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Vocabulary practice flashcards covering pulmonary gas exchange, diffusion versus perfusion limitation, ventilation equations and compartments, and regional pulmonary perfusion dynamics.
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Fick's Law of Diffusion
A physical principle stating that the net rate of gas transfer (V˙O2) across a membrane is proportional to the diffusing capacity (DL,O2) and the partial pressure gradient between alveolar gas and capillary blood (PAO2−PcO2) at a single point in space and time.
Diffusing Capacity (DL)
A composite physiological coefficient in Fick's law that incorporates barrier surface area (A), gas solubility (s), barrier thickness (a), and gas molecular weight (MW) into the net rate equation V˙net=DL⋅(P1−P2).
Henry's Law
A gas law stating that the concentration of a dissolved gas in liquid ([O2]Dis) is directly proportional to its partial pressure (PO2) and solubility coefficient (s), defined by the formula [O2]Dis=s⋅PO2.
![<p>A gas law stating that the concentration of a dissolved gas in liquid ($$[O_2]_{\text{Dis}}$$) is directly proportional to its partial pressure ($$P_{O2}$$) and solubility coefficient ($$s$$), defined by the formula $$[O_2]_{\text{Dis}} = s \cdot P_{O2}$$.</p>](https://assets.knowt.com/pdf-flow-prod/1c128dbb-2709-4a53-9310-4c52409eaea3-figures/2.jpg)
Type I Pneumocytes
The extremely thin epithelial cells that make up the vast majority of the alveolar wall barrier, providing an expansive surface area of approximately 100m2 (roughly half the size of a tennis court) to optimize passive gas diffusion.
Perfusion-Limited Gas Exchange
A condition of pulmonary gas transfer in which the total uptake of a gas depends strictly on pulmonary blood flow (Q˙) rather than diffusion capacity (DL), identified when partial pressure in the capillary reaches complete equilibration with alveolar gas before the end of the capillary.
Diffusion-Limited Gas Exchange
A condition of pulmonary gas transfer in which net gas uptake is restricted by the physical properties of the blood-gas barrier (DL), characterized by capillary partial pressure failing to reach alveolar partial pressure by the end of the pulmonary capillary.
Carbon Monoxide (CO) Uptake
A classic model of diffusion-limited gas transfer; because carbon monoxide binds with high affinity to hemoglobin, capillary PCO remains near zero, maintaining a continuous gradient where total uptake depends entirely on diffusing capacity (DL).
Nitrous Oxide (N2O) Uptake
A classic model of perfusion-limited gas transfer; because nitrous oxide does not bind to hemoglobin, capillary partial pressure rapidly equilibrates with alveolar partial pressure at the very beginning of the capillary, making uptake dependent entirely on blood flow (Q˙).
Pulmonary O2 Uptake at Rest
A perfusion-limited process in healthy individuals at sea level, in which capillary PO2 rises from mixed venous levels (40mmHg) to reach complete equilibration with alveolar PAO2 (100mmHg) approximately 1/3 of the way along the capillary length.

Effect of Vigorous Exercise on O2 Uptake
A physiological response where cardiac output increases 3-fold (Q˙=3), which increases total O2 uptake 3-fold; uptake remains perfusion-limited at sea level due to the lung's large capillary transit time reserve.
Effect of High Altitude on Resting O2 Uptake
A physiological state where low atmospheric barometric pressure reduces alveolar PAO2, diminishing the initial alveolar-capillary gradient from ≈60mmHg to ≈30mmHg and slowing diffusion, though equilibration is still achieved and uptake remains perfusion-limited at rest.
Exercise at High Altitude
A scenario where a reduced alveolar-capillary gradient (≈30mmHg) combines with shortened capillary transit time from elevated cardiac output, preventing capillary PcO2 from reaching alveolar PAO2 and rendering oxygen uptake diffusion-limited in healthy individuals.
Pulmonary CO2 Release
The transfer of carbon dioxide from pulmonary blood to alveolar air, which is normally perfusion-limited but can become diffusion-limited under pathological conditions such as pulmonary fibrosis, COPD, or severe anemia.
Total Ventilation (V˙T)
The total volume of gas entering or leaving the respiratory tract per minute (clinically called minute ventilation), calculated as the product of tidal volume and respiratory rate: V˙T=VT⋅f=(0.5L)⋅(12/min)=6L/min.
Anatomic Dead Space (VD)
The volume of the conducting airways (airway generations 0 through 16) that does not contain gas-exchanging alveoli, measuring approximately 150mL in an average adult.

