Respiratory System – Chapter 23

Respiratory System Overview

• Respiration = gas exchange of O2 and CO2 between atmosphere and body cells
  • Cells need O2 for aerobic ATP production; must expel metabolic CO2
• Respiratory system provides the passageways and structures for this exchange
  • Located in head, neck, trunk, plus lungs

General Functions

• Air passageway (conduits for airflow)
• Site of external gas exchange (alveolar–capillary interface)
• Detection of odors (olfactory epithelium in superior nasal cavity)
• Sound production (larynx & vocal folds)

Structural & Functional Organization

• Structural
  • Upper tract: nose, nasal cavity, pharynx, larynx
  • Lower tract: trachea → bronchi → bronchioles → alveolar ducts → alveoli
• Functional
  • Conducting zone: nose → terminal bronchioles (air transport only)
  • Respiratory zone: respiratory bronchioles, alveolar ducts, alveoli (gas exchange)

Respiratory Mucosa

• Mucosa = epithelium + basement membrane + areolar lamina propria
• Epithelium thins from nasal cavity (pseudostratified ciliated columnar) → alveoli (simple squamous)
• Mucus
  • Secreted by goblet cells + mucous/serous glands
  • Contains mucin (↑ viscosity), lysozyme, defensins, IgA
  • Daily production: ≈ 1–7 tbsp; called sputum when expectorated with saliva & debris

Upper Respiratory Tract

Nose & Nasal Cavity

• Nose = first conducting structure; external nares (nostrils) → internal choanae
• Nasal septum divides cavity; conchae (superior, middle, inferior) create turbulence for conditioning
• Functions: warm, humidify, filter air; extensive vascular plexus (epistaxis origin)

Paranasal Sinuses

• Lined by pseudostratified ciliated columnar epithelium; mucus swept to pharynx
• Blocked drainage → mucus accumulation → infection (sinusitis)

Pharynx

• Muscular funnel posterior to nasal/oral cavities & larynx
  • Nasopharynx: air only; pseudostratified ciliated columnar
  • Oropharynx & Laryngopharynx: air + food; non-keratinized stratified squamous (abrasion resistance)

Larynx (Voice Box)

• Cylindrical airway connecting laryngopharynx → trachea
• Functions
  • Air passage & protective sphincter (epiglottis, vestibular folds)
  • Sound production & speech modulation
  • Assists Valsalva maneuver (↑ abdominal pressure)
  • Participates in sneeze/cough reflexes

Vocal & Vestibular Ligaments

• Vocal ligaments (true cords): thyroid → arytenoid cartilages; covered by mucosa → vocal folds
  • Vibrate when air forced through rima glottidis → sound
• Vestibular ligaments (false cords): superior; protective; create rima vestibuli

Intrinsic Muscles & Sound Mechanics

• Skeletal muscles adjust tension & position of cords (adduction = narrower, abduction = wider)
• Range: cord length/thickness (males deeper voice)
• Pitch: ↑ tension → ↑ frequency
• Loudness: force of air across folds

Clinical – Laryngitis

• Inflammation from infection or overuse → hoarseness; severe pediatric cases may obstruct airway

Lower Respiratory Tract

Trachea

• Flexible, patent “windpipe”; mucosa = pseudostratified ciliated columnar

Bronchial Tree

• Main (primary) bronchi → lobar (secondary) → segmental (tertiary) → smaller bronchi → bronchioles → terminal bronchioles
• Cartilage rings/plates diminish; bronchioles lack cartilage & possess proportionally thick smooth muscle → bronchoconstriction/dilation

Clinical – Asthma

• Episodic bronchoconstriction + inflammation + excess mucus
• Triggers: allergens, exercise; chronic remodeling thickens walls
• Treatment: inhaled steroids & bronchodilators

Respiratory Zone

• Respiratory bronchioles → alveolar ducts → alveolar sacs (300–400 million alveoli/lung)
• Alveolar pores equalize pressure & provide collateral ventilation
• Pulmonary capillary network envelops alveoli

