The presence of an acid–base or an electrolyte disorder may explain a patient’s symptoms or may lead to a specific diagnosis.
Acid–Base Balance
(See Nelson Textbook of Pediatrics, p. 369.)
Normal acid–base balance is maintained by the lungs and kidneys. Carbon dioxide, a by-product of normal metabolism, is a weak acid. The lungs are able to prevent an increase in the partial pressure of carbon dioxide (P co 2 ) in the blood by excreting the carbon dioxide (CO 2 ) produced by the body. The pulmonary response to changes in the CO 2 concentration is fast, as it occurs via central sensing of the P co 2 , and there is a subsequent increase or decrease in ventilation to maintain a normal P co 2 (35-45 mm Hg). There is an inverse relationship between P co 2 and ventilation because an increase in ventilation decreases the P co 2 , and a decrease in ventilation increases the P co 2 .
The kidneys are responsible for excreting acid produced by the body. Sources of hydrogen ions include protein metabolism and incomplete metabolism of carbohydrates and fat; urine or stool losses of bicarbonate may contribute to acidemia. The hydrogen ions formed from endogenous acid production are neutralized by bicarbonate from the bicarbonate buffer system. The bicarbonate buffer system, based on the relationship between carbon dioxide and bicarbonate (HCO 3 − ), is displayed by the following equation:
CO 2 + H 2 O ↔ H + + HCO 3 −
This equation can help us understand how changes in CO 2 or HCO 3 − affect the acid–base balance.
Acid–Base Disorders
A pH <7.35 is defined as acidosis, and a pH >7.45 is defined as alkalosis. An acid–base disorder is respiratory in etiology when it is caused by a primary abnormality in respiratory function (a change in Pa co 2 ) and is metabolic when the primary change is due to a variation in bicarbonate concentration. Acid–base disorders may also be mixed, which occurs when 2 or even 3 primary events act to alter the acid–base state at the same time.
In metabolic disorders, extracellular buffers (bicarbonate) rapidly titrate the presence of strong acids or bases. Intracellular buffers chiefly accomplish the buffering of respiratory disorders. Secondary respiratory compensation for metabolic acid–base disorders begins within minutes by changes in ventilation and is usually complete in 12-24 hours. In contrast, secondary metabolic compensation for respiratory disorders occurs more slowly, beginning within hours but requiring 2-5 days for completion. The kidneys increase net acid excretion in response to a primary respiratory acidosis; renal net acid excretion also increases during a metabolic acidosis if the kidneys themselves are not the cause of the metabolic acidosis. The expected compensation for primary acid–base disorders is shown in Table 46.1 . These compensatory mechanisms never return the pH back to normal until the underlying disease process has subsided or has been effectively treated.
| Disorder | Primary Event | Degree of Initial Disturbance | Compensation | Degree of Compensation |
|---|---|---|---|---|
| Metabolic acidosis | ↓ [HCO 3 − ] | For every 10 mEq/L ↓ in HCO 3 – , pH ↓ by 0.15 | ↓ P co 2 | For 1 mEq/L ↓ [HCO 3 – ], P co 2 ↓ 1-1.5 mm Hg |
| Metabolic alkalosis | ↑ [HCO 3 − ] | For every 10 mEq/L ↑ in HCO 3 − , pH ↑ by 0.15 | ↑ P co 2 | For 1 mEq/L ↑ [HCO 3 − ], P co 2 ↑ 0.5-1 mm Hg |
| Respiratory acidosis | For every 10 mm Hg ↑ in P co 2 , pH ↓ by 0.08 | |||
| Acute (<12-24 hr) | ↑ P co 2 | ↑ [HCO 3 − ] | For 10 mm Hg ↑ P co 2 , [HCO 3 − ] ↑ 1 mEq/L | |
| Chronic (3-5 days) | ↑ P co 2 | ↑↑ [HCO 3 − ] | For 10 mm Hg ↑ P co 2 , [HCO 3 − ] ↑ 4 mEq/L | |
| Respiratory alkalosis | For every 10 mm Hg ↓ in P co 2 , pH ↑ by 0.08 | |||
| Acute (<12 hr) | ↓ P co 2 | ↓ [HCO 3 − ] | For 10 mm Hg ↓ P co 2 , [HCO 3 − ] ↓ 1-3 mEq/L | |
| Chronic (1-2 days) | ↓ P co 2 | ↓↓ [HCO 3 − ] | For 10 mm Hg ↓ P co 2 , [HCO 3 − ] ↓ 1-3 mEq/L |
* Normal serum [HCO 3 − ] is 24 mEq/L, and normal arterial partial pressure of carbon dioxide (P co 2 ) is 40 mm Hg.
