NORMAL ACID-BASE HOMEOSTASIS
Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (PaCO2) by the central nervous system (CNS) and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation:
Under most circumstances, CO2 production and excretion are matched, and the usual steady-state PaCO2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state PaCO2. Therefore, the PaCO2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in PaCO2 represent derangements of neural respiratory control or are due to compensatory changes in response to a primary alteration in the plasma [HCO3−].
DIAGNOSIS OF GENERAL TYPES OF DISTURBANCES
The most common clinical disturbances are simple acid-base disorders, that is, metabolic acidosis or alkalosis or respiratory acidosis or alkalosis.
SIMPLE ACID-BASE DISORDERS
Primary respiratory disturbances (primary changes in PaCO2) invoke compensatory metabolic responses (secondary changes in [HCO3−]), and primary metabolic disturbances elicit predictable compensatory respiratory responses (secondary changes in PaCO2). Physiologic compensation can be predicted from the relationships displayed in Table 51-1. In general, with one exception, compensatory responses return the pH toward, but not to, the normal value. Chronic respiratory alkalosis when prolonged is an exception to this rule and may return the pH to a normal value. Metabolic acidosis due to an increase in endogenous acid production (e.g., ketoacidosis) lowers extracellular fluid [HCO3−] and decreases extracellular pH. This stimulates the medullary chemoreceptors to increase ventilation and to return the ratio of [HCO3−] to PaCO2, and thus pH, toward, but not to, normal. The degree of respiratory compensation expected in a metabolic acidosis can be predicted from the relationship: PaCO2 = (1.5 × [HCO3−]) + 8 ± 2. Thus, a patient with metabolic acidosis and [HCO3−] of 12 mmol/L would be expected to have a PaCO2 of ∼26 mmHg. Values for PaCO2 <24 or="">28 mmHg define a mixed disturbance (metabolic acidosis and respiratory alkalosis or metabolic acidosis and respiratory acidosis, respectively). Compensatory responses for primary metabolic disorders move the PaCO2 in the same direction as the change in [HCO3−...24>