1. Overview and Fundamental Steps of Respiration

Respiration is the metabolic and mechanical process by which living organisms take in oxygen (O₂) from the atmosphere to oxidize organic substrates (such as glucose) for cellular energy (ATP) production, and eliminate the metabolic waste product carbon dioxide (CO₂).

Figure: The Five Sequential Steps of Respiration. Atmospheric air is drawn into the lungs by pulmonary ventilation, oxygen diffuses into pulmonary capillary blood while carbon dioxide diffuses out (external respiration), the gases are carried through the systemic circulation, oxygen and carbon dioxide are exchanged with tissue cells (internal respiration), and finally oxygen is consumed intracellularly during cellular respiration to generate ATP, releasing CO₂ and H₂O as byproducts that re-enter the transport cycle.

1.1 The Five Sequential Steps of Respiration

• Step 1
  Pulmonary Ventilation
  (Breathing)

  The physical movement of air into (inspiration) and out of (expiration) the lungs to maintain alveolar gas composition.

• Step 2
  External (Pulmonary) Respiration

  The passive diffusion of O₂ from alveolar air into pulmonary capillary blood, and CO₂ from pulmonary capillary blood into alveolar air across the respiratory membrane.

• Step 3
  Transport of Respiratory Gases

  The systemic circulation of oxygenated blood from lungs to body tissues, and deoxygenated blood returning CO₂ from body tissues to the lungs.

• Step 4
  Internal (Tissue) Respiration

  The exchange of O₂ and CO₂ between systemic capillary blood and surrounding tissue cells via interstitial fluid diffusion.

• Step 5
  Cellular Respiration

  Intracellular enzymatic oxidation of metabolic substrates (e.g., glucose + 6 O₂ → 6 CO₂ + 6 H₂O + ATP) within cell mitochondria.

1.2 Gas Exchange: External vs. Internal Respiration

Although both external and internal respiration involve passive diffusion of O₂ and CO₂ down their concentration gradients, they occur at opposite ends of the transport pathway and move gases in opposite net directions relative to the blood.

Figure: Gas Exchange at the Lungs vs. at the Tissues. In external respiration, O₂ diffuses from the O₂-rich alveolar air into the CO₂-laden pulmonary capillary blood, while CO₂ diffuses the opposite way to be exhaled. In internal respiration, the now oxygenated systemic capillary blood releases O₂ into the metabolically active tissue cells, which in turn release CO₂ into the blood for transport back to the lungs.

1.3 Cellular Respiration: The Final Step

Cellular respiration is the intracellular endpoint of the entire process: within cell mitochondria, oxygen delivered by the blood is used to enzymatically oxidize metabolic substrates such as glucose, releasing chemical energy captured as ATP.

Figure: Cellular Respiration Reaction. Glucose and oxygen delivered by the transport system are oxidized within the mitochondria, yielding carbon dioxide, water, and ATP: glucose + 6 O₂ → 6 CO₂ + 6 H₂O + ATP. The CO₂ produced diffuses back into the blood, re-entering the transport cycle for elimination via external respiration.

2. Gross and Microscopic Anatomy of the Respiratory System

The human respiratory system comprises conducting airways and respiratory zones extending from the nasal cavity down to the terminal alveolar sacs.

Figure: Anatomy of the Respiratory Tract. Air travels sequentially through the nasal cavity, the three regions of the pharynx, the larynx, and the trachea, then branches through the bronchial tree (primary → secondary → tertiary bronchi → bronchioles → terminal bronchioles) which together make up the conducting zone. Beyond the terminal bronchioles, the respiratory zone begins with respiratory bronchioles, alveolar ducts, and alveolar sacs, where individual alveoli serve as the site of gas exchange.

2.1 The Upper Respiratory Tract

• Structure
  Nose & Nasal Cavity

  Air enters via paired external nares (nostrils). The lined nasal cavity warms, humidifies, and filters incoming air via pseudostratified ciliated columnar epithelium and mucus.

