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Home , Alkalosis

World J. Surg. 7, 590-598, 1983 World Journal ol Sd ry

1983 by the Soci~t~ lnternationale de Chirurgie

Acid-Base Problems in

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 , 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 . jor surgery and in patients with multiple organ failure. There are several important acid-base pairs that , , respiratory acido- either liberate or receive protons depending on the sis, , 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 include carbonic acid/, 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 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 (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 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 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 . In certain metabolic states, typified 1.3 (approximately) x total CO2 (or actual bicar- by diabetic , organic anions are present bonate). There is no formula available for meta- in excess displacing HCO3- but plasma C!- is bolic alkal0sis because adaptive responses vary unchanged. The organic anions are unmeasured, so in extent. the anion gap is increased. The 2 broad categories of normal and increased anion gap acidosis may be recognized from the plasma electrolyte values. Clinical States of Acid-Base Imbalance Two conditions exist in which plasma CI- and HCO3- do not reciprocate in a simple fashion. In Once buffer systems have been overwhelmed, intra- dilutional states of fluid overload, the diluted cellular and extracellular fluid pH changes. Plasma HCO3- buffer system is inefficient and acidosis pH is measured directly, and the reason for the occurs, but C1- is also diluted and there is an disturbance can usually be deduced from the other apparent instead of the hyperchlore- components of the conventional "blood gas" analy- mia of acidosis. It is possible for hyperchloremia to sis and from the anion gap. For special applications, exist without a reduced plasma HCO3- leading to extracellular fluid pH may be measured directly by acidosis, as in chronic hyperventilation. In this pH probes inserted by skin puncture or implanta- condition, renal C1- reabsorption occurs because of tion. Recently, nuclear magnetic resonance tech- the unavailability of HCO3- which would normally niques have led to measurements of intracellular pH be reabsorbed preferentially. by estimations of the phosphate buffer system. Normal Anion Gap Acidosis. Enteric secretions from below the level of the pylorus contain bicar- Disorders of Metabolic Origin botiate and may be lost by aspiration, fistula, or diarrhea. The maximum capacity for renal reab- There are limits to the body's tolerance of changes sorption can accommodate short-term (48-h) losses in PCO2 and compensation fails when the bicarbon- of up to 600 ml/day, but it is unwise to allow even ate concentration continues to change after these lesser degrees of loss to accumulate or else acidosis limits have been reached. may suddenly become decompensated by even a small increase in enteric loss. In the presence of Metabolic Acidosis. This condition may be due to ileus, the loss of bicarbonate is always greater than excessive bicarbonate loss, excessive hydrogen ion observed by virtue of the sequestration of intralu- load, or reduced hydrogen ion excretion. Bicarbon- minal content. There is a variable electrolyte con- ate may be lost in enteric fluid or by failure of renal tent in intestinal fluid. The principle of replacement tubular reabsorption, there may be intrinsic (meta- is to administer a close approximation to the re- bolic) sources of excessive hydrogen ions, or ex- quirement and check the adequacy of by trinsic hydrogen ions may be administered as acid electrolyte measurements daily on the plasma and or as ammonium chloride. Renal failure results in once or twice weekly on 24-h specimens of urine failure of H + excretion. and the fluid that is being lost pathologically. In biological fluids, there is an equal number of Usually, the pancreas is not being stimulated positive and negative ions. Routine clinical bio- during surgical crises, and pancreatic and biliary chemical tests measure the cations sodium (- 140 loss should be replaced volume for volume by a mmol/L) and potassium (- 4 mmol/L) and anions solution containing approximately 25 mmol/L bicar- chloride (- 103 mmol/L) and bicarbonate (~ 25 bonate, or bicarbonate equivalent, in addition to mmol/L). There is, therefore, a 16 mmol/L short-fall normal plasma concentrations of sodium and chlo- in measured anion compared with the cations. This ride. Hartmann's and Ringer's lactate solutions is the anion gap. By convention, potassium is meet these requirements. Bicarbonate is provided omitted from the calculation because of its small, after metabolism of the lactate. These solutions also relatively stable value and the gap is, therefore, 12 contain a plasma equivalent of potassium, and it is mmol/L. In reality, the anion gap is even greater sensible to employ them as the salt-containing com- than 16 mmol/L because many minor cations are ponent (500 ml) of the normal daily body fluid unmeasured (Mg ++, Ca ++, Zn++). The unmea- requirement (2,500 ml) rather than the more usual J. Clark and W.F. Walker: Acid-Base Problems 593

