Acute respiratory failure can defined as a state in which the pulmonary system is no longer able to meet the metabolic demands of the body. It can be divided into hypoxaemic respiratory failure and hypercapnic respiratory failure. Hypoxaemic respiratory failure is defined as an arterial partial pressure of oxygen of less than or equal to 6.7 kPa when breathing room air and hypercapnic respiratory failure is defined as an arterial partial pressure of carbon dioxide of more than or equal to 6.7 kPa
The major function of the lung is to get oxygen into the body and carbon dioxide out
Getting oxygen into the body depends on the partial pressure of oxygen in the alveoli, the diffusing capacity of the alveolar membrane, ventilation, perfusion and the relationship between the two.
The partial pressure of each gas in a mixture of a gases is directly related to the proportions in which they are present. The sum of the partial pressures is equal to the total pressure inside the container. Thus the partial pressure of a particular gas can be increased by increasing the total pressure or by increasing the proportion of that gas in the mixture. Therefore increasing the alveolar pressure or the proportion of the alveolar gas that consists of oxygen increasing will increase alveolar PO2 Increasing the inspired concentration of oxygen increases the proportion of alveolar gas that is oxygen while reducing the proportion that consists of nitrogen. The proportion of alveolar gas that is water vapour remains constant and therefore water vapour has no effect on changes in alveolar PO2. On the other hand the proportion of alveolar gas that is CO2 does change and so alveolar PCO2 does affect alveolar PO2 Finally as oxygen diffuses out of the alveolus and carbon dioxide diffuses in the alveolar PO2 falls and PCO2 rises. Ventilation with fresh gas is necessary to restore these to their initial values
So to summarize, changes in alveolar PO2 result from changes in inspired oxygen concentration, alveolar PCO2, alveolar pressure and alveolar ventilation Alveolar PO2 is, however, not the only determinant of oxygenation. Diffusing capacity, perfusion of alveoli and ventilation-perfusion matching are also important. Perfusion of non-ventilated alveoli, also known as shunting, is the most common cause of hypoxic respiratory failure in ICU
The effectiveness of carbon dioxide elimination is largely dependent on alveolar ventilation. This in turn is dependent on the respiratory rate, the tidal volume and the volume of dead space. Physiological deadspace but not anatomical deadspace is variable and dependent on ventilation-perfusion matching. Ventilation of non-perfused alveoli increases phsyiological deadspace.
Thus carbon dioxide elimination is dependent on the respiratory rate, tidal volume and ventilation perfusion matching
This slide illustrates the various pathophysiological mechanisms which cause respiratory failure.
In the normal situation the alveolus is normally perfused and ventilated and blood is fully saturated with oxygen by the time it leaves the alveolus
Shunting is the most common cause for hypoxaemic respiratory failure in ICU patients. It is a form of ventilation-perfusion mismatch in which alveoli which are not ventilated (eg due to collapse or pus or oedema fluid) are still perfused.
As a result blood traversing these alveoli is not oxygenated before returning to the heart.
Respiratory failure due to shunting is relatively resistant to oxygen therapy. Increasing the inspired oxygen concentration has little effect because it can not reach alveoli where shunting is occurring and blood leaving normal alveoli is already 100% saturated
Subsequent hypoxic pulmonary vasoconstriction reduces the blood flow to non-ventilated alveoli and reduces the magnitude of the hypoxaemia by reducing the proportion of blood that perfuses non-ventilated alveoli
Shunting can also occur at an intra-cardiac level but this is an unusual cause of hypoxaemia in the ICU. Causes of intrapulmonary shunting include pneumonia, pulmonary oedema, atelectasis, collapse and pulmonary haemorrhage or contusion
The opposite extreme of ventilation-perfusion mismatch is deadspace ventilation
gas passes in and out of the alveoli but no gas exchange occurs because the alveoli are not perfused. and the ventilation is ineffective. In this respect these alveoli are behaving like other parts of the lung that are ventilated but do not take part in gas exchange (eg the major airways) and these alveoli therefore make up what is called physiological dead space unless the patient is able to compensate for it the reduction in effective ventilation results in an increase in PaCO2. causes include: a low cardiac output and high intra-alveolar pressure leading to compression or stretching of alveolar capillaries
These can result from a failure of diffusion across the alveolar membrane or a reduction in the number of alveoli resulting in a reduction in the alveolar surface area. Causes include ARDS and fibrotic lung disease
The alveolar gas is not adequately replenished with fresh gas as oxygen passes into the blood and carbon dioxide passes into the alveolus. This results in a fall in the alveolar PO2 and a rise in the alveolar PCO2 gradually eliminating any pressure gradients between the alveolus and blood. As a consequence gas exchange is impaired.
Hypoventilation can be caused by disease at any of the anatomical sites involved in ventilation. Brainstem injury or disease may result in impaired functioning of the respiratory centre, which may also be suppressed by depressant drugs
– Any cause of right to left shunt
• eg Fallot’s, Eisenmenger
– Pulmonary oedema
– Pulmonary haemorrhage or contusion