World J. Surg. 7, 590-598, 1983 World Journal ol Sd ry 1983 by the Soci~t~ lnternationale de Chirurgie Acid-Base Problems in Surgery John Clark, M.B., Ch.M., F.R.C.S., and William F. Walker, D.Sc., Ch.M., F.R.C.S. (Eng), F.R.C.S. (Ed), F.R.S. (Ed) Department of Surgery, Ninewells Hospital and Medical SchooL, Dundee, United Kingdom The identification and treatment of various clinical states of body's built-in defenses are designed to deal with acid-base imbalance assume particular significance in ma- the normal metabolic hazard of acidosis. jor surgery and in patients with multiple organ failure. There are several important acid-base pairs that Metabolic acidosis, metabolic alkalosis, respiratory acido- either liberate or receive protons depending on the sis, respiratory alkalosis, and mixed disorders of acid-base direction in which a reaction is driven according to balance are described and a management plan for each the law of mass action. Those that are soluble in entity is defined. intracellular and extracellular fluid include carbonic acid/bicarbonate, monobasic/dibasic phosphate, ammonium/ammonia, and lactic acid/lactate. The Disorders of acid-base metabolism are frequently acidic residues of many proteins are important encountered in major surgery, particularly in the buffers fixed in tissues. Because all buffer pairs very young and the elderly. This is especially so share the same hydrogen ions in a homogeneous when there is infection, shock, intestinal obstruc- system, acid-base changes may be monitored by tion, or fistula leakage and in those with cardiores- analyzing the components of one of the pairs, the piratory or renal failure. It may be difficult to dissociation constant of which is known. The com- identify the essential cause of an acid-base fault and posite effect of all these pairs is to absorb large full history-taking, clinical evaluation, and bio- quantities of hydrogen ions instantaneously by chemical investigation may be necessary. In pa- shifting the equilibrium in the direction of the acidic tients with multiple organ failure, mixed acid-base form in response to a rise in hydrogen ion concen- disorders present the clinician with a great chal- tration. The withdrawal of hydrogen ions or addi- lenge in which the stakes may be the life or death of tion of base shifts the reactions in the opposite the patient. direction. The result of adding hydrogen ions is a negligible change in hydrogen ion concentration at the expense of reducing the complement of basic Physiology components and increasing the complement of acid- ic components of the buffer system. The pH Acid-base homeostasis involves a 3-phase re- changes only when the supply of base is exhausted. sponse. Endogenous or exogenous acid or alkali is Hydrogen ions are transported harmlessly in solu- buffered immediately, then there is a respiratory ble buffer forms or on globin from the point of origin phase of rapid pH adjustment, and finally a slow to a point of hydrogen ion disposal, where the acidic renal phase of restoration of buffer systems. The form of the buffer dissociates to restore the original conditions. Hydrogen ions are secreted by the gastric mucosa and renal tubular epithelium. Buffer- m ing occurs in the urine as monobasic phosphate and Reprint requests: John Clark, Ysbyty Glan Clwyd, ammonium protect the urinary epithelium from acid Bodelwyddan, Rhyl, Clwyd LL18 5UJ, North Wales, damage. United Kingdom. The carbonic acid/bicarbonate pair contributes J. Clark and W.F. Walker: Acid-Base Problems 591 approximately 40% of the huge plasma and tissue basic groups in the globin moiety, and HCO3- buffer system and is unique in that independent diffuses back into the plasma in exchange for C1-. physiological mechanisms control the concentra- At low PO2 levels, the basic groups of globin have tion of each component. Buffering capacity can be an increased avidity for H § A lesser, but still extended by generating further acid by CO2 reten- significant, amount of CO2 forms carbamino com- tion or further base by bicarbonate reabsorption. pounds with globin and other proteins. The se- Most of the remaining plasm a and tissue buffer quence is reversed at the pulmonary alveolus and capacity lies in proteins and the phosphate pair. COz is excreted. This method of transport is in Proteins fixed in tissues buffer on site and then effect largely one of H § transport in the protein liberate hydrogen ions to soluble systems for trans- buffer system, and the capacity is greater than port. Hemoglobin provides protein buffer transport. would be possible for CO2 in solution. Changes in Plasma is readily accessible for analysis and the PCO2 are minimized. The arterial PCO2 is affected bicarbonate system is most easily assayed. Al- by the rate of CO2 production, the rate of alveolar- though interstitial fluid and plasma equilibrate rap- capillary diffusion, and the rate of pulmonary alveo- idly and hydrogen ions cross cell