Respiratory acidosis is characterized by an elevated PCO2 and reduced ECF pH. It results from decreased gas exchange across the alveoli as a result of either inadequate ventilation (e.g., drug-induced depression of the respiratory centers) or impaired gas diffusion (e.g., pulmonary edema, such as occurs in cardiovascular and lung disease). In contrast to the metabolic disorders, buffering during respiratory acidosis occurs almost entirely in the ICF compartment. The increase in PCO2 and the decrease in pH stimulate both HCO3 − reabsorption by the nephron and titratable acid and NH4 + excretion (renal compensation). Together these responses increase RNAE and generate new HCO3 − . The renal compensatory response takes several days to occur. Consequently, respiratory acid-base disorders are commonly divided into acute and chronic phases. In the acute phase the time for the renal compensatory response is not sufficient, and the body relies on ICF buffering to minimize the change in pH. In the chronic phase, renal compensation occurs. Correction of the underlying disorder returns the PCO2 to normal and RNAE decreases to its initial level.
Respiratory alkalosis is characterized by a reduced PCO2 and an increased ECF pH. It results from increased gas exchange in the lungs, usually caused by increased ventilation from stimulation of the respiratory centers (e.g., via drugs or disorders of the central nervous system). Hyperventilation also occurs at high altitude and as a result of anxiety, pain, or fear. Buffering is primarily in the ICF compartment. As with respiratory acidosis, respiratory alkalosis has both acute and chronic phases reflecting the time required for renal compensation to occur. The acute phase of respiratory alkalosis reflects intracellular buffering, whereas the chronic phase reflects renal compensation. With renal compensation, the elevated pH and reduced PCO2 inhibit HCO3 − reabsorption by the nephron and reduce titratable acid and NH4 + excretion. As a result of these effects, RNAE is reduced. Correction of the underlying disorder returns the PCO2 to normal, and renal excretion of acid then increases to its initial level.
Analysis of Acid-Base Disorders
Analysis of an acid-base disorder is directed at identifying the underlying cause so appropriate therapy can be initiated. The patient’s medical history and associated physical findings often provide valuable clues about the nature and origin of an acid-base disorder. In addition, analysis of an arterial blood sample is frequently required. Such an analysis is straightforward if approached systematically. For example, consider the following data: pH = .
The acid-base disorder represented by these values or any other set of values can be determined using the following three-step approach: 1.
Examination of the pH. When pH is considered first, the underlying disorder can be classified as either an acidosis or an alkalosis. The defense mechanisms of the body cannot correct an acid-base disorder by themselves. Thus even if the defense mechanisms are completely operative, the change in pH indicates the acid-base disorder. In the example provided, the pH of 7.35 indicates acidosis.
2.
Determination of metabolic versus respiratory disorder. Simple acid-base disorders are either metabolic or
Role of the Kidneys in the Regulation of Acid-Base Balance respiratory. To determine which disorder is present the clinician must next examine the ECF [HCO3 −] and PCO2. As previously discussed, acidosis could be the result of a decrease in [HCO3 −] (metabolic) or an increase in PCO2 (respiratory). Alternatively, alkalosis could be the result of an increase in ECF [HCO3 −] (metabolic) or a decrease in PCO2 (respiratory). For the example provided, the ECF [HCO3 −] is reduced from normal (normal = 24 mEq/L), as is the PCO2 (normal = 40 mm Hg). The disorder must therefore be metabolic acidosis; it cannot be a respiratory acidosis because the PCO2 is reduced.