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🫁 A&P II · Respiratory System

Memory tricks for breathing, gas exchange, and O₂ transport

Respiratory anatomy, pulmonary ventilation, gas exchange at the alveoli and tissues, oxygen and CO₂ transport in blood, lung volumes, and acid-base balance — these memory tricks unite the anatomy and physiology of every breath you take.

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🫁 Respiratory System

Memory Tricks

Proven Mnemonics & Acronyms — fast to learn, hard to forget.

Respiratory Anatomy
NPTLB → Alveoli — Nose · Pharynx · Trachea · Bronchi · Lungs
Conducting zone (no gas exchange) → Respiratory zone (gas exchange at alveoli)
Upper and lower respiratory tract — conducting zone vs respiratory zone
Conducting zone: nose → nasal cavity → pharynx → larynx → trachea → primary bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi → bronchioles → terminal bronchioles. Functions: warm, humidify, filter air. No gas exchange. Respiratory zone: respiratory bronchioles → alveolar ducts → alveolar sacs → alveoli. Gas exchange occurs here. ~300 million alveoli in adult lungs — massive surface area (~70 m²). Alveolar walls: Type I pneumocytes (thin, gas exchange), Type II pneumocytes (produce surfactant). Surfactant: reduces surface tension — prevents alveolar collapse on expiration. Respiratory distress syndrome in premature infants = surfactant deficiency.
Trachea
C-shaped cartilage rings (open posteriorly). Carina = where it splits into bronchi (cough reflex).
Type I pneumocytes
95% of alveolar surface. Thin squamous cells — gas exchange. Cannot divide.
Type II pneumocytes
5% of surface. Cuboidal. Produce surfactant. Can divide to replace Type I.
Surfactant
Phospholipid (DPPC). Reduces surface tension. Premature birth → RDS → CPAP or surfactant therapy.
Difficulty: Intermediate
Breathing Mechanics
Boyle's Law — Volume UP = Pressure DOWN = Air IN · Volume DOWN = Pressure UP = Air OUT
Inspiration: diaphragm contracts → thorax expands → pressure drops → air flows in
How breathing works — Boyle's Law drives every breath
Breathing follows Boyle's Law: pressure and volume are inversely proportional (at constant temperature). Inspiration (active): diaphragm contracts (flattens) + external intercostals contract → thoracic volume increases → intrapulmonary pressure drops below atmospheric (~758 mmHg) → air flows in. Forced inspiration adds scalene and sternocleidomastoid muscles. Expiration (passive at rest): diaphragm and intercostals relax → thoracic volume decreases → intrapulmonary pressure rises above atmospheric → air flows out. Forced expiration: internal intercostals + abdominal muscles contract. Intrapleural pressure: always slightly negative (−4 to −8 mmHg) — keeps lungs expanded against thoracic wall. Pneumothorax: air enters pleural space → lungs collapse.
Diaphragm
Primary breathing muscle. Innervated by phrenic nerve (C3-C5). "C3-4-5 keeps you alive."
Intrapleural pressure
Always negative (−4 to −8 mmHg). Prevents lung collapse. Pleural fluid surface tension.
Pneumothorax
Air in pleural space → intrapleural pressure equalizes → lung collapses. Tension = medical emergency.
Compliance
Lung stretchability. ↓ compliance (fibrosis) = harder to breathe in. ↑ compliance (emphysema) = hard to breathe out.
Difficulty: Intermediate
Lung Volumes
TVIR — Tidal · Inspiratory reserve · Expiratory reserve · Residual
Four lung volumes that combine into four capacities — know TLC and VC
Lung volumes and capacities — what a spirometer measures and why it matters
Tidal volume (TV): ~500 mL — air moved in one normal breath. Inspiratory reserve volume (IRV): ~3000 mL — extra air inhaled beyond TV with max effort. Expiratory reserve volume (ERV): ~1200 mL — extra air exhaled beyond TV with max effort. Residual volume (RV): ~1200 mL — air left after max exhalation — cannot be expelled. Capacities (sum of volumes): Vital capacity (VC) = TV + IRV + ERV = ~4700 mL — maximum usable range. Total lung capacity (TLC) = VC + RV = ~5900 mL. Functional residual capacity (FRC) = ERV + RV. Inspiratory capacity = TV + IRV. RV cannot be measured by spirometry — requires body plethysmography or helium dilution.
