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 systems and the control of the 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−].
The kidneys regulate plasma [HCO3−] through three main processes: (1) “reabsorption” of filtered HCO3−, (2) formation of titratable acid, and (3) excretion of NH4+ in the urine. The kidney filters ∼4000 mmol of HCO3− per day. To reabsorb the filtered load of HCO3−, the renal tubules must therefore secrete 4000 mmol of hydrogen ions. Between 80 and 90% of HCO3− is reabsorbed in the proximal tubule. The distal nephron reabsorbs the remainder and secretes H+ to defend systemic pH. While this quantity of protons, 40–60 mmol/d, is small, it must be secreted to prevent chronic positive H+ balance and metabolic acidosis. This quantity of secreted protons is represented in the urine as titratable acid and NH4+. Metabolic acidosis in the face of normal renal function increases NH4+ production and excretion. NH4+ production and excretion are impaired in chronic renal failure, hyperkalemia, and renal tubular acidosis.
The most common clinical disturbances are simple acid-base disorders; i.e., metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. Because compensation is not complete, the pH is abnormal in simple disturbances. More complicated clinical situations can give rise to mixed acid-base disturbances.
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 47-1. Metabolic acidosis due to an increase in endogenous acids (e.g., ketoacidosis) lowers extracellular fluid [HCO3−...