Alveolar-Capillary Gas Exchange

Course Overview: Respiratory Physiology

• The course covers the structure and function of the respiratory system and delves into ventilation mechanics and gas exchange. The process of gas exchange between alveoli and capillaries, gas transport in the blood, and the control of ventilation are also covered.

Alveolar-Capillary Gas Exchange

• This section covers the exchange of gases between the alveoli and capillaries exploring the composition of inspired and expired gases, the concept of dead space, and the properties of alveolar gases. Topics include alveolar-capillary diffusion, membrane transfer capacity, diffusion limits, ventilation/perfusion ratios, and methods for measuring pulmonary gas exchange.

Alveolar-Capillary Diffusion

• Pulmonary gases must diffuse across different structures between the alveoli and capillary blood
• Oxygen molecules move from alveolar gas into the pulmonary capillary blood and peripheral capillary blood toward tissues
• CO2 molecules move in the opposite direction

Oxygen Diffusion Across Alveolar-Capillary Barrier

• Substances in the alveolar capillary barrier Epithelial Cell, Alveollar basement membrane, epithelium membrane, Fluid and surfactant layer, Interstitial space, Capillary endothelium, Capillary basement membrane, Red blood cell

Atmospheric Pressure

• The total pressure exerted by atmospheric gas molecules is the barometric pressure and it decreases with altitude
• At sea level atmospheric pressure measures approximately 760 mmHg or 1 atm
• Partial pressure is the product of % concentration and the atmospheric pressure.

Factors Affecting Alveolar-Capillary Gas Exchange

• Efficiency depends on alveolar ventilation, alveolar-capillary diffusion, pulmonary circulation with capillary contact time and true shunt, and ventilation/perfusion ratio

Diffusion Factors

• Gas exchange relies on a pressure gradient between mixed venous blood and the alveolus, also surface area and thickness of the membrane A-cap.
• The anatomical surface area is 80-100 m^2
• Functional surface is 1 alveolus + 1 normal capillary
• The anatomical thickness is 0.5 µm and functional includes all the steps of diffusion

Ventilation-Perfusion Ratios

• Normal gas requires alveoli ventilation and adequate perfusion with pulmonary blood
• The ventilation/perfusion ratio (VA/Q = alveolar ventilation / pulmonary blood flow), determines the oxygenation level of capillary blood.
• Ventilation and perfusion distribution is uneven, with blood flow increasing progressively towards the lower regions of the lungs
• Ventilation increases 1-3x more from top to bottom of the lungs, perfusion is multiplied by 1-10.
• This results in VA/Q ratio being non-homogenous

Regional Ventilation Differences

• Lung volume is determined by transpulmonary pressure = alveolar pressure - pleural pressure.
• The base of the lung experiences greater gravity, resulting in higher pressure, whereas the top experiences less. (-10 cmH2O at the apex)
• With no airflow in the bronchi, the alveoli at the apex are more distended than at the base.
• During inspiration, volume increase is lower at the apex (already distended) compared to the base
• Lower pulmonary alveoli have better ventilation

Regional Ventilation/Perfusion Ratios

• VA/Q increases towards the apices but is low in the bases

  • Zone 1 (apex): High VA/Q, good alveolar ventilation, high PAO2 (132mmHg), low PACO2 (28mmHg)
  • Zone 2 (mid-lung): Ideal VA/Q and normal ventilation, alveolar ventilation matches capillary perfusion, PAO2 = PaO2 is near 100 mmHg and PACO2 and PaCO2 = 40 mmHg
  • Zone 3 (base): Low VA/Q ratio- high perfusion (89mmHg) , with PA02 and high (43mmHg) PACO2

Ventilation/Perfusion Imbalances

• Decreased ventilation in a group of alveoli results in higher PCO2 and lower P02 with blood not being oxygenated

Hypoxic Vasoconstriction

• The only circulation vasoconstriction is from hypoxia, from the drop of partial O2 pressure in alveolar gas below the threshold, around 60mmHg
• This is a self adaption mechanism that adjusts perfusion to alveolar ventilation and maintaining the V/P ration near its the optional value

Hypoxic Pulmonary Vasoconstriction

• It is a protective mechanism. The pressure will decrease and induce constriction in poorly ventilated parts of the lung
• Prefentially redistributes to optimized hematosis.
• Modulated by genetic factors by the “hypoxia included factor” or HIF. Those native to environments such as tibet can adapt using this pathway to reduce hypertension.

Ventilation-Perfusion Heterogeneity

• Alveoli either poorly ventilated + well perfuse or well ventilated and poorly perfuse

Impaired Alveoli

• Alveoli are ventilated but poorly perfused raises the VA/Q ration and the region participates incompletely in pulmonary gas exchanges
• This absence in gas exchanges results in elevated PAO2 and decreased PACO2
• Under severe conditions such as a pulmonary embolism, VA/Q can tend towards infinity and can change levels equal to the humidified air.