1. Chapter 23: The Respiratory System
BIO 211 Lecture
Instructor: Dr. Gollwitzer

2. Today in class we will:
Describe the functions of the organs and anatomical structures of the respiratory system
Distinguish between external respiration and internal respiration
Describe the key steps in external respiration
Define pulmonary ventilation and begin to describe the general roles of pressure changes, muscle movement and respiratory rates and volumes
Pressure changes
Discuss the general relationship between gas pressure, volume and airflow into/out of the lungs
Define respiratory cycle, inhalation/inspiration and exhalation/expiration
Define intrapulmonary pressure and intrapleural pressure
Discuss how intrapulmonary pressure and intrapleural pressure change during the respiratory cycle

3. Energy Produced by cells for:
Maintenance
Growth
Defense
Replication
Usually obtained through aerobic mechanisms
Requires O2 and produces CO2
O2 and CO2 exchange occurs in lungs
CVS = link between exchange surfaces of lungs and interstitial fluids

4. Functions of the Respiratory System
Provides large area for gas exchange between air and blood
Moves air to/from exchange surfaces of lungs (alveoli)
Protects respiratory surfaces
From dehydration, temperature changes, invasion by pathogens
Produces sounds, e.g., speaking, singing
Provides olfactory sensations to CNS
From olfactory epithelium in nasal cavity

5. Respiratory Physiology
Respiration = 2 integrated processes
Internal (cellular, mitochondrial) respiration (see Chapter 25)
O2 uptake and CO2 production by individual cells
External respiration
Exchange of O2 and CO2 between interstitial fluids and the external environment
Involves the respiratory system

6. External Respiration
Figure 23-12

7. 3 Processes of External Respiration
Pulmonary ventilation = breathing
Physical movement of air into/out of lungs
Gas diffusion (O2 and CO2)
Across respiratory membrane (between alveolar air spaces and alveolar capillaries)
Across capillary walls in peripheral tissues
Transport of O2 and CO2
Between alveolar capillaries and capillary beds in other tissues

8. 3 Processes of External Respiration
Any abnormality in one of these processes affects:
Gas concentration of interstitial fluids
Cellular activity
If O2 declines, affected tissue oxygen-starved (hypoxia)
If supply cut off entirely, results in anoxia

9. Pulmonary Ventilation
Physical movement of air into/out of lungs
Primary function
To maintain adequate alveolar ventilation (air into/out of alveoli)
Ensures continuous supply of O2
Keeps pace with absorption by bloodstream
Prevents build up of CO2 in alveoli
Process governed by basic principles/laws

10. Law of Gas Volume and Pressure (Boyle’s Law)
Inverse relationship between gas volume and pressure
If you decrease volume of a gas, its pressure rises
If you increase the volume of a gas, its pressure falls
Air flows from area of higher pressure to area of lower pressure (down a gradient)
Provides basis for pulmonary ventilation

11. Gas Volume and Pressure
Figure 23-13, 7th edition

12. Respiratory Cycle Consists of: Volume of thoracic cavity changes
An inspiration/inhalation
An expiration/exhalation
Volume of thoracic cavity changes
With expansion/contraction of diaphragm or rib cage
Causes volume changes in lungs that create changes in pressure
Creates pressure gradients that move air into/out of the respiratory tract

13. Mechanisms of Pulmonary Ventilation
Volume of thoracic cavity changes when:
Diaphragm changes position
Forms floor of thoracic cavity
Relaxed shape is dome that projects superiorly into thoracic cavity
Contracted shape flattens and moves inferiorly
Rib cage (ribs and sternum) moves
Elevated
Lowered

14. Figure 23-14, 7th edition

15. Mechanisms of Pulmonary Ventilation
Volume of thoracic cavity increases when:
Diaphragm contracts (flattens and moves inferiorly)
Rib cage is elevated (increases depth and width)
Volume of thoracic cavity decreases when:
Diaphragm relaxes and returns to dome shape
Rib cage is lowered

16. Mechanisms of Pulmonary Ventilation
Process of breathing
At start of breath:
Pressures inside and outside thoracic cavity are the same
No air moving in or out of lungs
When thoracic cavity enlarges, pleural cavities and lungs expand to fill additional space
Expansion of lungs lowers pressure inside lungs

