Respiratory acidosis occurs when acute or chronic derangements of the respiratory system lead to inefficient clearance of carbon dioxide. These derangements may involve:
- Primary disease of the lung parenchyma
- Problems with the chest wall
- Neuromuscular failure
- A disorder of central control of ventilation.
When alveolar gas exchange units are unable to sufficiently excrete carbon dioxide, this leads to an increase in the 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]
Respiratory acidosis may be acute or chronic. 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. Over time, more and more carbon dioxide is processed by carbonic anhydrase to bicarbonate (the Hamburger shift). This leads to chloride excretion by the kidney with ammonium, and the pH gradually rises.[2]
The consequences of failing to recognize acute respiratory failure include marked hypoxemia, hyperkalemia, cardiovascular instability, and cardiac arrest.