When only 1 primary acid–base abnormality occurs and its compensatory mechanisms are activated, the disorder is classified as a simple acid–base disorder. When a combination of acid–base disturbances occurs, the disorder is classified as a mixed acid–base disorder. The latter should be suspected if the compensation in a given patient differs from the predicted values (see Table 46.1 ). Interpretation of data in infants and young children requires caution. Crying results in hyperventilation and can quickly change P co 2 and consequently the pH.
Symptoms of Acid–Base Disorders
History and clinical evaluation are the 1st steps in assessing a patient with an acid–base disorder. Although the signs and symptoms associated with an acid–base abnormality can be nonspecific, there are certain clues that one can obtain from the signs and symptoms that can assist in the diagnosis of the acid–base disorder. Metabolic acidosis results in increased minute ventilation (manifesting as increased respiratory rate and/or effort) because of respiratory compensation. A patient may have tachypnea present with a metabolic acidosis from a diarrheal illness, metabolic disorder, ingestion, or infection. In more severe acidosis (pH <7.20), the respiratory pattern is characterized by deep and rapid breaths (Kussmaul respiration). Severe acidosis may also lead to hypotension, pulmonary edema, and asystole; its harmful effects are accentuated in the presence of hypoxia. Chronic metabolic acidosis leads to growth retardation and hypercalciuria with subsequent bone disease because bone buffering of acid produces marked mineral losses.
A child with metabolic alkalosis may be asymptomatic. In some cases, careful examination of the child may detect hypoventilation. One should consider metabolic alkalosis in a child who has been vomiting or in a child who has had chronic diuretic use. Severe alkalosis (pH >7.55) can lead to tissue hypoxia, mental confusion, obtundation, muscular irritability, tetany, and an increased risk of seizures and cardiac arrhythmias. Some of these signs and symptoms are related to decreased concentration of serum ionized calcium as a result of its increased binding to protein in the presence of alkalosis. Acid–base disturbances can be assessed through laboratory analysis by obtaining a basic chemistry panel and/or a blood gas analysis.
Renal Regulation of Acid–Base Balance
The kidneys are the principal regulator of bicarbonate homeostasis. The renal regulation of HCO 3 − can be divided into 2 processes: reabsorption of HCO 3 − and excretion of H + . The 1st role of the kidneys is to reabsorb the filtered HCO 3 − so that this important extracellular buffer is not excreted in the urine. The 2nd role of the kidneys is to excrete H + that is produced from protein and phospholipid catabolism.
Most (80-90%) of the filtered HCO 3 − is reabsorbed in the proximal tubule ( Fig. 46.1 ). Bicarbonate reabsorption at this site is increased by the contraction of the extracellular fluid (ECF) volume, activation of the renin-angiotensin system (mainly through the effect of angiotensin II), elevated P co 2 , and hypokalemia. Conversely, HCO 3 − reabsorption is decreased when there is expansion of the ECF volume, inhibition of angiotensin II, a fall in P co 2 , and an elevation of the parathyroid hormone level.
The distal tubule and collecting duct regenerate bicarbonate via H + ion secretion into the tubular lumen by an H + -adenosine triphosphatase (H + -ATPase) pump in the luminal membrane. This active secretion can generate an H + ion gradient of 1000 : 1 between tubular fluid and cells, permitting the urine pH to fall to as low as 4.5. The active H + secretion is significantly influenced by the luminal electronegativity caused by active Na + reabsorption in the cortical collecting duct. Thus, in the cortical collecting duct, H + excretion is influenced by distal Na + delivery and reabsorption. In contrast, in the outer medullary portion of the collecting duct, aldosterone stimulates the H + excretion independently of Na + delivery or reabsorption. Some of the H + secreted is consumed in reclaiming the small amount of HCO 3 − that escaped reabsorption at proximal sites; the rest of the H + is excreted in the urine. The ability to excrete large amount of H + ions is dependent on the presence of buffers. The H + ions are buffered by phosphates and, to a lesser extent, by other nonreabsorbable anions. The other very important urinary buffer is ammonia (NH 3 ), which combines with a secreted H + to generate an ammonium ion (NH 4 + ). The proximal tubular cells generate ammonia through the metabolism of the amino acid glutamine. For every H + that is finally excreted, an HCO 3 − is added to the ECF compartment. Metabolic acidosis by itself enhances NH 4 + production and excretion. Ammonia genesis by proximal tubular cells is also stimulated by hypokalemia, whereas hyperkalemia inhibits ammonia genesis. The ability of the kidney to produce ammonia is markedly decreased in conditions such as chronic renal failure as a result of reduced renal mass and in some types of renal tubular acidosis (RTA). The ability to lower urine pH and increase net acid excretion may not be achieved until 4-6 weeks of age.