17. Mechanisms of Pulmonary Ventilation
Process of breathing (continued)
Air enters RT because pressure inside is lower than outside (atmospheric pressure)
Air continues to enter until volume stops increasing and internal pressure = outside pressure
When thoracic cavity decreases in size, pressure rises inside lungs, forcing air out of RT

18. Mechanisms of Pulmonary Ventilation
Direction of air flow determined by relationship between:
Atmospheric pressure (760 mm Hg)
Intrapulmonary pressure (= intra-alveolar pressure)
When lungs expand (inhalation)
Pressure decreases (to 759 mm Hg) in alveoli
Air moves in
When lungs contract (exhalation)
Pressure increases (to 761 mm Hg)
Air moves out

19. Figure 23-15

20. Mechanisms of Pulmonary Ventilation
Size of pressure gradient increases when breathing heavily
-30 mm Hg during inhalation (730 mm Hg)
+100 mm Hg straining with glottis closed (860 mm Hg)
When lifting weights, exhale because this keeps intrapulmonary and peritoneal pressures from climbing so high that alveolar rupture or hernia could occur

21. Pulmonary Ventilation
Respiratory cycle
Single cycle of inhalation and exhalation
Tidal volume (TV)
Amount of air moved into/out of lungs during single cycle
Approx 500 mL
Amount in (inhalation) = amount out (exhalation)

22. Pleural Cavity Contains lung
Parietal and visceral pleura separated by thin film of pleural fluid
Pleurae can slide along each other but great force needed to pull apart
Fluid bond exists between parietal and visceral pleurae
Pulling apart creates suction (like wet glass on smooth surface)
RESULT: surface of lung sticks to inner wall of chest and superior surface of diaphragm

23. Intrapleural Pressure
= pressure in the pleural cavity
Measured in space between parietal and visceral pleurae
Always lower than atmospheric pressure throughout normal cycles of inhalation/ exhalation
Elastic fibers in lungs pull visceral pleura away from parietal pleura
Pull increases intrapleural space and lowers intrapleural pressure
Average = -4 mm Hg (756 mm Hg)
Decreases to -6 mm Hg during inhalation
Increases to -2.5 mm Hg during exhalation
Cyclical changes operate respiratory pump
Aids in venous return to heart

24. Pneumothorax Injury to chest wall that allows air into pleural cavity
Breaks fluid bond between pleurae
Allows elastic fibers to recoil
RESULT = atelectasis (collapsed lung)
Treatment
Remove as much air as possible and seal opening
Lowers intrapleural pressure and reinflates lung

25. Today in class we will:
Define pulmonary ventilation and continue our description of the general roles of pressure changes, muscle movement and respiratory rates and volumes
Discuss muscle movement
The mechanics of breathing
Define compliance and identify the factors that affect it
Discuss respiratory rates and volumes
Define respiratory rate, respiratory minute volume, alveolar ventilation and anatomic dead space
Distinguish between various pulmonary volumes, such as tidal volume, expiratory reserve volume, residual volume and inspiratory reserve volume
Define vital capacity and total lung capacity
Discuss gas exchange
Define partial pressure and describe the partial pressures of O2 and CO2 in alveolar air and capillaries, the systemic circuit and interstitial fluid.
Principles that govern the diffusion of gases into and out of the blood
Describe the important structural features and function of the respiratory membrane

26. Mechanics of Breathing
Inhalation
Always active
Exhalation
Active or passive

27. Modes of Breathing
Respiratory muscles used in various combinations, depending on volume of air to be moved into/out of system
2 modes of breathing
Eupnea
Quiet breathing
Hyperpnea
Forced breathing

28. Modes of Breathing: Eupnea
Inhalation active (uses muscular contractions)
Exhalation passive
Costal/shallow breathing
External intercostals contract
Elevate ribs and enlarge thoracic cavity
Diaphragmatic/deep breathing
Diaphragm contracts
Increases thoracic volume

29. Figure 23-16

30. Modes of Breathing: Hyperpnea
An abnormal increase in rate and depth of breathing
Active inhalation and exhalation
Involves accessory muscles
Internal intercostals
Pectoralis minor
Sternocleidomastoid
Serratus anterior