Dead-Space Ventilation (V˙D)
The volume of air per minute shuttled back and forth through non-gas-exchanging conducting airways, calculated as V˙D=VD⋅f=(0.150L)⋅(12/min)=1.8L/min, accounting for approximately 30% of total ventilation.
Alveolar Ventilation (V˙A)
The volume of fresh inspired air that reaches the respiratory zones and participates in gas exchange per minute, calculated as V˙A=(VT−VD)⋅f=(0.500L−0.150L)⋅(12/min)=4.2L/min.
Alveolar Dead Space
The volume of gas residing within alveoli that are ventilated with fresh air but receive no capillary blood perfusion, preventing gas exchange.
Physiological Dead Space
The total volume of gas in each respiratory cycle that does not participate in gas exchange, calculated as the sum of anatomic dead space and alveolar dead space.
Alveolar Ventilation Equation
A fundamental equation demonstrating that alveolar ventilation is inversely proportional to alveolar carbon dioxide partial pressure: V˙A=0.863⋅PACO2V˙CO2, where V˙CO2 is metabolic carbon dioxide production.

Hyperventilation
An increase in alveolar ventilation (V˙A) beyond metabolic needs that dilutes alveolar CO2, driving arterial PaCO2 down toward low levels, which leads to cerebral vasoconstriction, reduced brain perfusion, and dizziness.
Hypoventilation
A reduction in alveolar ventilation (V˙A) below metabolic requirement that causes alveolar and arterial PO2 to drop, while alveolar and arterial PCO2 double or rise proportionally due to diminished carbon dioxide excretion.

Alveolar Gas Equation
An equation defining the relationship between inspired oxygen, carbon dioxide excretion, and alveolar PAO2, expressed in the general case as PAO2=PIO2−PACO2(FIO2+RQ1−FIO2).
Physiological Non-Uniformity of Ventilation
The regional variation in airflow caused by gravity in an upright individual, where the base of the lung has lower resting volume and higher compliance than the apex, resulting in greater alveolar ventilation per unit volume at the base.

Pulmonary Vascular Resistance (Rpulmonary)
The low hydrodynamic resistance of the pulmonary bed, calculated as ΔP/Q˙=7mmHg/(83mL/s)=0.08PRU compared to systemic resistance of 1.1PRU, which protects alveolar air spaces from hydrostatic fluid transudation.
Physiological Non-Uniformity of Perfusion
The gravitational and hydrostatic pressure gradient in an upright lung that causes pulmonary blood flow per unit volume to be markedly higher at the base than at the apex.

West Zone 1
An apex lung zone where alveolar pressure exceeds pulmonary arterial and venous pressures (PA>PPA>PPV), collapsing capillaries and preventing blood flow; absent in normal upright individuals but seen during positive-pressure ventilation or hemorrhage.
West Zone 2
A middle lung zone where pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure exceeds venous pressure (PPA>PA>PPV), producing a waterfall effect where blood flow is determined by the arterial-alveolar pressure gradient (PPA−PA).
West Zone 3
A dependent lung zone where pulmonary arterial and venous pressures both exceed alveolar pressure (PPA>PPV>PA), keeping capillaries distended throughout and driving continuous flow governed by the arteriovenous pressure gradient (PPA−PPV).
West Zone 4
The extreme base of the lung where blood flow decreases slightly due to elevated intrapleural pressure (Pip), partial compression of extra-alveolar vessels, and reduced regional volume causing lower mechanical radial traction.