0.9% sodium chloride. The potassium content of mally. This results in 15% or more of the filtered these solutions is just adequate to replace normal load being excreted, compared with the normal daily losses in the short term, but to match the 1.5%. These patients require bicarbonate in. large concentration of potassium in enteric fluid (10-20 amounts to correct their normal anion gap acidosis. mmol/L), the appropriate supplement is added to Distal tubular failure results in the inability to each bottle of intravenous; replacement. generate a pH differential, so that urine is alkaline Small bowel content and diarrhea contain more (pH > 5.4) and there is a normal anion gap. In the bicarbonate (up to 70 mmol/L) and should be re- presence of an alkaline urine, the condition of the placed volume for volume by solutions containing distal tubules may be tested by administering am- 50 mmol/L. Formulations exist, such as Darrow's monium chloride, which should normally lower the solution for acidosis; otherwise the appropriate urinary pH to well below 5.4. If plasma acidosis volume of 8.4% is distributed already exists, a provocative test is unnecessar~r to between one or more isotonic components of the reach the diagnosis. Measurement of urinary bicar- daily intravenous fluid. Initially, potassium loss bonate before and after a bicarbonate load Will test should be estimated at 20 mmol/L but diarrhea can proximal tubular function. contain 40 mmol/L. Children require their daily Many patients with renal parenchymal disease, maintenance volume of 0.18% saline in 4.3% dex- such as pyelonephritis or polYCYstic kidneys, have a trose plus volume for volume replacement of enter- moderate degree of renal failure manifest by a ic loss by Ringer's lactate or Hartmann's solution. plasma creatinine level elevated to 150-350 ~mol/L, Fine adjustment of bicarbonate requirement can be with or without a normal anion gap acidosis. They made with 8.4% solution well diluted in the rest of have a normal or nearly normal glomerular filtration the day's fluids. Potassium supplements are given rate, normal urinary pH, normal ammonium, chlo- orally wherever possible. ride, and bicarbonate handling, but characteristical- Colonic loss of bicarbonate used to be promoted ly deficient ammonia excretion. Ammonia excre- by ureterosigmoidostomy and hyperchloremic aci- tion is low at around 14 mmol/day compared with dosis resulted. Regular ingestion of sodium bicar- the normal of about 50 mmol/day. Normal kidneys bonate tablets compensated for the loss, but current respond to nonrenal metabolic acidosis with an practice is to divert ureters into ileal conduits. ammonia excretion that may reach 400 mmol/day. These produce no acid-base problems unless they Low-grade renal failure is not uncommon in surgi- are excessively long or stagnant. cal practice, especially in an aged population. These Parenteral nutrition is commonplace in surgical kidneys are vulnerable to hypovolemia, hypoten- treatment, and acidosis can develop because of the sion, and hypoxia. predominance of cationic amino acids (arginine, Hyperchloremic acidosis occurring with hyper- lysine, histidine) in the synthetic amino acid mix- parathyroidism may be due to parathormone-in- tures. Before assimilation into protein, cationic duced impairment of proximal tubular reabsorption amino acids liberate H + which is buffered by bicar- of bicarbonate. A compensatory renal reabsorption bonate. Bicarbonate depletion occurs but it can be of chloride results and bicarbonate administration is offset to some extent by adding acetate or lactate, necessary. or by increasing the content of anionic amino acids in the mixture (aspartate, glutamate). Increased Anion Gap Acidosis. In the metabolic Renal failure may complicate surgical manage- acidosis that exists during exertion Or hypoxia, ment. Renal failure to excrete H + occurs in uremia lactate is the predominant unmeasured anion. Mild (end-stage kidney failure) or in disorders o~ renal degrees of are relatively common and tubular electrolyte handling (), correction occurs with the restoration of adequate or simply if the urine output falls to about 300 ml pulmonary ventilation. Infusions of sodium bicar- daily. In uremia, reduced glomerular filtration re- bonate are required (50-100 retool) to neutralize the sults in anion retention (phosphate, sulphate, creati- lactic acid bolus effect immediately prior to restora- nine) and an