By the end of this topic you should be able to:
Name and locate every muscle of respiration and state its role in inspiration/expiration.
Explain step‐by‐step how pressure gradients drive airflow in and out of the lungs and how the gradients are generated.
Reconstruct the full sequence of events (muscular, volumetric, pressure) during quiet inspiration, quiet expiration, forced inspiration, and forced expiration.
List and describe the three major physical factors that hinder or facilitate pulmonary ventilation.
Primary purpose: supply O₂ and remove CO₂.
Five inter-related steps (see figure reference):
Pulmonary ventilation — mechanical movement of air between atmosphere ↔ alveoli.
External respiration — gas exchange lung ↔ blood (O₂ into blood, CO₂ out).
Gas transport — circulation of gases: O₂ carried to tissues, CO₂ carried to lungs.
Internal respiration — exchange blood ↔ cells (O₂ into cells, CO₂ into blood).
Cellular respiration — mitochondrial use of O₂ to generate ATP ("ENERGY!").
Pulmonary ventilation is the entry point that makes all subsequent steps possible.
Quiet inspiration (ACTIVE):
Diaphragm (most important) – contracts & flattens ↓, increases superior-inferior dimension.
External intercostals – contract, lifting ribs & sternum (pump-handle & bucket-handle motions) → increases anterior-posterior & lateral dimensions.
Quiet expiration (PASSIVE):
No active muscle contraction; relaxation of diaphragm & external intercostals + elastic recoil of lungs & thoracic cage.
Forced inspiration (during exercise or COPD):
Accessory muscles: scalenes, sternocleidomastoid, pectoralis minor → further enlarge thoracic cavity.
Forced expiration (ACTIVE):
Abdominal wall muscles (obliques, transversus abdominis, rectus abdominis) → push viscera up against diaphragm.
Internal intercostals → depress rib cage.
Atmospheric pressure P_{atm} = 760\,\text{mmHg} (sea level) is reference (0).
Respiratory pressures expressed relative to P_{atm}:
Negative pressure < 0 ⇒ lower than atmospheric; e.g. -4\,\text{mmHg} \Rightarrow 756\,\text{mmHg absolute}.
Positive pressure > 0 ⇒ higher than atmospheric; e.g. +4\,\text{mmHg} \Rightarrow 764\,\text{mmHg absolute}.
Zero pressure = 0 ⇒ equal to atmospheric =760\,\text{mmHg}.
Boyle’s Law: for a fixed amount of gas at constant temperature, P \propto \frac{1}{V}.
Decreasing container volume → pressure rises.
Increasing container volume → pressure falls.
Intrapulmonary (intra-alveolar) pressure P_{pul}
Pressure inside alveoli.
Fluctuates with breathing; equals P_{atm} at end-inspiration & end-expiration.
Intrapleural pressure P_{ip}
Pressure within pleural cavity between visceral & parietal pleurae.
Always negative (≈ -4\,\text{mmHg}) under normal conditions.
Maintained by lymphatic drainage of pleural fluid.
Negative value results from opposing forces:
Inward (lung recoil + alveolar surface tension).
Outward (elasticity of chest wall).
Transpulmonary pressure
Keeps airways open; the larger P_{tp}, the larger & more inflated the lungs.
If P_{ip}= P_{pul} or P_{atm} → lung collapse (atelectasis).
Inspiratory muscles contract (diaphragm descends; external intercostals lift ribs).
Thoracic cavity volume ↑.
Lung surface follows thoracic wall (pleural coupling) → V_{pul} ↑.
P_{pul} drops to ≈ -1\,\text{mmHg}.
Air flows into lungs down its pressure gradient until P{pul}=P{atm}.
Inspiratory muscles relax.
Thoracic cavity volume ↓ (elastic recoil of costal cartilages & lungs).
V_{pul} ↓.
P_{pul} rises to ≈ +1\,\text{mmHg}.
Air flows out until P_{pul} =P_{atm}
Forced inspiration: accessory muscles enlarge thorax further, P_{pul} may fall to -2 to -3\,\text{mmHg} ⇒ larger tidal volume.
Forced expiration: active contraction of abdominals & internal intercostals sharply ↑ intrathoracic pressure, driving rapid airflow.
Atelectasis (lung collapse):
Causes: plugged bronchiole → alveolar collapse; pneumothorax (air in pleural cavity) from chest wound or visceral pleura rupture.
Treatment: remove intrapleural air via chest tube so pleural membranes reseal & lung reinflates.
Asthma: bronchoconstriction + mucus → ↑ airway resistance; treated with bronchodilators (e.g. albuterol, epinephrine).
Airway Resistance
Friction in airways; major non-elastic resistance.
Relationship: F = \frac{\Delta P}{R}.
Normally, \Delta P is only 1–2 mmHg; small radius changes (e.g. mucus, tumors, smooth muscle spasm) greatly ↑ R (Poiseuille’s law: R \propto \frac{1}{r^4}).
Medium-sized bronchi contribute most resistance; at terminal bronchioles, huge cross-sectional area → negligible R.
Alveolar Surface Tension
Water molecules lining alveoli attract, creating inward collapsing force.
Surfactant (produced by Type II pneumocytes) lowers surface tension, preventing collapse & stabilizing alveoli.
Deficiency → Infant Respiratory Distress Syndrome (IRDS); each breath requires re-inflation.
Lung Compliance ("stretchability")
Defined: CL = \frac{\Delta V}{\Delta P{tp}}.
High compliance = lungs expand easily.
Decreased by: fibrosis (scar tissue), low surfactant, thoracic cage stiffness (kyphosis, costal cartilage ossification), paralysis of intercostals.
Absolute pressures when P_{atm}=760\,\text{mmHg}:
Respiratory pressure -4 → 756\,\text{mmHg}.
Respiratory pressure 0 → 760\,\text{mmHg}.
Respiratory pressure +4 → 764\,\text{mmHg}.
Figure labels (slide 20):
A = Transpulmonary pressure (4 mmHg).
B = Intrapleural pressure (−4 mmHg).
C = Intrapulmonary pressure (0 mmHg).
Boyle’s law container question: container B (smaller volume) has higher pressure.
"Most important muscle for inspiration?" — the diaphragm.
Premature infants often lack surfactant → requires exogenous surfactant therapy and positive pressure ventilation.
COPD patients rely on accessory muscles; energy expenditure for breathing increases dramatically → caloric considerations for care.
Use of rescue inhalers (albuterol) & epinephrine auto-injectors illustrates pharmacological manipulation of airway smooth muscle tone.
Boyle’s Law: P1 V1 = P2 V2 (for a closed system at constant T).
Transpulmonary pressure: P{tp} = P{pul} - P_{ip}.
Compliance: CL = \frac{\Delta V}{\Delta P{tp}}.
Airflow: F = \frac{\Delta P}{R}.
[ ] I can diagram pressure changes during one full respiratory cycle.
[ ] I can explain why P_{ip} must remain negative and predict consequences if it becomes positive.
[ ] I can list every structure and muscle involved in forced breathing.
[ ] I can articulate how surfactant works and why its absence is devastating.
[ ] I can solve problems involving Boyle’s law and compliance calculations.
Marieb & Hoehn: Human Anatomy & Physiology, 13th ed.
Saladin: Anatomy & Physiology, 9th ed.