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Contents
Abstract
- Respiratory failure can be classified into two types. Type 1 has a low partial pressure of oxygen (pO2) with a normal or low partial pressure of carbon dioxide (pCO2). Type 2 has a high pCO2, usually with a low pO2.
- Type 1 respiratory failure can be caused by pulmonary embolism and by diffusion impairment (a gas exchange surface that is too thick or too small), such as in lung fibrosis or emphysema.
- Type 2 respiratory failure can be caused by respiratory pump failure (the chest wall, breathing muscles or nerves failing to move air in and out, or being unable to cope with the extra work of diseased lungs), in conditions such as chronic obstructive pulmonary disease (COPD) and chest wall deformities. It can also follow hypoventilation (breathing too little), for example after 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, respiratory failure can be identified by an arterial pO2 of below 8 kPa (kilopascals, the usual unit for blood gas pressures) 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 - high pCO2 (above the normal range of 4.6-6.1 kPa), usually with a low pO2
It is important to note that hypoxia is different to hypoxaemia. Hypoxia describes a reduced oxygen supply to the tissues. Hypoxaemia describes a reduced arterial oxygen tension (low pO2) 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 (a blue or grey colour of the tongue and lips)
- Cardiac arrhythmias (abnormal heart rhythms)
- 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 (sensors in the carotid and aortic bodies that detect low blood oxygen), resulting in hyperventilation (fast, deep breathing) with an increase in CO2 removal. The end result is a low pO2 and a low pCO2: the blood gas pattern of Type 1 Respiratory Failure.
People who live at high altitudes have numerous physiological adaptations to encourage oxygen transport in these conditions. These include polycythaemia (a raised red blood cell count), increased red cell 2,3-diphosphoglycerate (2,3-DPG, which helps haemoglobin release oxygen to the tissues) and increased capillary density in tissues.
A pulmonary embolus obstructs pulmonary arterial blood flow, creating ventilated alveoli with little or no perfusion: dead-space ventilation. Completely unperfused alveoli have no blood leaving them, so they do not themselves add poorly oxygenated blood to the arterial circulation. Blood is redirected to other lung regions. Where ventilation does not match the increased perfusion, low ventilation/perfusion (V/Q) ratios (too little airflow for the blood flow) can cause hypoxaemia. See the Properties of Gas Exchange article for an explanation of V/Q ratio. Alveolar collapse with shunt (blood passing through the lungs without picking up oxygen) may also contribute. Reduced mixed venous oxygen (low oxygen in the blood returning to the lungs) from low cardiac output may contribute too. Hyperventilation (fast, deep breathing) commonly lowers pCO2, but how far the pO2 falls varies from patient to patient. Oxygen levels can stay normal in pulmonary embolism. Only sufficiently severe hypoxaemia with normal or low pCO2 constitutes type 1 respiratory failure.
The barrier to diffusion between alveolar air and pulmonary capillary blood is normally extremely thin to allow efficient gas exchange. Diffusion will be impaired if this barrier is thickened, as in lung fibrosis or pulmonary oedema. It will also be impaired if the total area available for diffusion is reduced, as happens in emphysema. Emphysema is a form of COPD, which is also a common cause of type 2 respiratory failure (see Hypoventilation below). Oxygen diffuses much less readily than carbon dioxide, so isolated diffusion limitation generally affects oxygen transfer more. Mild impairment need not cause respiratory failure; sufficiently severe impairment can produce hypoxaemia with normal or low pCO2, consistent with Type 1 Respiratory Failure. Coexisting hypoventilation may instead cause carbon dioxide retention.
Examples of Type 2 Respiratory Failure
Type 2 respiratory failure is a condition with high pCO2, usually with a low pO2, 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 the hypoventilation needs urgent treatment. This may include mechanical ventilation (breaths delivered by a machine). Consciousness is often reduced after a head injury or overdose, so the airway may need to be secured with a breathing tube (invasive ventilation). If opioid poisoning (overdose of drugs such as morphine or heroin) is the cause, an antidote (naloxone) is given if available. If the hypoventilation has a chronic cause, such as COPD or chest wall deformity, then the respiratory failure will be better tolerated, because the patient will have adapted. These patients can still become acutely worse during an exacerbation (a flare-up of their disease). Some need assisted ventilation. In a COPD exacerbation, non-invasive ventilation (breaths delivered by a machine through a tight-fitting mask) is the treatment of choice if type 2 respiratory failure persists despite the best medical treatment. The adaptation occurs through renal compensation: the kidneys retain bicarbonate (HCO3-), which raises the bicarbonate level in the blood and buffers the extra acid from the raised CO2. If the hypercapnia is still persistent, then the choroid plexus (the tissue in the brain that makes cerebrospinal fluid) will import HCO3- into the cerebrospinal fluid (CSF) to restore the CSF pH to normal. This ‘resets’ the central chemoreceptors (brainstem cells that sense CO2 through the pH of the CSF). This means the body will continue to function at this increased CO2 level.
Patients with chronic hypercapnia are at risk of oxygen-induced hypercapnia: uncontrolled O2 therapy to correct acute hypoxia may worsen existing hypercapnia. Patients with COPD, or other known risk factors for hypercapnic respiratory failure, should be treated with controlled oxygen therapy with a target oxygen saturation (SaO2) of 88-92% until blood gas results are available. If the blood gas then shows a normal pH and pCO2, the target can be raised to 94-98%, unless the patient has needed assisted ventilation for hypercapnic respiratory failure before, or their usual saturation when well is below 94%. Arterial blood gases (a blood test from an artery that measures oxygen, carbon dioxide and pH) should be measured on arrival and repeated regularly according to the response to treatment, including 30 to 60 minutes after oxygen is started or sooner if the patient gets worse. This is because pulse oximetry (a finger probe that reads oxygen saturation) gives no information about the CO2 level or pH, so it cannot show dangerous hypercapnia. The worsening of hypercapnia has several causes, not just one. Reduced hypoxic respiratory drive (the urge to breathe that low blood oxygen triggers) may contribute in some patients. However, important mechanisms include worsening ventilation-perfusion mismatch and the Haldane effect (haemoglobin carrying more oxygen carries less CO2, so more CO2 stays in the blood). Together these can lead to a rise in pCO2 when high concentrations of oxygen are given. In an emergency, give oxygen to a patient with COPD who needs it, because hypoxia does more harm than raised CO2. Adjust the amount to keep the oxygen saturation within the individual target range.
Edited by: Dr. Maddie Swannack
Reviewed by: Dr. Thomas Burnell and Dr. Marcus Judge
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