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Respiratory System: Mechanics, Gas Exchange, and Pathology

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Types of Hypoxia

Overview of Hypoxia

Hypoxia refers to a deficiency in the amount of oxygen reaching the tissues. There are several types, each with distinct causes and physiological implications.

  • Hypoxic Hypoxia: Caused by low oxygen levels in the environment (e.g., high altitude, hypoventilation). Results in low arterial PO2.

  • Anemic Hypoxia: Due to problems with oxygen delivery by the blood (e.g., anemia, low hemoglobin, carbon monoxide poisoning).

  • Ischemic Hypoxia: Caused by reduced blood flow (ischemia) to tissues (e.g., heart attack, shock, thrombosis).

  • Histotoxic Hypoxia: Occurs when cells are unable to utilize oxygen, often due to poisoning (e.g., cyanide poisoning interfering with the electron transport chain).

Comparison Table of Hypoxia Types:

Type

Main Cause

Example

Hypoxic

Low environmental O2

High altitude

Anemic

Low O2 carrying capacity of blood

Anemia, CO poisoning

Ischemic

Reduced blood flow

Thrombosis, shock

Histotoxic

Cellular inability to use O2

Cyanide poisoning

Mechanics of Breathing

Pressure Changes and Lung Inflation

The process of breathing relies on pressure differences between the atmosphere, alveoli, and the pleural cavity. These differences drive inspiration and expiration.

  • Pleural Cavity: The pleural cavity surrounds the lungs and maintains a lower pressure than the lungs themselves, acting as a vacuum to keep the lungs inflated.

  • Intrapleural Pressure: Normally about 756 mmHg (lower than atmospheric and alveolar pressure), preventing lung collapse.

  • Pneumothorax: Loss of the vacuum in the pleural cavity (e.g., due to trauma) leads to lung collapse.

Boyle's Law and Breathing

Boyle's Law describes the inverse relationship between pressure and volume in a closed system:

  • During inspiration, thoracic volume increases, causing alveolar pressure to drop below atmospheric pressure, drawing air in.

  • During expiration, thoracic volume decreases, alveolar pressure rises above atmospheric, pushing air out.

Muscles of Respiration

  • Inspiration: Primarily the diaphragm (contracts and moves down), assisted by external intercostals for deeper breaths.

  • Expiration: Normally passive (diaphragm relaxes). Forced expiration uses internal intercostals and rectus abdominis.

Gas Laws Relevant to Respiration

Dalton's Law of Partial Pressures

Dalton's Law states that the total pressure of a gas mixture is the sum of the partial pressures of each individual gas:

  • At sea level, atmospheric pressure is 760 mmHg.

  • Nitrogen: ~78% (593 mmHg), Oxygen: ~21% (160 mmHg), CO2: ~0.3 mmHg.

  • Partial pressures drive diffusion of gases in the lungs and tissues.

Lung Structure and Function

Alveoli and Gas Exchange

The alveoli are the primary sites of gas exchange, featuring a thin barrier (one endothelial cell and one alveolar cell) and surrounded by capillaries.

  • Elastic Fibers: Allow alveoli to expand during inspiration and recoil during expiration.

  • Lung Compliance: Refers to the ease with which the lungs can expand. High compliance means the lungs are soft and easy to inflate; low compliance (e.g., in emphysema) means the lungs are stiff and hard to inflate.

  • Elasticity: The ability of the lungs to return to their original shape after being stretched.

Surface Tension and Surfactant

Surface tension in the alveoli, due to water lining their surfaces, tends to cause collapse. Surfactant reduces this tension, preventing collapse, especially in smaller alveoli.

  • Law of Laplace: The inward pressure in a sphere (alveolus) is given by:

  • T: Surface tension

  • r: Radius of the alveolus

  • Smaller alveoli have higher inward pressure and are more prone to collapse.

  • Surfactant: Produced by type II alveolar cells, surfactant (mainly dipalmitoyl phosphatidylcholine) reduces surface tension, equalizing pressure across alveoli of different sizes.

  • Infant Respiratory Distress Syndrome: Caused by insufficient surfactant production in newborns, leading to alveolar collapse and impaired gas exchange.

Assessment of Lung Function

Anatomical Dead Space

Not all inhaled air reaches the alveoli; some remains in the conducting airways (trachea, bronchi, bronchioles), known as anatomical dead space (~150 mL).

  • During each breath, only a portion of the tidal volume reaches the alveoli for gas exchange.

  • This mixing of fresh and stale air prevents alveolar PO2 from reaching atmospheric levels.

Spirometry and Lung Volumes

Spirometry measures the volume of air moved in and out of the lungs during various phases of breathing.

  • Tidal Volume (TV): Normal breath in and out (~500 mL).

  • Inspiratory Capacity (IC): Maximum volume inhaled after a normal exhalation.

  • Expiratory Capacity (EC): Maximum volume exhaled after a normal inhalation.

  • Vital Capacity (VC): Total volume of air that can be exhaled after a maximal inhalation.

  • Residual Volume (RV): Air remaining in the lungs after maximal exhalation.

  • Total Lung Capacity (TLC): Sum of all lung volumes.

Alveolar Ventilation Equation:

Example:

Gas Exchange Gradients

  • Alveolar PO2 is about 100 mmHg (lower than atmospheric due to dead space and mixing).

  • Alveolar PCO2 is about 40 mmHg (higher than atmospheric).

  • These gradients drive O2 into the blood and CO2 out of the blood.

Pulmonary Pathologies

Obstructive Pulmonary Diseases

Obstructive diseases are characterized by increased resistance to airflow, especially during expiration.

  • Examples: Asthma, bronchitis, chronic obstructive pulmonary disease (COPD).

  • Mechanism: Airway obstruction (e.g., mucus, inflammation) makes it harder to exhale; residual volume increases.

  • Spirometry Findings: Reduced expiratory capacity, increased residual volume, total lung capacity may remain unchanged.

Restrictive Pulmonary Diseases

Restrictive diseases (briefly mentioned) are characterized by reduced lung expansion, making inspiration more difficult.

  • Examples: Pulmonary fibrosis, black lung disease.

  • Mechanism: Stiff lungs reduce compliance, limiting inspiratory capacity.

Summary Table: Lung Volumes and Capacities

Volume/Capacity

Description

Typical Value (mL)

Tidal Volume (TV)

Normal breath in/out

500

Inspiratory Capacity (IC)

Max inhalation after normal exhale

~3,500

Expiratory Capacity (EC)

Max exhalation after normal inhale

~1,200

Vital Capacity (VC)

Max exhale after max inhale

~4,700

Residual Volume (RV)

Air left after max exhale

~1,200

Total Lung Capacity (TLC)

Sum of all volumes

~6,000

Key Equations

  • Boyle's Law:

  • Law of Laplace (Alveolus):

  • Alveolar Ventilation:

Additional info:

  • Birds use unidirectional (circular) airflow, unlike mammals' tidal breathing.

  • Type I alveolar cells form the gas exchange surface; Type II produce surfactant.

  • Obstructive diseases mainly affect expiration; restrictive diseases mainly affect inspiration.

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