• Structure
  Pharynx (Throat)

  A muscular funnel connecting nasal and oral cavities to the larynx and esophagus.

  • Nasopharynx: Posterior to nasal cavity; strictly an air passageway.
  • Oropharynx: Lies posterior to oral cavity; common pathway for both air and swallowed food/liquid.
  • Laryngopharynx (Hypopharynx): Inferior region opening into the larynx anteriorly and esophagus posteriorly.
• Structure
  Larynx (Voice Box)

  Cartilaginous housing connecting pharynx to trachea.

  • Contains vocal cords (vocal folds) that vibrate during expiration to generate phonation.
  • Opening between vocal folds is termed the glottis.
  • Superior flap called the epiglottis (elastic cartilage) acts as a mechanical switch, leafing down during swallowing to seal off the larynx and prevent aspiration into the airways.
  • Composed of 9 pieces of cartilage (including thyroid cartilage, cricoid cartilage, and paired arytenoid cartilages).

Figure: Larynx Structure (Anterior View). The epiglottis attaches via the thyrohyoid membrane to the thyroid cartilage (the largest laryngeal cartilage, forming the Adam's apple), which connects via the cricothyroid ligament to the cricoid cartilage — the only complete cartilaginous ring in the airway — which in turn continues inferiorly as the C-shaped tracheal cartilages.

2.2 The Lower Respiratory Tract & Bronchial Tree

• Airway
  Trachea (Windpipe)

  Rigid tube extending downward and bifurcating at the level of the 5th thoracic vertebra (T₅) at the carina into right and left primary bronchi. Supported by incomplete C-shaped hyaline cartilaginous rings.

Bronchial Tree Architecture

• Order 1
  Primary (Main) Bronchi

  Right (wider, shorter, more vertical) and Left primary bronchi enter respective lung hilum.

• Order 2
  Secondary (Lobar) Bronchi

  Supply individual lung lobes (3 in right lung, 2 in left lung).

• Order 3
  Tertiary (Segmental) Bronchi

  Supply distinct bronchopulmonary segments.

• Order 4
  Bronchioles

  Tiny airways (<1 mm diameter) devoid of cartilage, supported by smooth muscle.

• Order 5
  Terminal Bronchioles

  End of the conducting zone.

• Order 6
  Respiratory Bronchioles

  Beginning of the respiratory zone, featuring individual outpocketing alveoli.

• Order 7
  Alveolar Ducts & Sacs

  Clusters of grape-like thin-walled sacs called alveoli.

Figure: Alveolus and Capillary Microanatomy. Deoxygenated blood entering via a branch of the pulmonary artery surrounds the alveolus in a dense capillary network. Because alveolar Po₂ (≈100 mmHg) exceeds capillary Po₂, O₂ diffuses into the blood, while because capillary Pco₂ exceeds alveolar Pco₂ (≈40 mmHg), CO₂ diffuses into the alveolar air space to be exhaled. Freshly oxygenated blood then exits via a branch of the pulmonary vein.

2.3 Lung Gross Anatomy and Pleural Membranes

• Organ
  Lungs

  Paired organs situated inside the thoracic cavity.

  • Right Lung: 3 lobes (Superior, Middle, Inferior), separated by horizontal and oblique fissures.
  • Left Lung: 2 lobes (Superior, Inferior), separated by an oblique fissure; features the cardiac notch.
• Membrane
  Pleural Sac & Membranes
  • Visceral Pleura: Inner serous layer adhering directly to the lung outer surface.
  • Parietal Pleura: Outer serous layer lining the inner thoracic wall and superior diaphragm surface.
  • Pleural Cavity: Fluid-filled potential space between visceral and parietal pleurae containing lubricating intrapleural fluid. Prevents friction and maintains mechanical coupling between chest wall and lungs.

