Info
🌱 來自: Huppert’s Notes
Dynamics Flow, Resistance, and VQ Matching🚧 施工中
Dynamics: Flow, Resistance, and V/Q Matching
• Flow:
- Ohm’s Law (ΔP = Q × R)
P = pressure, Q = flow, R = resistance
• Laminar flow: ΔQ proportional to ΔP (peripheral airway). Reynold’s # < 2000.
• Turbulent flow: ΔQ proportional to √ΔP (central airway). Reynold’s # >2000.
• Reduce density of gas → favors turbulent over laminar flow → decrease work of breathing
- Breathing cycle
• At rest: Lung collapsing forces = Chest wall expanding forces; Intra-alveolar pressure = 0 cm H2O (i.e., equal to atmospheric pressure); pleural pressure negative (−5 cm H2O); Transmural pressure positive (+5 cm H2O); Lung volume = FRC.
• Inspiration: Inspiratory muscles contract → Thoracic volume increases → Intra-alveolar pressure <0 cm H2O (i.e., becomes lower than atmospheric pressure) → Air flows in → Intrapleural pressure becomes more negative; Lung volume = FRC + TV.
• Expiration (passive): Elastic forces of lungs compress greater volume of air in alveoli → Alveolar pressure > atmospheric pressure → Air flows out → Intrapleural pressure returns to baseline (−5 cm H2O)
• Forced expiration: Similar to passive expiration, except use of musculature (abdominal wall, internal intercostals) results in even more positive intrapleural pressure, which rapidly forces air out of the lungs
• Resistance/Poiseuille’s Law: R = 8ηl/πr4
R = Resistance to flow, η = viscosity of gas, l = length of airway, r = radius of airway
- Medium-sized airways = Highest resistance (small-sized bronchi exist in parallel, so less resistance)
- Resistance influenced by:
• Modification of airway radius via bronchial smooth muscle
- Sympathetic stimulation: β2 receptors → smooth muscle relaxation → airway dilation → decreased resistance (e.g., β2-agonist inhalers)
- Parasympathetic stimulation: Smooth muscle contraction → airway constriction → increased resistance (e.g., anticholinergic toxicity)
• Modification of airway radius by lung volume
- High volume = more traction holding airways open, thus decreased resistance (and vice versa)
• V/Q Matching:
- Calculating ventilation
• Minute ventilation = Tidal volume × breaths/min
• Alveolar ventilation = (Tidal volume – dead space) × breaths/min
- Dead space: Ventilation but no perfusion (Figure 2.5)
FIGURE 2.5: Dead space and shunt. Dead space refers to areas that are ventilated but not perfused, whereas shunt refers to areas that are perfused but not ventilated. V = ventilation; Q = blood flow.
• Types of dead space:
- Anatomic dead space: Volume of the conducting airways (i.e., areas that move air but do not participate in gas exchange; ~150 mL)
- Physiologic dead space: Functional measurement of the volume of the lungs that does not participate in gas exchange
• Calculating physiologic dead space: VD = VT × (PACO2 – PECO2)/(PACO2)
- VD = Physiologic dead space, VT = Tidal volume, PACO2 = PCO2 of arterial blood = PCO2 of alveolar gas, PECO2 = PCO2 expired air
• If physiologic dead space > predicted anatomic dead space, then pathology is present that increases dead space
- E.g., pulmonary embolism – clot disrupts blood flow (i.e., Q = 0) → V/Q = infinity; 100% O2 will help
- Shunt: Perfusion but no ventilation (Figure 2.5)
• E.g., airway obstruction (i.e., V = 0) → V/Q = 0; 100% O2 does NOT help
- V/Q mismatch is more likely to cause hypoxemia than hypercapnia
• O2 has a sigmoidal hemoglobin binding curve and thus is generally saturated in the alveolar–capillary bed (i.e., exchange only increases with increased blood flow) → hyperventilating does not help
• CO2 has a linear hemoglobin binding curve, and increased ventilation can increase removal from blood → hyperventilating can help/compensate for mismatch