Memory tricks for respiratory physiology

Breathing is driven entirely by pressure gradients — no suction, just physics. Inspiration: diaphragm contracts and flattens → thoracic volume increases → intrapulmonary pressure drops below atmospheric (~-1 mmHg) → air flows in. Expiration (quiet): elastic recoil → thoracic volume decreases → pressure rises above atmospheric → air flows out. Intrapleural pressure is always negative (-5 mmHg at rest, -8 mmHg during inspiration) — this keeps lungs inflated. Pneumothorax: intrapleural pressure equalizes with atmospheric → lung collapses.

Oxygen is transported in two ways: 98% bound to hemoglobin (oxyhemoglobin) and 2% dissolved in plasma. Each hemoglobin molecule carries 4 O2 molecules (one per heme group). Oxygen content = (Hgb × 1.34 × SaO2) + (0.003 × PaO2). Normal = ~20 mL O2/100 mL blood. SpO2 (pulse ox) measures saturation, not content — anemia patient can have 100% saturation but low O2 content (not enough Hgb). This is why Hgb level matters for oxygen delivery, not just SpO2.

The S-shaped oxyhemoglobin dissociation curve shows hemoglobin saturation vs PO2. Right shift: hemoglobin releases O2 more easily (good for exercising muscle). Causes: increased CO2 (Bohr effect), decreased pH (acidosis), increased 2,3-DPG, increased temperature, exercise. Left shift: hemoglobin holds O2 more tightly (Hgb grabs O2 at lungs). Causes: low CO2, alkalosis, fetal hemoglobin (HbF), CO poisoning, decreased temperature. P50 = PO2 at which Hgb is 50% saturated. Normal P50 = 27 mmHg. Increased P50 = right shift.

CO2 is transported in three forms. 70% as bicarbonate (HCO3-): CO2 + H2O → H2CO3 → H+ + HCO3- (catalyzed by carbonic anhydrase in RBCs). HCO3- exits RBC via chloride shift (Cl- enters). 23% as carbaminohemoglobin: CO2 binds amino groups of Hgb (not heme — different site from O2). 7% dissolved in plasma. Haldane effect: deoxygenated Hgb carries more CO2 — at tissues where O2 is released, Hgb picks up CO2 more efficiently.

Optimal gas exchange requires matching ventilation (V) to perfusion (Q). V/Q = 1 is ideal. Dead space: alveoli ventilated but not perfused (V/Q = ∞) — no gas exchange possible. Pulmonary embolism creates dead space. Shunt: alveoli perfused but not ventilated (V/Q = 0) — deoxygenated blood bypasses gas exchange. Pneumonia, atelectasis, pulmonary edema create shunt. Gravity: apex of lung has highest V/Q (least perfusion), base has lowest V/Q (most perfusion). V/Q mismatch is the most common cause of hypoxemia.

ROME is the fastest way to identify acid-base disorders. Respiratory: pH and CO2 move in OPPOSITE directions. pH down + CO2 up = respiratory acidosis. pH up + CO2 down = respiratory alkalosis. Metabolic: pH and HCO3 move in the SAME (Equal) direction. pH down + HCO3 down = metabolic acidosis. pH up + HCO3 up = metabolic alkalosis. Then check for compensation — the body always compensates in the same direction as the primary disorder to minimize pH change. Compensation never fully corrects pH to normal.

Hypoxic hypoxia: low PaO2 — altitude, lung disease, hypoventilation. Treat: supplemental O2. Anemic hypoxia: normal PaO2 but low O2 carrying capacity — anemia, CO poisoning. CO: give 100% O2 to displace CO. Stagnant (circulatory) hypoxia: low blood flow — heart failure, shock. Normal PaO2 and Hgb but inadequate delivery. Cytotoxic hypoxia: cells can't use O2 — cyanide poisoning blocks cytochrome c oxidase. PaO2 normal, Hgb normal but venous blood paradoxically well-oxygenated. Histotoxic: cells damaged and unable to utilize O2.

Surface tension in alveoli would cause them to collapse (smaller alveoli have higher pressure — LaPlace's Law). Surfactant (DPPC) is produced by type II alveolar cells — it reduces surface tension, preventing collapse. Without surfactant, the work of breathing increases dramatically. Premature infants (born before 34–36 weeks) lack surfactant → respiratory distress syndrome (RDS/hyaline membrane disease) → blue baby who grunts with each breath. Treatment: synthetic surfactant down the endotracheal tube and antenatal corticosteroids to accelerate surfactant production.

Breathing is controlled by the respiratory center in the medulla (pre-Bötzinger complex). Normal drive: central chemoreceptors in the medulla detect rising CO2 (as H+ in CSF) → increased ventilation. CO2 is the primary driver of breathing in healthy people. COPD exception: chronic CO2 retention → central chemoreceptors adapt and become insensitive to CO2 → the patient's ONLY drive to breathe is hypoxia (low O2) detected by peripheral chemoreceptors (carotid and aortic bodies). Giving high-flow O2 to a COPD patient may eliminate their hypoxic drive → apnea (the "hypoxic drive" phenomenon — controversial but clinically important to know).

TV (tidal volume) = ~500 mL normal breath. IRV (inspiratory reserve) = extra air you can inhale. ERV (expiratory reserve) = extra air you can exhale. RV (residual volume) = air always remaining in lungs (~1200 mL, can't be exhaled). TLC = TV + IRV + ERV + RV. VC = TLC - RV.

Right shift (↓ affinity, ↑ O2 delivery to tissues): ↑ CO2, ↑ H+ (acidosis), ↑ 2,3-DPG, ↑ temperature. Left shift (↑ affinity, ↓ O2 release): ↓ CO2, alkalosis, ↓ temp, fetal Hb. Bohr effect: acidosis shifts curve right → more O2 delivered to active tissues.

Normal V/Q = ~0.8. V/Q = 0 (shunt): perfusion but no ventilation (pneumonia, atelectasis) → deoxygenated blood passes through. V/Q = ∞ (dead space): ventilation but no perfusion (pulmonary embolism) → wasted ventilation. Lung apices have higher V/Q; bases have lower V/Q.

Central chemoreceptors (medulla): respond to CO2/H+ → primary breathing drive. Peripheral chemoreceptors (carotid + aortic bodies): respond to O2, CO2, pH. In healthy people, CO2 drives breathing. In COPD with chronic hypercapnia: body resets CO2 threshold → hypoxic drive takes over → giving high O2 can suppress breathing!