From the nasal cavity to the alveoli — the respiratory system's anatomy determines how air moves, where gas exchange occurs, and how the lungs are structured. These memory tricks help you navigate the airways from top to bottom.
How many lobes each lung has — and why they differ
The right lung has 3 lobes (upper, middle, lower) separated by the horizontal and oblique fissures. The left lung has only 2 lobes (upper and lower) separated by the oblique fissure — because the heart occupies space on the left side. The left lung has a cardiac notch and the lingula (corresponds to the right middle lobe). The right lung is larger and heavier. Memory trick: Right has 3 letters in "right" — 3 lobes. Left has 4 letters — but only 2 lobes (the heart took one!).
Tongue-like projection of left upper lobe — corresponds to right middle lobe.
Clinical
Right middle lobe syndrome — most common atelectasis site (narrow bronchus).
Gas Exchange
O2 in · CO2 out — Dalton's Law drives it all
Partial pressure gradient determines direction of gas diffusion
How gas exchange works at the alveoli — driven by pressure gradients
Gas exchange (external respiration) occurs at the alveolar-capillary membrane — only 0.5 micrometers thick. Gases move from high to low partial pressure. O2 partial pressure in alveoli (104 mmHg) is higher than in capillary blood (40 mmHg) — so O2 diffuses into blood. CO2 partial pressure in capillary blood (45 mmHg) is higher than in alveoli (40 mmHg) — so CO2 diffuses into alveoli. CO2 diffuses 20× faster than O2 across membranes.
Primary and accessory muscles of breathing — and when each is used
The diaphragm does 75% of the work during quiet breathing — it contracts and flattens, increasing thoracic volume. External intercostals elevate ribs during inspiration. During forced inspiration, accessory muscles kick in: SCM (sternocleidomastoid), scalenes, pectoralis minor. Forced expiration uses internal intercostals and abdominals — quiet expiration is passive (elastic recoil). Using accessory muscles at rest is a sign of respiratory distress.
Diaphragm
75% of breathing work — C3-C5 innervation (phrenic nerve). "C3,4,5 keeps you alive."
External intercostals
Elevate ribs — assist inspiration.
SCM + scalenes
Accessory muscles — only active in forced inspiration or distress.
Quiet expiration
Passive — elastic recoil of lungs. No muscles needed.
Forced expiration
Internal intercostals + abdominals — coughing, exercise, playing instruments.
Key lung volume measurements — what each one means
Tidal Volume (TV): air moved in one normal breath = ~500 mL. Inspiratory Reserve Volume (IRV): extra air you can inhale after normal breath = ~3000 mL. Expiratory Reserve Volume (ERV): extra air you can exhale after normal breath = ~1200 mL. Residual Volume (RV): air remaining after maximum exhalation = ~1200 mL (cannot be measured by spirometry). Vital Capacity = TV + IRV + ERV = ~4700 mL. Total Lung Capacity = VC + RV = ~5900 mL.
Tidal Volume
~500 mL — normal quiet breathing.
IRV
~3000 mL — extra you can breathe IN after normal breath.
ERV
~1200 mL — extra you can breathe OUT after normal breath.
Residual Volume
~1200 mL — always remains. Cannot be measured by spirometry.
Vital Capacity
TV + IRV + ERV = ~4700 mL. Reduced in restrictive disease.
Obstructive vs Restrictive
Obstructive = Can't get air OUT · Restrictive = Can't get air IN
Asthma · COPD · Emphysema vs Fibrosis · Sarcoidosis
Two categories of lung disease — opposite problems, different spirometry patterns
Obstructive diseases narrow the airways — air gets trapped. FEV1/FVC ratio is LOW (can't exhale fast enough). Examples: asthma, COPD, emphysema, chronic bronchitis. Restrictive diseases stiffen the lungs or chest wall — lungs can't expand fully. Total lung capacity is LOW. FEV1/FVC ratio is normal or HIGH. Examples: pulmonary fibrosis, sarcoidosis, pneumonia, obesity. Key test: FEV1/FVC ratio. Below 0.7 = obstructive.
