Respiratory acidosis and respiratory alkalosis are the two primary respiratory acid-base disorders commonly encountered in clinical practice, both resulting from primary changes in pCO2 due to various disorders.

Respiratory acidosis, also known as primary hypercapnia, is a clinical disorder characterized by a primary elevation in the PaCO2 (>45 mmHg) leading to a reduction in pH (<7.35) and variable compensatory increase in the plasma HCO3 concentration.

Respiratory acidosis occurs when the effective alveolar ventilation (CO2 excretion by the lung) fails to keep pace with the rate of CO2 production. Acute respiratory acidosis occurs rapidly within <48 hours, while chronic respiratory acidosis develops slowly over days to weeks (>48 hours).

Respiratory acidosis leads to renal compensation through increased urinary H+ secretion, resulting in acidic urine. This gradual process leads to a rise in plasma HCO3 levels, mitigating acidosis. Because renal compensation is a slow process, the compensatory increase in HCO3 is small in acute respiratory acidosis. In contrast, in chronic respiratory acidosis, the compensatory rise in HCO3 is more substantial over time due to robust and prolonged renal compensation.

Acute respiratory acidosis: Every 10 mm of Hg rise in PaCO2 causes 1 mEq/L rise in HCO3 and 0.1 fall in pH.

Chronic respiratory acidosis: Every 10 mm Hg rise in PaCO2 causes a 4 mEq/L rise in HCO3 and a 0.03 fall in pH.

Serum HCO3 usually does not exceed 38 mEq/L due to compensation. If HCO3 is >38 mEq/L, think of concomitant metabolic alkalosis.

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