increased anion gap; but, more impor- tion of regional blood flow after major arterial tantly, ammonia excretion is reduced because of the occlusion (emboius, major vascular cross-clamping, reduction in the number of functioning nephrons mesenteric ischemia). Severe lactic acidosis occurs and the failure of glutamine extraction by the tu- during circulatory arrest and an infusion of 100 bules. The reduction in filtered phosphate load is mmol sodium bicarbonate forms part of the resusci- the reason for the reduction in urinary titratable tative measure. Very severe acidosis of whatever acidity, but urine pH remains approximately normal cause may be treated in this way; but when time and the reduction in ammonium ion excretion is permits, the bicarbonate requirement is calculated characteristic. In renal tubular acidosis, the proxi- by multiplying the base deficit (mmol/L), which is mal tubules may fail to reabsorb bicarbonate nor- obtained from blood gas analysis, by an approxima- 594 World J. Surg. Vol. 7, No. 5, September 1983 tion of extracellular fluid volume, namely, 1/3 of the ed because, as the patient recovers, accumulated body weight (kg). Sodium bicarbonate is conve- lactate is metabolized and bicarbonate is generated. niently administered as 8.4% solution which con- Furthermore, hyperventilation often continues and tains 1 mmol/ml. The blood gas determination is PaCOz does not rise in parallel with bicarbonate repeated after an hour or so, and a further calcula- concentration. Extracellular fluid alkalosis results tion and correction is required for 3 reasons. Bicar- in increased protein binding of calcium, and bonate deficit underestimates the H + excess be- can occur. There is also a risk of sodium overload- cause approximately half of the excess is buffered ing. Cerebral deterioration can also occur if the by other systems. The calculation relates to extra- extracellular fluid glucose falls rapidly leaving intra- cellular fluid and there is also intracellular acidosis. cellular hypertonicity which leads to fluid shifts and Hydrogen ions continue to accumulate until the cerebral edema. Papilledema occurs. The mainstay primary disease process is halted. A fresh equilibri- of treatment is, therefore, rehydration and gentle um develops and more buffer is given, either as a correction of acidosis utilizing Ringer's lactate. bolus or by a slow infusion of an isotonic solution Insulin should be administered cautiously. A degree containing bicarbonate or its equivalent. Bolus re- of insulin resistance exists in the presence of acido- placement is indicated for initial therapy if the sis. patient's condition is critical, if plasma pH reaches As extracellular fluid acidosis builds up, H + 7.2, or if plasma bicarbonate falls below 10 mmol/L. passes into cells toward protein buffer sites and This is approaching the limits of compensation displaces potassium from the cells. The effect on because a further reduction in bicarbonate concen- plasma potassium is variable. Life-threatening hy- tration cannot be accompanied by a further fall in perkalemia can develop; or, if there is persistent PaCOz and, in addition, the buffer system is ineffi- loss of enteric secretions, or diuresis, normokale- cient at low concentration. Faced with lesser de- mia or may be found. The body devel- grees of acidosis, the decision to replenish buffer ops a total deficit of potassium and the sequence of depends on the likelihood of correction occurring events is the same whatever the cause of the spontaneously once therapy is initiated for the acidosis. During correction of acidosis, the ion primary and on the likelihood of contin- fluxes reverse d~rection and the potassium debt ued loss of buffer, must be repaid or else severe hypokalemia occurs. may follow surgery or sur- Potassium also shifts back into Cells during insulin gical complications. It can accompany a surgical therapy. For each unit of insulin, approximately 1.5 emergency and can mimic acute abdominal emer- mmol potassium is needed. The maximum rate of gencies. The prevention and control of ketoacidosis intravenous potassium administration is 50 mmol/h. are essential parts of surgical management. Ace- tone, acetoacetic and [3-hydroxybutyric acids ac- Metabolic Alkalosis. This occurs in 3 circum- count for the anion gap during diabetic ketoacidosis stances: excessive administration of alkali, chloride and also during starvation. Acetest | tablets react deficiency, and stimulation of renal tubular sodium- directly with plasma to ind!cate the magnitude of hydrogen exchange. In all circumstances, plasma the concentration of the first 2, but there is no bicarbonate excess is quantitatively matched by reaction with [3-hydroxybutyric. The latter keto chloride depletion. acid predominates in acute alcoholic acidosis during It is now rare to encounter the milk-alkali syn- which there is