Tidal volume
~500 mL. Normal quiet breathing. Dead space ~150 mL (conducting zone).
Vital capacity
TV + IRV + ERV. ~4700 mL. Reduced in restrictive diseases (fibrosis), preserved in obstructive.
FEV1/FVC ratio
Forced expiratory volume in 1 sec / forced vital capacity. Normal >70%. Obstructive = low ratio. Restrictive = normal ratio, low FVC.
Dead space
~150 mL anatomical dead space (conducting zone — no gas exchange). Alveolar dead space in disease.
Difficulty: Intermediate
Gas Exchange
Dalton's Law — each gas exerts its own partial pressure · diffuse from HIGH to LOW
O₂ diffuses into blood at lungs · CO₂ diffuses out · Opposite at tissues
Pulmonary and tissue gas exchange — partial pressures drive diffusion
Gas exchange follows Dalton's Law (partial pressures) and Fick's Law (diffusion rate). Atmospheric air: PO₂ = 159 mmHg, PCO₂ = 0.3 mmHg. Alveolar air: PO₂ = 104 mmHg, PCO₂ = 40 mmHg. Pulmonary capillary blood arriving: PO₂ = 40 mmHg, PCO₂ = 45 mmHg. Result: O₂ diffuses from alveoli (104) into blood (40). CO₂ diffuses from blood (45) into alveoli (40). Blood leaving lungs: PO₂ = 100 mmHg, PCO₂ = 40 mmHg. Tissue gas exchange (opposite): tissues have low PO₂ (~40) and high PCO₂ (~45) → O₂ leaves blood → CO₂ enters blood. Fick's law: rate ∝ surface area × concentration difference ÷ membrane thickness.
Dalton's Law
Total pressure = sum of partial pressures. PO₂ in atmosphere = 0.21 × 760 = 159 mmHg.
Alveolar PO₂
104 mmHg — lower than atmospheric because alveolar air is humidified and mixed with CO₂.
Fick's Law
↑ surface area, ↑ concentration gradient, ↓ membrane thickness → faster diffusion.
V/Q mismatch
Ventilation/perfusion mismatch → poor gas exchange. PE = perfusion without ventilation (dead space).
Difficulty: Advanced
Oxygen Transport
98.5% bound to Hb · 1.5% dissolved · Hb carries 4 O₂ · sigmoid curve
Hemoglobin (Hb) is the O₂ carrier — oxyhemoglobin dissociation curve shows loading and unloading
How oxygen is carried in blood — and what shifts the Hb-O₂ curve
Oxygen transport: 98.5% bound to hemoglobin (oxyhemoglobin), 1.5% dissolved in plasma. Each Hb molecule has 4 heme groups → binds 4 O₂. Cooperative binding: first O₂ makes subsequent binding easier → sigmoid (S-shaped) dissociation curve. Oxygen saturation (SpO₂): measured by pulse oximeter. Normal >95%. Right shift (decreased O₂ affinity — releases O₂ more readily at tissues): ↑ temperature, ↑ CO₂, ↑ H+ (↓ pH), ↑ 2,3-DPG (Bohr effect). Exercise shifts right → more O₂ delivered to muscles. Left shift (increased O₂ affinity — holds O₂ more tightly): ↓ temperature, ↓ CO₂, ↓ H+, fetal Hb (HbF). CO poisoning: CO binds Hb 200× tighter than O₂ → shifts curve left → tissues can't get O₂.
Right shift
↑ temp, ↑ CO₂, ↑ H+, ↑ 2,3-DPG → Hb releases O₂ more easily. Exercise effect.
