
Wilkes NJ, Wolf R, Mutch M, Mallett SV, Peachey T, Stephens R, Mythen MG (2001) The effects of balanced versus saline-based hetastarch and crystalloid solutions on acid-base and electrolyte status and gastric mucosal perfusion in elderly surgical patients. Anesth Analg 93:811–816
Zander R (2001) Nebenwirkungen von Volumenersatzmitteln—Einfluss auf den Säure-Basehaushalt. In: Boldt J (Hrsg) Volumenersatztherapie. Thieme, Stuttgart, S 127–140
Zander R, Lang W (2004) Base excess and strong ion difference: clinical limitations related to inaccuracy (letter). Anesthesiology 100:459–460
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Rehm, M., Conzen, P.F., Peter, K. et al. Das Stewart-Modell. Anaesthesist 53, 347–357 (2004). https://doi.org/10.1007/s00101-004-0660-x
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DOI: https://doi.org/10.1007/s00101-004-0660-x