Correction of respiratory acidosis with bicarbonate

When HCO3- is added to a closed system (e.g. venous blood) it is buffered by fixed buffer pairs A--AH (i.e. hemoglobin, proteins, and phosphates). This leads to generation of CO2, according to the following reaction: HCO3- + AH ® H2CO3 + A ® CO2 + H2O + A-.

However, not all the added HCO3- is transformed into CO2. For example, if 10 mmol of HCO3- are added to a closed system, 9.56 mmol are unchanged and only 0.44 mmol are transformed to CO2, so that PCO2 increases from 40 to 54.5 mmHg (5.33 to 7.27 kPa). The concurrent increases in HCO3- and PCO2 result in a change of pH from 7.40 to 7.41, which is clinically irrelevant.

This basic mechanism is important for the rational use of HCO 3- in correcting acidosis. For example, if the patient is in circulatory arrest or a severe low-flow state, i.e. approaching a closed system, HCO3- is ineffective in correcting pH as both HCO3- and PCO2 rise. The pH increases during HCO3- loading only if the newly generated CO2 can be cleared out of the system by appropriate transport (cardiac output) and elimination (ventilation).

Under these conditions, administration of HCO3- is equivalent to acceleration of the process naturally occurring in the kidneys, in which new HCO 3- is generated. Thus, when correcting the pH with HCO3- during CO2 retention, the rate of HCO3- administration and the resetting of mechanical ventilation to clear the extra CO 2 derived from HCO3- titration must be carefully balanced. It is important to avoid sudden changes in the acid-base status, and pH correction using alkalinizing agents should be restricted to conditions in which the pH decrease is believed to be responsible for severe clinical deterioration. In most cases artificial PCO2 control by mechanical ventilation and the natural kidney function (if present) is sufficient to restore an adequate acid-base balance.

Chapter References

Aubier, M. and Dombret, M.C. (1993). Acute exacerbation of chronic airflow obstruction. In Pathophysiology: foundations of critical care (ed. M.R. Pinsky and J.F.A. Dhainaut), pp. 427-46. Williams & Wilkins, Baltimore, MD.

Bidani, A., Tzounakis, A.E., Cardenas, V.J., and Zwischenberg, J.B. (1994). Permissive hypercapnia in acute respiratory failure. Journal of the American Medical Association, 272, 957-62. Brochard, L., et al. (1995). Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. New England Journal of Medicine, 333, 817-22. Darioli, R. and Perret, C. (1984). Mechanical controlled hypoventilation in status asthmaticus. American Review of Respiratory Disease, 129, 385-7.

Hikling, K.G., Henderson, S.J., and Jackson, R. (1990). Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. Intensive Care Medicine, 16, 372-7.

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