Bohr effect
↑ CO₂ / ↓ pH → right shift → Hb unloads O₂ at active tissues. Muscle benefits.
Fetal Hb (HbF)
Left shift — higher O₂ affinity than adult Hb. Steals O₂ from maternal blood across placenta.
CO poisoning
200× affinity for Hb. SpO₂ reads normal (false!). Treat with 100% O₂ or hyperbaric O₂.
Difficulty: Advanced
CO₂ Transport
70% as bicarbonate · 23% bound to Hb · 7% dissolved — chloride shift balances
CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻ — carbonic anhydrase in RBCs
Three ways CO₂ travels in blood — and the chloride shift explained
CO₂ is transported three ways: 70% as bicarbonate (HCO₃⁻): CO₂ enters RBC → carbonic anhydrase (CA) converts CO₂ + H₂O → H₂CO₃ → H⁺ + HCO₃⁻. H⁺ buffered by Hb. HCO₃⁻ exits RBC → Cl⁻ enters (chloride shift = Hamburger phenomenon — maintains electroneutrality). 23% as carbaminohemoglobin: CO₂ binds to amino groups of Hb (not heme). 7% dissolved in plasma. At lungs: process reverses — bicarbonate re-enters RBC → CA converts back to CO₂ → exhaled. H⁺ released → picked up by Hb → Bohr effect promotes O₂ release at tissues. Haldane effect: oxygenation of Hb reduces its CO₂-carrying capacity — promotes CO₂ unloading at lungs.
Carbonic anhydrase
In RBCs — catalyzes CO₂ + H₂O ↔ H₂CO₃. Acetazolamide inhibits it → altitude sickness treatment.
Chloride shift
HCO₃⁻ exits RBC → Cl⁻ enters. Maintains electrochemical balance. Hamburger phenomenon.
Haldane effect
Oxygenated Hb carries less CO₂. At lungs: O₂ loading → CO₂ unloading enhanced.
Carbaminohemoglobin
CO₂ + Hb amino groups (not heme). Accounts for 23% of CO₂ transport.
Difficulty: Advanced
Control of Breathing
CO₂ is the main driver — not O₂ · Central chemoreceptors sense pH · Peripheral sense O₂
Medullary respiratory centers + chemoreceptors control rate and depth of breathing
What controls breathing — the surprising answer is CO₂, not O₂
Respiratory centers in medulla oblongata: dorsal respiratory group (DRG) — rhythmic inspiration, ventral respiratory group (VRG) — forced breathing. Pontine centers: pneumotaxic (limits inspiration duration) and apneustic centers. Chemoreceptors control breathing: Central chemoreceptors (medulla): respond to H⁺ in CSF — CO₂ crosses BBB → reacts with water → H⁺ → stimulates breathing. Most powerful drive for breathing. Peripheral chemoreceptors (carotid and aortic bodies): respond to ↓ PO₂ (<60 mmHg), ↑ PCO₂, ↑ H⁺. O₂ drive only kicks in when PO₂ drops severely. COPD hypoxic drive: some COPD patients rely on low O₂ as breathing stimulus — giving high-flow O₂ can suppress breathing.
CO₂ = main driver
Even small ↑ PCO₂ → ↑ breathing rate. Normal PCO₂ = 40 mmHg. Very tightly regulated.
Central chemoreceptors
In medulla — respond to CSF pH (not directly CO₂). Most powerful respiratory stimulus.
Peripheral chemoreceptors
Carotid and aortic bodies — sense ↓ PO₂, ↑ PCO₂, ↑ H⁺. O₂ only matters below 60 mmHg.
Hering-Breuer reflex
Lung stretch receptors → inhibit inspiration when lungs fully inflated. Prevents overinflation.