Figure: Thoracic Cavity and Pleural Cavity. The lung is directly covered by the visceral pleura; the parietal pleura lines the inner surface of the ribcage and diaphragm. Between these two serous layers lies the fluid-filled intrapleural space, whose lubricating fluid prevents friction and mechanically couples the lung to the chest wall so that lung volume changes as the chest wall moves during breathing.

2.4 Pulmonary Blood Supply

• Circulation
  Pulmonary Circulation

  Pulmonary arteries carry deoxygenated blood from the right ventricle into lung capillary networks surrounding alveoli for gas exchange. Oxygenated blood leaves via 4 pulmonary veins to the left atrium.

• Circulation
  Bronchial Circulation

  Systemic arterial branches (bronchial arteries) providing oxygenated blood to nourish the structural tissues of the lungs and airways.

3. Mechanics of Breathing (Pulmonary Ventilation)

Ventilation operates on Boyle's Law, which states that the pressure of a gas in a closed container is inversely proportional to the volume of the container at constant temperature.

Figure: Inspiration vs. Expiration. During inspiration, contraction of the diaphragm and external intercostals actively increases thoracic volume, dropping intrapulmonary pressure below atmospheric so air flows in. During quiet expiration, these muscles relax and elastic recoil passively decreases thoracic volume, raising intrapulmonary pressure above atmospheric so air flows out — both processes continue until intrapulmonary pressure re-equilibrates with atmospheric pressure (760 mmHg).

3.1 Pressures Involved in Ventilation

• Pressure
  Atmospheric Pressure
  (P_atm)

  Pressure exerted by ambient air (760 mmHg at sea level).

• Pressure
  Intrapulmonary Pressure
  (P_pul, Intra-alveolar)

  Pressure inside the lung alveoli. Equilibrates to 760 mmHg between breaths.

  • Drops to 758 mmHg during inspiration.
  • Rises to 762 mmHg during expiration.
• Pressure
  Intrapleural Pressure
  (P_ip)

  Pressure within the pleural cavity. Always negative relative to P_pul (averages 756 mmHg at rest, i.e., −4 mmHg).

  • Drops further to 754 mmHg during inspiration as lungs stretch.
  • Returns to 756 mmHg during passive expiration.
• Pressure
  Transpulmonary Pressure
  (P_pul − P_ip)

  The transmural pressure gradient across the lung wall (760 − 756 = 4 mmHg) that prevents lung collapse.

Figure: Pressure Dynamics During Breathing. Intrapulmonary pressure oscillates a few mmHg on either side of atmospheric pressure (760 mmHg), driving airflow in and out of the lungs. Intrapleural pressure remains persistently below both, tracking the same rise and fall but offset by roughly 4 mmHg — the transpulmonary pressure that keeps the lung expanded against its own elastic recoil.

3.2 Mechanism of Inspiration

• Step 1
  Inspiratory Muscle Contraction
  • Diaphragm: Major muscle of quiet breathing (75% of volume change). Flattens downward upon contraction, increasing vertical thoracic dimensions.
  • External Intercostals: Elevate ribs and sternum upward and outward (bucket-handle and pump-handle mechanisms), expanding anteroposterior and lateral thoracic dimensions.
• Step 2
  Thoracic Cavity Expansion

  Thoracic cavity volume expands → parietal and visceral pleurae pull outward → intrapulmonary volume increases.

• Step 3
  Pressure Drop

  Intrapulmonary pressure drops below atmospheric pressure (758 mmHg).

• Step 4
  Airflow In

  Air rushes down the pressure gradient into alveoli until P_pul = P_atm (760 mmHg).

3.3 Mechanism of Expiration

• Passive
  Quiet Expiration
  • Inspiratory muscles relax; diaphragm ascends into its dome shape.
  • Elastic recoil of lung tissue and chest wall decreases thoracic volume.
  • Intrapulmonary volume decreases → intrapulmonary pressure rises above atmospheric (762 mmHg).
  • Air flows out of lungs down the pressure gradient until P_pul = 760 mmHg.
• Active
  Forced Expiration
  • Contraction of internal intercostals pulls ribcage down and inward.
  • Contraction of abdominal wall muscles forces abdominal viscera upward against the diaphragm, rapidly decreasing thoracic volume.

