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Learning objectives
At the end of this lecture, you will be able to:
1) Describe the contributions of lung elasticity and surfactants upon lung compliance. 2) List and describe the factors that affect airway resistance. 3) Differentiate between an obstructive and a restrictive pulmonary disorder based on changes in lung capacity. 4) Contrast minute ventilation with alveolar ventilation.
1) Lung compliance is defined as the change in lung volume (V) that results from a given change with transpulmonary pressure (Palv Pip) Ease in which lungs can be stretched V (Palv Pip)
Lung compliance =
formed by the thin layer of fluid lining the internal surface of the alveoli. As lung tissue expands, work is required not only to stretch the elastic tissue but also to increase the surface area of the fluid layer. Greater tension less compliant
Pulmonary surfactant (surface active agents) decreases the surface tension in alveoli.
Surfactant is a detergent secreted from type II alveolar cells that decreases surface tension by interfering with hydrogen bonding between water molecules. Surfactant increases lung compliance making inspiration easier. If surface tension were equal between two alveoli sharing a duct, the pressure would be higher in b, and air in b would move to the region of lower pressure in a causing b to collapse.
Surfactant stabilizes alveoli of different sizes by differentially altering surface tension allowing the alveoli to have the same pressure.
Babies who are born prematurely can develop newborn respiratory distress syndrome (NRDS).
Normally, surfactant synthesis begins about the 25th week of fetal development and reaches adequate levels by the 34th week, about 6 weeks before normal delivery. In addition to having stiff (lowcompliance) lungs, too little surfactant allows the alveoli to collapse and then they have to re-inflate every time. This is a huge energy drain. Treatment includes administration of steroid hormones to help stimulate surfactant production, aerosol administration of artificial surfactant, and artificial ventilation.
2) Airway resistance is the second major factor influencing the work of breathing.
The effect of airway resistance on breathing:
When resistance increases, a larger pressure gradient is required to produce a given rate of air flow.
3. In a normal person, what contributes more to the work of breathing: airway resistance or lung and chest wall elastance?
Three parameters contribute to resistance (R): the systems length (L), the viscosity of the substance flowing through the system (), and the radius (r) of the tubes in the system. 1. 8L Resistance (R) = r4 2.
air flow into and out of the lungs is low, because the radii of the tubes in the conducting zone are large and, in the respiratory zone, the total crosssectional area of the smaller tubes increases due to extensive branching. Consequently, lung and chest wall elastance provides more of the work of breathing.
The bronchioles have a total cross sectional area about 2000 times that of the trachea and do not normally contribute significantly to airway resistance.
The bronchioles, however, are collapsible tubes and a decrease in their diameter (bronchoconstriction) can contribute significantly to their resistance. Bronchioles, like arterioles, are subject to reflex control by the autonomic nervous system and by hormones. Most minute to minute changes occur in response to paracrines. For example, the paracrine signal Histamine acts as a powerful bronchoconstrictor. Histamine is released by mast cells in response to tissue damage or contact by allergens.
Spirometry is a technique for measuring the volumes of inspired and expired air using a device called a spirometer. An individual breathes into and out of a tube connected to a transducer that converts the volume of air to an electrical signal proportional to the volume. Using spirometry, three of the four nonoverlapping lung volumes that together make up the total lung capacity can be directly measured, including: tidal volume, inspiratory, and expiratory reserve volumes.
Use of spirometry to measure lung volumes and calculate lung capacities can differentiate between obstructive and restrictive pulmonary disorders.
Use of spirometry to measure lung volumes and calculate lung capacities can differentiate between obstructive and restrictive pulmonary disorders.
Restrictive pulmonary diseases involve an interference with lung expansion. Obstructive pulmonary diseases involve increases in airway resistance. In these cases, residual volume increases because an increase in resistance makes both expiration and inspiriation difficult. For egchronic obstructive pulmonary disease (COPD) refers to a combination of two lung diseases, chronic bronchitis and emphysema. The lungs become overinflated and ultimately the functional residual capacity and total lung capacity increase.
Restrictive disorders often involve structural damage to the lungs, plura, or chest wall that decrease the total lung capacity and vital capacity.
6000 ml/min =
Note only a fraction of this air is available for exchange with the blood. The air that remains in the upper airways does not get to the alveoli. The upper airways are thus referred to as dead space. The upper conducting airways have a volume of ~150ml, therefore the volume of fresh air reaching the alveoli (or the alveolar ventilation) is:
4200 ml/min =
350 ml/breath
12 breath/min
Ventilation
1 1
End of inspiration
2700 mL
Ventilation
2700 mL 1
The first exhaled air comes out of the dead space. 1 End of inspiration Only 350 mL leaves the alveoli. 2 Exhale 500 mL (tidal volume)
150 mL
2200 mL
KEY
Ventilation
2700 mL 1
The first exhaled air comes out of the dead space. 1 End of inspiration Only 350 mL leaves the alveoli. 2 Exhale 500 mL (tidal volume)
3 At the end of expiration, the dead space is filled with stale air from alveoli.
150 mL
2200 mL
KEY
2200 mL
Ventilation
2700 mL 1
Atmospheric air Dead space is filled with fresh air. Only 350 mL of fresh air reaches alveoli The first 150 mL of air into the alveoli is stale air from the dead space.
150 350 150 2200 mL 4
The first exhaled air comes out of the dead space. 1 End of inspiration Only 350 mL leaves the alveoli. 2 Exhale 500 mL (tidal volume)
3 At the end of expiration, the dead space is filled with stale air from alveoli.
150 mL
2200 mL
KEY
2200 mL
Ventilation
2700 mL 1
Atmospheric air Dead space is filled with fresh air. Only 350 mL of fresh air reaches alveoli The first 150 mL of air into the alveoli is stale air from the dead space.
150 350 150 2200 mL 4
The first exhaled air comes out of the dead space. 1 End of inspiration Only 350 mL leaves the alveoli. 2 Exhale 500 mL (tidal volume)
3 At the end of expiration, the dead space is filled with stale air from alveoli.
150 mL
2200 mL
KEY
2200 mL
Figure 17-14