Obstructive
Airway narrowing — air trapping. FEV1/FVC <0.7. Asthma, COPD, emphysema.
Restrictive
Reduced lung expansion — low TLC. Normal FEV1/FVC. Fibrosis, sarcoidosis.
FEV1
Forced expiratory volume in 1 second — key measure of airway obstruction.
FVC
Forced vital capacity — total air forcefully exhaled.
Two pleural layers and what happens when they fail
Visceral pleura covers the lung surface directly. Parietal pleura lines the thoracic wall, diaphragm, and mediastinum. Between them is the pleural cavity containing a thin film of pleural fluid — reduces friction during breathing. Pneumothorax = air enters pleural cavity — lung collapses. Pleural effusion = excess fluid in pleural cavity. Tension pneumothorax = one-way valve effect — air accumulates, shifts mediastinum — medical emergency.
Visceral pleura
Directly on lung — no pain fibers (lung itself doesn't hurt).
Parietal pleura
Lines thoracic wall — HAS pain fibers (pleurisy is painful).
Pneumothorax
Air in pleural space — lung collapses. Trachea deviates TOWARD affected side.
Tension pneumothorax
Emergency — trachea deviates AWAY from affected side. Needle decompression.
How breathing regulates blood pH — the fastest buffer system
CO2 dissolves in blood to form carbonic acid (H2CO3), which dissociates into H+ and bicarbonate. More CO2 = more H+ = lower pH (acidosis). The respiratory system is the fastest pH regulator — changes in breathing rate change CO2 levels within minutes. Hyperventilation = blows off CO2 = respiratory alkalosis. Hypoventilation = retains CO2 = respiratory acidosis. Chemoreceptors detect CO2/H+ and signal the medulla to adjust breathing rate.
Medulla — detect CO2/H+ in CSF. Primary driver of breathing rate.
Peripheral chemoreceptors
Carotid and aortic bodies — detect O2, CO2, pH in blood.
COPD hypoxic drive
Chronic CO2 retention — O2 becomes primary drive. Be cautious with high-flow O2.
Larynx Cartilages
TACE — Thyroid · Arytenoid · Cricoid · Epiglottis
Four major laryngeal cartilages
The four laryngeal cartilages and their clinical importance
Thyroid cartilage: the largest, forms the Adam's apple (laryngeal prominence). Cricoid cartilage: only complete ring of cartilage in the airway — landmark for cricothyrotomy. Arytenoid cartilages: paired, control vocal cord tension and position. Epiglottis: elastic cartilage — flips down to cover larynx during swallowing, preventing aspiration. The cricothyroid membrane between thyroid and cricoid is where emergency airway access is obtained.
Thyroid
Largest — Adam's apple. Protects vocal cords.
Cricoid
Only complete ring — below thyroid. Cricothyrotomy landmark.
Arytenoid
Paired — move to open/close glottis, tension vocal cords.
Q: What is V/Q mismatch and how does it cause hypoxemia?
A: Dead space (V/Q = infinity): ventilated not perfused — wasted ventilation. Example: pulmonary embolism. Shunt (V/Q = 0): perfused not ventilated — blood unoxygenated. Examples: pneumonia, atelectasis. Shunt NOT corrected by 100% O2. Normal variation: apices have higher V/Q; bases have lower V/Q. In PE: high V/Q → hypoxemia + low pCO2. In COPD: low V/Q areas → hypoxemia + hypercapnia.
Q: Compare chronic bronchitis (Blue Bloater) vs emphysema (Pink Puffer).
A: Chronic bronchitis: productive cough 3+ months for 2+ years. Hypersecretion, increased goblet cells. Retain CO2, hypoxic → cyanosis + edema (blue bloater). Emphysema: alveolar wall destruction → air trapping, loss of elastic recoil. Hyperventilate to compensate → normal pO2 but labored breathing (pink puffer). Centriacinar (upper lobes, smokers) vs panacinar (lower lobes, alpha-1-antitrypsin deficiency). Both: FEV1/FVC <70%.