1. Human Physiology Chapter 13 The Mechanisms of Body Function
Vander’s
Human Physiology
The Mechanisms of Body Function
Tenth Edition by
Widmaier • Raff • Strang
© The McGraw-Hill Companies, Inc.
Figures and tables from the book, with additional comments by:
John J. Lepri, Ph. D.,
The University of North Carolina at Greensboro

3. The major parts of the “airways,” along which
air movements (ventilation) occur during breathing.

4. Figure 13-2 The relaxation/contraction of circular smooth muscle
lining these “airways’”
determines how easily
airflow can occur
(bronchodilation vs.
bronchoconstriction).
Most gas exchange
occurs in the
~8,000,000
alveolar sacs.

6. Figure 13-3
Each of the clustered alveoli includes an abundance of pulmonary capillaries, thereby assuring that the ventilated air is brought into close proximity to the “pulmonary” blood, allowing efficient and thorough gas exchange between the air and the blood.

7. Figure 13-4 Extensive branching of alveoli produces
lots of surface area
for exchange between
air and blood.
Alveolar and capillary
walls are thin,
permitting rapid
diffusion of gases.

8. Figure 13-5 The space inside the lung is filled with air.
The intrapleural fluid is found between the lungs
and the thoracic wall.
Movement of the thoracic wall by
skeletal muscles drives the ventilation cycle.

9. pulmonary capillaries is driven by the contraction
Figure 13-6
Airflow in the lungs
is called ventilation.
[AIR]
[BLOOD]
EXCHANGE
Gases exchange
by diffusion.
Bloodflow through the
pulmonary capillaries is
driven by the contraction
of the right ventricle.

10. Airflow (F) is a function of the pressure differences
between the alveoli (Palv) and the atmosphere (Patm)
divided by airflow resistance (R).
Air enters the lungs when Palv < Patm
Air exits the lungs when Palv > Patm
F = Palv__-__Patm R

11. Figure 13-8
Boyle’s law states that the pressure of a fixed
number of gas molecules is inversely
proportional to the volume of the container.

12. Figure 13-12 Inspiration is the result of
the expansion of the thoracic
cage in response to skeletal
muscle contraction.
The expansion reduces
alveolar pressure (Palv) below
atmospheric pressure (Patm),
so air moves into the lungs.

13. Figure 13-15 Expiration is the result of reducing the volume of the
thoracic cage; in a resting
person, this occurs in
response to skeletal
muscle relaxation.
The volume reduction increases
alveolar pressure (Palv) above
atmospheric pressure (Patm),
so air moves out of the lungs.

14. Figure 13-16 Lung compliance is a measure of the
lung’s “stretchability.”
When compliance is
abnormally high, the
lungs might fail to
hold themselves open,
and are prone to collapse.
abnormally low, the
work of breathing is
increased.
Match color of high compliance curve and text describing it.

16. Figure 13-17 In the absence of surfactant, the attraction between
water molecules (H-bonds)
can cause alveolar collapse.
By reducing the surface
tension of water,
surfactant helps prevent
alveolar collapse.

17. Figure 13-18 The Heimlich maneuver increases the alveolar
pressure (Palv) by
supplementing
the upward movement
of the diaphragm, thus
compressing the
thoracic cavity to
dislodge foreign objects
in the airways.

18. The tidal volume is the amount of air moved in (or out) of the
airways in a single breathing cycle. Inspiratory and expiratory
reserve volumes, are, respectively, the additional volume that
can inspired or expired; all three quantities sum to the lung’s
vital capacity. The residual volume is the amount of air that
must remain in the lungs to prevent alveolar collapse.

19. Figure 13-20 “Fresh” inspired air is diluted by the left over air
remaining in the lungs from the previous breathing cycle.

21. Figure 13-21
In the lungs, the concentration gradients favor the inward
(toward the blood) diffusion of oxygen and the outward (toward
the alveolar air) diffusion of carbon dioxide; owing to the
metabolic activities of cells, these gradients are reversed
at the interface of the blood and the active cells.

22. Figure 13-22
Changes in the concentration of dissolved gases are indicated as the blood circulates in the body. Oxygen is converted to water in cells; cells release carbon dioxide as a byproduct of fuel catabolism.

24. Figure 13-23 Changes in the rate of ventilation alter the
concentration of gases
in the alveolar air.

26. Figure 13-24
Oxygen diffusion along the length of the pulmonary capillaries quickly achieves diffusional equilibrium, unless disease processes
in the lungs reduce the rate of diffusion.

28. Figure 13-26 Hemoglobin is the gas-transport molecule inside
erythrocytes.

29. Figure 13-27
Note that venous blood is typically 75% saturated with oxygen.
As the concentration of oxygen increases, the percentage of
hemoglobin saturated with bound oxygen increases until all
of the oxygen-binding sites are occupied (100% saturation).

30. Figure 13-28
Adding hemoglobin to compartment B substantially increases
the total amount of oxygen in that compartment, since the
bound oxygen is no longer part of the diffusional equilibrium.

31. Figure 13-30 Chemical and thermal factors that
alter hemoglobin’s affinity to bind
oxygen alter the ease of “loading”
and “unloading” this gas in the
lungs and near the active cells.

34. Chemosensory neurons
that respond to changes
in blood pH and gas
content are located in
the aorta and in the
carotid sinuses; these
sensory afferent
neurons alter CNS
regulation of
the rate of ventilation.

35. Figure 13-34 A severe reduction in the arterial concentration of
oxygen in the blood can stimulate hyperventilation.

36. Figure 13-35 Chemosensory neurons that respond to decreased
oxygen levels in the blood
“inform” the ventilation
control center in the
medulla to increase the rate of ventilation.

37. Figure 13-36 Small changes in the carbon dioxide content
of the blood quickly
trigger changes in
ventilation rate.

38. Figure 13-37 Central and peripheral
chemosensory neurons that respond to increased carbon dioxide levels in the blood are also stimulated by the acidity from carbonic acid, so they “inform” the ventilation control center in the medulla oblongata to increase the rate of ventilation.

39. Figure 13-38 Regardless of the source, increases in the acidity of
the blood cause
hyperventilation.

40. Figure 13-39
Regardless of the source, increases in the acidity of the blood cause hyperventilation, even if carbon dioxide levels are driven to abnormally low levels.

41. Figure 13-40 The levels of oxygen, carbon dioxide, and hydrogen ions
in blood and CSF
provide information
that alters the
rate of ventilation.

42. Figure 13-42
Absence of scale on ordinate axis
(1) Instantaneous hyperventilation with exercise onset suggests that learning allows the body to anticipate gas exchange needs during exercise.
(2) “Oxygen debt” after exercise includes restoration of myoglobin and creatin phosphate and acid cleanup.

43. Figure 13-43 An integrated perspective recognizes the variety and
diversity of factors that alter the rate
of ventilation.

46. The End.