4. Respiratory Volumes, Capacities, and Spirometry

Lung volumes and capacities are measured using a spirometer, generating a visual tracking trace known as a spirogram.

Figure: Spirogram of Lung Volumes. During quiet resting breathing the trace oscillates gently around the tidal volume band. A maximal forced inspiration recruits the inspiratory reserve volume, driving the trace to its peak, while a subsequent maximal forced expiration recruits the expiratory reserve volume, driving the trace to its trough. Residual volume, the air that can never be exhaled, is never seen directly on the trace but is inferred from the floor beneath the ERV excursion.

4.1 Respiratory Volumes

• Volume
  Tidal Volume
  (TV)

  Volume of air inhaled or exhaled with each normal quiet breath (~500 mL).

  Minute Ventilation = 500 mL × 12–16 breaths/min = 6000–8000 mL/min
• Volume
  Inspiratory Reserve Volume
  (IRV)

  Maximum volume of air that can be forcibly inhaled beyond normal tidal inspiration (~3100 mL in males, ~1900 mL in females).

• Volume
  Expiratory Reserve Volume
  (ERV)

  Maximum volume of air that can be forcibly exhaled after a normal tidal expiration (~1000–1100 mL).

• Volume
  Residual Volume
  (RV)

  Volume of air remaining in lungs even after maximal forced expiration (~1100–1200 mL). Keeps alveoli patent.

• Volume
  Anatomic Dead Space

  Volume of conducting airways where no gas exchange occurs (~150 mL or ~30% of tidal volume).

  Alveolar Ventilation = (500 mL − 150 mL) × 12 breaths/min = 4200 mL/min

4.2 Respiratory Capacities

Each respiratory capacity is the sum of two or more respiratory volumes.

• Capacity
  Inspiratory Capacity
  (IC)

  Total air volume inspired after normal tidal expiration.

  IC = TV + IRV = 500 + 3100 = 3600 mL
• Capacity
  Expiratory Capacity
  (EC)

  Total air volume expired after normal tidal inspiration.

  EC = TV + ERV = 500 + 1100 = 1600 mL
• Capacity
  Functional Residual Capacity
  (FRC)

  Air volume remaining in lungs after normal tidal expiration.

  FRC = ERV + RV = 1100 + 1200 = 2300 mL
• Capacity
  Vital Capacity
  (VC)

  Maximum volume of air that can be forcibly expired after maximal forced inspiration.

  VC = TV + IRV + ERV = 500 + 3100 + 1100 = 4700 mL
• Capacity
  Total Lung Capacity
  (TLC)

  Total volume of air accommodated in lungs after maximal inspiration.

  TLC = VC + RV = TV + IRV + ERV + RV = 5900–6000 mL

Figure: How Respiratory Volumes Combine into Capacities. The four primary volumes (IRV, TV, ERV, RV) stack to fill total lung capacity. Any two or more adjacent volumes summed together define a capacity: inspiratory capacity (TV+IRV), expiratory capacity (TV+ERV), functional residual capacity (ERV+RV), vital capacity (TV+IRV+ERV, everything that can be voluntarily moved), and total lung capacity (all four volumes combined).

5. Gas Laws and Mechanisms of Gas Exchange

Gas exchange across pulmonary and tissue capillary beds is governed by physical gas laws acting down partial pressure gradients.

Figure: The Two Gas Laws Governing Respiration. Dalton's Law determines how much of the total atmospheric pressure is contributed by each individual gas (its partial pressure), while Henry's Law determines how much of that gas actually dissolves into the blood or interstitial fluid, based on its partial pressure and its solubility in the liquid.

