Every breath only matters if blood is there to meet it. Build up how air and blood share each tiny air sac in the lung, then watch what extra oxygen, airway drugs, a clot and an infection do to the match.
Educational, not for clinical use
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Air and blood meet in the lungs
Each breath carries air down branching tubes, the airways, to millions of tiny air sacs called alveoli (one is an alveolus). Blood pumped from the heart flows past them. This is where your body picks up oxygen.
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Each air sac is wrapped in tiny blood vessels
Each alveolus is wrapped in a mesh of capillaries: blood vessels so narrow that red blood cells pass in single file. Only an extremely thin wall separates the air from the blood, so gases cross it easily.
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Oxygen goes in, carbon dioxide comes out
Gas exchange happens across that wall. Oxygen moves from the air into the blood. Carbon dioxide, the waste gas cells make, moves from the blood into the air to be breathed out. Each gas moves from more to less.
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Ventilation: fresh air in, used air out
Ventilation is the flow of air in and out of the alveoli. Each breath brings in oxygen-rich air and carries carbon dioxide away. The more air a sac gets, the closer its gas stays to fresh air.
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Perfusion: blood flowing past
Perfusion is the flow of blood past the alveoli. Blood arrives from the body low in oxygen and high in carbon dioxide, and leaves topped up with oxygen. The more blood flows past a sac, the more oxygen it takes from that sac.
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Air and blood need to match
Each alveolus works best when its air and its blood are in balance. The ventilation–perfusion ratio compares the two: air delivered against blood flowing past. When they balance, the match is good and blood leaves full of oxygen.
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Too little air: blood leaves short of oxygen
If a sac gets too little air for its blood, its oxygen runs low and blood leaves only partly loaded. With no air at all, blood passes through unchanged: a shunt, blood that crosses the lungs without meeting air.
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Too little blood: air is wasted
If a sac gets plenty of air but little blood, most of that air is not used. With no blood at all, air goes in and out for nothing: dead space, air that reaches the lungs but never meets blood.
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Blood from every sac mixes
Blood from every alveolus mixes into arterial blood, which the heart pumps to the body. Well-aired sacs cannot make up for a poorly aired one: their blood is already nearly full of oxygen (Lesson 9). So a little oxygen-poor blood drags the whole mix down.
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The lung steers blood toward air
When an alveolus runs low on oxygen, the small blood vessels around it tighten. This hypoxic vasoconstriction, meaning vessels narrowing where oxygen is low, steers blood toward better-aired sacs, so the mismatch shrinks.
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The whole picture
Ventilation brings air, perfusion brings blood, and each alveolus needs the two in balance. Two key measures: the ventilation–perfusion ratio, which says how well air and blood match, and the oxygen in arterial blood, the result of every sac mixed together.
What changes it
Supplemental oxygen: richer air
Supplemental oxygen means breathing air with extra oxygen added, through a mask or soft nasal tubes. Every ventilated sac fills with more oxygen, so arterial blood carries more. It cannot reach blood in a shunt, because that blood never meets the air.
What changes it
Beta-2 agonists: switching on the relax signal
In asthma, the muscle around the airways tightens, so some sacs get too little air. Bronchodilators widen airways. Beta-2 agonists, one kind, switch on the muscle’s relaxing signal (Lesson 6), so the airway opens and air reaches the sacs again.
What changes it
Muscarinic antagonists: blocking the tighten signal
Nerves tighten airway muscle by releasing a messenger that lands on muscarinic receptors, the muscle’s receiving sites for it. Muscarinic antagonists, the other kind of bronchodilator, block those receptors, so the tightening signal cannot land. The muscle eases and air returns to the sacs.
What changes it
Pulmonary embolism: blood flow blocked
A pulmonary embolism is a blood clot, often from a leg vein, stuck in a lung artery. Sacs beyond it keep their air but lose their blood: dead space. Their blood is pushed to other sacs, which now get too little air, so oxygen falls.
What changes it
Pneumonia: air sacs fill with fluid
Pneumonia is a lung infection. Infected alveoli fill with fluid and pus, so no air reaches them, yet blood still flows past: a shunt. That blood leaves without fresh oxygen, and extra oxygen in the air cannot reach it.
Step 1 of 16
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Reference values, beside the model.
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Normal teaching baseline.
The blue line on each bar is an illustrative two-air-sac teaching model, not a patient measurement. Where a source gives a range, the bar shades it; where it gives a single value, the bar shows that value as a black tick and the model is called close when it is within a tenth of it. Arrows come from the cited source for the selected state. Every number in the rows comes from the open textbook and StatPearls passages quoted under each row.
Sources
Mismatch the lung yourself.
An illustrative teaching model with two air sacs sharing one blood supply. The left sac stays healthy; change the air breathed in, the right sac’s airway, its blood flow and how much of it is filled with fluid. The faint dashed shapes and ticks are the normal state.
Where each sac sits on the ventilation–perfusion line
How this teaching model works
Two air sacs share the blood that leaves the heart, after a small bypass that skips them both. Each sac normally gets half the air and half the remaining blood. Its ventilation–perfusion ratio is scaled so that a normal sac has the whole-lung ratio from the Clinical values data file. For each sac, alveolar carbon dioxide follows a simple balance, PACO2 = PvCO2 ÷ (1 + k × ratio), and alveolar oxygen is solved by bisection from the oxygen balance k′ × ratio × (PIO2 − PAO2) = content(PAO2) − content(venous). The two constants k and k′ are set so that a normal sac reproduces OpenStax’s alveolar gas exactly, so a sac with no air holds the gas of blood arriving from the body and a sac with no blood holds the air breathed in.
Oxygen content here is hemoglobin saturation only, on a Hill-shaped curve. Its steepness is an illustrative choice of the model; its position is set so that blood at OpenStax’s pulmonary-vein oxygen pressure sits at the middle of OpenStax’s saturation range. Oxygen dissolved directly in the blood is left out, so with supplemental oxygen the model understates how far the oxygen pressure of blood leaving the lungs rises. The bypass is sized at load time so that the healthy model’s mixed blood lands exactly on OpenStax’s pulmonary-vein value; it stands in for the small mismatches of a real lung and is not a reference value. Blood leaving each sac is fully equilibrated with that sac’s gas, and carbon dioxide content is treated as proportional to its pressure.
A clot sends blood away from the right sac to the left one, so total blood flow stays the same. Fluid fills part of the right sac, taking away its air and turning the blood past it into shunt. With hypoxic vasoconstriction switched on, blood flow to the right sac shrinks toward three tenths of its set value as that sac’s oxygen falls toward the level of arriving blood (an illustrative rule, found by repeated adjustment until it settles).
Left out: breathing harder to compensate, the heart and the tissues (blood always arrives with the same gases), diffusion limits, gravity and the many sacs of a real lung. The sizes of the drug and disease changes are illustrative; only their directions are meant to teach.