The human body tightly regulates its acid–base environment, keeping the serum pH close to 7.40 (normal values = 7.35–7.45). As pH is a negative logarithmic scale, this corresponds to a concentration of H⁺ in serum of 0.00004 mEq/L¹—which is dramatically less than the concentration of sodium (135–145 mEq/L) and other ions. Significant shifts away from the normal pH result in cellular alterations that lead to changes to systemic and pulmonary vascular resistance, reduced cardiac output and sensitivity to inotropes, precipitates arrhythmias,¹ and can put the patient at risk of death. Carbonic acid (H₂CO₃) and its buffering salt bicarbonate play key roles in the metabolic component of pH.

When the usual homeostatic mechanisms ultimately become overwhelmed with the production of acid or base, acidosis or alkalosis develops. The nearly immediate compensatory response of the body to this change in pH occurs through chemoreceptors in the brain resulting in increases in minute ventilation, lowering the pCO₂ in response to a metabolic acidosis (trying to maintain a more normal pH). The renal system is also activated to help correct the acidosis/alkalosis but this process is slower and may take hours to days. The body does not overcompensate such that changes occurring in pCO₂ through changes in ventilation or metabolic changes via the kidneys will only bring the pH toward neutral but will not convert an acidosis to alkalosis or vice versa.²

KEY CONCEPTS

The states of having an abnormally low or high pH are referred to as acidemia and alkalemia, respectively. The term compensation refers to the homeostatic mechanism the body uses to generate a compensatory acidosis or alkalosis as an attempt to normalize pH when faced with a pathologic acid–base disturbance.²

The pH, pCO₂, and pO₂ are measured, while the bicarbonate level and base excess/deficit are calculated estimations. A serum bicarbonate measurement in the chemistry laboratory is an actual measurement rather than a calculation, but in most instances the calculated and measured values should be very close to each other. Recent literature in adult trauma victims suggests the base deficit may be very useful in predicting transfusion requirements and risk of mortality, and may better identify shock severity than current Advanced Trauma Life Support (ATLS) classification based on clinical signs.^3,4

The gold standard for blood gas measurement remains an arterial specimen but this often proves difficult to obtain, is unnecessarily invasive for most children, and carries a small risk of complications.⁵ Venous or capillary specimens are generally easier to obtain and there is good correlation for pH, pCO2, base excess, and bicarbonate.⁶ An arterial specimen should be obtained when pO₂ or co-oximetry measurement is required (e.g., when the pulse oximeter has a poor perfusion signal due to severe shock, or when it is unreliable, as in a patient with carbon monoxide poisoning or methemoglobinemia).⁷

INTERPRETATION

The first step in analyzing the blood gas is to look at the pH. A value less than 7.4 reflects an acidosis and regardless of what other processes may be simultaneously occurring, the primary process is an acidosis. Similarly, a pH value of greater than 7.4 reflects a primary alkalosis with a primary process of an alkalosis. The next step should be look at the pCO₂ and bicarbonate. In the context of an acidosis, an elevated pCO₂ suggests the primary process is a respiratory acidosis, and a low bicarbonate suggests a metabolic acidosis (the combination of both suggests mixed respiratory and metabolic acidosis). Conversely, in an alkalemic presentation, a low pCO₂ indicates respiratory alkalosis and a high bicarbonate indicates a metabolic alkalosis.

The next step should determine if the compensation is appropriate. If not, there may be multiple acid–base disturbances occurring simultaneously. In acute respiratory acidosis, an increase of 10 mmHg usually decreases the pH by 0.08, and a compensatory bicarbonate increase of 1 mEq/L is an attempt to normalize the pH. For chronic changes in pCO₂ the kidney is better able to compensate and the bicarbonate will increase by 3.5 mEq/L for the same 10 mmHg increase in pCO₂.⁸ This difference in compensation may help the clinician determine the chronicity of the patient’s symptoms when it is not readily apparent on history. As an example, a 5-month old former 26-week premature infant with chronic lung disease presenting with a pCO₂ of 60 mmHg and a bicarbonate 31 mEq/L likely has chronic CO₂ retention compared to an infant with a pCO₂ of 60 mmHg and a bicarbonate of 26 mEq/L who has an acute process that will require more aggressive therapy.