Pulmonary alveoli

Alveoli pulmonis

Also known as: alveolus, air sacs, alveolar wall, interalveolar septum

≈480 million thin-walled air sacs (≈200 µm across) providing ≈70 m² of surface, wrapped in capillaries, where O2 and CO2 are exchanged.

Overview

Number≈480 million (≈270–790 million)

Diameter≈200 µm

Total surface≈70 m² (≈50–100 m²)

Capillary blood volume≈70–100 mL at rest

Each alveolus is a polyhedral pouch opening into a respiratory bronchiole, alveolar duct or sac. Neighbouring alveoli share interalveolar septa containing one of the densest capillary networks in the body, elastic and reticular fibres, fibroblasts and interstitial macrophages. The alveolar surface is lined by type I pneumocytes (flat, ≈95% of the surface) and type II pneumocytes (cuboidal, surfactant-secreting), and patrolled by alveolar macrophages. Small pores of Kohn connect adjacent alveoli, allowing collateral ventilation around blocked airways (and spread of infection).

Each septal capillary has a thin side, where epithelial and endothelial basement membranes fuse to form the blood–gas barrier (≈0.2–0.6 µm) for gas exchange, and a thick side with interstitium, where fluid exchange and lymphatic drainage occur. The alveolar surface is covered by a thin liquid layer with surfactant at the air–liquid interface. At any instant only ≈70–100 mL of capillary blood is spread across this vast surface, allowing very rapid equilibration.

Location

Throughout the respiratory zone of both lungs.

Parts & subdivisions

Type I pneumocytes

Squamous gas-exchange cells.

Type II pneumocytes

Cuboidal surfactant-producing progenitor cells.

Alveolar macrophages

Phagocytes on the alveolar surface.

Pores of Kohn

Interalveolar pores (≈10–15 µm) allowing collateral ventilation.

Respiratory membrane

The thin blood–gas barrier.

Septal capillaries

Pulmonary capillary network in the interalveolar septa.

Anatomy

Arterial supply

Pulmonary capillaries fed by branches of the pulmonary arteries (deoxygenated blood) and drained by pulmonary veins (oxygenated).

Lymphatic drainage

No lymphatics in the alveolar walls; interstitial fluid moves to lymphatics beginning at the level of the terminal bronchioles and interlobular septa.

Histology

Type I and II pneumocytes on a basement membrane; interstitium with elastic and collagen (type I and III) fibres, fibroblasts, pericytes; continuous capillary endothelium.

Function

Gas exchange between alveolar air and pulmonary capillary blood.

Production of surfactant.

Immune defence of the distal lung.

Contribute elastic recoil (elastic fibres and surface tension).

Physiology

PAO2 ≈100–104 mmHg and PACO2 ≈40 mmHg are maintained by alveolar ventilation. Capillary hydrostatic pressure (≈7–10 mmHg) is lower than plasma oncotic pressure (≈25 mmHg), and surfactant reduces the suction of fluid into the alveoli, so the alveoli stay dry.

Clinical significance

Pulmonary oedema

Fluid floods the interstitium and then the alveoli when capillary hydrostatic pressure rises (cardiogenic, e.g. left heart failure, pulmonary capillary wedge pressure > 18 mmHg) or when the barrier becomes leaky (non-cardiogenic, e.g. ARDS). Signs: dyspnoea, orthopnoea, basal crackles, Kerley B lines and bat's-wing opacities; J-receptor stimulation causes rapid shallow breathing.

Emphysema

Destruction of alveolar walls reduces surface area and capillary bed (↓DLCO), and loss of elastic tissue increases compliance and causes airway collapse.

Atelectasis

Collapse of alveoli (post-operative, obstruction, compression, surfactant deficiency) creates shunt and hypoxaemia; deep breathing, incentive spirometry and early mobilisation help prevent it.