Mechanics of human respiration Factors controlling respiration

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Here is a comprehensive overview of both topics, drawn from Guyton and Hall Textbook of Medical Physiology.

Mechanics of Human Respiration

1. Muscles of Ventilation

The lungs expand and contract by two mechanisms:

Downward/upward movement of the diaphragm — lengthens or shortens the chest cavity (vertical diameter).
Elevation/depression of the rib cage — increases or decreases the anteroposterior (AP) diameter.

Figure 38.1 — Thoracic cage contraction and expansion during expiration (left) and inspiration (right), showing diaphragmatic contraction, external intercostal contraction, and rib cage elevation

Muscles of Inspiration

Diaphragm — primary muscle; its contraction pulls the lung bases downward.
External intercostals — pull upper ribs forward, raising the rib cage.
Accessory muscles (used in heavy breathing): sternocleidomastoid (lifts sternum), anterior serrati (lifts ribs), scaleni (lifts first two ribs).

Muscles of Expiration

Normal quiet expiration is passive — driven by elastic recoil of lungs and chest wall.
Forced expiration recruits: abdominal recti (pull lower ribs down, compress abdomen upward) and internal intercostals.

2. Pressures Governing Airflow

Figure 38.2 — Changes in lung volume, alveolar pressure, pleural pressure, and transpulmonary pressure during normal breathing

Pressure	Resting	Inspiration	Expiration
Pleural pressure	−5 cm H₂O	−7.5 cm H₂O	returns to −5
Alveolar pressure	0 (= atm)	−1 cm H₂O	+1 cm H₂O
Transpulmonary pressure	~5 cm H₂O	increases	decreases

Pleural pressure is a slight suction (negative) that holds the lung apposed to the chest wall. During inspiration, thoracic expansion pulls this to a more negative value, expanding the lungs.
Alveolar pressure must drop below atmospheric (−1 cm H₂O) to draw 0.5 L of air in during quiet inspiration; it rises to +1 cm H₂O during expiration to push air out.
Transpulmonary pressure = alveolar pressure − pleural pressure; it represents the elastic recoil force tending to collapse the lung.

3. Lung Compliance

Compliance = the volume change per unit change in transpulmonary pressure.

Normal lungs alone: ~200 mL/cm H₂O
Lungs + thoracic cage together: ~110 mL/cm H₂O (about half, because the chest wall adds its own resistance to expansion)

Two components determine lung elastic forces:

Tissue elasticity — elastin and collagen fibers in lung parenchyma.
Surface tension of alveolar fluid — the dominant factor (~2/3 of total); counteracted by surfactant (secreted by type II pneumocytes), which dramatically lowers surface tension and prevents alveolar collapse (atelectasis).

4. Work of Breathing

The work of inspiration has three fractions:

Compliance (elastic) work — expanding lungs and chest against elastic recoil.
Tissue resistance work — overcoming viscosity of lung and chest wall.
Airway resistance work — overcoming friction of airflow through airways.

At rest, respiration uses only 3–5% of total body energy expenditure. During heavy exercise, this can rise up to 50-fold, becoming a limiting factor when airway resistance is elevated or compliance is reduced.

5. Pulmonary Volumes and Capacities (Spirometry)

Parameter	Typical Value
Tidal volume (TV)	~500 mL
Inspiratory reserve volume (IRV)	~3,000 mL
Expiratory reserve volume (ERV)	~1,100 mL
Residual volume (RV)	~1,200 mL
Inspiratory capacity (IC)	TV + IRV ≈ 3,500 mL
Functional residual capacity (FRC)	ERV + RV ≈ 2,300 mL
Vital capacity (VC)	IRV + TV + ERV ≈ 4,600 mL
Total lung capacity (TLC)	~5,800 mL

Factors Controlling Respiration

1. The Respiratory Center

Located bilaterally in the medulla oblongata and pons, it is divided into three main groups:

Group	Location	Function
Dorsal Respiratory Group (DRG)	Dorsal medulla (nucleus tractus solitarius)	Generates inspiratory rhythm; receives input from chemoreceptors, baroreceptors, lung receptors
Ventral Respiratory Group (VRG)	Ventrolateral medulla	Active in both inspiration and expiration; drives accessory muscles during heavy breathing
Pneumotaxic Center	Superior pons (dorsal)	Limits duration of inspiration → increases respiratory rate; "switches off" inspiration

The pre-Bötzinger complex (rostral VRG) contains spontaneously firing pacemaker neurons and is considered the key component of the central pattern generator for respiratory rhythm.

2. Chemical Control — CO₂ and H⁺ (Central Chemoreceptors)

The most important chemical driver of ventilation is CO₂/H⁺, acting on central chemoreceptors located on the ventral surface of the medulla.

CO₂ diffuses across the blood–brain barrier → combines with water → carbonic acid → H⁺
Rising H⁺ (falling pH) powerfully stimulates the respiratory center → increased rate and depth.
A rise of just a few mm Hg in arterial PCO₂ can double ventilation.
Conversely, CO₂ changes have virtually no direct effect on O₂ sensing at the central level — that is handled peripherally.

3. Peripheral Chemoreceptors — O₂, CO₂, H⁺

Figure 42.4 — Peripheral chemoreceptor system: carotid bodies (via glossopharyngeal nerve) and aortic bodies (via vagus nerve) projecting to the medullary respiratory center

Located in the carotid bodies (at carotid bifurcations, signaling via CN IX) and aortic bodies (along aortic arch, signaling via CN X vagus).

Stimulated primarily by low arterial PO₂ — response is most sensitive when PO₂ falls below 60 mm Hg.
Also respond to elevated PCO₂ and elevated H⁺ (though these are secondary roles compared with central chemoreceptors).
Receive direct arterial blood supply; blood flow is ~20× their body weight per minute, so they always sample arterial (not venous) blood.

Why O₂ is a secondary controller: Hemoglobin's buffering capacity means that adequate O₂ delivery to tissues is maintained across a wide range of pulmonary PO₂ (60–1000 mm Hg). CO₂, by contrast, changes directly and proportionally with ventilation rate — making it the primary feedback signal.

4. Hering–Breuer Inflation Reflex

Stretch receptors in bronchial/bronchiolar walls → signals via the vagus to the DRG → terminate inspiration when lungs are over-inflated. This reflex is strongest in infants; in adults it plays only a minor role during normal breathing but becomes active during tidal volumes >1.5 L.

5. Other Factors Affecting Respiration

Factor	Effect
Exercise	Ventilation rises 20-fold; largely neurogenic (motor cortex collateral signals); also arterial PCO₂ is tightly maintained near 40 mm Hg by a learned cortical response
Irritant receptors (airway epithelium)	Triggered by capsaicin, particulates, inflammatory mediators → cough, sneeze, bronchospasm (relevant in asthma)
J receptors (juxtacapillary, alveolar wall)	Stimulated by pulmonary capillary engorgement/edema → dyspnea and increased respiratory rate
Brain edema	Compresses cerebral arteries → depresses respiratory center → hypoventilation
Anesthetics / narcotics	Depress respiratory center; overdose → respiratory arrest
High altitude	Low PO₂ stimulates peripheral chemoreceptors → hyperventilation → blows off CO₂ → respiratory alkalosis → partially limits hyperventilation
Voluntary cortical control	Cerebral cortex can override the automatic rhythm (e.g., breath-holding, speech, singing)

Source: Guyton and Hall Textbook of Medical Physiology, Chapters 38 & 42

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