31. Apnea Cessation of breathing Often occurs during sleep
Signaled by snoring followed by tiredness next day
Can lead to: heart disease, high BP, clots, stroke
Important to treat, e.g., continuous pressure air pump (CPAP) that keeps airways open

32. Compliance
= expandability; the ability of the lungs to tolerate changes in volume (how easily the lungs expand)
Lower compliance requires more force to fill the lungs
Greater compliance requires less force to fill the lungs
Factors affecting compliance:
Connective tissue (Ct) of lungs
Loss of supporting Ct due to alveolar damage increases compliance
Level of surfactant production
Inadequate surfactant can cause alveoli to collapse upon exhalation
Mobility of thoracic cage
Arthritis and other skeletal disorders can affect expandability of ribcage

33. Respiratory Terminology/Values
Respiratory rate = number of breaths/min
Normal, resting adult = 12-18
Child = 18-20
Tidal volume (TV) = amount of air moved in and out of lungs in single respiratory cycle
500 mL/breath
350 mL travels along passageways and enters alveoli
150 mL remains in conducting passages; never gets further than passageways = anatomic dead space

34. Respiratory Terminology/Values
Respiratory minute volume = amount of air moved (L/min)
= respiratory rate (breaths/min) X tidal volume (L/breath)
At rest = 12 breaths/min X 500 mL/breath = 6000 mL/min or 6L/min
Can be increased by increasing respiratory rate and/or tidal volume
Alveolar ventilation = amount of air reaching alveoli each minute
= respiratory rate X (TV – anatomic dead space)
At rest = 12 breaths/min X 350 mL = 4.2 L/min
Can be increased by increasing the respiratory rate and/or TV

35. Respiratory Volumes/Capacities
Fig

36. Respiratory Volumes Inspiratory reserve volume (IRV)
= Amount of air you can take in over and above TV
Expiratory reserve volume (ERV)
= Amount of air expelled after a complete and normal respiratory cycle
Residual volume (RV)
= Amount of air that remains in lungs after maximum exhalation

37. Respiratory Volumes Vital capacity (VC)
= absolute maximum amount of air you can move into or out of lungs in a single respiratory cycle
= TV + IRV + ERV
Total lung capacitance (TLC) = total volume of lungs
= VC + RV

38. Pulmonary Function Tests
Measure rate/volumes of air movements
Use spirometer, peak flow meter, pneumotachometer
Values abnormal in:
Asthmatics (asthma = reversible constriction of smooth muscle around respiratory passageways)
Smokers

39. Gas Diffusion/Exchange at Respiratory Membrane
Pulmonary ventilation ensures alveoli are supplied with O2, removes CO2
Gas exchange
Occurs between blood and alveolar air spaces across respiratory membrane
Depends on:
Partial pressures of gases
Diffusion of molecules between gas and liquid

40. Gas Laws Diffusion occurs in response to:
Concentration gradients
Pressure gradients
Cause gases to move from high pressure to low pressure
Cause gases to move in and out of solution
Rate of diffusion depends on physical principles or gas laws, e.g., gas volume and diffusion
Also determined by:
Law of Partial Pressures (Dalton’s Law)
Law of Solubility and Pressure (Henry’s Law)

41. Law of Partial Pressures (Dalton’s Law)
Air we breathe is mixture of gases
N2 (Nitrogen) = 78.6%
O2 (Oxygen) = 20.9%
H2O (water) = 0.5%
CO2 (Carbon dioxide)= 0.04%
Atmospheric pressure = 760 mm Hg
= Combined effects of different molecules colliding in air
Each gas contributes a partial pressure (P) to the total
Because we know the percentage for each gas, we can calculate the P for each
PN2+PO2 +PH2O+PCO2 = 760 mm Hg
= mm Hg

42. Law of Solubility and Pressure (Henry’s Law)
Amount of a gas in solution:
Is directly proportional to partial pressure of that gas (at a given temperature)
When gas under pressure comes in contact with liquid:
Pressure forces gas molecules into solution until equilibrium reached
At equilibrium, molecules that diffuse in = molecules that diffuse out
If P increases, more gas molecules go in
e.g. soda can (CO2 put in under pressure and can sealed)
If P decreases, more gas molecules come out of solution
e.g., open soda can, CO2 starts coming out until totally gone ( flat soda)

