Respiratory acidosis is a condition that raises the serum partial pressure of carbon dioxide (pCO2 > 45) and lowers the serum pH (< 7.35). Presentation varies based on the acuity of onset as well as on the underlying cause.
Typical symptoms associated with a rapid increase in pCO2 include anxiety, dyspnea, confusion, hallucination, and psychosis; this can progress to coma.
A more gradual increase, as is seen with chronic respiratory acidosis, may cause memory impairment, sleep disturbances, personality changes, daytime somnolence, coordination impairment, tremors, myoclonic jerks, or asterixis.
Increased carbon dioxide production (eg, fever, thyrotoxicosis, sepsis, steroids, overfeeding, exercise) – Unless a patient has limited pulmonary reserve, this will rarely result in clinically important hypercapnia.
Respiratory acidosis can occur as an acute or a chronic process. Depending on the acuity of the condition, the body will compensate in different ways.
Acute respiratory acidosis – Acute hypercapnia typically follows sudden obstruction of the airway or generalized bronchospasm. The acute compensatory response for respiratory acidosis is an increase in the serum bicarbonate concentration by 1 mEq/L for every 10 mm Hg elevation in pCO2.
Chronic respiratory acidosis – Chronic hypercapnia (defined as respiratory acidosis persisting after 3-5 days) occurs in end-stage COPD, restrictive lung disease with ventilatory muscle fatigue, or advanced states of intrapulmonary and extrapulmonary restrictive lung disease. With chronic acidosis, the kidneys increase acid excretion, allowing for generation of additional HCO3, and the renal tubule increases HCO3 reabsorption, a process that takes 3-5 days to complete. The chronic response leads to a 4 mEq/L increase in the serum bicarbonate concentration per 10 mm Hg elevation in pCO2.
Codes
ICD10CM: E87.29 – Other acidosis
SNOMEDCT: 12326000 – Respiratory acidosis
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