Alveolar Cell Types

1. Type I (squamous): 95 % surface; thin diffusion barrier
2. Type II (septal): secrete surfactant → ↓ surface tension, prevent collapse
3. Alveolar macrophages (dust cells): fixed or free, phagocytose debris & microbes

Respiratory Membrane

• Type I cell epithelium + fused basement membrane + capillary endothelium
• Thickness ≈ 0.5\,\mu m; large area ≈ 70\,m^2 → efficient diffusion

Lungs & Pleura

• Paired organs flanking mediastinum; each in its own pleural cavity
• Bronchopulmonary segments: autonomous units (10 right; 8–10 left) with own tertiary bronchus & vascular supply; surgically resectable

Pleural Membranes & Cavity

• Visceral pleura (on lung) & parietal pleura (thoracic wall); serous fluid lubricates
• Intrapleural pressure < intrapulmonary → lungs stay inflated (outward pull vs elastic recoil)

Inflation Mechanics

• Chest wall tends to expand; lungs recoil inward; surface tension of fluid couples motions

Clinical – Smoking & Lung Cancer

• Smoking ↑ risk of infections, emphysema, atherosclerosis, ulcers, cancers (lung 85 %, esophagus, stomach, pancreas), low-birth-weight infants, secondhand effects
• Lung cancer: aggressive; symptoms—chronic cough, hemoptysis, excess mucus

Pulmonary Ventilation (Breathing)

• Four integrated processes of respiration
  1. Pulmonary ventilation
  2. Pulmonary gas exchange
  3. Gas transport
  4. Tissue gas exchange
• Breathing phases
  • Inspiration (inhalation)
  • Expiration (exhalation)
  • Quiet (eupnea, restful) vs forced (vigorous/exercise)

Mechanics & Boyle’s Law

• Volume ↔ pressure (inverse) at constant T: P1 V1 = P2 V2
• Thoracic cavity changes
  • Vertical (diaphragm), lateral, anterior-posterior (rib movements)
• Air flows down pressure gradient until equalization

Pressures

• Atmospheric P_{atm} ≈ 760\,mm\,Hg at sea level
• Intrapulmonary (alveolar) P{alv} fluctuates; = P{atm} at end phases
• Intrapleural P_{ip} about -4\,mm\,Hg (between breaths)

Quiet Breathing Sequence

1. MRC inspiratory neurons fire (~2 s) → diaphragm & external intercostals contract → thoracic V ↑ → P_{alv} ↓ → air in
2. Inspiratory neurons inhibited (~3 s) → muscles relax → thoracic V ↓ → P_{alv} ↑ → air out

Forced Breathing

• Recruit accessory muscles (sternocleidomastoid, scalenes, abdominal, etc.) → larger ΔV and ΔP → greater airflow; visible chest movement

Nervous Control of Breathing

• Respiratory center (brainstem)
  • Medullary Respiratory Center (MRC)
  • Ventral RG (VRG) – rhythm generation; motor output
  • Dorsal RG (DRG) – sensory integration
  • Pontine Respiratory Center (pneumotaxic) – smooth transitions
• Neural pathways
  • Phrenic nerves → diaphragm; intercostal nerves → intercostals

Receptors & Reflexes

• Chemoreceptors
  • Central (medulla) sense CSF pH (reflects P{CO2})
  • Peripheral (aortic, carotid bodies) respond to blood H^+, P{CO2}, P{O2}
• Others: irritant receptors, baroreceptors (Hering–Breuer), proprioceptors
• Higher centers: hypothalamus (temperature), limbic (emotion), cortex (voluntary override)

Key Stimulus

• P{CO2} rise of 5\,mmHg → breathing rate doubles; P{O2} less sensitive (must fall to <60\,mmHg)
• Hypoxic drive: in chronic hypercapnia (e.g.
  emphysema) P{O2} becomes primary stimulus; supplemental O_2 can depress respiration

