Diagnosing Mixed Acid-Base Disorders

The following section is adapted from Chapter 8 of Dr. Martin's book All You Really Need to Know to Interpret Arterial Blood Gases, 2nd edition, published February 1999 by Lippincott Williams & Wilkins. Click on the title to see the Preface and Table of Contents. The book is available for purchase from the publisher at 1-800-638-0672 or 1-410-528-4223 and also at the following web sites:
Lippincott Williams & Wilkins and Amazon.com

Does the patient have a mixed acid-base disorder?

There is perhaps no more confusing topic related to blood gases than mixed acid-base disorders. This topic has already been discussed in Chapter 7 in regards to the serum electrolytes. As was pointed out, calculation of the anion and bicarbonate gaps can help uncover mixed metabolic disorders (e.g., anion gap metabolic acidosis and metabolic alkalosis). Of course, to accurately diagnose the specific disorders and their relative severity at least one set of blood gases is usually necessary.

When there is significant deviation from the expected changes for a single disorder, a mixed disorder is usually present. I have found the following four "tips" especially helpful in diagnosing mixed acid-base disorders.

These rules are quite useful in diagnosing a mixed acid-base disorder when there is respiratory acidosis or respiratory alkalosis. These two conditions of course describe acute changes in PaCO₂, and therefore acute changes in the dissolved CO₂ in the blood. Changes in PaCO₂, i.e., in the dissolved fraction of CO₂, affect the hydration of dissolved CO₂ with H₂O, which is a reversible reaction:

Acute CO₂ retention (i.e., acute respiratory acidosis) drives the hydration reaction more than normal to the right; as a result, HCO₃^- increases slightly. Acute CO₂ excretion (i.e., acute respiratory alkalosis) drives the hydration reaction more than normal to the left, and HCO₃^- decreases slightly. These changes in HCO₃^- are instantaneous by virtue of changes in the CO₂ hydration reaction, and have nothing to do with the kidneys or renal compensation. Thus:

a) A normal or slightly low HCO₃^- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27, PaCO₂ 50 mm Hg, HCO₃^- 22 mEq/L;

b) A normal or slightly elevated HCO₃^- in the presence of hypocapnia suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO₂ 30 mm Hg, HCO₃^- 26 mEq/L.

In a), the bicarbonate is lower than expected for acute hypo-ventilation; the patient has respiratory acidosis and metabolic acidosis. In b), bicarbonate is higher than expected for acute hyperventilation; the patient has respiratory alkalosis and metabolic alkalosis. In c), PaCO₂ is higher than expected for fully compensated metabolic acidosis, suggesting a concomitant respiratory disorder or very early metabolic acidosis.

Always keep in mind that any isolated measurement of pH and PaCO₂ can be explained by two or more co-existing acid-base disorders. Thus, even when blood gas values fall into one of the 95% confidence bands, the patient may still have a mixed disorder. Often, the only way to know for sure is by detailed analysis of all the clinical and laboratory information and close patient follow up.

His pH and PaCO₂ fit into the band of acute respiratory alkalosis. He has moderate hypoxemia and the blood gas data alone could be explained by acute hyperventilation due to pneumonia. But the anion gap is elevated at 26 mEq/L, indicating a concomitant metabolic acidosis. The delta anion gap is 14 mEq/L, giving an expected serum CO₂ of 13 mEq/L, and a bicarbonate gap +8 mEq/L. Thus the patient manifests three separate acid-base disorders: respiratory alkalosis (from pneumonia); metabolic acidosis (from renal disease); and hypokalemic metabolic alkalosis (from excessive diuretic therapy). The result of all this acid-base abnormality? Blood gas values that are indistinguishable from those of simple acute respiratory alkalosis.

Summary: Clinical and laboratory approach to acid-base diagnosis

Each primary acid-base disorder should be viewed as a physiologic process caused by a specific clinical condition or disease, not simply as changes in blood gas and electrolyte values. This view allows for unraveling complex or mixed acid-base disorders. Points to remember for proper acid-base diagnosis and management can be summarized as follows (Figure 8-3).

• Determine existence of acid-base disorder from arterial blood gas and/or serum electrolyte measurements. For electrolytes, follow steps outlined in Figure 7-2. Check serum CO₂ for abnormal value. Calculate AG and, if elevated, calculate the bicarbonate gap.

• If the measured pH and/or PaCO₂ are abnormal, you should be able to discern at least one primary acid-base disorder from the observed changes (Table 8-1).
  The changes for each primary disorder are straightforward and should be committed to memory.

• Examine pH, PaCO₂ and HCO₃^- for deviations that may indicate mixed acid-base disorders (TIPS 2 through 4, Table 8-3.)

• Use a full clinical assessment (history, physical exam, other lab data including previous arterial blood gases and serum electrolytes) to explain each acid-base disorder (Table 8-1).

• Remember that co-existing clinical conditions may lead to opposing acid-disorders, so that pH can be high when there is an obvious acidosis, or low when there is an obvious alkalosis.

• Treat the underlying clinical condition(s); this will usually suffice to correct most acid-base disorders. If there is concern that acidemia or alkalemia is life-threatening, aim toward correcting pH into the range of 7.30-7.52 ([H⁺] 50-30 nM/L).

• Clinical judgment should always apply. See Pitfalls 12-14 in Chapter 13.

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