(See also Acid-Base Regulation.)
Acid-base disorders are pathologic changes in arterial pH and carbon dioxide partial pressure (Pco2), and in serum bicarbonate (HCO3−).
Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present.
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
Metabolic alkalosis is serum HCO3−> 24 mEq/L. Causes are
Respiratory acidosis is Pco2> 40 mm Hg (hypercapnia). Cause is
Respiratory alkalosis is Pco2< 40 mm Hg (hypocapnia). Cause is
Whenever an acid-base disorder is present, compensatory mechanisms begin to correct the pH (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders). Compensation cannot return pH completely to normal and never overshoots.
A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response.
Mixed acid-base disorders comprise ≥ 2 primary disturbances.
Primary Changes and Compensations in Simple Acid-Base Disorders
Compensated or mild acid-base disorders cause few symptoms or signs. Severe, uncompensated disorders have multiple cardiovascular, respiratory, neurologic, and metabolic consequences (see Table: Clinical Consequences of Acid-Base Disorders and see Figure: Oxyhemoglobin dissociation curve.).
Clinical Consequences of Acid-Base Disorders
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; HCO3− levels on serum chemistry panels are directly measured and are considered more accurate in cases of discrepancy. Acid-base balance is 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.
Complex or mixed acid-base disturbances involve more than one primary process. In these mixed disorders, values may be deceptively normal. Thus, it is important when evaluating acid-base disorders to determine whether changes in Pco2 and HCO3− show the expected compensation (see Table: Primary Changes and Compensations in Simple Acid-Base Disorders). If not, then a second primary process causing the abnormal compensation should be suspected. Interpretation must also consider clinical conditions (eg, chronic lung disease, renal failure, drug overdose).
The anion gap (see 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 chloride (Cl−) indicates a non-anion gap (hyperchloremic) metabolic acidosis. If metabolic acidosis is present, a delta gap is calculated (see The Anion Gap) to identify concomitant metabolic alkalosis, and Winters formula is applied to determine 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).
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 a primary metabolic alkalosis coexists. 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.
Acidosis and alkalosis refer to physiologic processes that cause accumulation or loss of acid and/or alkali; blood pH may or may not be abnormal.
Acidemia and alkalemia refer to an abnormally acidic (pH < 7.35) or alkalotic (pH > 7.45) serum pH.
Acid-base disorders are classified as metabolic if the change in pH is primarily due to an alteration in serum HCO3−and respiratory if the change is primarily due to a change in Pco2 (increase or decrease in ventilation).
The pH establishes the primary process (acidosis or alkalosis), changes in Pco2reflect the respiratory component, and changes in HCO3− reflect the metabolic component.
All acid-base disturbances result in compensation that tends to normalize the pH. Metabolic acid-base disorders result in respiratory compensation (change in Pco2); respiratory acid-base disorders result in metabolic compensation (change in HCO3− ).
More than one primary acid-base disorder may be present simultaneously. It is important to identify and address each primary acid-base disorder.
Initial laboratory evaluation of acid-base disorders includes ABG and serum electrolytes and calculation of the anion gap.
Use one of several formulas, rules-of-thumb, or acid-base nomogram to determine if laboratory values are consistent with a single acid-base disorder (and compensation) or if a second primary acid-base disorder is also present.
Treat each primary acid-base disorder.