Ventilation and perfusion matching

What it normally does

• Standing up, both ventilation and perfusion increase from apex to base, but perfusion varies far more steeply than ventilation. Ventilation favours the base because the weight of the lung makes pleural pressure less negative there, so basal alveoli start smaller and expand more with each breath; perfusion favours the base because of the hydrostatic pressure gradient in the pulmonary arteries. The result is that the apex is relatively over-ventilated (V/Q around 3) and the base relatively over-perfused (V/Q around 0.6), averaging about 0.8 across the whole lung — roughly 4 L/min of alveolar ventilation against 5 L/min of cardiac output.

  the bases do most of the gas exchange, so basal collapse after surgery costs far more oxygen than the same collapse at the apex — and it explains why sitting a breathless patient up, or lying them with the good lung down, actually changes their saturations.

• When an alveolus goes low on oxygen, the pulmonary arteriole beside it constricts (hypoxic pulmonary vasoconstriction). Systemic arterioles do the opposite and dilate when the tissue they supply is hypoxic.

  blood is automatically diverted away from a poorly ventilated region towards lung that still works — which is why a lobe of pneumonia often drops saturations less than you would expect, and why hypoxia across the WHOLE lung raises pulmonary artery pressure and eventually fails the right ventricle.

• The oxygen-haemoglobin curve is flat at the top: blood leaving a well-ventilated alveolus is already close to fully saturated and cannot pick up meaningfully more bound oxygen. The carbon dioxide curve, by contrast, is steep and nearly straight over the whole working range.

  good lung can blow off extra carbon dioxide for bad lung, but it cannot carry much extra oxygen for it — only the small amount that dissolves in plasma as alveolar PO2 rises. That asymmetry is the main reason V/Q problems make people hypoxic long before they make them hypercapnic, and the reason oxygen cannot rescue a large shunt.

• About 150 mL of every 500 mL breath never reaches an alveolus — it sits in the conducting airways (anatomical dead space). Any alveolus that is ventilated but not perfused adds to that total; the two together are physiological dead space.

  fast shallow breathing moves mostly dead space and achieves little, and a blocked pulmonary artery converts working lung into dead space — so exhaled gas is diluted by carbon dioxide-free gas and the end-tidal carbon dioxide falls below the arterial value, which is the fingerprint of a pulmonary embolism.

What goes wrong

• True shunt — pneumonia, pulmonary oedema, lobar collapse← from “The oxygen-haemoglobin curve is flat at the to…”

  Pus, fluid or collapse fills the alveolus, so no air enters, but the capillary next to it keeps carrying blood. That blood leaves the lung with the oxygen content it arrived with and mixes into the pulmonary veins — venous admixture. Oxygen helps little, because the alveoli that are open are already producing nearly fully saturated blood and the flat top of the haemoglobin curve means they can add only the small dissolved fraction to compensate. The larger the shunt fraction, the less oxygen achieves; re-opening the alveolus is what actually fixes it.

  Perfusion without ventilation. V/Q = 0. Hypoxia that corrects poorly with oxygen. Pneumonia, pulmonary oedema, lobar collapse.

  You would find: Saturations of 85 to 90% that rise much less than you expect when you go from nasal prongs to a non-rebreather mask, in a patient with bronchial breathing and dullness over one lobe, or with crackles to the mid-zones and pink frothy sputum. The arterial blood gas shows a wide alveolar-arterial oxygen gradient.

• Dead space — pulmonary embolism← from “About 150 mL of every 500 mL breath never reac…”

  A clot lodges in a pulmonary artery. The alveoli it supplied are still ventilated but no longer perfused, so that breath does no gas exchange — it has been converted into dead space, which is why end-tidal carbon dioxide falls below the arterial value. Dead space by itself does not lower the arterial oxygen; the hypoxaemia comes from what happens to the blood that was displaced. It is forced through the remaining vascular bed, over-perfusing regions relative to their ventilation and creating low V/Q units, while released mediators cause bronchoconstriction, surfactant loss and small areas of atelectasis that behave as true shunt. Shortened capillary transit time in the over-perfused regions and, if cardiac output falls, a low mixed venous oxygen make it worse; occasionally a rise in right atrial pressure opens a patent foramen ovale and shunts blood right to left. The patient breathes faster, which is why the carbon dioxide is low rather than high.

  Ventilation without perfusion. V/Q approaches infinity. Hypoxia plus hypocapnia, clear chest, clear film. That combination is a PE until proven otherwise.

  You would find: Sudden breathlessness and pleuritic pain with a clear chest on auscultation and often a normal chest x-ray. The gas shows low oxygen with a LOW carbon dioxide and a wide A-a gradient — the patient is over-breathing to compensate. On a ventilator, end-tidal carbon dioxide sits well below the arterial value.

• Low V/Q mismatch — asthma and COPD← from “The oxygen-haemoglobin curve is flat at the to…”

  Mucus, bronchospasm and airway collapse reduce but do not abolish ventilation to a region that is still fully perfused. Those units produce blood that is under-saturated, but they are still open, so raising the inspired oxygen concentration does reach them and does raise their alveolar oxygen — which is exactly what a true shunt unit cannot offer. This is the mismatch that responds to oxygen, and the reason a small increase in flow can transform a hypoxic asthmatic.

  Partly blocked airways, so V/Q is low but not zero. Oxygen works here — because some air still gets in.

  You would find: Hypoxia that corrects easily with a modest increase in inspired oxygen, in a wheezy patient. Saturations of 89% on room air become 95% on 2 L/min through nasal prongs.

• Basal atelectasis and positional hypoxia← from “Standing up, both ventilation and perfusion in…”

  Gravity already sends the most blood to the lung bases. Pain, sedation and lying flat make breaths shallow and reduce functional residual capacity, and the basal alveoli — which are the ones receiving most of the blood — collapse first. The heavily perfused bases are now unventilated, which is shunt in the worst possible place, so oxygenation falls much further than the size of the collapse would suggest.

  Gravity sends most blood to the bases, so shallow breathing and basal collapse cost more oxygen than the same collapse at the apex. Sit them up. Good lung down.

  You would find: Day two after an abdominal operation, the patient desaturates when lying flat and improves sitting up. In one-sided lung disease, an adult breathing spontaneously usually oxygenates better lying with the GOOD lung down — gravity sends more blood to the lung that can actually ventilate it. (Infants behave the opposite way, for reasons of chest wall compliance.)

• Cor pulmonale from chronic hypoxic vasoconstriction← from “When an alveolus goes low on oxygen, the pulmo…”

  Hypoxic pulmonary vasoconstriction is a local tool for diverting blood away from one bad region. When the whole lung is hypoxic, as in advanced COPD, the entire pulmonary vascular bed constricts. Pulmonary artery pressure rises, the vessels remodel, and the thin-walled right ventricle — built for a low-pressure circuit — hypertrophies, then dilates and fails, backing pressure up into the systemic veins.

  Local hypoxic vasoconstriction is useful; global hypoxic vasoconstriction raises pulmonary artery pressure and eventually fails the right ventricle. Cor pulmonale.

  You would find: A COPD or bronchiectasis patient with a loud pulmonary component of the second heart sound, a raised jugular venous pressure and pitting ankle oedema. Both COPD and bronchiectasis are markedly more common in Aboriginal and Torres Strait Islander communities and present at younger ages, so this is not a picture reserved for the elderly.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.