Lungs

The lungs are the primary organs of the human gas exchange system, located in the thorax (chest cavity). Their vital function is to supply the blood with oxygen for respiration and remove carbon dioxide from the body.

Structure of the Human Gas Exchange System (Lungs)

Air enters the system through the nasal cavity or mouth, passing through the pharynx and larynx, then into the trachea (windpipe). The trachea then divides into two bronchi (singular: bronchus), one leading to each lung. The bronchi further branch into smaller tubes called bronchioles, which continue to divide, becoming progressively narrower. The smallest bronchioles, known as terminal bronchioles, end in tiny air sacs called alveoli. The lungs have a spongy texture due to the air trapped in the alveoli.

Various tissues and cells contribute to the structure and function of the lungs and airways:

• Cartilage provides support and prevents the trachea and bronchi from collapsing. The trachea has C-shaped rings of cartilage, while bronchi have irregular blocks. Cartilage is absent in smaller bronchioles and alveoli.

• Ciliated epithelium lines the trachea, bronchi, and some bronchioles. These cells have small, hair-like extensions called cilia.

• Goblet cells and mucous glands are found within the ciliated epithelium. They produce sticky mucus.

• Smooth muscle is present in the walls of the bronchi and bronchioles.

• Elastic fibres (containing elastin) are found in the walls of the alveoli and terminal bronchioles.

• Squamous epithelium (thin, flat cells) forms the walls of the alveoli.

• Capillaries (lined by endothelium) surround the alveoli.

• Surfactant cells produce a lipoprotein that lines the inner surface of the alveoli.

• Macrophages (dust cells), a type of phagocytic white blood cell, patrol the alveolar surfaces.

Adaptations for Efficient Gas Exchange

The alveoli are highly specialized for rapid gas exchange due to several adaptations:

• Large Surface Area: Millions of alveoli provide a vast surface area (estimated at 70–75 m² in an adult human), maximizing the area for gas diffusion.

• Thin Exchange Surface: The walls of each alveolus are a single layer of thin, flat alveolar epithelium (squamous epithelial cells), and the walls of the surrounding capillaries are also very thin. This creates a very short diffusion pathway for gases.

• Good Blood Supply: Alveoli are enveloped by a dense network of capillaries. The continuous flow of blood constantly removes oxygenated blood and brings deoxygenated blood, maintaining steep concentration gradients for both oxygen and carbon dioxide.

• Moist Surface: Oxygen must first dissolve in a thin film of moisture lining the alveolar surface before it can diffuse into the blood.

• Elasticity: The presence of elastin in the alveolar walls allows them to stretch during inspiration and then recoil during expiration, aiding the expulsion of air.

• Surfactant: The lung surfactant reduces surface tension within the alveoli, preventing them from collapsing during expiration.

Ventilation (Breathing Mechanism)

Ventilation involves inspiration (breathing in) and expiration (breathing out). It is controlled by the movements of the diaphragm, external intercostal muscles, internal intercostal muscles, and ribcage.

• Inspiration (Active Process): The external intercostal muscles and the diaphragm contract. This causes the ribcage to move upwards and outwards, and the diaphragm to flatten and move downwards. As a result, the volume of the thoracic cavity (and thus the lungs) increases, leading to a decrease in lung pressure below atmospheric pressure, causing air to flow into the lungs.

• Expiration (Passive, or Active for Forced Expiration): In normal quiet breathing, expiration is passive, as the diaphragm and external intercostal muscles relax. This decreases the volume of the thoracic cavity and increases lung pressure, forcing air out. During forced expiration, the internal intercostal muscles contract, pulling the ribcage further down and in. The elastic recoil of the lungs also assists in expelling air.

The Medulla Oblongata, a part of the brain, contains ventilation centers that control the rate of breathing. Chemoreceptors in the medulla, aortic bodies, and carotid bodies are sensitive to changes in blood pH and can influence breathing rate and depth.

