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Acid-base disorders are changes in arterial Pco₂, serum HCO₃ ⁻, and serum pH.

• Acidemia is serum pH < 7.35.
• Alkalemia is serum pH > 7.45.
• Acidosis refers to physiologic processes that cause acid accumulation or alkali loss.
• Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss.

Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present.

Classification

Primary acid-base disturbances are defined as metabolic or respiratory based on clinical context and whether the primary change in pH is due to an alteration in serum HCO₃ ⁻ or in Pco₂.

Metabolic acidosis is serum HCO₃ ⁻ < 24 mEq/L. Causes are

• Increased acid production
• Acid ingestion
• Decreased renal acid excretion
• GI or renal HCO₃ ⁻ loss

Metabolic alkalosis is serum HCO₃ ⁻ > 24 mEq/L. Causes are

• Acid loss
• HCO₃ ⁻ retention

Respiratory acidosis is Pco₂ > 40 mm Hg (hypercapnia). Cause is

• Decrease in minute ventilation (hypoventilation)

Respiratory alkalosis is Pco₂ < 40 mm Hg (hypocapnia). Cause is

• Increase in minute ventilation (hyperventilation)

Whenever an acid-base disorder is present, compensatory mechanisms begin to correct the pH (see Table 1: Acid-Base Regulation and Disorders: Primary Changes and Compensations in Simple Acid-Base Disorders). Compensation cannot return pH completely to normal and never overshoots.

Table 1
Primary Changes and Compensations in Simple Acid-Base Disorders Primary Disturbance pH HCO3 − Pco2 Compensation Metabolic acidosis < 7.35 Primary decrease Compensatory decrease 1.2-mm Hg decrease in Pco2 for every 1-mmol/L decrease in HCO3 − or Pco2 = (1.5 × HCO3 −) + 8 (± 2) or Pco2 = HCO3 − + 15 or Pco2 = last 2 digits of pH × 100 Metabolic alkalosis > 7.45 Primary increase Compensatory increase 0.6–0.75 mm Hg increase in Pco2 for every 1-mmol/L increase in HCO3 −. Pco2 should not rise above 55 mm Hg in compensation Respiratory acidosis < 7.35 Compensatory increase Primary increase Acute: 1–2 mmol/L increase in HCO3 − for every 10-mm Hg increase in Pco2 Chronic: 3–4 mmol/L increase in HCO3 − for every 10-mm Hg increase in Pco2 Respiratory alkalosis > 7.45 Compensatory decrease Primary decrease Acute: 1–2 mmol/L decrease in HCO3 − for every 10-mm Hg decrease in Pco2 Chronic: 4–5 mmol/L decrease in HCO3 − for every 10-mm Hg decrease in Pco2

A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response.

Mixed acid-base disorders comprise 2 or more primary disturbances.

Symptoms and Signs

Compensated or mild acid-base disorders cause few symptoms or signs. Severe, uncompensated disorders have multiple cardiovascular, respiratory, neurologic, and metabolic consequences described below (see Table 2: Acid-Base Regulation and Disorders: Clinical Consequences of Acid-Base Disorders; see Fig. 4: Tests of Pulmonary Function (PFT): Oxyhemoglobin dissociation curve.).

Table 2
Clinical Consequences of Acid-Base Disorders System Acidemia Alkalemia Cardiovascular Impaired cardiac contractility Arteriolar dilation Venoconstriction Centralization of blood volume Increased pulmonary vascular resistance Decreased cardiac output Decreased systemic BP Decreased hepatorenal blood flow Decreased threshold for cardiac arrhythmias Attenuation of responsiveness to catecholamines Arteriolar constriction Reduced coronary blood flow Reduced anginal threshold Decreased threshold for cardiac arrhythmias Metabolic Insulin resistance Inhibition of anaerobic glycolysis Reduction in ATP synthesis Hyperkalemia Protein degradation Bone demineralization (chronic) Stimulation of anaerobic glycolysis Formation of organic acids Decreased oxyhemoglobin dissociation Decreased ionized Ca Hypokalemia Hypomagnesemia Hypophosphatemia Neurologic Inhibition of metabolism and cell-volume regulation Obtundation and coma Tetany Seizures Lethargy Delirium Stupor Respiratory Compensatory hyperventilation with possible respiratory muscle fatigue Compensatory hypoventilation with hypercapnia and hypoxemia

Diagnosis

• ABG
• Serum electrolytes
• Anion gap calculated
• If metabolic acidosis is present, delta gap is calculated and Winter's formula applied
• Search for compensatory changes

Evaluation is with ABG and serum electrolytes. The ABG directly measures arterial pH and Pco₂. HCO₃ ⁻ levels on ABG are calculated using the Henderson-Hasselbalch equation; levels on serum chemistry panels are directly measured and are more accurate. Acid-base balance is generally most accurately assessed with measurement of pH and pCO₂ on arterial blood. In cases of circulatory failure or during cardiopulmonary resuscitation, measurements on venous blood may more accurately reflect conditions at the tissue level and may be a more useful guide to bicarbonate administration and adequacy of ventilation.

The pH establishes the primary process (acidosis or alkalosis), although it moves toward the normal range with compensation. Changes in Pco₂ reflect the respiratory component, and changes in HCO₃ ⁻ reflect the metabolic component. However, several calculations may be required to determine whether changes in Pco₂ and HCO₃ ⁻ are primary or compensatory and whether a mixed disorder is present; in mixed disorders, values may be deceptively normal. Interpretation must also consider clinical conditions (eg, chronic lung disease, renal failure, drug overdose).

