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Abstract
- Respiratory failure can be classified into type 1 (low pO2 with a normal or low pCO2) or type 2 (low pO2 with a high pCO2).
- Type 1 respiratory failure can be caused by pulmonary embolism and diffusion impairment such as emphysema.
- Type 2 respiratory failure can be caused by respiratory pump failure, in conditions such as chronic COPD, chest wall deformities, or hypoventilation caused by head trauma or drug overdose.
Core
Respiratory failure is a broad term used to describe a condition of impaired gas exchange, leading to hypoxaemia (decreased oxygen levels) with or without hypercapnia (increased carbon dioxide levels). Clinically this can be classified as an arterial pO2 of below 8 kPa when breathing air at sea level.
Respiratory failure can be further divided into two categories:
- Type 1 Respiratory Failure - low pO2 with a normal or low pCO2
- Type 2 Respiratory Failure - low pO2 with a high pCO2
It is important to note that hypoxia is different to hypoxaemia, as hypoxia describes a reduced oxygen supply to the tissues and hypoxaemia describes a reduced arterial oxygen tension in the blood. It is possible to be hypoxic without hypoxaemia - for example after a myocardial infarction, when poor perfusion may cause hypoxia despite the blood carrying enough oxygen.
The effects of hypoxia can include:
- Impaired central nervous system function
- Central cyanosis
- Cardiac arrhythmias
- Vasoconstriction of pulmonary vessels
Examples of Type 1 Respiratory Failure
At high altitudes, the air naturally has a lower pO2. This means that people acutely exposed to high altitudes develop hypoxaemia. This hypoxaemia stimulates the peripheral chemoreceptors in the body, resulting in hyperventilation with an increase in CO2 removal. The end result is a low pO2 and a low pCO2 - Type 1 Respiratory Failure.
People who live at high altitudes have numerous physiological adaptations to encourage oxygen transport in these conditions, including polycythaemia, increased red cell 2-3 DPG, and increased capillary density in tissues.
When a pulmonary embolus obstructs a branch of pulmonary artery, it leaves a section of alveoli without blood supply. The ventilation of the under-perfused alveoli is therefore wasted as no gas exchange occurs there. Initially, this means that there is a decrease in pO2 of the blood. The diversion of blood means that there is increased perfusion to functioning parts of the lung, so increased ventilation is required to maintain the V/Q ratio (see Properties of Gas Exchange article for an explanation of V/Q ratio). This is achieved through hyperventilation, which decreases CO2 levels, but cannot compensate fully for the lack of oxygen, therefore causing Type 1 Respiratory Failure.
The barrier to diffusion between alveolar air and pulmonary capillary blood is normally extremely thin to allow efficient gas exchange. If this barrier is thickened, such as in lung fibrosis or pulmonary oedema, or the total area available for diffusion is reduced, as happens in emphysema, diffusion will be impaired. Oxygen diffuses much less readily than carbon dioxide, so is always affected more by any change to the diffusion barrier. This means that diffusion impairment causes Type 1 Respiratory Failure.
Examples of Type 2 Respiratory Failure
Type 2 respiratory failure is a condition with low pO2 and high pCO2, and the main cause is hypoventilation. The reduced movement of air both in and out of the lungs causes reduced oxygen intake and decreased carbon dioxide removal.
If the hypoventilation has an acute cause, such as head injury or overdose, then this needs urgent treatment which may include mechanical ventilation. If the hypoventilation has a chronic cause, such as COPD or chest wall deformity, then the respiratory failure will be better tolerated, and the patient will have adapted. This occurs through renal compensation which increases HCO3- levels. If the hypercapnia is still persistent, then the choroid plexus will import HCO3- into the cerebrospinal fluid (CSF), to restore the CSF pH to normal and ‘reset’ the central chemoreceptors. This means the body will continue to function at this increased CO2 level.
Because of this, the use of uncontrolled O2 therapy to correct acute hypoxia may worsen existing hypercapnia. These patients should be treated with controlled oxygen therapy with a target SaO2 of 88-92%. CO2 should be closely monitored to avoid the risk of dangerous hypercapnia. The worsening of hypercapnia is multifactorial. Although reduced hypoxic respiratory drive may contribute in some patients, important mechanisms include worsening ventilation-perfusion mismatch and the Haldane effect, which together can lead to a rise in pCO2 when high concentrations of oxygen are given. However, it is important to note that in an emergency setting, oxygen should not be withheld from patients with COPD, as hypoxia will do the patient more harm in the acute setting.
Edited by: Dr. Maddie Swannack
Reviewed by: Dr. Thomas Burnell
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