Respiratory Acidosis

RESPIRATORY ACIDOSIS

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.

Acute 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.

Chronic Respiratory Acidosis

“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.

Treatment of Respiratory Acidosis

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 Carbicarb^TM 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.