1. Respiratory physiology

2. Respiration is the process by which the body takes in and utilizes oxygen (O2) and gets rid of carbon dioxide (CO2).

3. Respiration can be divided into four major functional events
Ventilation: Movement of air into and out of lungs
Gas exchange between air in lungs and blood
Transport of oxygen and carbon dioxide in the blood
Internal respiration: Gas exchange between the blood and tissues

4. Respiratory System Functions
Gas exchange: Oxygen enters blood and carbon dioxide leaves
Regulation of blood pH: Altered by changing blood carbon dioxide levels
Voice production: Movement of air past vocal folds makes sound and speech
Olfaction: Smell occurs when airborne molecules drawn into nasal cavity
Protection: Against microorganisms by preventing entry and removing them

5. Section 1 Pulmonary Ventilation
Pulmonary ventilation means the inflow and outflow of air between the atmosphere and the lung alveoli, which is determined by the activity of the airways, the alveolus and the thoracic cage.

6. I Functions of the Respiratory Passageways

7. Respiratory System Divisions
Upper tract
Nose, pharynx and associated structures
Lower tract
Larynx, trachea, bronchi, lungs

8. Conducting Zone
All the structures air passes through before reaching the respiratory zone.
Cartilage holds tube system open and smooth muscle controls tube diameter
Warms and humidifies inspired air.
Filters and cleans:
Insert fig. 16.5

9. Respiratory Zone Region of gas exchange between air and blood.
Includes respiratory bronchioles and alveolar sacs.

10. Airway branching

11. Bronchioles
and Alveoli

12. Thoracic Walls and Muscles of Respiration

13. Breathing Occurs because the thoracic cavity changes volume
Insipiration uses external intercostals and diaphragm
Expiration is passive at rest, but uses internal intercostals and abdominals during severe respiratory load
Breathing rate is breaths / minute at rest, at maximum exercise in adults

14. Thoracic Volume

15. Pleura

16. Pleural fluid produced by pleural membranes
Acts as lubricant
Helps hold parietal and visceral pleural membranes together

17. Ventilation Movement of air into and out of lungs
Air moves from area of higher pressure to area of lower pressure
Pressure is inversely related to volume

18. Alveolar Pressure Changes During Respiration

19. Principles of Breathing
Functional Unit: Chest Wall and Lung
Conducting
Airways
Follows Boyle’s Law: Pressure (P) x Volume (V) = Constant
Pleural Cavity Imaginary Space between
Lungs and chest wall
Pleural Cavity
Very small space
Maintained at negative pressure
Transmits pressure changes
Allows lung and ribs to slide
Chest Wall
(muscle, ribs)
Lungs
Gas Exchange
Diaphragm
(muscle)

20. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0 Pb
Airway Open A CW Pi PS D 1

21. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0
Inhalation:
Increase Volume of Rib cage
Decrease the pleural cavity pressure - Decrease in Pressure inside (Pi) lungs Pb
Airway Open A Pi CW PS D 2

22. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0
Inhalation:
Pb outside is now greater than Pi - Air flows down pressure gradient
Until Pi = Pb Pb
Airway Open A Pi CW PS D 3

23. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0
Exhalation: Opposite Process
Decrease Rib Cage Volume Pb
Airway Open A Pi CW PS D 4

24. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0
Exhalation: Opposite Process
Decrease Rib Cage Volume
Increase in pleural cavity pressure - Increase Pi Pb
Airway Open A Pi CW PS D 5

25. Pb Pi Principle of Breathing At Rest with mouth open Pb = Pi = 0
Follows Boyle’s Law: PV= C
At Rest with mouth open Pb = Pi = 0
Exhalation: Opposite Process
Decrease Rib Cage Volume
Increase Pi
Pi is greater than Pb
Air flows down pressure gradient
Until Pi = Pb again Pb
Airway Open A Pi CW PS D 6

26. Mechanisms of Breathing: How do we change the volume of the rib cage ?
To Inhale is an ACTIVE process
Diaphragm
External Intercostal Muscles
Intercostals Contract to Lift
Rib
Spine
Ribs
Volume
Rib Cage
Contract
Diaphragm
Volume
Both actions occur simultaneously – otherwise not effective

30. II Respiratory Resistance
Including Elastic Resistance and Inelastic resistance

31. Elastic Resistance
A lung may be considered as an elastic sac. The thoracic wall also can be considered as an elastic element.
So during inspiration the inspiratory muscles must expand the thoracic cage which are together with the elastic resistance.

