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Acid-base disorders are changes in arterial P co 2 , serum HCO 3 − , and serum pH.
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 HCO 3 − or in P co 2 .
Metabolic acidosis is serum HCO 3 − < 24 mEq/L. Causes are
Metabolic alkalosis is serum HCO 3 − > 24 mEq/L. Causes are
Respiratory acidosis is P co 2 > 40 mm Hg (hypercapnia). Cause is
Respiratory alkalosis is P co 2 < 40 mm Hg (hypocapnia). Cause is
Whenever an acid-base disorder is present, compensatory mechanisms begin to correct the pH (see Primary Changes and Compensations in Simple Acid-Base Disorders). Compensation cannot return pH completely to normal and never overshoots.
Primary Changes and Compensations in Simple Acid-Base Disorders
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.
Compensated or mild acid-base disorders cause few symptoms or signs. Severe, uncompensated disorders have multiple cardiovascular, respiratory, neurologic, and metabolic consequences (see 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 P co 2 . HCO 3 − levels on ABG are calculated using the Henderson-Hasselbalch equation; HCO 3 − 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 P co 2 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 P co 2 reflect the respiratory component, and changes in HCO 3 − 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 P co 2 and HCO 3 − show the expected compensation (see 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 HCO 3 − (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 The Anion Gap) to identify concomitant metabolic alkalosis, and Winter’s formula is applied to determine whether respiratory compensation is appropriate or reflects a 2nd acid-base disorder (predicted P co 2 = 1.5 [HCO 3 − ] + 8 ± 2; if P co 2 is higher, there is also a primary respiratory acidosis—if lower, respiratory alkalosis).
Respiratory acidosis is suggested by P co 2 > 40 mm Hg; HCO 3 − should compensate acutely by increasing 3 to 4 mEq/L for each 10 mm Hg rise in P co 2 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 HCO 3 − implies a primary metabolic alkalosis; lesser increase suggests no time for compensation or coexisting primary metabolic acidosis.
Metabolic alkalosis is suggested by HCO 3 − > 28 mEq/L. The P co 2 should compensate by increasing about 0.6 to 0.75 mm Hg for each 1 mEq/L increase in HCO 3 − (up to about 55 mm Hg). Greater increase implies concomitant respiratory acidosis; lesser increase, respiratory alkalosis.
Respiratory alkalosis is suggested by P co 2 < 38 mm Hg. The HCO 3 − should compensate over 4 to 12 h by decreasing 5 mEq/L for every 10 mm Hg decrease in P co 2 . 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, HCO 3 − , and P co 2 .
Acidosis and alkalosis refer to physiologic processes that cause accumulation or loss of acid and/or alkali; serum 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 HCO 3 − and respiratory if the change is primarily due to a change in P co 2 (increase or decrease in ventilation).
All acid-base disturbances result in compensation that tends to normalize the pH. Metabolic acid-base disorders result in respiratory compensation (change in pCO 2 ); respiratory acid-base disorders result in metabolic compensation (change in HCO 3 − ).
The pH establishes the primary process (acidosis or alkalosis), changes in P co 2 reflect the respiratory component, and changes in HCO 3 − reflect the metabolic component.
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 anion gap.
Use one of several formulas, rules-of-thumb or acid-base nomogram to determine if lab 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.
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