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Respiratory acidosis is primary increase in Pco₂ with or without compensatory increase in HCO₃ ⁻; pH is usually low but may be near normal. Cause is a decrease in respiratory rate, volume (hypoventilation), or both from CNS, pulmonary, or iatrogenic conditions. Respiratory acidosis can be acute or chronic; the chronic form is asymptomatic, but the acute, or worsening, form causes headache, confusion, and drowsiness. Signs include tremor, myoclonic jerks, and asterixis. Diagnosis is clinical and with ABG and serum electrolyte measurements. The cause is treated; O₂ and mechanical ventilation are often required.

Respiratory acidosis is CO₂ accumulation (hypercapnia) from a decrease in respiratory rate, respiratory volume (hypoventilation), or both. Causes of hypoventilation are discussed under Ventilatory Failure (Respiratory Failure and Mechanical Ventilation: Ventilatory Failure) and include

• Conditions that impair CNS respiratory drive
• Conditions that impair neuromuscular transmission and other conditions that cause muscular weakness
• Obstructive, restrictive, and parenchymal pulmonary disorders

Hypoxia typically accompanies hypoventilation.

Respiratory acidosis may be acute or chronic. Distinction is based on the degree of metabolic compensation; CO₂ is initially buffered inefficiently, but over 3 to 5 days the kidneys increase HCO₃ ⁻ reabsorption significantly.

Symptoms and Signs

Symptoms and signs depend on the rate and degree of Pco₂ increase. CO₂ rapidly diffuses across the blood-brain barrier. Symptoms and signs are a result of high CNS CO₂ concentrations (low CNS pH) and any accompanying hypoxemia.

Acute (or acutely worsening chronic) respiratory acidosis causes headache, confusion, anxiety, drowsiness, and stupor (CO₂ narcosis). Slowly developing, stable respiratory acidosis (as in COPD) may be well tolerated, but patients may have memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes. Signs include gait disturbance, tremor, blunted deep tendon reflexes, myoclonic jerks, asterixis, and papilledema.

Diagnosis

• ABG and serum electrolytes
• Diagnosis of cause usually clinical

Recognition of respiratory acidosis and appropriate renal compensation discussed in Acid-Base Regulation and Disorders: Diagnosis requires ABG and measurement of serum electrolytes. Causes are usually obvious from history and examination. Calculation of the alveolar-arterial (A-a) O₂ gradient (inspired Po₂ − [arterial Po₂ + ⁵⁄₄ arterial Pco₂]) can help distinguish pulmonary from extrapulmonary disease; a normal gradient essentially excludes pulmonary disorders.

Treatment

• Adequate ventilation
• NaHCO₃ almost always contraindicated

Treatment is provision of adequate ventilation by either endotracheal intubation or noninvasive positive pressure ventilation (for specific indications and procedures, see Respiratory Failure and Mechanical Ventilation). Adequate ventilation is all that is needed to correct respiratory acidosis, although chronic hypercapnia generally must be corrected slowly (eg, over several hours or more), because too-rapid Pco₂ lowering can cause a posthypercapnic “overshoot” alkalosis when the underlying compensatory hyperbicarbonatemia becomes unmasked; the abrupt rise in CNS pH that results can lead to seizures and death. Any K⁺ and Cl⁻ deficits are corrected.

NaHCO₃ is almost always contraindicated, because HCO₃ ⁻ can be converted to Pco₂ in serum but crosses the blood-brain barrier slowly, thus increasing serum pH without affecting CNS pH. One exception may be in cases of severe bronchospasm, in which HCO₃ ⁻ may improve responsiveness of bronchial smooth muscle to β-agonists.

Last full review/revision July 2008 by James L. Lewis, III, MD

Content last modified July 2008