43. Figure 23-18, 7th edition

44. Decompression Sickness
Caused by sudden drop in atmospheric pressure
Because N2 has a high partial pressure it
Comes out of solution
Forms bubbles in joint cavities, CSF, bloodstream (like shaken soda can)
Causes great pain  curl up  “bends”
Affects:
Scuba divers (breathing air under greater than normal pressures)
People in airplanes with sudden loss of cabin pressure

45. Gas Diffusion/Exchange at Respiratory Membrane
Site of gas exchange
Very efficient
Rapid diffusion because:
Gases lipid soluble, travel easily across membrane
Substantial differences in P across respiratory membrane
Distances very small
Large total surface area
Figure 23-11c

46. Gas Diffusion/Exchange at Respiratory Membrane
Blood flow and air flow coordinated
Blood flow greatest around alveoli with highest PO2 values
Coordination lost when one part impaired
Blood flow impairment, e.g., pulmonary embolism
Air flow impairment, e.g., pulmonary obstruction

47. Partial Pressures
Figure 23-19

48. Blood Gas Analysis Measurement of pH, PCO2, PO2 Useful in monitoring:
Heart attack victims
Asthmatics (COPD = chronic obstructive pulmonary disease)

49. Today in class we will: Discuss O2 and CO2 transport
Describe how O2 is transported in the blood
Describe a normal oxygen-hemoglobin saturation curve and the effects of pH and temperature on that curve
CO2 transport
Describe how CO2 is transported in the blood
Discuss the effects of carbon monoxide (CO)
Discuss control of respiration
Describe how changes in blood flow and O2 delivery are regulated at the local level
Name the 3 respiratory centers, their locations and their basic functions
Discuss the respiratory reflexes and describe their role in respiration

50. Transport of O2 and CO2 O2 and CO2 have limited solubility in plasma
Problem solved by RBCs
Remove O2 from plasma and bind to hemoglobin
Remove CO2 from plasma and convert to soluble compounds
Reactions are temporary and completely reversible
If tissue gases high, excess removed by RBCs
If too low, RBCs release stored reserves

51. O2 Transport In blood leaving alveolar capillaries:
1.5 % of O2 in solution
Rest bound to Fe ions in center of heme units of hemoglobin molecules
Each Hb can bind 4 molecules of O2  oxyhemoglobin
Hb + O2   HbO2
(reversible reaction)
> 1 billion O2 molecules/RBC!

52. Figure 19-3, 7th edition

53. Hemoglobin Saturation
O2 carrying capacity of Hb
= % of total heme units bound to O2
Presented in a graph
Curved (vs. straight) line because:
Hb changes shape each time O2 molecule bound
Each O2 bound makes next O2 binding easier
Factors that affect saturation
Blood PO2
Blood pH
Temperature

54. Hemoglobin Saturation
Blood PO2
High PO2  % saturation of hemoglobin increases
e.g., at PO2 = 100 mm Hg, Hb sa = 98%
Low PO2  % saturation of hemoglobin decreases
e.g., at PO2 = 40 mm Hg, Hb sa = 75%
Automatically regulates O2 delivery

55. Figure 23-20

56. Hemoglobin Saturation
Blood pH
Active tissues generate acids that lower pH of interstitial fluid and blood
CO2   HCO3   H+ + HCO3-
When PCO2 increases, H+ increases, pH decreases (more acidic)
Decreased blood pH 
Change in shape of hemoglobin  releases O2 more readily
% Hb saturation decreases
“ Bohr Effect”

57. Figure 23-21, 7th edition

58. Hemoglobin Saturation
Temperature
Increase in temp  Hb releases more O2
Decrease in temp  Hb binds O2 more tightly
Significant only in active tissues where heat is generated, e.g., skeletal muscles

59. CO2 Transport After entering bloodstream, CO2 is:
Converted to carbonic acid (70%)
Bound to Hb inside RBCs  carbaminohemoglobin (23%)
Remains dissolved in plasma (7%)
Completely reversible reactions