Metabolic Acidosis
A metabolic acidosis can result from addition of H + to the body, failure to excrete H + , or loss of HCO 3 − . The differential diagnosis of metabolic acidosis is simplified by classifying the causes into those associated with a normal anion gap (also known as a hyperchloremic metabolic acidosis) and those associated with an increased anion gap ( Table 46.2 ).
| Normal Anion Gap |
| Increased Anion Gap |
| Lactic Acidosis |
|
* Along with these genetic disorders, distal RTA may be secondary to renal disease or medications.
† Most cases of proximal RTA are not caused by this primary genetic disorder. Proximal RTA is usually part of Fanconi syndrome, which has multiple etiologies.
‡ Hyperkalemic RTA can be secondary to a genetic disorder (some of the more common are listed) or other etiologies.
The anion gap is easily calculated: Na + − (Cl − + HCO 3 − ). The anion gap is normally 8-16 mEq/L. When a strong acid (e.g., lactic acid) is added to or produced in the body, hydrogen ions are neutralized by bicarbonate, HCO 3 − is consumed by the H + , and the bicarbonate concentration falls. The accompanying anion, such as lactate, is a new unmeasured anion, which increases the anion gap. The increase in the anion gap is usually proportional to the fall in serum (HCO 3 − ). In contrast, when HCO 3 − is lost from the body, no new anion is generated. In this situation, there is a reciprocal increase in the serum Cl − to maintain electroneutrality. The anion gap does not change; the rise in (Cl − ) is proportional to the fall in (HCO 3 − ).
Normal Anion Gap (Hyperchloremic) Metabolic Acidosis
Renal Tubular Acidosis
RTA is a group of disorders characterized by impairment of renal HCO 3 − reabsorption and/or H + excretion in the presence of a relatively normal glomerular filtration rate (GFR). On the basis of the distinctive pathophysiologic features, 3 types of RTA—type I (distal or classic), type II (proximal or bicarbonate wasting), and type IV (hyperkalemic) are recognized ( Table 46.3 ).
| Factor | Type 1 | Type 2 | Type 4 |
|---|---|---|---|
| Serum K + | Low | Low | High |
| Renal function | Normal or near normal | Normal or near normal | Stage 3, 4, or 5 chronic kidney disease |
| Urine pH during acidosis | High | Low | Low or high |
| Serum HCO 3 − (mmol/L) | 10-20 | 16-18 | 16-22 |
| Urine P co 2 (mm Hg) | <40 | <40 | >70 |
| Urine citrate | Low | High | Low |
| Fanconi syndrome | No | May be present | No |
Type I RTA is caused by the inability to secrete H + in the distal tubule, resulting in hypokalemic hyperchloremic metabolic acidosis. These patients have a tendency to develop nephrocalcinosis and nephrolithiasis, which results from the excretion of large quantities of calcium, combined with an alkaline urine pH and hypocitraturia. In addition to the deficient H + secretion, these patients are unable to increase ammonia genesis. The patient’s urine pH remains alkaline (>5.5) despite extreme systemic metabolic acidosis. Type I RTA may occur as an isolated condition or may develop secondary to several diseases, medications, or toxins ( Table 46.4 ).
| Proximal Renal Tubular Acidosis |
| Primary |
|
| Secondary |
|
| Distal Renal Tubular Acidosis |
| Primary |
|
| Secondary |
|
| Hyperkalemic Renal Tubular Acidosis |
| Primary |
|
| Secondary |
|
Type II RTA is caused by an impairment of HCO 3 − reabsorption in the proximal tubule, resulting in hypokalemic hyperchloremic metabolic acidosis. Because the distal acidification mechanisms are intact, these patients can lower the urine pH to less than 5.5 and can excrete adequate amounts of NH 4 + when the serum HCO 3 − is below the filtration threshold. As a result, their acidosis is usually less profound than that which occurs in distal RTA. In some patients, there may be an increase in urinary calcium excretion, but because citrate excretion is normal, nephrocalcinosis is uncommon. Type II RTA may rarely occur as an isolated defect, but it usually coexists with other defects in proximal tubule function. Fanconi syndrome is the combination of multiple defects in proximal tubule reabsorption and, in addition to type II RTA, includes excessive urinary losses of glucose, amino acids, phosphate, and uric acid. The excessive losses of phosphate often cause hypophosphatemic rickets. There are many causes of type II RTA (see Table 46.4 ).
