Metabolic acidosis is usually accompanied by respiratory compensation (tachypnea).
Chronic respiratory acidosis is usually accompanied by gradual metabolic compensation (increases in serum bicarbonate).
Acute respiratory acidosis is usually not accompanied by immediate metabolic compensation.
The most common cause of a non–anion-gap metabolic acidosis is bicarbonate loss from diarrhea.
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
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 ...