Resp

• CO2 & O2 exchange

  Acute regulation of blood pH
• Recall from cardiovascular:

  muscle contraction → Δ size → Δ pressure → bulk flow

  resistance to flow (friction)

  diameter of tubes

  length of tubes

  viscosity
• Branching of the airways

  • Multiple, small branches = ↑ surface area = better diffusion
  • Multiple, small branches = ↓ diameter = ↑ resistance (friction)
• Limited bulk flow at exchange surfaces = diffusion moves gases
• Partial pressure gradients


  Drive diffusion
• Most important factor for gas exchange: concentration gradients (partial pressures)
• total pressure ≈ osmolarity

  partial pressure ≈ molarity
• Conditioning of air = maximum diffusion


  1. Adding water vapor

  2. Warming air to body temperature

  3. Filtering out foreign material
• Your lungs always want to collapse


  • Alveolar inner walls must have a layer of H2O
  • Cohesion = surface tension within alveolus
  • Compounded by recoil of elastin in connective tissue

  
• What stops your lungs from collapsing

  1. Pulmonary surfactant

  2. Alveolar interdependence

  3. Transmural pressure gradient

  
• Pulmonary surfactant


  • Type II alveolar cells → phospholipoprotein
  • Disrupts air-water interface
  • Reduced surface tension & cohesion = reduced recoil

  
• La Place: smaller alveoli = more likely to collapse
• Smaller alveoli = ↑ pulmonary surfactant

  
• Alveolar interdependence


  • Mutual walls prevent individual collapse/expansion
  • Collateral ventilation = pressure equalisation
  • Interbronchiolar channels (of Martin)
  • Interalveolar pores (of Kohn)
  • Bronchoalveolar channels (of Lambert)

  
• Transmural pressure gradient


  • Pressure difference between 2 cavities
  • Intrapleural = between parietal & visceral pleurae
  • Intrapulmonary = inside the lungs

  
• • Surface tension = recoil (even with surfactant & interdependence)
  • creates lower pressure in pleural cavity
  • Surface tension = recoil
  • = low pressure = expansion
  • Forces balance each other (≈ K+ at resting membrane potential)
• Summary of lung dynamics (rank order)


  • Collapsing forces:

  1. Alveolar surface tension
  2. Elastic recoil

  Expanding forces:

  1. Pulmonary surfactant
  2. Transmural pressure gradient
  3. Alveolar interdependence

  
• Tidal ventilation


  1. Inspiratory muscles contract

  2. Inspiratory muscles relax
• Compliance


  • Ability to stretch
  • High compliance = expands easily
  • Low compliance = requires ↑ pressure gradient (↑↑ muscle force)
  • Restrictive lung diseases = ↓ compliance
• Elastance


  • Ability to regain shape (recoil)
  • Return to resting size
  • Surface tension > elastic fibers
• Forced exhalation (exhale more than normal)

  1. Expiratory muscles contract

  2. Friction in small airways

  3. Once intrapleural pressure ≥ bronchial pressure: dynamic bronchial compression

  
• Dynamic bronchial compression


  • Prevents excessive LaPlace (like heart, or blowing up a balloon)
  • Restricts maximum volume exchange
  • Obstructive lung diseases = ↑ resistance = faster loss of pressure = early dynamic bronchial compression = ↑ RV
• Pulmonary ventilation ( )


  • ≈ cardiac output
  • = respiratory rate (RR) * tidal volume (VT)
  • No gas exchange within conducting system
  • Gas exchange = alveoli & compliant bronchioles
  • Alveolar volume (VA) = tidal volume (VT) - dead space (VD)

  
• Problems if VT ≈ VD:

  ↓ VT = anesthesia, lung disorders, respiratory paralysis

  ↑ VD = ventilation tubes, unperfused alveoli
• • VA is low in humans (≈ 350 ml for tidal breathing)
  • RV stale air reduces PO2 inside the lungs
  • Prevents sudden changes in PO2 & PCO2 in lungs
  • Minimizes impact of toxins & dust

  
• Matching ventilation (VA) & blood flow (Q)

  • O2 delivered to alveoli must enter blood
  • Airflow should therefore equal blood flow (VQ matching)
  • VA / Q = 1

  
• Systemic control


  1. Parasympathetic (Ach + muscarinic → ↑ IP3 & DAG → ↑ Ca2+ in ICF)

  2. Sympathetic (E + β2 → ↑ cAMP → ↓ MLCK activity)

  3. Thoracic pressure
• Local alveolar ventilation controlled by PCO2

  Airflow < blood flow to alveolus → ↑ PCO2 in alveolus → Local bronchodilation → ↑ ventilation to alveolus

  
• Local alveolar blood flow controlled by PO2

  Blood flow > airflow to alveolus → ↓ PO2 in alveolus → Local vasoconstriction → ↓ blood flow to alveolus

  
• Gravity has a greater effect on blood flow (liquid)
• VA/Q inequality = ↓ vascular PO2
• Oxygen transport


  • Dissolved (2%)
  • Bound (98%)
• Bohr effect


  • At lungs, shift curve left = maximize O2 loading
  • At tissues, shift curve right = maximize O2 release

  
• Carbon dioxide transport


  1. Dissolved (7%)

  2. Bound (23%)

  3. Bicarbonate (70%)
• Reflex control of ventilation

  1. Central chemoreceptors

  2. Peripheral chemoreceptors