CHAPTER 38

1. Introduction to Pulmonary Ventilation

Definition: Pulmonary ventilation is the process of moving air into and out of the lungs, ensuring
continuous supply of oxygen (O₂) and removal of carbon dioxide (CO₂).

Physiological significance:
• Oxygen is crucial for cellular respiration, where it is used in the mitochondria to
generate ATP.
• Carbon dioxide, a byproduct of cellular metabolism, must be expelled to prevent acid-
base disturbances.

Two main components:

• Inspiration: The process of drawing air into the lungs.
• Expiration: The process of expelling air out of the lungs.
• Regulation: Controlled by both the autonomic nervous system and central respiratory
centers in the brainstem, ensuring proper gas exchange to meet the body’s metabolic demands.

2. Mechanics of Pulmonary Ventilation

Inspiration mechanics:
• Diaphragm contraction: This is the main driver of inspiration. When the diaphragm
contracts, it moves downward, expanding the thoracic cavity’s volume and creating a negative
pressure that draws air into the lungs.
• External intercostal muscles: Assist by elevating the ribs and increasing the
anteroposterior and lateral dimensions of the chest cavity.

Expiration mechanics:
• Quiet expiration is largely a passive process, driven by the natural elastic recoil of the
lungs and relaxation of the diaphragm.
• Forced expiration (e.g., during exercise) requires active contraction of the internal
intercostal muscles and abdominal muscles to push the diaphragm upward and force air out of
the lungs.

Pleural pressure:
 • Normally negative in the pleural cavity, which helps keep the lungs inflated by
maintaining a pressure gradient between the atmosphere and the lungs.
• During inspiration, this pressure becomes even more negative, helping to pull the lungs
outward with the chest wall.
• If this pressure becomes positive, as in a pneumothorax (air entering the pleural
cavity), lung collapse can occur.

Transpulmonary pressure: The difference between alveolar pressure and pleural pressure,
which determines the extent of lung inflation. Greater transpulmonary pressure results in greater
lung expansion.

3. Alveolar Pressure and Airflow

• Alveolar pressure is the pressure of the air inside the alveoli of the lungs.

• At rest (between breaths), alveolar pressure is equal to atmospheric pressure (0 cm

H₂O), meaning no airflow occurs.

• During inspiration, alveolar pressure drops below atmospheric pressure (typically

around -1 cm H₂O), allowing air to flow into the lungs.

• During expiration, alveolar pressure becomes slightly positive (around +1 cm H₂O),

which forces air out of the lungs.

• Airflow: Directly proportional to the pressure gradient between the atmosphere and
the alveoli. Higher pressure gradients result in greater airflow.

• Resistance in the airways, such as in asthma (bronchoconstriction), increases airway

resistance, reducing airflow despite the pressure gradient.

4. Compliance of the Lungs

• Lung compliance is the measure of how easily the lungs can expand when subjected to
pressure changes.

• High compliance means the lungs easily expand with small changes in pressure, as
seen in diseases like emphysema.
 • Low compliance indicates stiff lungs, requiring more effort to inflate, as in pulmonary
fibrosis.

Elastic forces:
• The lungs have two major sources of elasticity:
1. Tissue elasticity: Provided by elastin and collagen fibers in lung parenchyma.
2. Surface tension: The tendency of the alveoli to collapse due to the liquid lining their
surface. The liquid molecules have a natural attraction to each other (cohesion), which creates a
force trying to pull the alveoli closed.

Clinical relevance:
• In pulmonary fibrosis, scar tissue builds up in the lungs, making them stiff and less
compliant.
• In emphysema, the alveolar walls are destroyed, reducing the elastic recoil and
increasing compliance, but making exhalation more difficult.

5. Surfactant and Surface Tension

Surfactant:
• Produced by type II alveolar epithelial cells and primarily composed of
dipalmitoylphosphatidylcholine (DPPC).
• Surfactant reduces surface tension in the alveoli, preventing alveolar collapse,
especially during expiration when the lung volume is low.

Role of surfactant:
• By reducing surface tension, surfactant lowers the work of breathing and prevents
atelectasis (collapse of alveoli).
• Surfactant is particularly important in preventing infant respiratory distress syndrome
(IRDS), which occurs in premature infants who lack adequate surfactant.

