Dead space and alveolar ventilation !

Concept
Exam priority: high

Part of every breath stays in the airway tubes and never reaches the alveoli. What matters for CO₂ is the air that does arrive.

Updated 2026-11-01

Also called: Physiological dead space, Bohr equation

See it in 3D: Trachea · Main bronchi · Lobar bronchi · Segmental bronchi

What it is

Anatomical dead space is the volume of the conducting airways (≈ 150 mL), where no gas exchange happens. Alveolar dead space is alveoli that are ventilated but not perfused; together they make the physiological dead space. Alveolar ventilation, not total ventilation, sets the PaCO₂.

How it works, step by step

CO₂ reaches the alveoli from the blood at a rate set by metabolism.
Only fresh air that reaches the alveoli dilutes and carries away that CO₂.
If tidal volume approaches dead space, most air just moves in the tubes and CO₂ builds up.
Doubling alveolar ventilation halves PaCO₂, and vice versa.

Lung volumes and capacities

TLC 6.0 LVC 4.8 LFRC 2.4 LRV 1.2 LFEV1/FVC 0.80

Normal adult pattern (approximate values: they vary with height, age and sex).

Tap a volume, a capacity or FEV1.

IRV · Inspiratory reserve volume
TV · Tidal volume
ERV · Expiratory reserve volume
RV · Residual volume
Capacity (sum of volumes)
Current forced expiration
Normal

Tidal volume: about 150 of its 500 mL stays in the conducting airways.

Equations

Minute ventilationV_E = V_T × RR

V_T: tidal volume
RR: respiratory rate

Alveolar ventilationV_A = (V_T − V_D) × RR

V_D: dead space

The ventilation that actually exchanges gas.

Bohr equationV_D/V_T = (PaCO₂ − P_ECO₂) / PaCO₂

P_ECO₂: PCO₂ of mixed expired gas

Measures physiological dead space.

Reference values (resting adult)

Parameter	Value	Note
Anatomical dead space	≈ 150 mL
Minute ventilation	≈ 6 L/min	500 mL × 12
Alveolar ventilation	≈ 4.2 L/min	(500 − 150) × 12
VD/VT	≈ 0.2–0.35
PaCO₂ at sea level	35–45 mmHg	usually lower in Bogotá, ≈ 30–35 mmHg

Approximate values for a healthy adult at rest; each laboratory sets its own ranges.

Clinical notes

Pulmonary embolism: ventilated alveoli with no blood flow; dead space rises and end-tidal CO₂ falls (capnography).
Sedation or opioids: slow, shallow breathing; alveolar ventilation falls and PaCO₂ rises.
On a ventilator, long tubing between the Y-piece and the patient adds dead space.

Test yourself

Think of the answer, then tap the question to see it.

Two patients both ventilate 6 L/min: one at 500 mL × 12, the other at 250 mL × 24. Which retains CO₂, and why?

The second: alveolar ventilation is (250 − 150) × 24 = 2.4 L/min against 4.2 L/min for the first, so PaCO₂ rises.

What happens to end-tidal CO₂ in a massive pulmonary embolism?

It falls: unperfused alveoli receive no CO₂ and their CO₂-free gas dilutes the exhaled air; dead space increases.

If alveolar ventilation halves while CO₂ production stays constant, what happens to PaCO₂?

It doubles (e.g. from 40 to 80 mmHg), because PaCO₂ is inversely proportional to alveolar ventilation.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Pharmacology

Opioids and antagonists

← All of physiology

Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 22.3 The Process of Breathing (OpenStax (Rice University), 2022); 22.4 Gas Exchange (OpenStax (Rice University), 2022); Acute Pulmonary Embolism (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 38). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.