Respiratory Acidosis

CO2 + H2O H2CO3 H+ + HCO3

In respiratory acidosis there is raised pCO2 as the respiratory system is unable to remove enough CO2 from the body. The reaction is driven to the right, causing a rise in [H+], (i.e. a fall in pH). This inability to remove CO2 is often coupled with a failure to keep up with O2 demand. This is respiratory failure. There are two types of respiratory failure essentially distinguished by the levels of CO2 within the blood and the main driver for ventilation.

Normally, as pCO2 increases, only a small increase (0.1 kPa) will produce a 1-2 litre/minute rise in alveolar ventilation. This effect can be blunted by medication (e.g. opiates and barbiturates), where the CO2 must rise further before ventilation increases. It is also depressed during sleep allowing slightly higher levels of CO2 than normal. In contrast, pO2 levels must fall significantly below normal (i.e. <8 kPa) to stimulate increased ventilation. This hypoxic ventilatory drive is also reduced in sleep and with drugs.

Type 1 respiratory failure is hypoxia with a low or normal PaCO2 due to failure of gas exchange or increased oxygen consumption.

Type 2 respiratory failure is ventilatory failure resulting in hypoxia with a raised PaCO2.

Traditional thinking about the hypoxic respiratory drive has been largely debunked. Worsening hypercapnoea when oxygen is administered in type 2 failure is due to V/Q mismatch and the Haldane effect. Explained here in depth.

A typical arterial blood gas result in acute type 2 failure:

  • pH 7.22
  • pCO2 8.3 kPa
  • pO2 7.2 kPa
  • bicarbonate 25 mmol/L

The pH is low indicating an acidosis. There is hypoxia, indicating a problem with oxygenation and the CO2 is high indicating a problem with ventilation. The bicarbonate is normal indicating that this is an acute problem. Therefore this is an acute respiratory acidosis.

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