We received four samples in a span of one year, from December 2011 to November 2012, for ABG analysis, in which the BcHCO₃^- was not displayed by the ABG analyzer, RL 348 from Siemens Diagnostics Ltd., installed in our laboratory. The operating manual of the ABG analyzer was studied to find out the display range for BcHCO₃^-. Similar information was obtained about other models of ABG analyzers.

By using information from literature and by performing mathematical operations, the formula for calculating BcHCO₃^- from pH and pCO₂ was obtained. By using this formula, BcHCO₃^- for the four samples mentioned above was calculated. To verify the correctness of the formula, BcHCO₃^- of 10 other samples falling within the measuring range of the ABG analyzer were also calculated using the formula. These values were compared with the values displayed by the analyzer. Clinical and laboratory data pertaining to the four samples mentioned above was collected from hospital and laboratory records.

BcHCO₃^- can be obtained by calculation from the values of pH and pCO₂ or by measurements using analytical methods. The calculated value is advantageous, as it is not affected by electrolyte exclusion effects and reflects BcHCO₃^- as measured with an ion selective electrode [2]. In most of the ABG analyzers, the BcHCO₃^- is calculated from the measured pH and pCO₂ values. Different ABG analyzers have different upper and lower limits for displaying BcHCO₃^-. Values falling beyond the display limits are not displayed by the analyzers, though they may sometimes be encountered in patients. In such instances, laboratory personnel may suspect analyzer malfunction and reporting may be delayed while trying to get the analyzer repaired. To prevent this, it is necessary to know

(1) The formula, by using which BcHCO₃^- can be calculated from the pH and pCO2 values [2].

The relation between pH, pCO₂, and bicarbonate ion concentration (cHCO₃^-) is given by the Handerson-Hasselbalch’s equation as follows:

pH = 6.103 + log [cHCO₃^- / (0.0306 X pCO₂ )] ------- formula 1

Here, cHCO₃^- is expressed in mmol/L, while pCO₂ is expressed in mmHg.

We modified formula 1 by using simple mathematical operations to get the following formula for directly calculating the cHCO₃^-_:

cHCO₃^- (mmol/L) = 24.1 X pCO₂ (mmHg)/10^9-pH ------- formula 2

Another modified form of formula 1 that can be found in literature is as follows [3]:

cHCO₃^- = 0.03 X pCO₂ x 10^pH-6.1

The BcHCO₃^- can also be directly obtained on entering pH and pCO₂ values in software programs available on the internet [3]. BcHCO₃^- for ten other samples calculated using formula 2 matched exactly with the values displayed by the analyzer, thus confirming the validity of formula 2. Literature shows that there is no significant difference between cHCO₃^- values obtained by measurements or by calculation [4]. This obviates the need to measure such undisplayed BcHCO3^- by another method and the calculated value can be treated as correct.

(2) The types of patients in whom BcHCO₃^- may fall beyond the display range of the ABG analyzer:

Relevant data pertaining to the four samples mentioned above has been presented in [Table/Fig-1]. The value for actual BcHCO₃^- mentioned in the [Table/Fig-1] was not displayed by the analyzer and it was calculated manually using formula 2, which has been given above. As is evident from the table, the calculated BcHCO₃^- values were above 60mmol/L and hence, they were not displayed by our analyzer (RL 348), that has a measuring range of 3-60 mmol/L. All patients mentioned in the [Table/Fig-1] had chronic respiratory disease leading to increased pCO₂ (hypercapnea) and chronic respiratory acidosis. Excess CO₂, on undergoing the following reaction, is converted in the blood to H⁺ and HCO₃^- : .

H₂O + CO₂ → H₂CO₃ → H⁺ + HCO₃^-

The excess H⁺ ions generated are buffered mainly by the protein buffer systems, leaving behind an excess of HCO₃^- ions. This may manifest as metabolic alkalosis, especially immediately following a rise in pCO₂. With passage of time, renal compensation of acidosis will occur and it may fully restore the pH to normal, in spite of high pCO₂ values. During renal compensation, the renal tubular cells promote H⁺ ion excretion and bicarbonate retention, thus further increasing the cHCO₃^- values [5]. In chronic compensated respiratory acidosis, the expected rise in cHCO₃^- is 3.5 mmol/L for every 10mm Hg rise in pCO₂, while the expected fall in pH is 0.05 units for every 15 mmHg rise in pCO₂. Using the above information, the expected pH and BcHCO₃^- in our patients were calculated from pCO₂ values [5]. [Table/Fig-1] shows that the actual pH and BcHCO₃^- in our patients were higher than the values expected, due to pure renal compensation, suggesting that an additional factor was causing metabolic alkalosis which was superimposed on compensated respiratory acidosis. There was no record of any intravenous bicarbonate being administered, which could have led to the superimposed metabolic alkalosis. Hospital records of these patients showed administration of furosemide and/or dexamethasone. Furosemide blocks Na⁺ and K⁺ absorption from the ascending limb of loop of Henle, resulting in a sodium rich fluid reaching the distal convoluted tubule. This stimulates aldosterone secretion that causes loss of K⁺ and H⁺ in the urine, leading to alkalosis. Similarly, in case of exogenous mineralocorticoid or glucocorticoid administration, K⁺ and H⁺ ions are excreted by the kidney as a consequence of increased Na⁺ reabsorption. Decreased tubular K⁺ concentration stimulates ammonia production and thus, renal H⁺ excretion as NH₄⁺. This is accompanied by enhanced HCO₃^- reabsorption, causing alkalosis [5]. Thus, the superimposed metabolic alkalosis in our patients could have been caused by administration of furosemide and dexamethasone.

The blood concentrations of electrolytes could be traced only for sample 1, as they were requested along with the ABG analysis and were mentioned in the records. They were, Na⁺=123mEq/L, K⁺=3.1mEq/L and Cl^-=75mEq/L. The anion gap (AG) was calculated by the formula, Na⁺- (Cl^-+HCO₃^-) and in this case, it was minus 14.29mEq/L. The delta gap was calculated by the formula, (AG -12) – (24 – HCO₃^-) and in this case, it was 12mEq/L, confirming the presence of metabolic alkalosis [6].

To summarize, BcHCO₃^- may be increased in patients with chronic respiratory disease due to hypercapnoea and renal compensation. Such a rise may be further augmented by treatment with loop diuretics like furosemide and/or glucocorticoids and mineralocorticoids. Sometimes, the raised bicarbonate values may not be displayed by the ABG analyzers, as they may be beyond the display range of the instrument. In such cases, the BcHCO₃^- values may be calculated accurately from the modified form of Handerson –Hasselbalch’s equation, which has been given above.

The aim of this article was to draw attention to the fact that whenever BcHCO₃^- is not displayed on the ABG analyzer, the cause may be found in the medical condition of the patient. Hence, instead of suspecting analyzer malfunction, in such situations, it is worthwhile, probing into the patient history, and calculating the BcHCO₃^- manually, so that critical time is saved.