Respiratory acidosis

Respiratory acidosis is characterized by a primary increase in PCO2 _with or without a compensatory increase in HCO3 ^{~; pH is usually low but may be near normal. Diagnosis is based on clinical findings and arterial blood gas and plasma electrolyte measurements. The underlying cause should be treated:}_O2 and mechanical ventilation are often required.

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Causes respiratory acidosis

The cause is a decrease in respiratory rate and/or tidal volume (hypoventilation) due to disorders of the central nervous system, respiratory system, or iatrogenic causes.

Respiratory acidosis is the accumulation of CO2 ₍ hypercapnia) due to a decrease in respiratory rate and/or tidal volume (hypoventilation). Causes of hypoventilation include conditions that impair the function of the respiratory center of the central nervous system; impaired neuromuscular transmission and other causes of muscle weakness, obstructive, restrictive, and parenchymatous lung diseases. Hypoxia usually accompanies hypoventilation.

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Symptoms respiratory acidosis

The symptoms of respiratory acidosis depend on the rate and degree of increase in PCO2 _. CO2 _rapidly crosses the blood-brain barrier; symptoms and signs result from high CNS _{CO2 concentrations (low CNS pH) and any accompanying hypoxia.}

Acute (or acutely progressive chronic) respiratory acidosis causes headache, impaired consciousness, anxiety, drowsiness, stupor (CO2 _narcosis ). Slowly developing, stable respiratory acidosis (as in COPD) can be well tolerated, but patients may experience memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes. Signs include gait disturbance, tremor, decreased deep tendon reflexes, myoclonic seizures, "flutter tremor," and optic nerve edema.

Forms

Respiratory acidosis may be acute or chronic: the chronic form is asymptomatic, but the acute or progressive form is characterized by headache, impaired consciousness, and drowsiness. Signs include tremor, myoclonic seizures, and "flutter tremor."

The difference in forms is based on the degree of metabolic compensation: initially, CO2 _is ineffectively corrected, but after 3-5 days the kidneys significantly increase the reabsorption of ^HCO3.

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Diagnostics respiratory acidosis

Arterial blood gases and plasma electrolyte levels should be measured. History and examination data usually suggest a cause. Calculation of the alveoloarterial O2 gradient _[ inspiratory PO2 (arterial PO2 _+5/4 arterial PCO2 ₎ ] may help differentiate pulmonary from extrapulmonary disease; a normal gradient virtually excludes pulmonary disease.

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Treatment respiratory acidosis

Treatment consists of providing adequate ventilation by endotracheal intubation or noninvasive positive pressure ventilation. Adequate ventilation is sufficient to correct respiratory acidosis, but chronic hypercapnia must be corrected slowly (e.g., over several hours or longer) because too rapid a reduction in PCO2 _may cause posthypercapnic alkalosis, when the initial compensatory hyperbicarbonatemia becomes apparent; the resulting sharp increase in CNS pH may lead to seizures and death. K and CI deficits are corrected as needed.

Administration of NaHCO ³ is usually contraindicated because HCO ³ ~ can be converted to plasma PCO ₂ but slowly penetrates the blood-brain barrier, increasing plasma pH and not affecting pH in the CNS. An exception is cases of severe bronchospasm, when HCO ³ increases the sensitivity of bronchial smooth muscles to beta-agonists.