5.1 Dalton's Law of Partial Pressures

The total pressure exerted by a mixture of non-reactive gases is the sum of the partial pressures exerted by each individual gas.

Calculation of atmospheric P_O₂ at sea level (760 mmHg):

• Gas
  Oxygen (O₂)

  Concentration = 21% (0.21)

  P_O₂ = 0.21 × 760 mmHg = 159.6 mmHg ≈ 160 mmHg
• Gas
  Nitrogen (N₂)

  Concentration = 78% (0.78)

  P_N₂ = 0.78 × 760 mmHg = 592.8 mmHg ≈ 593 mmHg
• Gas
  Carbon Dioxide (CO₂)

  Concentration = 0.04% (0.0004)

  P_CO₂ = 0.0004 × 760 mmHg = 0.3 mmHg

5.2 Henry's Law

The quantity of gas that dissolves in a liquid is directly proportional to the partial pressure of that gas and its specific liquid solubility coefficient.

CO₂ is roughly 20 times more soluble in plasma/water than O₂. Nitrogen has extremely low solubility.

Figure: Relative Solubility of Respiratory Gases. Although alveolar air contains far more N₂ and O₂ than CO₂, CO₂'s much higher solubility in plasma allows it to dissolve and diffuse efficiently despite its low partial pressure, while N₂'s negligible solubility keeps it essentially inert during normal gas exchange.

Figure: Partial Pressure Gradients Through the Body. Alveolar Po₂ and Pco₂ equilibrate with pulmonary capillary blood during external respiration; that oxygenated blood is carried unchanged as systemic arterial blood to the tissues. During internal respiration, tissues (with lower Po₂ and higher Pco₂ from ongoing metabolism) exchange gases with the capillary blood, producing venous blood with Po₂ ≈ 40 mmHg and Pco₂ ≈ 46 mmHg, which then returns to the lungs to repeat the cycle.

5.3 Partial Pressures Summary Table

Summary of O₂ and CO₂ partial pressures (in mmHg) at each stage of the respiratory and circulatory pathway.

6. Transport of Oxygen in Blood

Oxygen is poorly soluble in water; 100 mL of blood plasma dissolves only 0.3 mL of O₂.

6.1 Oxygen Transport Forms

• Form
  Dissolved in Plasma

  ≈1.5% of total oxygen.

• Form
  Bound to Hemoglobin (Hb)

  ≈98.5% carried as oxyhemoglobin (HbO₂) inside Red Blood Cells (RBCs).

6.2 Structural Types of Human Hemoglobin

Hemoglobin is a tetrameric protein containing 4 globin polypeptide chains, each conjugated to an iron-containing (Fe²⁺) heme group.

6.3 Oxygen-Hemoglobin Dissociation Curve

A plot of percent hemoglobin saturation versus P_O₂ yields a characteristic S-shaped (sigmoidal) curve due to cooperative binding — binding of the first O₂ molecule changes Hb conformation, increasing affinity for subsequent O₂ molecules.

Figure: Oxygen-Hemoglobin Dissociation Curve. The sigmoidal shape reflects cooperative binding among the four heme sites. The flat alveolar plateau (Po₂ 80–100 mmHg) means hemoglobin stays well-saturated despite altitude-related drops in alveolar Po₂, while the steep middle portion (around Po₂ 40 mmHg, typical of resting tissue) allows large amounts of O₂ to be released for only a small drop in Po₂.

Figure: Factors Shifting the Oxygen-Hemoglobin Dissociation Curve. A left shift increases hemoglobin's affinity for O₂, favoring loading in the lungs; a right shift decreases affinity, favoring unloading in metabolically active tissues.

6.4 Physiological Modulators of Affinity

• Modulator
  The Bohr Effect
  (pH and P_CO₂)

  Decreased blood pH (acidosis) or increased P_CO₂ shifts the dissociation curve to the RIGHT. H⁺ ions bind globin chains, stabilizing the deoxygenated state and promoting O₂ unloading in active tissues.

