In one breath
Alveolar ventilation (VA) is the volume of fresh air that actually reaches the alveoli each minute: (tidal volume − dead space) × rate, or (500 − 150) × 12 = 4200 mL/min at rest. The dead space takes the same bite out of every breath, so deep, slow breathing ventilates the alveoli far better than rapid, shallow breathing at the same minute ventilation. VA sets the arterial PCO₂: halve it and PCO₂ doubles, so a high PaCO₂ means hypoventilation and a low one means hyperventilation.
Builds on: Dead space · Leads to: Gas exchange in the lungs · Chemical control of breathing · Asphyxia, hypercapnia and hypocapnia · Hypoxia
What it is and how to work it out
- Alveolar ventilation (VA): the volume of air that reaches the alveoli per minute. Only this air takes part in gas exchange.
- VA = (tidal volume − dead space) × respiratory rate
| Step | Value |
|---|---|
| Tidal volume | 500 mL |
| minus dead space | 150 mL |
| Air reaching alveoli per breath | 350 mL |
| × respiratory rate | 12/min |
| Alveolar ventilation | 4200 mL/min |
- Worth knowing, though not in your pages: minute (pulmonary) ventilation is tidal volume × rate, 500 × 12 = 6000 mL/min. It counts the dead-space air too, which VA leaves out. Ch114 lists the same 6000 mL as the normal minute volume (Lung volumes, capacities and spirometry).
Significance
Clinical importance
- VA, not minute ventilation, is the air that does the gas exchange.
- Anything that enlarges the anatomical dead space lowers VA, even when the lungs themselves are healthy.
- Mechanical ventilation: the tubing adds dead space, so VA falls. If the minute ventilation is left unchanged, alveolar gas exchange suffers. See Artificial respiration.
Physiological significance
- Rapid, shallow breathing: minute ventilation barely changes, but most of each small breath only fills the anatomical dead space. VA is badly cut, and the result is hypoxia and hypercapnia.
- Deep, slow breathing: again the minute ventilation is about the same, but VA is adequate, and it can even exceed that of normal breathing.
- So, to raise VA, increasing the depth of breathing pays more than increasing the rate.
- A trained athlete in moderate to severe exercise reaches the needed VA mainly by breathing more deeply rather than faster.
Worth knowing, though not in your pages: the arithmetic, with made-up breathing patterns that all give a minute ventilation of 6000 mL/min and a dead space of 150 mL:
| Pattern | Tidal volume × rate | VA (mL/min) |
|---|---|---|
| Normal | 500 × 12 | 350 × 12 = 4200 |
| Rapid, shallow | 200 × 30 | 50 × 30 = 1500 |
| Deep, slow | 1000 × 6 | 850 × 6 = 5100 |
Applied: pranayama raises alveolar ventilation
Yogic breathing exercises such as pranayama train slow, deep breaths, which raise VA. Your book adds that they also aim to take in prana, universal energy, by breathing consciously.
Fast breathing is not hyperventilation
Hyper- and hypoventilation are judged by the VA and the PaCO₂, not by the rate. A patient breathing fast and shallow can be hypoventilating, with a high PaCO₂.
Measuring alveolar ventilation
- The formula above needs the dead space, and that is hard to measure in a person. So the pulmonary function laboratory works VA out from CO₂ instead.
- The logic: the conducting airways exchange no gas, and inspired air has practically no CO₂. So every molecule of expired CO₂ came from the alveoli.
- CO₂ breathed out per minute = VA × the fraction of CO₂ in alveolar gas:
- V̇ECO₂ = VA × FACO₂
- rearranged, VA = V̇ECO₂ ÷ FACO₂ (the alveolar ventilation equation).
- FACO₂ is sampled from the end-tidal air, the last part of an expiration, which is alveolar gas.
| Symbol | Meaning |
|---|---|
| V̇ECO₂ | CO₂ expired per minute |
| FACO₂ | fraction of CO₂ in alveolar gas |
| VA | alveolar ventilation |
VA sets the PaCO₂
- VA and PaCO₂ are inversely related: halve VA and the alveolar PCO₂ doubles.
- So the arterial PCO₂ is the clinical yardstick of whether VA is adequate. Its normal value is 40 mmHg (Table 105.1, on Gas exchange in the lungs).
| PaCO₂ | Means |
|---|---|
| ↑ | hypoventilation |
| ↓ | hyperventilation |
Hypoventilation and hyperventilation
Hypoventilation
- Its causes fall into two groups:
- central: the respiratory centres are depressed by disease or drugs;
- peripheral: the ventilatory apparatus (lungs, chest wall, muscles) fails.
- Common causes:
| Group | Examples |
|---|---|
| Chronic lung disease flaring up | asthma, chronic bronchitis, emphysema |
| Depressed respiratory centres | head injury; barbiturates, opiates |
| Weak respiratory muscles | myasthenia gravis, poliomyelitis, acute polyneuritis, tetanus |
- The result is hypoxia (less O₂ brought in) together with hypercapnia (less CO₂ removed).
- The CO₂ retained causes respiratory acidosis, covered in ch112 (Asphyxia, hypercapnia and hypocapnia).
Hyperventilation
- Usually caused by stimulation of the respiratory centres.
- Common physiological causes: voluntary hyperventilation and exercise.
- Too much CO₂ is washed out, which causes respiratory alkalosis.
- Worth knowing, though not in your pages: in moderate exercise, ventilation rises in step with CO₂ output, so PaCO₂ stays normal; strictly, that is hyperpnea. PaCO₂ falls, a true hyperventilation, mainly in heavy exercise.
Exam-answer skeleton: "Alveolar ventilation: definition, calculation and significance" (short note)
- Definition, and how it differs from minute ventilation (the dead space).
- The formula and the worked example: (500 − 150) × 12 = 4200 mL/min.
- Clinical importance: a bigger dead space, ventilator tubing.
- Physiological significance: rapid shallow vs deep slow breathing; depth beats rate; athletes; pranayama.
- Measurement from expired CO₂: VA = V̇ECO₂ ÷ FACO₂, with end-tidal sampling.
- The inverse link with PaCO₂: halving VA doubles PCO₂.
- Hypoventilation and hyperventilation: causes and results.
Asked in exams
- Alveolar ventilation, and working it out: May 2022, 2 marks · Mar 2024, MCQ