Respiratory acidosis is defined as a primary increase in Paco2. This increase drives the reaction
to the right, leading to an increase in [H+] and a decrease in arterial pH. For the reasons described above, [HCO3−] is minimally affected.
Paco2 represents the balance between CO2 pro-duction and CO2 elimination:
CO2 is a byproduct of fat and carbohydrate metabolism. Muscle activity, body temperature, and thyroid hormone activity can all have major influ-ences on CO2 production. Because CO 2 production does not appreciably vary under most circum-stances, respiratory acidosis is usually the result of alveolar hypoventilation (Table 50–3). In patients
with a limited capacity to increase alveolar ventila-tion, however, increased CO 2 production can pre-cipitate respiratory acidosis.
The compensatory response to acute (6–12 h) elevations in Paco2 is limited. Buffering is primar-ily provided by hemoglobin and the exchange of extracellular H+ for Na+ and K+ from bone and the intracellular fluid compartment (see above). The renal response to retain more bicarbonate is acutely very limited. As a result, plasma [HCO3−] increases only about 1 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.
“Full” renal compensation characterizes chronic respiratory acidosis. Renal compensation is appre-ciable only after 12–24 hr
and may not peak until 3–5 days. During that time, the sustained increase in Paco2 has been present long enough to permit maximal renal compensation. During chronic respiratory acidosis, plasma [HCO 3−] increases approximately 4 mEq/L for each 10 mm Hg increase in Paco2 above 40 mm Hg.
Respiratory acidosis is treated by reversing the imbalance between CO 2 production and alveolar ventilation. In most instances, this is accomplished by increasing alveolar ventilation. Measures aimed at reducing CO2 production are useful only in specific instances (eg, dantrolene for malignant hyperther-mia, muscle paralysis for tetanus, antithyroid medi-cation for thyroid storm, and reduced caloric intake in patients receiving enteral or parenteral nutrition). Potential temporizing measures aimed at improv-ing alveolar ventilation (in addition to controlled mechanical ventilation) include bronchodilation, reversal of narcosis, or improving lung compliance (diuresis). Severe acidosis (pH <7.20), CO2 narcosis, and respiratory muscle fatigue are indications for mechanical ventilation. An increased inspired oxy-gen concentration is also usually necessary, as coex-istent hypoxemia is common. Intravenous NaHCO3 is rarely necessary, unless pH is <7.10 and HCO3− is <15 mEq/L. Sodium bicarbonate therapy will tran-siently increase Paco2:
H+ + HCO3−↔ CO2+ H2O
Buffers that do not produce CO 2, such as CarbicarbTM or tromethamine (THAM), are theoret-ically attractive alternatives; however, there is almost no evidence showing that they have greater efficacy than bicarbonate. Carbicarb TM is a mixture of 0.3 M sodium bicarbonate and 0.3 M sodium carbonate;
buffering by this mixture mainly produces sodium bicarbonate instead of CO2. Tromethamine has the added advantage of lacking sodium and may be a more effective intracellular buffer.
Patients with a baseline chronic respiratory acidosis require special consideration. When such patients develop acute ventilatory failure, the goal of therapy should be to return Paco2 to the patient’s “normal” baseline. Normalizing the patient’s Paco2 to 40 mm Hg will produces the equivalent of a respi-ratory alkalosis . Oxygen therapy must also be carefully controlled, because the respiratory drive in these patients may be dependent on hypox-emia, not Paco2. “Normalization” of Paco2 or relative hyperoxia can precipitate severe hypoventilation.