The pulmonary circulation and hypoxic vasoconstriction !
- Regulation
- Exam priority: medium
The right heart pumps all the blood through the lungs at low pressure. Where oxygen is missing, the vessels narrow to send blood to well-aired areas.
Updated 2026-11-01
Also called: Hypoxic pulmonary vasoconstriction, Pulmonary vascular resistance
See it in 3D: Pulmonary trunk · Pulmonary arteries · Pulmonary veins · Segmental lung vessels · Right ventricle
What it is
The pulmonary circulation takes the entire right-ventricular output, but at pressures about five times lower than the systemic circulation, thanks to short, thin-walled, highly distensible vessels. Unlike systemic vessels, pulmonary arterioles constrict when alveolar oxygen is low: blood is diverted away from poorly ventilated areas and ventilation–perfusion matching improves. When hypoxia is widespread, the same reflex raises pulmonary pressure.
How it works, step by step
- Alveolar PO₂ falls in one region (atelectasis, pneumonia, bronchospasm).
- Smooth muscle of nearby arterioles senses the hypoxia: potassium channels close, the cell depolarizes and calcium enters.
- The arterioles constrict and blood is diverted toward better-ventilated alveoli.
- This limits shunt and protects PaO₂ when the problem is local.
- If hypoxia is global (altitude, hypoventilation), all arterioles constrict: pulmonary pressure and right-ventricular load rise.
- With sustained hypoxia the arteriolar wall remodels and pulmonary hypertension becomes fixed.
Reference values (resting adult)
| Parameter | Value | Note |
|---|---|---|
| Pulmonary artery pressure | ≈25/8 mmHg | mean ≈15 mmHg |
| Pulmonary capillary pressure | ≈7–10 mmHg | |
| Wedge pressure (left atrium) | ≈6–12 mmHg | |
| Pulmonary blood volume | ≈450 mL | ≈9 % of total |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- −Alveolar hypoxia: Constricts pulmonary arterioles and raises resistance.
- −Acidosis and hypercapnia: Strengthen hypoxic vasoconstriction.
- +Endothelial nitric oxide and prostacyclin: Dilate; their loss contributes to pulmonary hypertension.
- +Capillary recruitment and distension: Lower resistance as cardiac output rises.
- −Embolism or thrombosis: Obstructs the bed and raises pulmonary artery pressure.
Clinical notes
- At Bogotá's altitude (≈2,600 m) pulmonary pressure is somewhat higher than at sea level; at greater heights, uneven vasoconstriction can cause high-altitude pulmonary edema.
- Massive pulmonary embolism: the right ventricle cannot handle the sudden afterload rise and dilates.
- Systemic vasodilators can worsen oxygenation by abolishing hypoxic vasoconstriction in poorly ventilated areas.
Test yourself
Think of the answer, then tap the question to see it.
Why does hypoxic vasoconstriction improve PaO₂ in lobar pneumonia?
It diverts blood away from the consolidated lobe, which does not ventilate, toward healthy lung, reducing shunt and venous admixture.
Why does pulmonary pressure barely rise when cardiac output triples during exercise?
Previously closed capillaries open and open ones distend; resistance falls almost in proportion to the rise in flow.
How does COPD with chronic hypoxemia lead to right-ventricular failure?
Diffuse alveolar hypoxia constricts and then remodels pulmonary arterioles; pulmonary pressure rises and the right ventricle hypertrophies and eventually fails.
Why does pulmonary vascular resistance rise at both very high and very low lung volumes?
At high volume, stretched alveoli compress alveolar capillaries; at low volume, extra-alveolar vessels lose radial traction and narrow.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Ventilation–perfusion matching and West zones
- High altitude and acclimatization
- Physiology of pulmonary edema
- The bronchial circulation
- Fetal circulation and the transition at birth
- The causes of hypoxemia
Related conditions
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: 20.5 Circulatory Pathways (OpenStax (Rice University), 2022); 22.4 Gas Exchange (OpenStax (Rice University), 2022); Acute Pulmonary Embolism (StatPearls (NCBI Bookshelf), 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 39). 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.