32. Elasticity Tendency to return to initial size after distension.
High content of elastin proteins.
Very elastic and resist distension.
Recoil ability.
Elastic tension increases during inspiration and is reduced by recoil during expiration.

33. Compliance Distensibility (stretchability):
Ease with which the lungs can expand.
The compliance is inversely proportional to elastic resistance
Change in lung volume per change in transpulmonary pressure.
DV/DP
100 x more distensible than a balloon.

34. Static lung compliance
C = DV/DP
100
deflation
Lung
volume
(%TLC) 50
normal
breathing
inflation
Transpulmonary pressure (cmH2O) 30

35. The elastic forces can be divided into two parts:
the elastic forces of the lung tissue itself
2) the elastic forces caused by surface tension of the fluid that lines the inside wall of the alveoli.
The elastic forces caused by surface tension are much more complex. Surface tension accounts for about two thirds of the total elastic forces in a normal lungs.

36. Surface Tension Force exerted by fluid in alveoli to resist distension
Lungs secrete and absorb fluid, leaving a very thin film of fluid.
This film of fluid causes surface tension..
H20 molecules at the surface are attracted to other H20 molecules by attractive forces.
Force is directed inward, raising pressure in alveoli.

37. What is Surface Tension ?
At surface
Unbalanced forces
Generate Tension
Within Fluid
All forces balance

38. Surface Tension Law of Laplace:
Pressure in alveoli is directly proportional to surface tension; and inversely proportional to radius of alveoli.
Pressure in smaller alveolus would be greater than in larger alveolus, if surface tension were the same in both.
Insert fig

39. Effect of Surface Tension on Alveoli size
Air Flow
Expand
Collapse

40. Surfactant Phospholipid produced by alveolar type II cells.
Lowers surface tension.
Reduces attractive forces of hydrogen bonding by becoming interspersed between H20 molecules.
Surface tension in alveoli is reduced.
As alveoli radius decreases, surfactant’s ability to lower surface tension increases.

41. Area dependence of Surfactant action
Low S/unit Area
Saline
Decrease Area
Saline
Slider - Change Surface Area
Increase Area
High S/unit Area
Tension
Area
Surfactant

42. Surfactant prevents alveolar collapse

43. Factors Contributing to Compliance
- Hysteresis
Volume L 6
Saline Filled
Normal (with surfactant) 3
Without surfactant RV
- 30 cm H2O
Pleural Pressure
- 15

44. Inelastic Resistance
The inelastic resistance comprises the airway resistance (friction) and pulmonary tissue resistance (viscosity, and inertia).
Of these the airway resistance is by far the more important both in health and disease. It account for 80%-90% of the inelastic resistance.

45. Airway Resistance
Airway resistance is the resistance to flow of air in the airways and is due to :
1) internal friction between gas molecules
2) friction between gas molecules and the walls of the airways

46. Types of Flow

47. Laminar flow
… is when concentric layers of gas flow parallel to the wall of the tube. The velocity profile obeys Poiseuille’s Law (pg 43:11)

48. Poiseuille and Resistance
Airway Radius or diameter is KEY.
 radius by 1/2  resistance by 16 FOLD - think bronchodilator here!!

49. Airway resistance increase
Any factor that decreases airway diameter, or increases turbulence will increase airway resistance, eg:
Rapid breathing: because air velocity and hence turbulence increases
Narrowing airways as in asthma, parasympathetic stimulation, etc.
Emphysema, which decreases small airway diameter during forced expiration

50. Control of Airway Smooth Muscle
Neural control
Adrenergic beta receptors causing dilatation
Parasympathetic-muscarinic receptors causing constriction
NANC nerves (non-adrenergic, non-cholinergic)
Inhibitory release VIP and NO  bronchodilitation
Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation”

51. Control of Airway Smooth Muscle (cont.)
Local factors
histamine binds to H1 receptors-constriction
histamine binds to H2 receptors-dilation
slow reactive substance of anaphylaxsis-constriction-allergic response to pollen
Prostaglandins E series- dilation
Prostaglandins F series- constriction

52. Control of Airway Smooth Muscle (cont)
Environmental pollution
smoke, dust, sulfur dioxide, some acidic elements in smog
elicit constriction of airways
mediated by:
parasympathetic reflex
local constrictor responses

53. III Pulmonary Volume and Capacity

55. Pulmonary Volumes Tidal volume Inspiratory reserve volume
Volume of air inspired or expired during a normal inspiration or expiration (400 – 500 ml)
Inspiratory reserve volume
Amount of air inspired forcefully after inspiration of normal tidal volume (1500 – 2000 ml)
Expiratory reserve volume
Amount of air forcefully expired after expiration of normal tidal volume (900 – 1200 ml)
Residual volume
Volume of air remaining in respiratory passages and lungs after the most forceful expiration (1500 ml in male and 1000 ml in female)