• Modulator
  2,3-Bisphosphoglycerate
  (2,3-BPG)

  An intermediate of RBC glycolysis. BPG binds deoxygenated β-chains, shifting the curve to the RIGHT to facilitate O₂ release.

• Modulator
  Fetal Hemoglobin
  (HbF)

  γ-chains of HbF do not bind BPG efficiently. Consequently, HbF displays a LEFT-shifted curve compared to adult HbA, enabling oxygen transfer across the placenta from maternal to fetal blood.

7. Transport of Carbon Dioxide in Blood

Carbon dioxide is carried in arterial and venous blood via three distinct physiological mechanisms.

Figure: Relative Proportions of CO₂ Transport Mechanisms. The majority of CO₂ is converted to bicarbonate ions inside red blood cells; smaller fractions bind directly to hemoglobin or remain physically dissolved in plasma.

7.1 Mechanisms of CO₂ Transport

• ≈7%
  Dissolved in Plasma

  Physically dissolved gas carried in plasma solution.

• ≈23%
  Carbamino Compounds

  CO₂ combines directly with terminal amino groups of globin proteins inside RBCs, forming carbaminohemoglobin (HbCO₂).

• ≈70%
  Bicarbonate Ions
  (HCO₃⁻)

  CO₂ reacts with H₂O inside RBCs, catalyzed by the rapid enzyme Carbonic Anhydrase (CA).

7.2 The Chloride Shift (Hamburger Phenomenon)

At the systemic tissue level, as HCO₃⁻ accumulates rapidly inside RBCs, it exits down its concentration gradient into plasma via an anion exchange antiport protein (Band 3). To maintain electrical neutrality across the RBC membrane, chloride ions (Cl⁻) move from plasma into the RBC cytosol. This process reverses completely in pulmonary capillaries.

Figure: The Chloride Shift (Hamburger Phenomenon). Inside the RBC, CO₂ combines with H₂O (catalyzed by carbonic anhydrase) to form carbonic acid, which dissociates into H⁺ and HCO₃⁻. HCO₃⁻ exits the RBC into plasma via the Band 3 antiporter, while Cl⁻ simultaneously enters the RBC to preserve electrical neutrality. This exchange reverses in the pulmonary capillaries.

7.3 The Haldane Effect

The degree of CO₂ loading into blood is inversely dependent on the oxygenation state of hemoglobin. Deoxygenation of blood increases its capacity to carry CO₂ (and vice versa). In pulmonary capillaries, high O₂ loading promotes CO₂ displacement from Hb.

7.4 Summary Table of Key Respiratory Terminology

8. Neural and Chemical Control of Respiration

Breathing is an involuntary rhythmic process generated and coordinated by neurons in the brainstem, which set the basic rate and depth of ventilation and continuously adjust it in response to chemical signals from the blood and cerebrospinal fluid.

Figure: Brainstem Respiratory Control Centers. The medulla oblongata contains the neurons that generate the basic breathing rhythm (DRG, VRG), while the pons refines and smooths the transition between inspiration and expiration (Pneumotaxic and Apneustic centers).

8.1 Medullary Respiratory Centers

• Center
  Dorsal Respiratory Group (DRG)

  Contains primarily inspiratory neurons; generates the basic rhythm of quiet breathing by firing in a repeating cyclical pattern that drives the diaphragm and external intercostals.

• Center
  Ventral Respiratory Group (VRG)

  Contains both inspiratory and expiratory neurons; largely inactive during quiet breathing but becomes active during forced (active) breathing, driving accessory muscles for both forced inspiration and forced expiration.

8.2 Pontine Respiratory Centers

• Center
  Pneumotaxic Center

  Sends inhibitory signals to the DRG to limit inspiration, helping to fine-tune respiratory rate and prevent overinflation of the lungs; a stronger pneumotaxic signal produces faster, shallower breaths.