Type IV RTA results from low circulating aldosterone concentrations, partial or complete end-organ resistance to aldosterone, or aldosterone antagonism. Because of the lack of aldosterone effect, there is decreased distal acidification and decreased distal sodium reabsorption with hyperkalemic hyperchloremic acidosis. The hyperkalemia seen in type IV RTA is the most characteristic feature and differentiates it from the other 2 types.
The examination of a child with RTA may be normal. Poor skin turgor may be present from dehydration. Muscle weakness and muscle aches from hypokalemia may occur. Low back pain and bone pain may be present in patients with abnormalities of calcium metabolism (type II). All forms of RTA are associated with growth failure. Patients with Fanconi syndrome have severe rickets/osteomalacia and malnutrition.
Laboratory work-up in all patients with RTA shows metabolic acidosis with hyperchloremia and a normal anion gap. The urine pH always exceeds 5.5 in type I RTA but can be less than 5.5 in type II and type IV RTA.
Type I and II RTA are treated with oral sodium bicarbonate titrated to correct the acidosis. Potassium supplementation is needed in hypokalemic patients. Type IV RTA can be treated with furosemide to lower elevated potassium levels, along with sodium bicarbonate to correct significant acidosis. Fludrocortisone can be used to correct mineralocorticoid deficiency. In patients with secondary proximal RTA, treatment should be aimed at the primary disorder.
There needs to be frequent monitoring of potassium levels in type IV RTA. Because of the common occurrence of nephrocalcinosis and nephrolithiasis in type I RTA, renal ultrasound can be used to monitor these patients. A skeletal survey to look for bone disease should also be done, especially in cases of type II RTA. Patients with Fanconi syndrome should be evaluated for cystinosis, the most common cause of Fanconi syndrome in children. Some patients with inherited distal RTA have sensorineural deafness; therefore, infants and children with established distal RTA need routine audiograms.
Additional Causes of Renal Loss of Bicarbonate
Carbonic anhydrase inhibitors such as acetazolamide inhibit the carbonic anhydrase present in the proximal tubule, thus preventing the reabsorption of HCO 3 − . The net effect is similar to that of proximal RTA.
Potassium-sparing diuretics such as spironolactone or amiloride can impair H + secretion by the distal nephron by blocking Na + absorption in this segment.
Gastrointestinal Loss of Bicarbonate
Diarrhea is the most common cause of non–anion gap hyperchloremic metabolic acidosis in children. The acidosis is secondary to loss of stool bicarbonate. The degree of dehydration should be assessed and appropriate fluid resuscitation should be given, which should help correct the acidosis. If there is persistent acidosis, one should consider additional etiologies such as worsening infection/sepsis, an inborn error of metabolism, or bacteria-associated methemoglobinemia, or production of D-lactate.
Miscellaneous Causes of Hyperchloremic Acidosis
Recovery from ketoacidosis.
During recovery from diabetic ketoacidosis (DKA), many patients may eliminate the organic anions (through increased renal clearance and utilization) faster than their acidosis resolves. The clinical picture can resemble normal anion gap acidosis. Excessive fluids with isotonic chloride levels may contribute to this acidemia.
Dilutional acidosis.
The rapid expansion of ECF volume with fluids that do not contain HCO 3 − leads to a dilution of HCO 3 − and mild metabolic acidosis. In addition, the expansion of ECF volume by itself promotes urinary HCO 3 − loss, possibly contributing to the dilutional acidosis.
Parenteral alimentation.
Amino acid infusions without concomitant administration of alkali (or alkali-generating precursors) may produce a normal anion gap acidosis in a manner similar to that of addition of HCl.
Increased Anion Gap Acidosis
Increased Acid Production
Diabetic ketoacidosis.
In DKA, the lack of insulin and excess of glucagon shunts free fatty acids into ketone body formation. The rate of formation of ketone bodies, principally β-hydroxybutyrate and acetoacetate, exceeds the capacity for their peripheral utilization and renal excretion. Accumulation of ketoacids (both of which are relatively strong acids and dissociate rapidly into H + and the ketoacid anions) results in metabolic acidosis. Acetone is formed by nonenzymatic conversion of acetoacetate and is responsible for the fruity odor of the patient’s breath.