membranes readi- lar ventilation. The last is the dominant influence. ly, plasma pH does not necessarily reflect pH in Because the gas diffuses freely, alveolar partial cells, cellular organelles, or cerebroSpinal fluid. The pressure of carbon dioxide (PACO2) equilibrates concentration of CO2 dissolved in plasma is propor- extremely rapidly with capillary and hence the tional to the arterial partial pressure of CO2 systemic arterial partial pressure of CO2 (PaCO2). (PaCO2). Approximately 0.12% of this CO2 is con- Arterial PCO2 is easily measured. verted at once into carbonic acid by the ubiquitous Respiratory depression leads to a rise in PaCO2 carbonic anhydrase. When carbonic acid is re- and acidOsis, but the normal adaptive response moved, it is replaced at once from the carbon occurs partly from further dissociation of carbonic dioxide store in solution. Carbonic acid dissociates acid and partly from increased renal reabsorption of as a weak acid and the relationship between the bicarbonate, so that in compensated respiratory concentration of carbonic acid, hydrogen ions, and acidosis the plasma has a normal or low pH, high bicarbonate ions is expressed in the Henderson- PaCO2, and high bicarbonate. Respiratory stimula- Hasselbalch equation: tion leads to a low PaCO2 and high pH (respiratory alkalosis), and the normal adaptive response is to pH = 6.1 + log [HCO3-/(0.03 PaCO2)] decrease renal reabsorption of bicarbonate and de- Factors that affect PaCO2 and bicarbonate concen- crease plasma bicarbonate concentration. Metabol- tration have a direct bearing on the pH of tissue ic events that lead to.a reduction in plasma bicar- fluids, and pathological or physiological events that bonate cause metabolic acidosis. The respiratory alter one of these components have 4 conse- center is stimulated by cerebrospinal fluid acidosis quences. First, the change in ratio of PaCO2 to resulting in compensatory hyperventilation and a bicarbonate concentration results in an alteration of reduction in PaCO2. This tends to redress the pH. Second, the law of mass action dictates that the balance in the Henderson-Hasselbalch equation and dissociation reaction of H2CO3 proceeds in the return the pH toward normal. Metabolic alkalosis direction of the component that has become rela- results from metabolic events that lead to an accu- tively lowered. Third, immediate readjustment of mulation of plasma bicarbonate. Plasma pH rises the ratio is obtained by respiratory readjustment of but respiratory center depression results from the PaCO2 and pH is restored. Fourth, and less rapidly, low concentration of hydrogen ions in cerebroSpinal renal tubular adjustment of both H § excretion and fluid, so alveolar CO2 accumulates leading to a bicarbonate reabsorption restores the total body compensatory rise in PaCO2. The origin of the 4 complement of H § and bicarbonate buffer toward types of pH disturbance can, therefore, be deduced normal. There follows reversal of the previous shift from the arterial pH. PaCO2, and bicarbonate, in the dissociation of H2CO3 Until both the ratio and provided a single acid-base disorder is present. This the concentration of carbon dioxide and bicarbon- deduction may not be so simple if adaptive respons- ate are normal again. Renal reabs0rption of bicar- es are not normal because of the operation of 2 or bonate takes 6-12 h to be initiated and 3-5 days for more acid-base disorders, for example, metabolic a complete response. alkalosis in a patient in chronic respiratory failure. Approximately 20,000 mmol CO2 is produced As a guide as to whether an acid-base disturbance daily, depending on the metabolic rate. Carbon is of single origin, a number of formulae have been dioxide is transported by diffusion gradients in developed. In simple acute respiratory acidosis and tissues. In the bloodstream, COe enters red cells alkalosis, the appropriate deviation of pH (ApH) and carbonic anhydrase mediates conversion to from the normal 7.40 should be 0.7 times the carbonic acid which dissociates, H + attaches to observed deviation (APaCO2) of PaCO2 from the 592 World J. Surg. Vol. 7, No. 5, September 1983 normal 40 mm Hg. In chronic respiratory acidosis, sured anions that account for the gap are sulphate, adaptive mechanisms are established and a lesser phosphate, lactate, and other organic anions. Pro- pH change occurs in response to a change in PaCO2 teins contribute and have zwitterion properties, that so that A pH = 0.3 x A PaCO2. Chronic respiratory is, the charge varies with the pH. Usually, in alkalosis is the most completely compensated acid- acidosis the fall in plasma bicarbonate is replaced base disorder and A pH = 0.17 x A PaCO2. The pH by an increase in chloride and there is no change in can become normal. In metabolic acidosis, pH= the anion gap. In certain metabolic states, typified 1.3 (approximately) x total CO2 (or actual bicar- by diabetic ketoacidosis, organic anions are present bonate).