Respiratory Physiology Calculators
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Lung Volumes and Capacities
- Tidal volume (TV): ~500 mL per breath at rest
- Inspiratory reserve volume (IRV): ~3000 mL (maximum additional air inspired beyond TV)
- Expiratory reserve volume (ERV): ~1200 mL (maximum air expelled beyond TV)
- Residual volume (RV): ~1200 mL (air remaining after maximum exhalation — cannot be exhaled)
- Vital capacity (VC) = TV + IRV + ERV ≈ 4700 mL
- Total lung capacity (TLC) = VC + RV ≈ 5900 mL
- FEV₁: forced expiratory volume in 1 second; FEV₁/FVC ratio < 0.70 = obstructive disease (asthma, COPD)
Alveolar Gas Exchange
Governed by Fick's law: V̇gas ∝ A × D × (P₁ − P₂)/T, where A = surface area; D = diffusion coefficient; P₁−P₂ = partial pressure difference; T = membrane thickness. Alveolar–arterial PO₂ gradient (A-a gradient) normally < 15 mmHg; elevated in V/Q mismatch, diffusion impairment.
Oxygen Transport
Hemoglobin: 4 heme groups/molecule; each binds one O₂. Oxyhemoglobin dissociation curve: sigmoidal (cooperative binding); P50 = 26.5 mmHg (O₂ pressure giving 50% saturation). Bohr effect: decreased pH or increased CO₂ shifts curve right → lower O₂ affinity → facilitates O₂ release to tissues.
Respiratory Control
Central pattern generator in medulla (pre-Bötzinger complex) drives rhythmic breathing. Central chemoreceptors (medulla): respond to CSF pH (from PCO₂). Peripheral chemoreceptors (carotid bodies): respond to PaO₂, PaCO₂, pH. Hypercapnia is the primary drive; hypoxia stimulates mainly via carotid bodies.
Glossary
Frequently Asked Questions
Tidal volume (TV) ≈ 500 mL: air moved per normal breath. Inspiratory reserve volume (IRV) ≈ 3000 mL: extra air inspireable above TV. Expiratory reserve volume (ERV) ≈ 1200 mL: extra air expellable below TV. Residual volume (RV) ≈ 1200 mL: air remaining after maximum exhalation (prevents alveolar collapse). Vital capacity (VC) = TV + IRV + ERV ≈ 4700 mL: maximum breath volume. Total lung capacity (TLC) ≈ 5900 mL. Spirometry measures all volumes except RV (requires gas dilution or plethysmography). FEV₁/FVC < 0.70 indicates obstructive disease; reduced FVC with normal ratio indicates restrictive disease.
Each hemoglobin molecule contains four heme groups, each binding one O₂. Binding is cooperative (positive cooperativity) — binding of the first O₂ increases affinity for subsequent O₂ molecules, producing the sigmoidal oxyhemoglobin dissociation curve. At arterial PO₂ ≈ 100 mmHg: Hb is ~98% saturated. At venous PO₂ ≈ 40 mmHg: Hb is ~75% saturated. ~25% of O₂ is extracted per circulation pass at rest. Bohr effect: decreased pH or increased CO₂ (both in exercising tissues) shifts the curve right (lower affinity), facilitating O₂ unloading exactly where it is needed.
The Bohr effect describes how CO₂ and H⁺ (decreased pH) decrease hemoglobin's affinity for oxygen — shifting the oxyhemoglobin dissociation curve to the right. In exercising muscle: high CO₂ production → CO₂ enters red blood cells → carbonic anhydrase converts CO₂ to H₂CO₃ → H⁺ + HCO₃⁻ → H⁺ binds globin chains → changes Hb conformation → decreases O₂ affinity → more O₂ released to muscle. In the lungs: CO₂ is exhaled → PCO₂ falls → pH rises → Hb affinity for O₂ increases (Bohr effect reversed) → Hb fully loads with O₂. The Bohr effect is a beautiful physiological mechanism that automatically delivers more O₂ to the tissues that need it most.
Respiratory rhythm is generated by the pre-Bötzinger complex in the medulla. Rate is regulated by: (1) Central chemoreceptors (medulla): sense PCO₂ via CSF pH — hypercapnia (↑PCO₂ → ↓pH) is the strongest normal stimulus for increased ventilation. (2) Peripheral chemoreceptors (carotid bodies at carotid bifurcation; aortic bodies): sensitive to PaO₂ (hypoxic drive below PaO₂ 60 mmHg), PaCO₂, and pH. Carotid bodies mediate the hypoxic ventilatory response. At high altitude: hypoxia stimulates carotid bodies → hyperventilation → ↓PCO₂ → respiratory alkalosis → partially compensated by renal HCO₃⁻ excretion over days.