E3: Pulmonary 1 Compliance Resistance & hypoxic vasoconstriction

Name and describe the functions of the lungs.

• Provides oxygen

• Eliminates carbon dioxide

• Regulates blood pH (with the kidneys)

• Forms speech sounds (phonation)

• Defends against microbes

• Influences arterial concentrations of chemical messengers

• Traps and dissolves blood clots from systemic veins

Explain how the tissue characteristics of lung/chest wall and surface tension contribute to compliance and the work of breathing.

Compliance (the change in pressure needed to inflate the lungs to a certain volume)= ΔV / ΔP_tp (change in lung volume per change in transpulmonary pressure).

• Lung tissue is a weave of elastin and collagen fibers ("the sweater")

• More compliant = stretchier = less pressure needed to inflate

• Stiff lungs (lots of crosslinking) → restrictive lung disease → high work of breathing

• High surface tension in alveoli also opposes inflation, increasing work of breathing

Describe how the Law of LaPlace can be applied to the pulmonary system.

Law of LaPlace: P = 2T / r

• P = collapsing pressure, T = surface tension, r = radius

• Smaller alveoli (smaller r) have a higher collapsing pressure if surface tension is equal

• Without surfactant: small alveoli (b) have higher pressure than large (a), so air flows from b → a and b collapses into a

• This is why alveoli would collapse without surfactant (no net air flow between alveloi)

Describe the characteristics of surfactant and explain how surfactant reduces surface tension and equalizes inflation pressures in the lung.

• Produced by type II alveolar cells

• Composed mainly of DPPC made from glucose, fatty acids, choline

• Sits at the gas–liquid interface with hydrophobic tails in gas, hydrophilic heads in liquid

• Lowers surface tension — and lowers it more in smaller alveoli (T_a > T_b)

• Result: P_a = P_b → pressures equalize → small alveoli do not collapse into large ones

Apply the principles of airway resistance to lung function.

Flow = ΔP / R  (F = [P_alv − P_atm] / R)

• Most important determinant of airway resistance: airway size (radius)

• High resistance → reduced airflow for the same pressure gradient

• Asthma and COPD cause high airway resistance

Discuss how compliance changes occur with restrictive lung disease.

• Decreased compliance (stiffer lungs) = shifted right on the compliance curve

• Much more transpulmonary pressure needed to achieve the same volume

• Causes: fibrosis, tuberculosis, interstitial lung disease, ARDS, pulmonary edema

• Clinical pattern: small tidal volume, high respiratory rate

• Both vital capacity and flow rate are reduced; work of breathing is increased

Discuss how airway resistance changes with obstructive lung disease.

• Increased airway resistance = obstruction to airflow

• Causes: asthma, chronic bronchitis, emphysema

• Emphysema paradox: destroys lung matrix → airways very collapsible → especially collapses on forced expiration

• FEV₁/FVC is decreased (normal 70–80%); e.g. 3L/4L = 75% normal

• Treatment: pursed-lip breathing to slow expiration; vital capacity and flow rate both reduced

Explain the mechanism of hypoxic vasoconstriction. Describe the benefit of this mechanism.

• Low O₂ in airways → decreased PO₂ in pulmonary blood → vasoconstriction of pulmonary vessels in that region → decreased blood flow

• Opposite of systemic circulation (which vasodilates with low O₂)

• Benefit: diverts blood flow away from poorly ventilated (diseased) areas to healthy, well-ventilated areas → better matching of ventilation and perfusion → more efficient gas exchange

• Also: decreased PCO₂ in alveoli → bronchoconstriction → matches air flow to perfusion from the other direction

• Harmful: at high altitude (globally low O₂), causes widespread pulmonary vasoconstriction → pulmonary hypertension