Difficulty: Intermediate
Respiratory Acid-Base
CO₂ = respiratory acid · HCO₃⁻ = metabolic base · pH 7.35–7.45
Respiratory acidosis (↑CO₂) · Respiratory alkalosis (↓CO₂) · Compensated by kidneys
Four acid-base disorders — respiratory vs metabolic and compensation
CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻. CO₂ is the respiratory acid — lungs control it. HCO₃⁻ is the metabolic base — kidneys control it. Respiratory acidosis: ↑ CO₂ (hypoventilation, COPD, pneumonia) → ↓ pH. Kidneys compensate: retain HCO₃⁻. Respiratory alkalosis: ↓ CO₂ (hyperventilation, anxiety, altitude) → ↑ pH. Kidneys compensate: excrete HCO₃⁻. Metabolic acidosis: ↓ HCO₃⁻ (diabetic ketoacidosis, renal failure) → ↓ pH. Lungs compensate: hyperventilate (Kussmaul breathing) → blow off CO₂. Metabolic alkalosis: ↑ HCO₃⁻ (vomiting, antacid overuse) → ↑ pH. Lungs compensate: hypoventilate → retain CO₂.
Respiratory acidosis
↑ CO₂, ↓ pH. COPD, sleep apnea, opioids. Renal compensation: retain HCO₃⁻.
Respiratory alkalosis
↓ CO₂, ↑ pH. Hyperventilation, anxiety, altitude. Renal compensation: excrete HCO₃⁻.
Metabolic acidosis
↓ HCO₃⁻, ↓ pH. DKA, renal failure, lactic acidosis. Kussmaul breathing compensates.
Metabolic alkalosis
↑ HCO₃⁻, ↑ pH. Vomiting, diuretics. Hypoventilation compensates.
Difficulty: Advanced
Obstructive vs Restrictive
Obstructive = flow out blocked · Restrictive = can't expand fully
Obstructive (↓ FEV1/FVC) · Restrictive (↓ TLC, normal or ↑ FEV1/FVC ratio)
Two categories of lung disease — how spirometry tells them apart
Obstructive lung diseases: airflow OUT is obstructed — airways narrow. FEV1 markedly reduced, FVC relatively preserved → FEV1/FVC ratio less than 70%. TLC increased (air trapping). Examples: asthma (reversible bronchospasm — treat with bronchodilators), COPD/emphysema (irreversible — alveolar destruction, loss of elastic recoil), chronic bronchitis (hypersecretion, Blue Bloater), cystic fibrosis. Restrictive lung diseases: lungs cannot fully expand — small volumes. FVC and TLC reduced, but FEV1/FVC ratio normal or increased. Examples: pulmonary fibrosis (stiff lungs), sarcoidosis, obesity, neuromuscular disease (can't generate force), pleural effusion, pneumothorax. Pink Puffer (emphysema) vs Blue Bloater (chronic bronchitis) distinction.
FEV1/FVC ratio
Key spirometry ratio. Normal >70%. Obstructive <70%. Restrictive = normal or high ratio.
Pink Puffer
Emphysema — thin, pursed-lip breathing, barrel chest, hyperinflated. Maintaining O₂ with effort.
Blue Bloater
Chronic bronchitis — overweight, cyanotic, productive cough, hypoxic. Right heart failure risk.
Asthma
Reversible bronchospasm. Treat: short-acting β2 agonist (albuterol) + inhaled corticosteroids.
Difficulty: Intermediate
🎓 Common Exam Questions
Q: Explain ventilation-perfusion matching and how it affects gas exchange.
A: Ideal V/Q = 1.0. Normal lung has gradient: apex V/Q ~3 (over-ventilated relative to perfusion); base V/Q ~0.6 (over-perfused relative to ventilation). Lung disease extremes: Dead space (V/Q → ∞): ventilated alveoli not perfused — wasted ventilation. Arterial pCO2 may be normal (other alveoli compensate), pO2 low. Example: PE. Shunt (V/Q → 0): perfused alveoli not ventilated — venous blood bypasses oxygenation. Causes hypoxemia not correctable by 100% O2. Examples: atelectasis, pneumonia, ARDS, intracardiac shunts. Clinical: PE → increase dead space → hypoxemia + low pCO2 (hyperventilating to compensate). COPD → low V/Q regions → hypoxemia + high pCO2 (cannot compensate due to airway obstruction).
