Exam 4 Flashcards
Alveolar-Capillary
Gas exchange in the lungs occurs
in air sacs, known as alveoli.
- Type I alveolar cells
- Type II alveolar cells (surfactant)
- Alveolar epithelium
- Epithelial basement membrane
- Capillary basement membrane
- Capillary lumen
- RBC
Gas exchange
A. Dalton’s law of partial pressures:
Partial pressure= Total pressure X Fractional gas concentration
In dry inspired air, PO2=160 mm Hg, PCO2=0 mm Hg
In humidified tracheal air at 37 C. (H2O) PO2=150 mmHg, PCO2=0 mmHg
Partial pressures of O2 and CO2 in inspired air, alveolar air, PAO2=100 mmHg, PACO2=40 mmHg (A=Alveolar)
In blood (Pulmonary a.) PO2=40 mmHg, PCO2=46 mmHg
In blood (Pulmonary v.) PO2=100 mmHg, PCO2=4o mmHg
Gas Laws
Diffusion of gases-Fick’s law
Transfer of gases across cell membranes or capillary walls occurs by simple diffusion, For gases, the rate of transfer by diffusion is directly proportional to the driving force, a diffusion coefficient, and the surface area available for diffusion, it is inversely proportional to the thickness of membrane barrier.
Gas Laws
Lung diffusing capacity (DL)
DL combines:* the diffusion coefficient of the gas, *the surface area of the membrane, and *the thickness of the membrane.
DL also takes into account the time required for the gas to combine with proteins in pulmonary capillary blood (e.g., binding of O2 to hemoglobin in red cells).
DL can be measured with carbon monoxide (CO) because CO transfer across the alveolar/pulmonary capillary barrier is limited exclusive by the diffusion process.
Lung diffusing capacity (DL)
In various diseases,
In various diseases, DL changes: in emphysema, DL deceases because destruction of alveoli results in a decreased surface area for gas exchange.
In fibrosis or pulmonary edema, DL decreases because the diffusion distance (membrane thickness or interstitial volume) increases.
In anemia, DL decreases because the amount of hemoglobin in red blood cells is reduced (recall that DL includes the protein-binding component of O2 exchange).
During exercise, DL increases because additional capillaries are perfused with blood, which increases the surface area for gas exchange.
Diffusion of gases such as O2 and CO2
The diffusion rates of O2 and CO2 depend on the partial pressure differences across the membrane and the area available for diffusion.
For example, the diffusion of O2 from alveolar air into the pulmonary capillary depends on the partial pressure difference for O2 between alveolar air and pulmonary capillary blood. Normally, capillary blood equilibrates with alveolar gas, when the partial pressures of O2 become equal, then there is no more net diffusion of O2.
Perfusion-limited and diffusion-limited gas exchange:
- Perfusion-limited exchange
In perfusion-limited exchange, the gas equilibrates early along the length of the pulmonary capillary. The partial pressure of the gas in arterial blood becomes equal to the partial pressure in alveolar air.
Thus, for a perfusion-limited process, diffusion of the gas can be increased only if blood flow increases.
- Diffusion-limited exchange *****
In fibrosis, the diffusion of O2 is restricted because thickening of the alveolar membrane increases diffusion distance.
In emphysema, the diffusion of O2 is decreased because the surface area for diffusion of gases is decreased.
Lung volumes
Tidal volume (TV)
is the volume inspired or expired with each normal breath.
Lung volumes
Inspiratory reserve volume (IRV)
- is the volume that can be inspired over and above the tidal volume.
- is used during exercise.
Lung volumes
Expiratory reserve volume (ERV)
is the volume that can be expired after the expiration of a tidal volume.
Lung volumes
Residual volume (RV)
is the volume that remains in the lungs after a maximal expiration.
Can not be measured by spirometry.
Lung volumes
Dead space
a. Anatomic dead space
- is the volume of the conducting airways.
- is normally approximately 150ml.
Lung volumes
Dead space
b. Physiologic dead space
- is a functional measurement.
- is defined as the volume of the lungs that does not participate in gas exchange.
- is approximately equal to the anatomic dead space in normal lungs.
- may be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects.
