Occurs when pulmonary gas exchange is sufficiently impaired to cause hypoxaemia with or without hypercarbia.
It is defined as a PaO2 < 8 kPa (60 mmHg) and subdivided into two types according to the PaCO2 level.
It can be divided into two main categories:
Type I or "acute hypoxaemic" respiratory failure, in which the PaO2 is < 8 kPa and the PaCO2 is normal or low.
Occurs with diseases that damage lung tissue, with hypoxaemia due to right-left shunts or V/Q mismatch.
- Pneumonia (i.e. as in this case)
- Pulmonary oedema
- Adult respiratory distress syndrome
- Pulmonary fibrosing alveolitis
Type II or "ventilatory failure", with hypoxia (PaO2 < 8 kPa) and a PaCO2 of > 6 kPa.
Occurs when alveolar ventilation is insufficient to excrete the volume of CO2 being produced by tissue metabolism.
Inadequate alveolar ventilation due to reduced respiratory effort, inability to overcome an increased resistance to ventilation, failure to compensate for an increase in dead space and/or CO2 production.
- Chronic bronchitis and emphysema
- Chest wall deformities
- Respiratory muscle weakness (e.g. Guillain-Barre syndrome)
- Depression of respiratory centre (e.g. opioids)
A diagnosis of respiratory distress should be made on the following:
The most sensitive indicator of increasing respiratory difficulty is a rising respiratory rate. Tidal volume is a less sensitive indicator.
Minute ventilation rises initially in acute respiratory failure and then falls precipitously only at a late stage, when the patient is exhausted. Vital capacity is often a better guide to deterioration and is particularly useful in patients with respiratory inadequacy due to neuromuscular problems such as Guillain-Barre syndrome, where the vital capacity decreases as weakness increases.
Blood gas measurement should be performed.
H+: 35-45 nmol/L (pH 7.35-7.45)
PO2: 10-13.3 kPa (75-100 mmHg)
PCO2: 4.8-6.0 kPa (36-46 mmHg)
Plasma HCO3-: 22-26 mmol/L
O2 saturation: 95-100%