Q: What are the lung volumes and capacities and which cannot be measured by spirometry?
A: Volumes (cannot overlap): TV (tidal volume, ~500mL) — normal breath. IRV (inspiratory reserve volume, ~3000mL) — extra air after normal inspiration. ERV (expiratory reserve volume, ~1200mL) — extra air after normal expiration. RV (residual volume, ~1200mL) — air remaining after maximal exhalation. Capacities (sum of volumes): TLC = TV + IRV + ERV + RV = ~6000mL. VC = TV + IRV + ERV = ~4800mL. IC = TV + IRV. FRC = ERV + RV = ~2400mL (lung volume at rest). FRC and RV cannot be measured by spirometry (contain RV) — require helium dilution or body plethysmography. Clinical: Obstructive disease → increased RV, FRC, TLC (air trapping). Restrictive disease → decreased all volumes, TLC most affected.
Q: How is CO2 transported in the blood?
A: Three forms: (1) Dissolved in plasma (7%) — drives diffusion. (2) Carbaminohemoglobin (23%) — CO2 binds to globin chains of Hgb (different site from O2). (3) Bicarbonate (70%) — CO2 + H2O → H2CO3 → H+ + HCO3- (catalyzed by carbonic anhydrase in RBCs). H+ buffered by Hgb; HCO3- exits RBC via chloride shift (Cl- enters). In the lungs: process reverses — HCO3- re-enters RBC, combines with H+ to form CO2 → exhaled. Haldane effect: deoxygenated Hgb carries more CO2 (both carbamino and as bicarbonate — deoxyHgb is better buffer). Bohr effect (opposite): increased CO2 → decreased O2 affinity of Hgb → O2 released to tissues.
Q: What is the control of breathing and what happens in COPD hypoxic drive?
A: Central chemoreceptors (medulla): respond to CSF pH changes caused by CO2 diffusion. Primary driver of breathing. Peripheral chemoreceptors (carotid and aortic bodies): respond to pO2 (<60mmHg), pCO2, and pH. Only ones sensitive to hypoxia. Normal drive: CO2 rise → pH falls → medullary chemoreceptors → increased ventilation → CO2 normalizes. COPD and hypoxic drive myth: Chronic CO2 retainers reset central chemoreceptors — pCO2 chronically high, so chemoreceptors reset to higher set point. Peripheral chemoreceptors then become more important but are not the 'only drive.' High-flow O2 in COPD causes hypercarbia mainly due to: Haldane effect (O2 displaces CO2 from Hgb) and V/Q mismatch worsening (hypoxic pulmonary vasoconstriction lost). Clinical: target SpO2 88-92% in COPD, not 100%.
Q: What is ARDS and what are the Berlin criteria?
A: Acute Respiratory Distress Syndrome: diffuse alveolar damage causing severe hypoxemia. Berlin criteria (2012): (1) Acute onset within 1 week of known clinical insult. (2) Bilateral opacities on CXR/CT not fully explained by effusions, atelectasis, or nodules. (3) Respiratory failure not fully explained by cardiac failure or fluid overload. (4) PaO2/FiO2 ratio: Mild 201-300, Moderate 101-200, Severe ≤100 (on PEEP ≥5). Pathophysiology: neutrophil-mediated injury → capillary leak → protein-rich fluid in alveoli → surfactant dysfunction → diffuse atelectasis → shunt → refractory hypoxemia. Causes: sepsis (most common), aspiration pneumonia, trauma, transfusion (TRALI), pancreatitis. Treatment: lung-protective ventilation (low tidal volume 6 mL/kg ideal body weight, PEEP), prone positioning for severe ARDS, treat underlying cause.