Patients with DKA typically present with polyuria and polydipsia in addition to altered mental status (ranging from confusion and drowsiness, which can progress to obtundation and loss of consciousness), and deep, sighing respirations (Kussmaul respirations). Additional clinical manifestations of DKA can be dehydration, nausea, vomiting, abdominal pain, and tachypnea. Laboratory analysis of a patient with DKA is significant for a severely increased anion gap metabolic acidosis with pH values that may be lower than 7.0. Initially, the increase in the anion gap is in proportion to the decrease in HCO 3 − , but once the patients start recovering with successful management, the kidneys clear the ketoacid anions, and the increase in the anion gap becomes less than the fall in HCO 3 − . The loss of ketoacid anions in urine increases the urinary losses of Na + and K + as the accompanying cations.
The diagnosis of DKA is made by the combination of increased anion gap metabolic acidosis, hyperglycemia, and demonstration of serum (or urine) ketoacid anions. The therapy for DKA includes careful volume repletion, insulin, and correction of electrolyte disturbances. Severe acidosis is reversible by fluid and insulin replacement. Insulin inhibits ketosis and allows ketoacids to be metabolized, which generates bicarbonate. Treatment of hypovolemia improves tissue perfusion and renal function thereby increasing the excretion of organic acids. Most patients with DKA present with considerable total body deficits of potassium, magnesium, and phosphorus, even though serum levels, particularly of potassium, may actually be high on presentation.
Lactic acidosis.
Under normal conditions, lactate is formed in relatively small amounts and is further metabolized by the liver. Pathologic conditions associated with either local or systemic hypoxia or ischemia, hypotension (shock), impaired oxidative metabolism, or impaired hepatic clearance can cause significant lactic acidosis.
The diagnosis of lactic acidosis must be considered in all forms of increased anion gap metabolic acidosis. The diagnosis can be confirmed by measuring the serum lactate level. Treatment must be directed at the underlying pathophysiologic process.
Inborn errors of metabolism.
Most patients with inborn errors of metabolism that cause a metabolic acidosis present in the neonatal period or shortly thereafter. Organic acidemias, aminoacidopathies, disorders of fatty acid oxidation, mitochondrial disorders, and defects in carbohydrate metabolism are associated with acidosis. Associated presenting signs and symptoms may include vomiting, failure to thrive, lethargy, seizures, developmental abnormalities, hepatomegaly, and elevated blood or urine levels of a particular metabolite. Some of these disorders will be detected by the state newborn screening protocols. In contrast, urea cycle disorders during the 1st few days of life manifest with respiratory alkalosis because of stimulation of the respiratory center by increased ammonia levels.
Poisonings.
A variety of toxic agents may be associated with increased anion gap metabolic acidosis; these include salicylate intoxication, ethylene glycol (a component of antifreeze), and methanol. Carbon monoxide, cyanide poisoning, or methemoglobinemia induces hypoxic acidosis.
Classically, salicylate intoxication is described as causing respiratory alkalosis (stimulation of the respiratory center), followed by increased anion gap metabolic acidosis (accumulation of salicylic acid itself and lactic acidosis as a result of uncoupling of mitochondrial oxidative phosphorylation). However, children may present with simple increased anion gap metabolic acidosis. Nausea, tinnitus, noncardiogenic pulmonary edema, and prolonged prothrombin time are other associated features. Alkalization of the blood and urine with sodium bicarbonate is beneficial despite the potential problems associated with its use in acute metabolic acidosis. Alkalization of the plasma decreases the diffusion of salicylate into the central nervous system, and alkaline urine improves renal excretion. In severe poisoning, hemodialysis is quite effective at removing salicylate from the body. In cases of poisonings, dialysis serves the dual purposes of removing the poison (if dialyzable) and correcting the acid–base and electrolyte abnormalities.
Failure of Acid Excretion
In both acute and chronic renal failure, the kidneys fail to excrete the acid produced from normal daily metabolism. Both H + and anions accumulate in the body, resulting in slow consumption of bicarbonate stores. However, the acidosis is generally not severe unless a markedly catabolic state occurs or other associated conditions coexist. In acute renal failure, there is abrupt and complete inhibition of acid excretion, whereas in chronic renal failure, there initially is enhanced ammonia genesis by the remaining nephrons. As renal failure progresses, excretion of both NH 4 + and phosphate declines. In addition, the secondary hyperparathyroidism seen with chronic renal failure decreases proximal tubular HCO 3 − reabsorption and adds a component of hyperchloremic acidosis to the increased anion gap acidosis.
