Critical care: respiratory pathophysiology and support

Summary

The function of the respiratory system is to transport oxygen to the blood and remove carbon dioxide from it. Success requires an adequate volume of gas to ventilate the alveoli and close matching of the degree of ventilation and perfusion of each lung unit. Failure results in hypoxaemia, hypercarbia or both.

Hypercarbia is caused by a reduction in alveolar minute ventilation, due to:

1. ▪ Decreased minute ventilation (respiratory rate or tidal volume) such as in drug overdose and neuromuscular disorders

2. ▪ Increased dead space ventilation (e.g. rapid shallow breathing, COPD)

3. ▪ Increased physiological dead space ventilation

4. ▪ Increased CO₂ production (e.g. sepsis, fever, seizure).

All of these can be corrected or compensated by an increase in the respiratory rate.

Hypoxaemia may be caused by:

Hypoventilation: if the rate at which fresh inspiratory gas is presented to the alveoli falls but oxygen consumption remains the same, the partial pressure of oxygen within the alveoli falls. The oxygen tension within the pulmonary capillary and systemic arteries (PaO₂) is reduced. Postoperative surgical patients are vulnerable to hypoxaemia due to pain from upper abdominal incisions and opioid analgesia causing respiratory suppression. Hypoxaemia from hypoventilation can be corrected by:

1. ▪ Increasing the respiratory rate, either pharmacologically or mechanically

2. ▪ Increasing the inspired FiO₂ (oxygen fraction).

Shunting:true anatomical shunting cannot be corrected by an increased FiO2, because by definition no gas exchange occurs. Physiological shunting caused by imperfect V/Q matching can be partially corrected by increasing the FiO₂. Postoperative surgical patients are vulnerable to shunting due to basal atelectasis, ARDS, pulmonary oedema, and chest infection.