VD = dead space VT = tidal volume PaCO2 = partial pressure of carbon dioxide in arteries PECO2 = partial pressure of carbon dioxide in exhaled air
-In words, the equation states that physiologic dead space is tidal volume multiplied by a fraction. The fraction represents the dilution of alveolar Pco2 by dead-space air, which does not participate in gas exchange and does not therefore contribute CO2 to expired air.
VD = dead space VT = tidal volume PaCO2 = partial pressure of carbon dioxide in arteries PECO2 = partial pressure of carbon dioxide in exhaled air
-In words, the equation states that physiologic dead space is tidal volume multiplied by a fraction. The fraction represents the dilution of alveolar Pco2 by dead-space air, which does not participate in gas exchange and does not therefore contribute CO2 to expired air.
Ventilation rate
a. Minute ventilation is expressed as follows
:Minute ventilation=Tidal volume x Breath/min
b. Aveolar ventilation is expressed as follow:
Alveolar ventilation= (Tidal volume –Dead space) x Breath/min
Lung capacities
Inspiratory capacity
-is the sum of tidal volume and inspiratory reserve volume (IRV).
Lung capacities
Functional residual capacity (FRC)
-is the sum expiratory reserve volume (ERV) and residual volume (RV).
Is the volume remaining in the lungs after a tidal volume is expired.
-includes the residual volume, so it cannot be measured by spirometry.
Lung capacities
Vital capacity (VC) or forced vital capacity (FVC)
- is the sum of tidal volume, IRV, and ERV.
- is the volume of air that can be forcibly expired after a maximal inspiration.
Lung capacities
Total lung capacity (TLC)
- is the sum of all four lung volumes.
- is the volume in the lungs after a maximal inspiration.
- includes residual volume, so it cannot be measured by spirometry.
Forced expiratory volume (FEV1)
- is the volume of air that can be expired in the first second of a forced maximal expiration.
- is normally 80% of the forced vital capacity, which is expressed as:
FEV1/FVC=0.8
- In obstructive lung disease, such as asthma, FEV1 is reduced more than FVC so that FEV1/FVC is decreased.
- In restrictive lung disease, such as fibrosis, both FEV1 and FVC are reduced.
Mechanics of Breathing
Muscles of inspiration
- Diaphragm
- is the most important muscle for inspiration.
-When the diaphragm contracts, the abdominal contents are pushed downward, and the ribs are lifted upward and outward, increasing the volume of the thoracic cavity.
- External intercostals and accessory muscles
- are not used for inspiration during normal quiet breathing.
- are used during exercise.
Mechanics of Breathing
Muscles of Expiration
- Expiration is normally passive.
- Because the lung-chest wall system is elastic, it returns to its resting position after inspiration.
- Expiratory muscles are used during exercise or when airway resistance is increased because of disease (e.g., asthma).
- Abdominal muscles
- compress the abdominal cavity, push the diaphragm up, and push air out of the lungs. - Internal intercostal muscles
- pull the ribs downward and inward.
Surface tension of alveoli and surfactant
Surface tension of alveoli
- results from the attractive forces between molecules of liquid lining the alveoli.
- creates a collapsing pressure that is directly proportional to surface tension and inversely proportional to alveolar radius (Laplace’s law), as shown in the following equation:
P=2xT/r
P=collapsing pressure on alveolus (or pressure required to keep alveolus open)
T= surface tension
r= radius of alveolus (cm)
a. Large alveoli have low collapsing pressures and are easy to keep open.
b. Small alveoli have high collapsing pressures and are more difficult to keep open.
- In the absence of surfactant, the small alveoli have a tendency to collapse (atelectasis).
Surface tension of alveoli and surfactant
Surfactant
- lines the alveoli.
- reduces surface tension by disrupting the intermolecular forces between molecules of liquid. This reduction is surface tension prevents small alveoli from collapsing and increases compliance.
- is synthesized by type II alveolar cells and consists primarily of the phospholipid dipalmitoryl phosphatidylcholine (DPPC).
- In the fetus, surfactant synthesis is variable. Surfactant may be present as early as gestational week 24 and is almost always present by gestational week 35.
- Neonatal respiratory distress syndrome can occur in premature infants because of the lack of surfactant. The infant exhibits atelectasis (lung collapse), difficulty reinflating the lungs (as a result of decreased compliance), and hypoxemia because of the V/Q defect.(Glucocorticoid)