57. Pulmonary Capacities Inspiratory capacity Functional residual capacity
Tidal volume plus inspiratory reserve volume
Functional residual capacity
Expiratory reserve volume plus the residual volume
Vital capacity
Sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume
Total lung capacity
Sum of inspiratory and expiratory reserve volumes plus the tidal volume and residual volume

59. Minute and Alveolar Ventilation
Minute ventilation: Total amount of air moved into and out of respiratory system per minute
Respiratory rate or frequency: Number of breaths taken per minute
Anatomic dead space: Part of respiratory system where gas exchange does not take place
Alveolar ventilation: How much air per minute enters the parts of the respiratory system in which gas exchange takes place

60. Dead Space Area where gas exchange cannot occur
Includes most of airway volume
Anatomical dead space (=150 ml)
Airways
Physiological dead space
= anatomical + non functional alveoli

61. DEAD SPACE Basic Structure of the Lung VD VA NO GAS EXCHANGE
A tube = Airway (Trachea – Bronchi – Bronchioles)
NO GAS EXCHANGE
DEAD SPACE
A thin walled Sac = Alveolus
Blood Vessels
GAS EXCHANGE
OCCURS HERE VA
Formula: Total Ventilation = Dead Space + Alveolar Space VT = VD + VA

62. Similar Concept: Physiological Dead Space
Healthy Lungs:
Anatomical Dead Space = Airways (constant) VA VD
Diseased lungs:
Physiological = Anatomical Dead Space Dead Space +
Blocked Vessel
Additional Dead Space

63. FVC - forced vital capacity
defines maximum volume of exchangeable air in lung (vital capacity)
forced expiratory breathing maneuver
requires muscular effort and some patient training
initial (healthy) FVC values approx 4 liters
slowly diminishes with normal aging
significantly reduced FVC suggests damage to lung parenchyma
restrictive lung disease (fibrosis)
constructive lung disease
loss of functional alveolar tissue (atelectasis)
FVC volume reduction trend over time (years) is key indicator
intra-subject variability factors
age
sex
height
ethnicity

64. FEV1 - forced expiratory volume (1 second)
defines maximum air flow rate out of lung in initial 1 second interval
forced expiratory breathing maneuver
requires muscular effort and some patient training
FEV1/FVC ratio
normal FEV1 about 3 liters
FEV1 needs to be normalized to individual’s vital capacity (FVC)
typical normal FEV1/FVC ratio = 3 liters/ 4 liters = 0.75
standard screening measure for obstructive lung disease (COPD)
FEV1/FVC reduction trend over time (years) is key indicator
calculate % predicted FEV1/FVC (age and height normalized)
reduced FEV1/FVC suggests obstructive damage to lung airways
episodic, reversible by bronchodilator drugs
probably asthma
continual, irreversible by bronchodilator drugs
probably COPD

65. Spirometry
1 sec
Total Lung Capacity
Forced Vital Capacity - FVC
Volume (litres)
Time (sec)
Forced Expiratory Volume in 1 sec - FEV1
Residual Volume

66. Lung Volume in Restrictive Disease
Assessment of RESTRICTIVE Lung Diseases
These are diseases that reduce the effective surface area available for gas exchange
Normal Lung Volume
Lung Volume in Restrictive Disease
eg fibrosis / pulmonary oedema

67. RESTRICTIVE lung disease
Volume (litres)
Time (sec)
Vital Capacity
Total Lung Capacity
Residual Volume
Spirometry
RESTRICTIVE lung disease
REDUCED

68. Assessment of OBSTRUCTIVE Lung Diseases
These are diseases that reduce the diameter of the airways and increase airway resistance -
remember Resistance increases with 1/radius 4
Normal Airway Calibre
Airway Calibre in Obstructive Disease
eg asthma / bronchitis

69. FEV1 > 80% of FVC is Normal Forced Vital Capacity - FVC
or in words - you should be able to forcibly expire more than 80% of your vital capacity in 1 sec.
Forced Expiratory Volume in 1 sec - FEV1

70. OBSTRUCTIVE lung disease
Volume (litres)
Time (sec)
Total Lung Capacity
Residual Volume
Spirometry
1 sec
OBSTRUCTIVE lung disease
Forced Vital Capacity - FVC
Forced Expiratory Volume in 1 sec - FEV1
FEV1 < 80% of FVC