Two or three simultaneous disorders can be present in a mixed acid-base disorder, but there can never be two primary respiratory disorders. Uncovering a mixed acid-base disorder is clinically important and requires a methodical approach to acid-base analysis (see box Step-by-Step Analysis of Acid-Base Status). Once the primary disturbance has been determined, the clinician should assess whether the compensatory response is appropriate (Table 21–11). An inadequate or an exaggerated response indicates the presence of another primary acid-base disturbance.
STEP-BY-STEP ANALYSIS OF ACID-BASE STATUS
Step 1: Determine the primary (or main) disorder—whether it is metabolic or respiratory—from blood pH, HCO3–, and PCO2 values.
Step 2: Determine the presence of mixed acid-base disorders by calculating the range of compensatory responses (see Table 21–11).
Step 3: Calculate the anion gap (see Table 21–12).
Step 4: Calculate the corrected HCO3– concentration if the anion gap is increased.
Step 5: Examine the patient to determine whether the clinical signs are compatible with the acid-base analysis.
Table 21–11.Primary acid-base disorders and expected compensation. ||Download (.pdf) Table 21–11. Primary acid-base disorders and expected compensation.
|Disorder ||Primary Defect ||Compensatory Response ||Magnitude of Compensation |
|Respiratory acidosis |
| Acute ||↑ PCO2 ||↑ HCO3– ||↑ HCO3– 1 mEq/L per 10 mm Hg ↑ PCO2 |
| Chronic ||↑ PCO2 ||↑ HCO3– ||↑ HCO3– 3.5 mEq/L per 10 mm Hg ↑ PCO2 |
|Respiratory alkalosis |
| Acute ||↓ PCO2 ||↓ HCO3– ||↓ HCO3– 2 mEq/L per 10 mm Hg ↓ PCO2 |
| Chronic ||↓ PCO2 ||↓ HCO3– ||↓ HCO3– 5 mEq/L per 10 mm Hg ↓ PCO2 |
|Metabolic acidosis ||↓ HCO3– ||↓ PCO2 ||↓ PCO2 1.3 mm Hg per 1 mEq/L ↓ HCO3– |
|Metabolic alkalosis ||↑ HCO3– ||↑ PCO2 ||↑ PCO2 0.7 mm Hg per 1 mEq/L ↑ HCO3– |
Table 21–12.Anion gap in metabolic acidosis.1 ||Download (.pdf) Table 21–12. Anion gap in metabolic acidosis.1
Decreased (< 6 mEq)
Hypoalbuminemia (decreased unmeasured anion)
Plasma cell dyscrasias
Monoclonal protein (cationic paraprotein accompanied by chloride and bicarbonate)
Increased (> 12 mEq)
Chronic kidney disease (advanced stages) (PO43–, SO42–)
Metabolic alkalosis (increased number of negative charges on protein)
5-oxoproline acidosis from acetaminophen toxicity
Drug or chemical anion
Sodium carbenicillin therapy
Methanol (formic acid)
Ethylene glycol (oxalic acid)
Normal (6–12 mEq)
Loss of HCO3
Recovery from diabetic ketoacidosis
Pancreatic fluid loss, ileostomy (unadapted)
Carbonic anhydrase inhibitors
Renal tubular acidosis
Ileal loop bladder
Administration of HCl equivalent or NH4Cl