Pulmonary embolism: V/Q mismatch and hypoxaemia
In pulmonary embolism, a clot lodges in a lung artery, and ventilation-perfusion (V/Q) mismatch, where ventilation does not match blood flow, mainly explains the hypoxaemia (low blood oxygen).
Remember
A clot leaves ventilated alveoli with little or no blood, and the redirected blood causes V/Q mismatch, which can lower the oxygen level, while fast breathing commonly lowers the carbon dioxide. The typical pattern is low oxygen with a normal or low carbon dioxide.
A pulmonary embolus is a clot, usually from the leg veins, that lodges in an artery of the lung. It blocks the blood flow to part of the lung, but breathing carries on. The alveoli (the air sacs where gas exchange happens) in that part of the lung are still ventilated, yet they get little or no blood. This is dead-space ventilation: air reaches alveoli that cannot exchange gas, because there is no blood flow for gas exchange.
The blood is redirected to other regions of the lung. In regions where ventilation does not match the extra blood flow, the ventilation-perfusion (V/Q) ratio is low (too little air for the blood), and the blood leaving them is not fully oxygenated. This V/Q mismatch mainly explains the hypoxaemia (low blood oxygen) of pulmonary embolism. A completely unperfused alveolus has no blood leaving it, so it does not itself add poorly oxygenated blood to the circulation.
Hyperventilation (fast, deep breathing) is the body's response, and it commonly lowers the carbon dioxide level. The typical pattern is therefore a low oxygen level with a normal or low carbon dioxide level. If the hypoxaemia is severe enough, with a normal or low carbon dioxide, that is called type 1 respiratory failure.
Other factors, such as collapsed alveoli with shunt (blood passing through the lung without meeting ventilated alveoli) and a low cardiac output, may also contribute, but they are not the main mechanism.
Key facts
- Blocked artery
- A clot in a lung artery leaves ventilated alveoli with little or no blood flow.
- Dead space
- Air reaches alveoli that have no blood flow and so cannot exchange gas.
- Redirected blood
- Blood goes to other lung regions, where low V/Q ratios (too little air for the blood) can cause hypoxaemia.
- Carbon dioxide
- Hyperventilation commonly lowers it, so the level is normal or low.
- Respiratory failure
- Severe enough hypoxaemia with a normal or low carbon dioxide is type 1 respiratory failure.
- Oxygen level
- It varies, and a normal level is possible.
Exam traps
- A fall in the drive to breathe does not explain the low oxygen of pulmonary embolism, because the drive is usually increased, with fast breathing, and the carbon dioxide is normal or low rather than high.
- Airway obstruction is not the problem in pulmonary embolism, because the airways are open and the problem lies in the blood supply to the alveoli. Reduced ventilation from airway obstruction is the mechanism in asthma.
- A thickened barrier between air and blood, as in lung fibrosis or pulmonary oedema, impairs diffusion, but it does not explain the low oxygen of pulmonary embolism, because the barrier is thin and normal and it is the blood flow that is disturbed.
Read the full notes
Tested in 6 SimpleMed+ questions
Practice it in Respiratory System, with the answer and a full explanation after every question.
Practice these questions