Gas Exchange Process in Alveoli

Air (containing oxygen) moves down the trachea, bronchi, and bronchioles into the alveoli. Oxygen then moves from the alveoli, across the alveolar epithelium and the capillary endothelium, and into the blood (specifically, into haemoglobin in red blood cells), moving down a concentration gradient. Simultaneously, carbon dioxide moves from the blood into the alveoli, down its own diffusion and pressure gradients, to be exhaled. These gradients are constantly maintained by the flow of blood and continuous ventilation.

Lung Function Measures

Several terms are used to assess lung function:

• Tidal volume is the volume of air in each normal breath, typically 0.4–0.5 dm³ for adults.

• Ventilation rate is the number of breaths per minute, usually around 15 breaths for a healthy person at rest.

• Forced Expiratory Volume1 (FEV1) is the maximum volume of air that can be exhaled in 1 second.

• Forced Vital Capacity (FVC) is the maximum volume of air that can be forcefully exhaled from the lungs after a deep inspiration. Lung function can be measured using a spirometer.

Protection of the Gas Exchange System

The lungs are protected from dust particles, pathogens (like bacteria and viruses), and other foreign matter by several mechanisms:

• The airways warm and moisten incoming air.

• Hairs in the nostrils trap large dust particles.

• Goblet cells and mucous glands produce sticky mucus that traps fine particles, bacteria, and pathogens.

• Cilia constantly sweep this mucus (and trapped foreign matter) upwards towards the throat, where it is swallowed and destroyed by stomach acid.

• Macrophages in the alveoli engulf and digest any remaining dust or pathogens that reach them.

• Cartilage rings in the trachea and bronchi also provide structural support, preventing airway collapse.

Effects of Lung Disease

Lung diseases significantly affect both ventilation and gas exchange, reducing lung function. This leads to less oxygen diffusing into the bloodstream, less oxygen reaching body cells, and a reduction in aerobic respiration, resulting in fatigue and weakness.

• Emphysema: Caused by smoking or air pollution. Inflammation leads to phagocytes breaking down elastin in the alveolar walls. This loss of elasticity impairs alveolar recoil, trapping air. It also causes the destruction of alveolar walls, which reduces the surface area for gas exchange. Symptoms include shortness of breath and wheezing. Alveoli may appear enlarged or merged. Oxygen tents can benefit patients by increasing the oxygen concentration gradient.

• Chronic Bronchitis: Caused by components in cigarette smoke (e.g., tar) that stimulate increased mucus production by goblet cells and inhibit cilia function. This leads to mucus accumulation, trapping dirt, bacteria, and viruses, obstructing the airways. Airways become inflamed and narrower. Symptoms include a persistent cough (often with phlegm), chest pain, shortness of breath, and wheezing.

• Asthma: A respiratory condition where airways become inflamed and irritated, causing the smooth muscle lining the bronchioles to contract and excessive mucus to be produced. This constricts the airways, severely reducing airflow and FEV1. Symptoms include wheezing, a tight chest, and shortness of breath.

• Pulmonary Tuberculosis (TB): A lung disease caused by the bacterium Mycobacterium tuberculosis. Immune cells form tubercles around the bacteria, leading to tissue death and damage to the gas exchange surface. It reduces tidal volume and can cause fibrosis. Symptoms include a persistent cough (sometimes with blood or mucus), chest pains, shortness of breath, and fatigue. TB can spread to other organs and be fatal if untreated.

• Fibrosis: Involves the formation of thick, less elastic scar tissue in the lungs, reducing lung expansion and thus tidal volume and FVC. Diffusion of gases is slower across the thicker scarred membrane, reducing the rate of gaseous exchange.

• Cystic Fibrosis (CF): An inherited disorder where a faulty protein (CFTR) leads to the production of abnormally thick, sticky mucus in the airways. Cilia cannot effectively move this mucus, causing it to build up and block airways. This reduces the surface area for gas exchange, causing breathing difficulties and increasing susceptibility to lung infections.

Water loss from the lungs during gas exchange is a significant issue for terrestrial organisms, accounting for about 10-15% of total daily water loss in humans.