no hyperglycemia. The metabolites drome in peptic ulcer patients and accidental over- of other organic poisons add to the anion gap: administration of bicarbonate is the most common salicylate, methyl alcohol, ethylene glycol, and cause of overloading. This results in expansion of paraldehyde. It is possible for these metabolic prob- the extracel!ular fluid space and, in response, renal lems to complicate surgical management in accident reabsorption of filtered sodium is inhibited. Be- and emergency units. cause of the linked reciprocal transport of sodium In the control of ketoacidosis, a bolus of bicar- and hydrogen, H + excretion into the tubule is bonate is given only if acidosis is life-threatening, inhibited, no reaction occurs with tubular HCO3-, because such treatment can occasionally worsen and this anion is excreted. The excess bicarbonate coma. This is because extracellular fluid pH re- is normally excreted efficiently and alkalosis results moves the acidotic respiratory drive and PaCO2 only when the load is massive and continuous or in rises. Carbon dioxide crosses the blood brain barri- the presence of renal tubular failure. The compen- er faster than bicarbonate, hence cerebrospinal satory respiratory depression and hypercapnea that fluid acidosis intensifies as its PCOz rises before the accompanies metabolic alkalosis is limited in extent bicarbonate concentration (Henderson-Hasselbalch by the attendant hypoxia. It is also limited in effect equation). There are further potential hazards of by the proportionately high change in PCO2 re- bicarbonate therapy. Acidosis may be over-correct- quired to effect pH changes in the presence of high J. Clark and W.F. Walker: Acid-Base Problems 595 concentrations of buffer. Respiratory compensation alkalosis commences rapidly but is completed over is, therefore, little in evidence unless plasma bicar- several days. The absence of chloride from the bonate reaches high levels. At a plasma bicarbonate urine (<10 retool/L) is diagnostic of inadequate concentration of up to 50 retool/L, PCO2 should be replacement therapy; but if oliguria has been treat- 50 mm Hg or less. Narcosis occurs when PCO2 ed by the administration of tubular blocking diuret- reaches 65-80 mm Hg in response to a bicarbonate ics instead of the requisite fluid load, chloride will concentration of 50-60 mmol/L. A disproportion- be present in the urine. The body cannot afford to ately high PCO2 is indicative of coincident pulmo- lose this chloride and the diuretic serves to intensify nary failure. the alkalosis. The most common cause of metabolic alkalosis is Inadequate restitution of sodium loss has several chloride depletion resulting from the loss of gastric consequences. In order to maintain extracellular juice or the effect of diuretics. The deficient plasma fluid volume, renal reabsorption of sodium is stimu- anion is replaced by bicarbonate. The ionic content lated and, consequently, H + is excreted. Very little of gastric secretions depends on the rate of secre- sodium appears in the urine and that which is tion. Hydrogen ion concentration varies from 10 absorbed is accompanied by bicarbonate in the mmol/L at low secretion rates to 150 mmol/L at high absence of sufficient chloride. Acid-base balance is rates, and sodium varies reciprocally from 100 to 5 subordinate to volume homeostasis. Continued ad- mmol/L. Potassium is fairly constant at I0 to 20 ministration of water produces extracellular, then mmol/L. There is a small bicarbonate secretion (up intraceUular, fluid hypotonicity and intracellular to 30 mmol/L), but chloride is the dominant anion, fluid volume expansion, but total body water re- which varies from a concentration of I00 to a mains reasonably normal and absolute hyponatre- maximum of 160 mmol/L. At maximal secretion mia develops. Mental confusion and apathy are rates, gastric juice is hypertonic. The H + for secre- noted. Coma and circulatory collapse are late and tion is generated by carbonic anhydrase and the very serious events but rapidly recoverable. Once it HCO3- produced at the same time passes into the has been established from analysis of the fluid plasma in exchange for C1- which is secreted into balance charts and clinical examination that the the gastric lumen. Normally, the chloride is reab- patient is not suffering from fluid overload (dilu- sorbed further down the intestinal tract, and the tional hyponatremia), correction of absolute hypo- plasma chloride and bicarbonate balance is restored natremia is best commenced with 1.8, 3.0, or even by the renal tubules unless their function is serious- 5.0% saline. This rapidly reduces intracellular over- ly inadequate or gastric fluid is lost and not re- hydration, expands extracellular fluid volume, and placed. permits renal adjustment of water and sodium ex- When the intravenous route is the sole source of cretion to