60. Figure 23-23

61. Figure 23-24

62. CO (Carbon Monoxide) Poisoning
CO produced from burning fuels, e.g., combustion in engines, space heaters, etc.
CO competes with O2 for binding sites on Hb
CO “wins” because has greater affinity than O2
Very strong attachment
Makes Hb unavailable for O2
Treatment
Administer pure O2 to force CO off and O2 on Hb
Transfuse RBCs

63. Control of Respiration
O2 absorption and delivery =
CO2 production and removal
If unbalanced, homeostatic mechanisms restore equilibrium
Mechanisms involved
Local factors
Control blood flow and O2 and CO2 exchange and transport
Respiratory centers
Control depth and rate of respiration

64. Control of Respiration: Local Factors
Regulate O2 delivery to and CO2 removal from tissues
Active tissues  dec PO2 and inc PCO2
Inc PCO2  relaxed smooth muscle in arterioles and capillaries  vasodilation  inc blood flow
More PO2 delivered, more CO2 carried away
Coordinate alveolar blood flow
Low alveolar PO2  alveolar capillaries constrict
Blood flows toward alveolar capillaries where PO2 is high
Coordinate alveolar airflow
Inc PCO2 in bronchioles  relaxed smooth muscle in bronchioles  bronchodilation  inc air flow out of lungs; dec PCO2  bronchoconstriction

65. Control of Respiration: Respiratory Centers
In brain stem (i.e., pons, medulla oblongata)
Body’s autopilot
Also has centers for HR, BP, temp
3 pairs of nuclei that regulate respiratory muscles
Respiratory rhythmicity centers (in medulla oblongata) – set rate
Apneustic centers (in pons) – cause inspiration
Pneumotaxic centers (in pons) – inhibit apneustic and promote exhalation

66. Respiratory Centers and Reflex Controls
Figure 23–26, Part 4

67. Control of Respiration: Respiratory Reflexes
Baroreceptors
Chemoreceptors

68. Control of Respiration: Baroreceptor Reflexes
Baroreceptors
Monitor amount of stretch in walls of
Arteries
R atrium
Located in
Carotid sinuses (expanded chambers near base of internal carotid arteries) (Fig 21-22)
Aortic sinuses (sac-like dilations at base of ascending aorta) (Fig 20-8b)
Respond to changes in BP (see Chapter 21)
Affect respiratory rhythmicity centers
Inc BP  dec respiratory rate
Dec BP  inc respiratory rate

69. Figure 21-22

70. Figure 20-8b, 7th edition

71. Control of Respiration: Chemoreceptor Reflexes
Chemoreceptors
Respond to inc CO2, dec pH, dec O2 in arteries or CSF
Located in
Carotid bodies (near carotid sinuses)
Aortic bodies (near aortic arch)
Stimulate respiratory rhythmicity centers (in medulla oblongata), e.g., inc CO2 
Inc respiratory rate
Inc elimination of CO2 at alveoli
Dec PCO2

72. Control of Respiration: Voluntary Control
Conscious and unconscious thought processes also affect respiration
Fear  stimulates sympathetic system  bronchodilation and inc respiratory rate
Relaxation has opposite effect
Cannot override respiratory center activity or chemoreceptor reflexes by holding breath
When PCO2 increases to critical level, forced to breathe

73. Aging and the Respiratory System
Respiratory system less efficient in elderly
Elastic tissue deteriorates  dec vital capacity of lungs
Chest movements restricted by:
Arthritic changes
Decreased flexibility of costal cartilages
Some degree of emphysema usually present

74. Emphysema Chronic, progressive condition
Characterized by shortness of breath and inability to tolerate physical exertion
Alveoli expand, merge  larger air spaces supported by fibrous tissue without capillaries
Loss of respiratory surface restricts O2 absorption
Associated with cigarette smoke and aging

75. Respiratory Performance
Figure 23-28

76. Lung Cancer Aggressive cancer
Originates in epithelial cells of bronchioles or alveoli
Diagnosis usually delayed until tumor masses restrict airflow
Signs/symptoms: chest pain, shortness of breath, cough/wheeze, weight loss
Treatment: surgery, radiation exposure, chemotherapy
Associated with smoking