Treatment of Metabolic Acidosis
The morbidity and mortality caused by metabolic acidosis are determined not only by the severity of acidosis but also by the amenability of the underlying disorder to medical management. During treatment of metabolic acidosis, the primary effort should focus on the management of the underlying condition. The recommendations and goals of buffer therapy differ for acute acidotic disorders such as DKA and for chronic acidotic states such as RTA.
During the correction of acute metabolic acidosis, particular attention should be paid to ensure an appropriate potassium balance. During an episode of metabolic acidosis, potassium shifts from the intracellular space to the extracellular space in exchange for H + , and thus the presence of a total body potassium deficit may not be appreciated. Hypokalemia may become evident only as the pH increases and potassium returns to the intracellular space. Chronic metabolic acidosis slows linear growth and interferes with bone mineralization. In chronic metabolic acidosis, there is a need for alkali therapy.
Metabolic Alkalosis
(See Nelson Textbook of Pediatrics, Table 55.11.)
Metabolic alkalosis (pH >7.45) occurs as a result of a primary increase in the serum HCO 3 − , which may occur as a result of (1) net loss of H + , (2) net gain of HCO 3 − (or its precursors), or (3) loss of fluid with more Cl − than HCO 3 − . Normally functioning kidneys can excrete large amounts of HCO 3 − and should offset any increase in serum HCO 3 − resulting from these causes. Therefore, factors that prevent the kidneys from excreting HCO 3 − also must be present to maintain the metabolic alkalosis.
Factors Initiating Metabolic Alkalosis
The H + can be lost externally, either through the gastrointestinal tract or through the kidneys. For every H + lost at these sites, the body gains 1 HCO 3 − ion. This is because H + production at both these sites (gastric parietal cell and renal tubular cells) is associated with generation of an equivalent number of HCO 3 − molecules. H + can also be “lost” internally, by shifting into the intracellular compartment. This occurs in states of severe potassium depletion (H + moves in, whereas K + exits the cell, to maintain electroneutrality).
The administration of HCO 3 − or its precursors (such as lactate, citrate, and acetate), at a rate greater than normal metabolic production of acid can lead to net gain of HCO 3 − by the body.
External loss of fluid (gastric fluid) containing more Cl − than HCO 3 − raises the concentration of HCO 3 − in the body. One of the factors responsible for this type of alkalosis is the associated volume contraction, which leads to increased bicarbonate reabsorption by the proximal tubule of the kidney.
Factors Responsible for Sustaining Alkalosis
Decrease in effective blood volume and kidney perfusion causes increased Na + reabsorption, in both the proximal tubule (angiotensin II effect) and the distal renal tubule (mineralocorticoid effect), thereby increasing H + excretion.
Increased mineralocorticoid levels directly increase H + secretion in the outer medullary collecting duct.
Chloride depletion increases HCO 3 − reabsorption in the proximal tubule. This effect is independent of ECF volume status.
Hypokalemia sustains metabolic alkalosis by decreasing bicarbonate loss. Hypokalemia promotes hydrogen ion secretion in the distal nephron and stimulates ammonia genesis in the proximal tubular cells. When produced, ammonia enhances renal excretion of hydrogen ions.
Hypercapnia induces a state of intracellular acidosis, which increases H + secretion. Although P co 2 increases as a normal compensatory response to metabolic alkalosis, the elevated P co 2 prevents the renal correction of alkalosis.
Differential Diagnosis of Metabolic Alkalosis
The causes of metabolic alkalosis can be divided into 2 categories on the basis of the urinary chloride level. The alkalosis in patients with low urinary chloride is maintained by volume depletion; volume repletion is needed to correct the alkalosis. In the process of volume depletion, there are losses of sodium, potassium, and chloride, but the loss of chloride is usually greater than the losses of sodium and potassium combined. Since chloride losses are the main cause of the volume depletion, these patients require chloride to correct the volume deficit and metabolic alkalosis; these patients have chloride-responsive metabolic alkalosis. Conversely, patients with alkalosis and an elevated urinary chloride concentration do not respond to volume repletion and have chloride-resistant metabolic alkalosis. Blood pressure can also be useful when considering the etiology of a patient’s chloride-resistant metabolic alkalosis ( Table 46.5 ).
| Chloride-Responsive (Urinary Chloride <15 mEq/L) |
| Chloride–Resistant (Urinary Chloride >20 mEq/L) |
|
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