restore balance. fluid replacement, the input must match the losses Potassium is lost in gastric juice and also in urine for volume and ionic content. It is necessary to where, along with hydrogen, it is exchanged for estimate the loss prior to admission and make this sodium reabsorption. Serum potassium also falls in good over the first 24-48 h and at the same time alkalosis because the ion shifts into cells in ex- replace the daily visible and insensible fluid losses. change for hydrogen, which leaves intracellular Physiological saline solution containing 20 mmol/L buffer sites and passes into the extracellular fluid. potassium chloride is given in a volume equal to the Hypokalemia increases in severity with the alkalo- gastric loss. There is no need to administer H + as 1/6 sis, and both must be corrected simultaneously. M ammonium chloride, hydrochloric acid, or argi- Potassium is administered safely if the daily re- nine hydrochloride for maintenance, but on rare quirement is calculated as for an extracellular fluid occasions it may be needed to treat tetany or ion, but this is an underestimate and the calculation established alkalosis of life-threatening degree will require repeating twice daily until the intracel- (plasma pH > 7.60). Should it be necessary, the lular potassium complement is restored. This is dose of H + is calculated by multiplying the base particularly important in the preparation of babies excess by 1/3 of the body weight in kilograms. This for pyloromyotomy. Alkalosis and are adjustment ignores intracellular acidosis, and bio- corrected by the infusion of 0.9% saline in a volume chemical reassessment must follow in an hour or so. equal to 5% of the body weight for moderate and Hydrogen ions are readily generated by carbonic severe dehydration and 2.5% of the body weight for anhydrase and homeostasis is achieved, if chloride mild dehydration. About half of this volume is given is available to replace the bicarbonate that is pro- over the first 4 hours and the remainder given with duced at the same time. Under these circum- the maintenance volume of 0.18% saline and 4.3% stances, normal renal tubules avidly reabsorb chlo- glucose solution over the rest of the day. When ride in preference to bicarbonate so that, once rehydration is well under way, potassium is added chloride is available, the reversal of established to the infusate (as chloride) to achieve a concentra- 596 World J. Surg. Vol. 7, No. 5, September 1983 tion of 20 mmol/L. Hypovolemia requires plasma, portasystemic shunting. It is essential to administer 20 ml/kg body weight. As the plasma potassium large quantities of K +, in the region of 100 mmol/ approaches normal, the potassium concentration in day, to keep pace with excretion, replenish the the infusate is halved and the infusion continues up continuous drain on intracellular potassium, and-- to the time of surgery, reducing the concentration most importantly--to compete with H + for the again as necessary. If the continuous input of obligatory distal tubular excretion in order to con- potassium stops, hypokalemia will recur. Occasion- serve H § This is the only way the body can counter ally, the plasma potassium rises very rapidly before alkalosis. Chloride administration increases alkalo- replacement is complete, and its shift into the cells sis because it is excreted in preference to bicarbon- needs to be accelerated by soluble insulin and ate, and sodium administration increases still fur- glucose therapy (1 unit/3 g). To this regimen is ther the total body sodium overload. Established added calcium gluconate 5 mmol/kg per day. Potas- severe metabolic alkalosis of this type is likely to sium replacement in babies should rarely exceed 3 require H + treatment in order to initiate the trend mmol/kg per day. High rates of infusion must be toward a normal plasma pH. accompanied by ECG monitoring and the rate is reduced when T waves revert to normal. Finally, the least common form of metabolic Disorders of Respiratory Origin alkalosis results from stimulation of renal tubular Na+-H + exchange due to hypermineralocorticoi- dism. This occurs in Cushing's and Conn's syn- These acid-base changes occur as a result of failure dromes, ectopic ACTH production, hepatocellular of respiratory control of arterial PCO2. By the law failure, and severe potassium depletion. Unlike the of mass action, plasma bicarbonate rises when COs conditions discussed previously, correction does is retained. The change is approximately I mmol/L not occur following the administration of chloride. for each 10 mm Hg change in PCO2. If blood gas The mechanism is the enforced reabsorption ofNa + analysis demonstrates a greater or lesser bicarbon- and the linked excretion of H +. In the tubule H § ate in proportion to the deviation of PCO2 from reacts with bicarbonate, CO2 is absorbed, recon- normal, then metabolic