Respiratory acidosis occurs when acute, acute-on-chronic, or chronic derangements of the respiratory system lead to inefficient carbon dioxide clearance and pathologic accumulation of carbon dioxide.
When alveolar gas exchange units are unable to sufficiently excrete carbon dioxide, this leads to an increase in arterial carbon dioxide levels above the normal range of 35 to 45 mmHg (4.7-6.0 kPa). With the increase in carbon dioxide, hydrogen ions accumulate, causing the arterial pH to fall below the normal range (i.e., <7.35).[1]
Acute respiratory acidosis is usually secondary to acute respiratory failure.
In acute respiratory failure, there is insufficient buffering capacity to handle the dramatic increase in arterial and venous carbon dioxide. In chronic derangements, however, carbon dioxide is processed by carbonic anhydrase to bicarbonate (the Hamburger shift). This leads to chloride excretion (with ammonium) by the kidney, and the pH gradually rises.[2]
Common pathophysiologic mechanisms in the development of respiratory acidosis include:
- Alveolar hypoventilation
- Central alveolar hypoventilation
- Neuromuscular disorders
- Increase of dead space ventilation (V/Q mismatching)
- Overproduction of carbon dioxide
The consequences of failing to recognize acute respiratory failure include marked hypoxemia, hyperkalemia, cardiovascular instability, and cardiac arrest.