Law of LaPlace:
• The pressure tending to collapse an alveolus is inversely proportional to the radius of
the alveolus (P = 2T/r).
• Smaller alveoli tend to have higher pressures, but surfactant equalizes the surface
tension, allowing alveoli of different sizes to coexist without smaller ones collapsing into larger
ones.
6. Work of Breathing

The total work of breathing consists of overcoming three primary factors:

• Elastic work: The energy required to overcome the elasticity of the lung and chest
wall. This is primarily dependent on lung compliance.

• Tissue resistance work: The energy needed to overcome the viscosity of lung tissues
and chest wall structures during their movement.

• Airway resistance work: The energy required to overcome resistance to airflow in the
airways.

Clinical significance:
• In conditions such as asthma and COPD, airway resistance increases, leading to an
increased work of breathing.
• In fibrotic lung diseases, increased stiffness of the lungs results in higher elastic work,
leading to rapid, shallow breathing patterns to minimize the effort.

7. Pulmonary Volumes and Capacities

. Tidal volume (TV): The amount of air moved in and out of the lungs during a normal
breath (~500 mL).

. Inspiratory reserve volume (IRV): The additional air that can be inhaled after a normal
inspiration (~3000 mL).

. Expiratory reserve volume (ERV): The additional air that can be forcibly exhaled after a
normal expiration (~1100 mL).

. Residual volume (RV): The volume of air remaining in the lungs after maximal exhalation
(~1200 mL).

. Vital capacity (VC): The total amount of air that can be exhaled after maximal inhalation.
VC = TV + IRV + ERV.

. Total lung capacity (TLC): The total volume of air in the lungs after a maximal inhalation.
 .
TLC = VC + RV.

Clinical applications:
• In restrictive lung diseases (e.g., pulmonary fibrosis), all lung volumes are reduced
because the lungs are stiff and difficult to expand.
• In obstructive lung diseases (e.g., COPD), residual volume increases due to air
trapping, leading to a barrel-shaped chest.

8. Dead Space and Alveolar Ventilation

● Anatomical dead space: This refers to the portions of the respiratory system where gas
exchange does not occur, such as the trachea, bronchi, and bronchioles (~150 mL).

● Physiological dead space: Includes the anatomical dead space plus any alveoli that are
ventilated but not perfused (i.e., alveolar dead space). In healthy individuals, physiological
dead space is roughly equivalent to anatomical dead space.

● Alveolar ventilation: Alveolar ventilation refers to the amount of fresh air that reaches the
alveoli and participates in gas exchange per minute.

● It is more relevant to gas exchange than minute ventilation because minute ventilation
includes dead space air, which does not contribute to gas exchange.

9. Control of Pulmonary Ventilation

Medullary respiratory centers:

• The dorsal respiratory group (DRG) is primarily responsible for initiating inspiration by
stimulating the diaphragm.
• The ventral respiratory group (VRG) is activated during heavy breathing and controls
both inspiration and expiration, particularly during forced breathing.

Pneumotaxic center:
• Located in the pons, the pneumotaxic center regulates the duration of inspiration and
indirectly influences the respiratory rate.
• It acts as an “off-switch” for inspiration, limiting the size of the tidal volume and
preventing overinflation of the lungs.

Hering-Breuer reflex:
Hering-Breuer reflex:
• Stretch receptors in the walls of the bronchi and bronchioles are activated during lung
inflation.
• These receptors send inhibitory signals to the brainstem to terminate inspiration and
prevent overinflation of the lungs.

10. Factors Influencing Respiratory Rate

Chemical control:
• Central chemoreceptors: Located in the medulla, they primarily respond to elevated
levels of CO₂ (via increased H⁺ concentration in the cerebrospinal fluid) and stimulate an increase
in ventilation to expel CO₂ and restore normal pH.

• Peripheral chemoreceptors: Located in the

carotid bodies and aortic bodies, they primarily respond to low oxygen levels (hypoxia),
stimulating increased ventilation when oxygen levels drop below a critical threshold.

Voluntary control:
• The cerebral cortex can override automatic breathing for activities like talking, singing,
or holding one’s breath.
• However, automatic control will resume if blood gases deviate too much from normal,
such as during hypercapnia (high CO₂) or hypoxia (low O₂).