The anion gap ( see Sidebar 1: Acid-Base Regulation and Disorders: The Anion Gap) should always be calculated; elevation almost always indicates a metabolic acidosis. A normal anion gap with a low HCO₃ ⁻ (eg, < 24 mEq/L) and high serum Cl⁻ indicates a non-anion gap (hyperchloremic) metabolic acidosis. If metabolic acidosis is present, a delta-gap is calculated (see Sidebar 1: Acid-Base Regulation and Disorders: The Anion Gap) to identify concomitant metabolic alkalosis, and Winter's formula is applied to see whether respiratory compensation is appropriate or reflects a 2nd acid-base disorder (predicted Pco₂ = 1.5 [HCO₃ ⁻] + 8 ± 2; if Pco₂ is higher, there is also a primary respiratory acidosis—if lower, respiratory alkalosis).

Sidebar 1
The Anion Gap The anion gap is defined as plasma Na concentration minus the sum of Cl− and HCO3 − concentrations; Na+ − (Cl− + HCO3 −). The term “gap” is misleading, because the law of electroneutrality requires the same number of positive and negative charges in an open system; the gap appears on laboratory testing because certain cations (+) and anions (−) are not measured on routine laboratory chemistry panels. Thus: Na+ + unmeasured cations (UC) = Cl− + HCO3 − + unmeasured anions (UA) and the anion gap, Na+ − (Cl− + HCO3 −) = UA − UC. The predominant unmeasured anions are PO4 3 −, sulfate (SO4 −), various negatively charged proteins, and some organic acids, accounting for 20 to 24 mEq/L. The predominant unmeasured extracellular cations are K+, Ca++, and Mg++ and account for about 11 mEq/L. Thus the typical anion gap is 23 − 11 = 12 mEq/L. The anion gap can be affected by increases or decreases in the UC or UA. Increased anion gap is most commonly caused by metabolic acidosis in which negatively charged acids—mostly ketones, lactate, sulfates, or metabolites of methanol, ethylene glycol, and salicylate—consume (are buffered by) HCO3 −. Other causes of increased anion gap include hyperalbuminemia and uremia (increased anions) and hypocalcemia or hypomagnesemia (decreased cations). Decreased anion gap is unrelated to metabolic acidosis but is caused by hypoalbuminemia (decreased anions); hypercalcemia, hypermagnesemia, lithium Some Trade Names ESKALITH LITHOBID LITHONATE Click for Drug Monograph intoxication, and hypergammaglobulinemia (increased cations); or hyperviscosity or halide (bromide or iodide) intoxication. The effect of low albumin can be accounted for by adjusting the normal range for the anion gap 2.5 mEq/L upward for every 1-g/dL fall in albumin. Negative anion gap occurs rarely as a laboratory artifact in severe cases of hypernatremia, hyperlipidemia, and bromide intoxication. The delta gap: The difference between the patient's anion gap and the normal anion gap is termed the delta gap. This amount is considered an HCO3 − equivalent, because for every unit rise in the anion gap, the HCO3 − should lower by 1 (by buffering). Thus, if the delta gap is added to the measured HCO3 −, the result should be in the normal range for HCO3 −; elevation indicates the additional presence of a metabolic alkalosis. Example: A vomiting, ill-appearing alcoholic patient has laboratory results showing Na, 137; K, 3.8; Cl, 90; HCO3 −, 22; pH, 7.40; Pco2, 41; Po2, 85 At first glance, results appear unremarkable. However, calculations show elevation of the anion gap 137 − (90 + 22) = 25 (normal, 10), indicating a metabolic acidosis. Respiratory compensation is evaluated by Winter's formula: Predicted Pco2 = 1.5 (22) + 8 ± 2 = 41 ± 2 Predicted = measured, so respiratory compensation is appropriate. Because there is metabolic acidosis, the delta gap is calculated, and the result is added to measured HCO3 −: 25 − 10 = 15 15 + 22 = 37 The resulting corrected HCO3 − is above the normal range for HCO3 −, indicating a primary metabolic alkalosis is also present. Thus, the patient has a mixed acid-base disorder. Using clinical information, one could theorize a metabolic acidosis arising from alcoholic ketoacidosis combined with a metabolic alkalosis from recurrent vomiting with loss of Cl– and volume.

Respiratory acidosis is suggested by Pco₂ > 40 mm Hg; HCO₃ ⁻ should compensate acutely by increasing 3 to 4 mEq/L for each 10-mm Hg rise in Pco₂ sustained for 4 to 12 h (there may be no increase or only 1 to 2 mEq/L, which slowly increases to 3 to 4 mEq/L over days). Greater increase in HCO₃ ⁻ implies a primary metabolic alkalosis; lesser increase suggests no time for compensation or coexisting primary metabolic acidosis.

Metabolic alkalosis is suggested by HCO₃ ⁻ > 28 mEq/L. The Pco₂ should compensate by increasing about 0.6 to 0.75 mm Hg for each 1 mEq/L increase in HCO₃ ⁻ (up to about 55 mm Hg). Greater increase implies concomitant respiratory acidosis; lesser increase, respiratory alkalosis.

Respiratory alkalosis is suggested by Pco₂ < 38 mm Hg. The HCO₃ ⁻ should compensate over 4 to 12 h by decreasing 5 mEq/L for every 10-mm Hg decrease in Pco₂. Lesser decrease means there has been no time for compensation or existence of a primary metabolic alkalosis. Greater decrease implies a primary metabolic acidosis.

Nomograms (acid-base maps) are an alternative way to diagnose mixed disorders, allowing for simultaneous plotting of pH, HCO₃ ⁻, and Pco₂.

Last full review/revision July 2008 by James L. Lewis, III, MD

Content last modified July 2008