An aid for interpreting blood gas results in acid-base disturbance

Blood gas analysis includes measurement or calculation of four blood parameters – pH, pCO₂, bicarbonate and base excess – that together allow assessment of patient acid-base status, which is disturbed in different ways in many acute and some chronic illnesses. Interpretation of blood gas results is widely perceived to be one of the more challenging aspects of laboratory medicine, but help is at hand with publication of this most recent paper, which aims to provide a systematic approach to diagnosis of acid-base disorders from the four blood parameters.

The core of this paper, which is authored by critical care physicians with specialist interest and clinical experience in blood gas interpretation, is the algorithm they have developed that provides a step-by-step approach to the diagnosis of each of the following four principal acid-base disorders:

• Metabolic acidosis – characterized by primary decrease in bicarbonate and compensatory (secondary) decrease in pCO₂
• Respiratory acidosis – characterized by primary increase in pCO₂ and compensatory (secondary) increase in bicarbonate
• Metabolic alkalosis – characterized by primary increase in bicarbonate and compensatory (secondary) increase in pCO₂
• Respiratory alkalosis – characterized by primary decrease in pCO₂ and compensatory (secondary) decrease in bicarbonate

The algorithm, which is supported by referenced explanatory text, begins with application of the Henderson-Hasselbalch equation to confirm internal consistency of pH, pCO₂ and bicarbonate results; this is a safety step intended to identify/rule out analytical error. Assuming the results are found to be internally consistent, the next step in the algorithm focuses on pH and identification of either acidemia (pH <7.35) or alkalemia (pH >7.45). Then the remaining three parameters (pCO₂, bicarbonate and base excess) are used to determine if the acidemia or alkalemia is due to primary abnormality in pCO₂ (respiratory) or primary abnormality in bicarbonate and base excess (metabolic).

The algorithm includes application of the means to establish if results are consistent with expected compensation (i.e. secondary change in bicarbonate for primary respiratory disturbance, and secondary change in pCO₂ for primary metabolic disturbance). This step allows final diagnosis of one of the four acid-base disorders or alternatively, a more complex, mixed acid-base disorder, for example: metabolic acidosis and respiratory alkalosis.

The authors also incorporate a range of non-blood gas laboratory results into their algorithm that allow further classification of acid-base disturbances and point to the cause of the identified acid-base disturbance. So, for example, the following tests are helpful in further classifying metabolic acidosis and identifying its cause: albumin-corrected anion gap, calculated ratio of change in anion gap to change in bicarbonate (delta anion gap/delta bicarbonate), serum potassium and urine osmolal gap. Just how results of these additional tests are applied is described in the algorithm and discussed more fully in the text of the article.

In a similar way, the differential diagnosis of metabolic alkalosis is aided by the following: assessment of intravascular volume, measurement of urine electrolytes (sodium and chloride) and serum renin/angiotensin/aldosterone. Once again, just how these additional clinical details/tests are applied to patients with metabolic alkalosis is described in the algorithm, and discussed in the text.

The text that accompanies the algorithm provides a wealth of clinical detail about the multiple causes and consequences of both single and mixed acid-base disorders. The article is published in a Spanish critical care journal; an English translation is provided.