Respiratory acid-base disorders are commonly seen in the intensive care unit, and can occur independently or coexist with metabolic acid-base disorders (see Chapter 24). Respiratory acid-base disorders are characterized by altered plasma carbon dioxide levels, measured on arterial blood gas (ABG) analysis as the partial pressure of carbon dioxide (PaCO₂). Respiratory acidosis is characterized by an elevated PaCO₂ and decreased pH, and respiratory alkalosis by a decreased PaCO₂ and elevated pH. The PaCO₂ in healthy adults is 35 to 45 mm Hg and the normal pH is 7.35 to 7.45. For calculation purposes, it is reasonable to use 40 mm Hg as the baseline PaCO₂ level and 7.4 as the baseline pH. In general, each acute 10 mm Hg change in the PaCO₂ causes a 0.08 change in the arterial pH. For example, in a patient with a plasma pH of 7.4, an acute increase in the PaCO₂ from 40 to 50 mm Hg would be expected to decrease the plasma pH from 7.4 to 7.32. An acute 10 mm Hg decrease in the PaCO₂ from 40 to 30 mm Hg would be expected to increase the pH from 7.4 to 7.48.

In respiratory acid-base disorders, the kidneys compensate for changes in the PaCO₂ by increasing the plasma bicarbonate (HCO₃⁻) in respiratory acidosis, or decreasing the plasma HCO₃⁻ in respiratory alkalosis. Acute respiratory acid-base disorders result in small changes in the HCO₃⁻ concentration, and cellular buffering predominates. Chronic renal compensation occurs during days to weeks, and results in a larger change in plasma HCO₃⁻. Table 26.1 shows the expected change in the plasma HCO₃⁻ level in acute and chronic respiratory acidosis and alkalosis. The serum HCO₃⁻ in a healthy adult is approximately 22 to 26 mEq/L. Thus, it is reasonable to use a level of 24 mEq/L for calculation purposes. Compensatory change in HCO₃⁻ is associated with a shift in the pH back toward normal. A normal pH is not achieved by compensation alone and overcompensation does not occur. Therefore, a mixed respiratory and metabolic disorder is present if the pH is normal and the PaCO₂ is altered. For example, a pH of 7.4 with a PaCO₂ of 60 mm Hg means that, in addition to the respiratory acidosis, a metabolic alkalosis is present that has moved the pH back to normal (see Step 4). Mixed acid-base disorders do not include the renal HCO₃⁻ compensation that occurs for acute and chronic respiratory acid-base disorder.

Evaluation of respiratory acid-base disorders can be relatively straightforward in patients with an isolated acute primary respiratory acidosis or alkalosis, such as occurs in a young patient with an acute asthma exacerbation or in an otherwise healthy patient with anxiety-induced hyperventilation, or more difficult when superimposed metabolic acid-base disorders are present in a critically ill patient. Further complicating evaluation is the change that occurs in the serum HCO₃⁻ in acute and chronic
respiratory acidosis and alkalosis. Algorithm 26.1 and steps 1 through 6 can aid in analyzing a respiratory acid-base disorder. However, these are general rules, and when evaluating a given ABG in a primary respiratory acid-base disorder, the patient’s clinical history and physical examination have to be incorporated to arrive at the correct diagnosis (see step 5 for further explanation).

Respiratory acidosis results from hypercapnia induced by alveolar hypoventilation. The approach to hypercapnia and the differential diagnosis is outlined in Chapter 7, Algorithm 7.1 and includes disorders in any component of the ventilatory mechanism, such as the central or peripheral nervous system, neuromuscular junction, respiratory muscles, chest wall, pleura, upper airway, or lungs.

Respiratory acidosis treatment is directed at the underlying cause, outlined in various other chapters in this manual. In general, treatment is aimed at improving alveolar ventilation and includes bronchodilators for patients with asthma and chronic obstructive pulmonary disease (COPD), bilevel positive airway pressure, mechanical ventilation (used with caution in patients with chronic respiratory acidosis with an elevated serum HCO₃⁻ as rapid correction can cause a life-threatening metabolic alkalosis), reversal of drug effects, treatment of pulmonary edema, and addressing neuromuscular diseases. Sodium HCO₃⁻ is not recommended in respiratory acidosis as it may worsen hypercapnia and pulmonary edema, or cause a metabolic alkalosis. Small doses of sodium HCO₃⁻ can be considered in cases of severe acidosis (pH <7.1) with intractable hypercapnia.