alkalosis or metabolic aci- verted to carbonic acid from which bicarbonate is dosis exists in addition to the respiratory acid-base absorbed, and H + excreted again. Effectively, sodi- change. Several days elapse before renal retention um bicarbonate is retained in the body and much of of bicarbonate becomes established in pure respira- the chloride passes unabsorbed into the urine. Uri- tory acidosis, and the plasma pH settles at about nary electrolyte analysis reveals this fundamental 7.36. Plasma pH settles at 7.48 in pure respiratory difference compared to chloride responsive alkalo- alkalosis. sis. Potassium is almost completely reabsorbed in the proximal renal tubule, and in the distal tubule a small amount is excreted along with H + in exchange Respiratory Acidosis. Retention of carbon dioxide for sodium absorption. Normally, the proportion of up to a level of 50 mm Hg stimulates the respiratory hydrogen to potassium excreted depends on the centers, but above this level carbon dioxide has a relative abundance of each. In acidosis, H + excre- depressant effect and hypoxia becomes the domi- tion predominates and potassium is retained. The nant respiratory drive. In patients suffering from opposite obtains in alkalosis. Potassium excretion is chronic carbon dioxide retention, the administra- regulated by aldosterone by 3 mechanisms. The tion of oxygen depresses respiratory drive and renin-angiotensin-aldosterone system is stimulated acute respiratory failure ensues. Alveolar hypoven- by hyponatremia, hypovolemia, and hypoperfusion tilation promotes hypercapnea, while increased res- of the juxtaglomerular apparatus. Aldosterone is piratory muscle work increases COs production. secreted in response to ACTH and brief peaks of Ultimately, these problems develop in patients with secretion can be obtained in this way. Aldosterone chronic obstructive airways disease and those with is secreted in rapid response to increases in plasma thoracic deformities; but in patients who were oth- potassium to which the zona glomerulosa is sensi- erwise within the limits of compensation, the onset tive. Primary over-activity of these mechanisms of a surgical emergency may precipitate respiratory results in excessive excretion of potassium and H + failure. This is because of increased CO2 production and in hypokalemic alkalosis. The alkalosis is usual- resulting from hypercatabolism and reduced venti- ly mild but assumes great significance during hyper- latory capacity due to pain, muscle spasm, dia- aldosteronism secondary to hepatocellular failure, phragmatic splinting, disruption of the thoracic because ammonia remains non-ionized, is readily cage, or the collection of air or fluid within the absorbed from the colon, and crosses the blood pleural cavity. Pre- or postoperative chest infection brain barrier. The problem is exacerbated after can be disastrous and intensive physiotherapy, J. Clark and W.F. Walker: Acid-Base Problems 597 though itself exhausting, is essential. Preoperative- Mixed Disorders of Acid-Base Balance ly, physiotherapy techniques and breathing exer- cises must be practiced, particularly before thoracic Mixed disorders are obvious when both systems are procedures are undertaken. Prompt recognition of producing a pH change in the same direction, sputum retention and treatment by intratracheal because the concentration of the buffer component catheter suction, intubation, and suction or bron- primarily at fault is accompanied by a quite inappro- choscopic aspiration, can be lifesaving. Aspects of priate direction of change in the buffer component treatment that might precipitate respiratory failure which should be compensating. For example, the include the administration of respiratory depressant hypokalemic patient who is in hepatocellular failure analgesics, persistence of muscle relaxant drug ef- has a metabolic alkalosis (bicarbonate increased) fects postoperatively, and restrictive bandaging (for and Should have a compensatory hypercapnea (res- example, after mastectomy). Obesity lowers the piratory acidosiS). Not infrequently, the PCO2 is threshold at which the respiratory workload be- low because there is a separate pathological respira- comes critical, Patients whose forced expiratory tory stimulus in operation which is resulting in an volume is, or would be reduced to, l L or less inappropriate respiratory alkalosis. Therapy needs cannot tolerate resection of any residual functional to be directed at both pathological mechanisms. lung tissue. Other more usual causes of hyperventilafion may The management of respiratory acidosis centers coexist with metabolic alkalosis, which is common- on improving these mechanical aspects of pulmo- ly due to hypokalemia or loss of gastric juice. As a nary function and not by the administration of rule, mixed acid-base disorders result from meta- bicarbonate. When maximum