Airflow, Resistance & Compliance

• Airflow formula: F = \dfrac{\Delta P}{R}
  • \Delta P = P{atm} - P{alv} (pressure gradient)
  • R = resistance (airways, lung/chest elasticity, alveolar state)
• Factors ↑ R
  • ↓ chest wall elasticity (age, disease)
  • Bronchoconstriction or lumen occlusion (mucus, inflammation)
  • Alveolar collapse (surfactant deficiency)
• Compliance = ease of expansion; ↓ compliance → ↑ work (respiratory disorders may raise energy cost from 5 % to 25 % of total metabolism)

Gas Exchange Principles

Partial Pressures & Dalton’s Law

• P_{gas} = \text{Total pressure} \times \text{\% of gas}
• Each gas diffuses independently down its own gradient
• Alveolar gas differs from atmospheric due to dead space mixing, diffusion, humidity

Henry’s Law & Solubility

• Gas in liquid ∝ P_{gas} & solubility coefficient
• CO2 24× more soluble than O2; N_2 least soluble (requires high pressure to dissolve)
• Decompression sickness: rapid surfacing → N2 bubbles; treated with hyperbaric chambers (↑P{O_2})

Pulmonary Gas Exchange (External Respiration)

• Efficiency aided by huge surface area & thin membrane
• Ventilation–perfusion coupling: local control matches airflow (bronchioles) with blood flow (arterioles)
  • ↓ airflow → bronchoconstriction & arteriole constriction
  • ↑ airflow → bronchodilation & arteriole dilation

Tissue Gas Exchange (Internal Respiration)

• Systemic cells consume O2, produce CO2 → gradients drive diffusion opposite of lungs

Gas Transport in Blood

Oxygen

• 98 % bound to hemoglobin (HbO2); 2 % dissolved
• Saturation curve (sigmoid)
  • Cooperative binding; steep portion facilitates unloading in tissues
  • Sea-level arterial P{O2} = 104\,mmHg → 98 % saturation
  • Oxygen reserve: after systemic circuit at rest, Hb still 75 % saturated; provides margin for ↑ demand
• Influences on Hb-O2 affinity
  • ↑CO_2, ↑H^+ (Bohr effect), ↑temperature, 2,3-BPG → right shift (easier unloading)

Carbon Dioxide

• Transport forms
  1. Dissolved in plasma (7 %)
  2. Carbaminohemoglobin (23 %) – binds globin amino groups
  3. Bicarbonate in plasma (70 %)
  • In RBCs: CO2 + H2O \xrightarrow{carbonic\ anhydrase} H2CO3 \rightarrow H^+ + HCO_3^-
  • Chloride shift exchanges HCO_3^- with Cl^-

Hemoglobin as Multi-solute Carrier

• Binds O2 (iron), CO2 (globin), and H^+
• Binding of one modulates affinity for others (allosteric regulation)

Breathing & Homeostasis

• Normal set-point: 12–15 breaths/min, tidal volume ≈ 500\,mL

Hyperventilation

• Breathing > metabolic need → ↓P{CO2} (hypocapnia) & respiratory alkalosis
• Cerebral vasoconstriction → dizziness, paresthesias; prolonged → coma/death

Hypoventilation

• Bradypnea/hypopnea → ↑P{CO2} (hypercapnia) & ↓P{O2} (hypoxemia)
• Leads to respiratory acidosis, cyanosis, polycythemia; severe → convulsions/death

Exercise (Hyperpnea)

• Depth ↑, rate stable; proprioceptors, motor commands, and anticipation stimulate respiratory center
• Enhanced ventilation + cardiac output keeps arterial P{O2} & P{CO2} stable despite ↑ metabolism

Clinical Correlations Summary

• Asthma: reversible bronchoconstriction; immune hypersensitivity
• Emphysema: smoking-induced destruction of alveoli & elastic tissue → ↓ surface area & recoil
• Respiratory diseases (CHF, PE, cancer) impair diffusion, surface area, or V/Q matching → ↓P{O2}, ↑P{CO2}
• Hypoxic drive caution in chronic CO2 retainers; oxygen therapy must be titrated