• Center
  Apneustic Center

  Sends stimulatory signals that prolong inspiration and delay expiration, promoting deep, sustained inhalation; normally held in check by the pneumotaxic center.

8.3 Chemoreceptor Control Mechanisms

Chemoreceptors continuously monitor blood and cerebrospinal fluid chemistry and relay signals to the DRG, which adjusts the rate and depth of breathing to maintain homeostatic Po₂, Pco₂, and pH.

Figure: Chemoreceptor Feedback Loop. Central chemoreceptors respond primarily to CO₂-driven changes in CSF pH, while peripheral chemoreceptors respond directly to arterial Po₂, Pco₂, and pH; both converge on the DRG, which adjusts minute ventilation to restore homeostasis.

• Receptor
  Central Chemoreceptors

  Located on the surface of the medulla oblongata; separated from arterial blood by the blood-brain barrier, which is freely permeable to CO₂ but not to H⁺ or HCO₃⁻.

  • CO₂ diffuses from blood into the CSF, where it combines with H₂O to form carbonic acid, which dissociates into H⁺ and HCO₃⁻.
  • Rising H⁺ directly stimulates the chemoreceptors, increasing ventilation.
  • This is the single most powerful drive for ventilation under normal physiological conditions.
• Receptor
  Peripheral Chemoreceptors

  Located in the carotid bodies (at the carotid artery bifurcation) and aortic bodies (along the aortic arch); directly exposed to arterial blood.

  • Detect changes in arterial Po₂, Pco₂, and pH.
  • Become the dominant stimulus for ventilation when arterial Po₂ falls substantially (severe hypoxia, e.g., high altitude), since the central chemoreceptors cannot directly sense O₂ levels.
  • Also respond rapidly to acute changes in blood pH independent of CO₂ (e.g., metabolic acidosis).

9. Pathophysiology and Disorders of the Respiratory System

Disruption of normal ventilation, gas exchange, or airway patency underlies a wide range of clinically significant respiratory disorders, broadly grouped into obstructive diseases and infections of the respiratory tract.

Figure: COPD Subtypes. COPD is an umbrella term encompassing chronic bronchitis (airway-centered inflammation and mucus obstruction) and emphysema (alveolar wall destruction and loss of elastic recoil); most patients show overlapping features of both.

9.1 Chronic Obstructive Pulmonary Disease (COPD)

• Disorder
  Asthma

  Chronic inflammatory disorder causing reversible bronchospasm, bronchial hyperresponsiveness, and airway edema, often triggered by allergens, exercise, or irritants; presents with wheezing, coughing, and dyspnea during acute exacerbations.

• Disorder
  Emphysema

  Irreversible destruction of alveolar walls and the pulmonary capillary bed, causing the fusion of adjacent alveoli into fewer, larger air spaces with markedly reduced surface area for gas exchange and loss of the elastic recoil needed to passively empty the lungs; strongly linked to cigarette smoking.

• Disorder
  Chronic Bronchitis

  Persistent inflammation of the bronchi with excessive mucus production, defined clinically by a productive cough on most days for at least three months in at least two consecutive years; the excess mucus and airway swelling narrow the airway lumen and obstruct airflow.

9.2 Respiratory Infections

• Infection
  Acute Bronchitis

  Short-term inflammation of the bronchial airways, most commonly caused by viral infection; produces cough (often productive), chest discomfort, and mild dyspnea that typically resolves within one to three weeks.

• Infection
  Pneumonia

  Infection (bacterial, viral, or fungal) of the lung parenchyma causing inflammation and fluid or pus accumulation within the alveoli, which impairs gas exchange; presents with fever, productive cough, pleuritic chest pain, and dyspnea.

• Infection
  Tuberculosis (TB)

  Chronic granulomatous infection caused by Mycobacterium tuberculosis, most often affecting the lungs; can remain latent for years before reactivating to cause progressive tissue destruction, cavitation, chronic cough, hemoptysis, weight loss, and night sweats.