effort has not been bolic upset in patients suffering from chronic pul- rewarded by a reduction in plasma PCO2, or when monary failure, but in this context one final cause of there is a distressing increase in pulmonary work, simultaneous metabolic and respiratory alkalosis then ventilatory assistance is indicated. Mechanical needs to be mentioned. ventilation is adjusted until the PCO2 is in the Chronic pulmonary failure results in hypercapnea normal or near normal range, and blood gas moni- (respiratory acidosis) and an adaptive increase in toring ensures that respiratory acidosis or alkalosis renal bicarbonate reabsorption (compensatory met- is not induced by incorrect ventilator settings. Pro- abolic alkalosis). Over-enthusiastic mechanical phylactic postoperative ventilation saves lives in ventilation in an intensive care situation reduces high-risk patients, but it can be very difficult to PCO2 creating respiratory alkalosis, but it is many terminate ventilatory assistance in patients who days before there is any change in renal bicarbonate depend on a hypoxic respiratory drive. excretion and metabolic alkalosis persists. The treatment is to improve pulmonary function as Respiratory Alkalos&. Stimulation of the respira- much as possible and reduce the ventilatory rate to tory centers may be psychogenic brought on by restore the normal state of compensated respiratorY anxiety or fear, and the extent of hyperventilation acidosis, or else the patient will never be indepen- may not be obvious because of its rapid, shallow dent of the ventilator. The ventilatory rate is deter- nature. Hyperventilation also results from organic mined in this case by the plasma pH, not PCO2. brain disease, pulmonary embolism, or interstitial Very many patients are open to this risk because of pulmonary disease. Arterial hypoxemia is a com- the frequency with which chronic respiratory acido- mon cause encountered in surgical patients in shock sis provides the background to major surgical prob- states and anemia. Hyperventilation is frequently lems. The usual and dangerous mixed acid-base found in patients in hepatocellular failure or after disorder seen in these patients is chronic respira- portasystemic shunting. Respiratory alkalosis ex- tory acidosis and acute metabolic acidosis due to ists in spite of metabolic alkalosis. The reason for hypoxia or shock. Bicarbonate therapy, respiratory the respiratory center drive is not clear. It may be support, and treatment of the precipitating surgical due to a direct toxic effect of metabolites, to cere- condition are urgently required. bral extracellular fluid acidosis because of the dif- The recognition of coincident metabolic and res- ferent rates of transport of CO2 and bicarbonate piratory disorders influencing the pH in opposite across the blood brain barrier, or to cerebral intra- directions depends on identifying the dominant in- cellular acidosis. The hyperventilation persists for fluence and deciding whether the compensatory several days after correction of the metabolic alka- response is normal or excessive. Formulae have losis by potassium therapy. Some degree of correc- been presented that define the normal range of tion may be obtained by increasing the dead space compensatory responses. Any of the causes of in the ventilatory circuit, either by mask or by metabolic alkalosis may occur in patients with increasing the effective length of an endotracheal respiratory acidosis due to chronic pulmonary fail- tube. ure. Respiratory center depression is enhanced, so 598 World J. Surg. Vol. 7, No. 5, September 1983 therapy is directed to the cause of the metabolic L'acidose mdtabolique, l'alcalose m6tabolique, alkalosis, and sometimes dilute hydrochloric acid or l'acidose respiratoire, l'alcalose respiratoire et les ammonium chloride is required. Acetazolamide en- d6sordres varids de l'6quilibre acide-base sont d6- hances renal bicarbonate excretion. Finally, hyper- crits et un plan de traitement de chaque entit6 ventilation (reSpiratory alkalosis) may complicate particuli~re est propos6 par les auteurs. metabolic acidosis as a result of anxiety, hypoxia, or circulatory failure. Resumen

La identificaci6n y tratamiento de varios estados Re~um6 clfnicos de desequilibrio ~cido-base asurne impor- tancia de particular significaci6n en cirug/a mayor y L'identification et le traitement des diff6rentes var- en pacientes con falla de mtitiples 6rganos. La i6t6s cliniques de d6s6quilibre acide-base, qui acidosis metab61ica, la alcalosis metab61ica, la aci- jouent un r61e particuli6rement important en cas de dosis respiratoria, la alcalosis respiratoria y los chirurgie majeure et chez les malades qui pr6sen- des6rdenes mixtos del balance ~icido-base son de- tent de multiples d~faillances organiques, sont scritos; se define un plan de tratamiento para cada d'une importance considdrable. entidad.