This chapter describes a practical approach to the clinical evaluation and treatment of acid-base disorders. We discuss the traditional approach recognizing that acid-base homeostasis is maintained by respiratory control of the partial pressure of carbon dioxide (PCO2) through changes in alveolar ventilation and control of HCO3– reabsorption and H+ excretion by the kidneys.1,2 The traditional bicarbonate-centered model continues to be the most commonly used at the bedside.3
Plasma [H+]* is influenced by the rate of endogenous production, the rate of excretion, exogenous addition (e.g., acetylsalicylic acid ingestion), and the buffering capacity of the body.1 Buffers mitigate the impact of large changes in available hydrogen ion on plasma pH.
Buffer systems that are effective at physiologic pH include hemoglobin, phosphate, proteins such as albumin, and bicarbonate (Figure 15-1). One can consider the [H+] to be the result of all physiologic buffers acting on the common pool of hydrogen ions.
Schematic representation of hydrogen ion homeostasis.
The quantity of [HCO3–] in relation to carbonic acid buffer in the system is not fixed, but varies according to physiologic need. This flexibility is largely provided by pulmonary exhalation of carbon dioxide (CO2), which can vary significantly and change rapidly as required by alterations in the underlying acid-base status.
The kidney regulates HCO3– excretion and the formation of new HCO3–. The rate of these processes is dependent on the underlying acid-base status. The renal response to pulmonary acid-base disturbances begins within 30 minutes of onset, but requires hours to days to achieve equilibrium.4
Any condition that acts to increase [H+]—whether through endogenous production, decreased buffering capacity, decreased excretion, or exogenous addition—is known as acidosis. Similarly, any condition that acts to decrease [H+] is termed alkalosis. The terms acidemia and alkalemia refer to the net imbalance of [H+] in the blood.
Acid-base disturbances are further classified as respiratory or metabolic. Respiratory acid-base disorders are due to primary changes in PCO2, and metabolic acid-base disorders reflect primary changes in [HCO3–]. Compensatory mechanisms are, by definition, not “disorders,” but rather normal physiologic responses to acid-base derangements. Failure of appropriate compensatory response implies the presence of another primary acid-base disturbance.
The principle of electrical neutrality requires that plasma have no net charge. The charge of the predominant plasma cation, Na+, must therefore be “balanced” by the charge of plasma anions.5 Although HCO3– and Cl– constitute a significant fraction of plasma ...