Distribution of Ventilation

Transpulmonary Pressure = (alveolar - pleural surface pressure); keeps lung inflated and determines volume

must change in order for lung inflation or deflation to occur
relationship between transpulmonary pressure and volume the same for all alveoli in the lung

Pleural Pressure Gradient

pleural pressure in apex is more negative than that in base, due to gravity

pressure increases approx. 0.25 cmH₂O per centimeter of vertical distance from top to bottom of lung
since alveolar pressure same throughout lung, transpulmonary pressure also changes from apex to base

Effect of the pleural pressure gradient on lung volume at rest

transpulmonary pressure is higher at the top of the lung compared to the bottom of the lung
pleural pressure is more negative at apex
alveoli at the top of the lung are more fully expanded at FRC than those at the bottom

Effect of the pleural pressure gradient on distribution of ventilation during tidal breathing

pressure-volume curve of the alveoli is the same in all regions of the normal lung
pressure gradient means different alveoli operate on different portions of the pressure volume curve

alveoli at the bottom of the lung expand considerably more than those at the top (better ventilated)
matched by increase in blood flow to the base of the lung

Effect of the pleural pressure gradient on alveolar volume after inspiration to total lung capacity (TLC)

at TLC, all alveoli are same size (gradient still exists, but alveoli are at flat portion of P-V curve)

Effect of pleural pressure gradient on lung volume after expiration to residual volume (RV)

at RV, pleural pressure at the base of the lung becomes positive, so transpulmonary pressure is negative
pleural pressure now acts as a compressing force that begins to close airways (if <1 mm)

as exhalation continues, airway closure moves upward in the lung and involves more and more airways
premature airway closure in emphysema, obesity, or elderly at FRC (especially if lying flat)

Closing Volume – lung volume at which the lower lung zones stop ventilating as a result of airway closure

Measurement: Single Breath Oxygen Method (single breath nitrogen washout test)

[N₂] at the mouth is plotted against expired lung volume after full inspiration of 100% O₂ (RV Þ TLC)

during inspiration: first to enter (dead space gas, N₂-rich) goes to apex, remainder (O₂-rich) to base

during expiration: four phases

phase I – first to exit (dead space) contains no N₂
phase II – [N₂] concentration rises sharply as alveolar gas containing N₂ begins to be washed out
phase III – [N₂] plateau since gas leaves all regions of the lung synchronously and equally
phase IV – [N₂] rises again, since gas is coming from alveoli with different [N₂] (bottom closed)

Effects of Age—closing volume relative to vital cap. high in infants, decreases, then increases during aging

due to differences in distending pressure acting on small airways
thus, the airways of a young child or an older person are not held open as well as those of a young adult

Other Factors Influencing Distribution of Ventilation

Regional Differences in Airway Resistance – high inspiratory flow rate: mostly to apical alveoli

airways at apex more distended than base, so greater cross sectional area and decreased resistance

Regional Differences in Compliance – low inspiratory flow rate: mostly to basilar alveoli

alveoli at the base expand more at a given change in pleural pressure, so higher compliance

Respiratory Muscles – distribution of inspired air can be altered by using different groups of muscles

Change in Distribution of Ventilation with Exercise – use more apical alveoli (to match increased blood flow)

blood CO₂ concentration rises, so chemoreceptors increase respiratory rate and tidal volume so use more apical alveoli
intercostal and accessory muscles are progressively recruited so use more apical alveoli
at rest, air mostly goes to base; during exercise, more even distribution