1. Overview of Respiration and Respiratory Mechanics
Dr Shihab Khogali
Ninewells Hospital & Medical School, University of Dundee

2. See blackboard for detailed learning objectives
This lecture is the first of four-linked lectures …in this lecture:
Understand what is meant by the terms “internal respiration” and “external respiration”
Know the four steps of external respiration
Understand Ventilation - the first step of external respiration
What is
This
Lecture
About?
See blackboard for detailed learning objectives

3. Understand ventilation (Step 1 of external respiration).
Know that gases move from higher to lower pressure, with the Boyle’s Law.
Understand the respiratory mechanics and the relationship between atmospheric, intra-alveolar, and intrapleural pressures.
understand the significance of transmural pressure gradient. Know that peumothorax abolishes the transmural pressure gradient.
Understand that inspiration is an active process and that normal resting expiration is a passive process.
Know the inspiratory muscles and the accessory muscles of respiration (link with anatomy).
Describe the role and importance of pulmonary surfactant, with the Law of Laplace and alveolar stability.
Know the lung volumes and capacities. Understand the changes in dynamic lung volumes in obstructive and restrictive lung disease.
Know the factors which influence airway resistance.
Define the compliance of lungs and thorax.
Understand what is meant by the term work of breathing.

4. Internal Respiration ‘energy’ + CO2 Our body systems are made of cells
These cells need a constant supply of oxygen (O2) to produce energy and function
The carbon dioxide (CO2) produced by the cellular reactions must continuously be removed from our bodies
The internal respiration refers to the intracellular mechanisms which consumes O2 and produces CO2
Internal Respiration
‘food’ O2
‘energy’ CO2

5. External Respiration Atmosphere
The term external respiration refers to the sequence of events that lead to the exchange of O2 and CO2 between the external environment and the cells of the body
External respiration is the topic for our four-linked physiology lectures
External respiration involves four steps O2
CO2
Alveoli of lungs
CO2 O2
Pulmonary
circulation
Systemic
circulation
CO2 O2
Food + O2
CO2 + HO2 + HTP
Tissue cell

6. Steps of external respiration
Atmosphere
Steps of external respiration 1
Ventilation or gas exchange between
the atmosphere and air sacs (alveoli)
in the lungs O2
CO2
Alveoli of lungs 2
Exchange of O2 and CO2 between air
in the alveoli and the blood
CO2 O2
Pulmonary
circulation 3
Transport of O2 and CO2 between the
lungs and the tissues
Systemic
circulation
CO2 O2 4
Exchange of O2 and CO2 between the
blood and the tissues
Food + O2
CO2 + HO2 + ATP
Internal respiration
Tissue cell
Fig. 13-1, p. 452

7. The Four Steps of External Respiration
Ventilation
The mechanical process of moving gas in and out of the lungs
Gas exchange between alveoli and blood
The exchange of O2 and CO2 between the air in the alveoli and the blood in the pulmonary capillaries
Gas transport in the blood
The binding and transport of of O2 and CO2 in the circulating blood
Gas exchange at the tissue level
The exchange of O2 and CO2 between the blood in the systemic capillaries and the body cells

8. Three body systems are involved in external respiration
Atmosphere
Three body systems are involved
in external respiration
The Respiratory System
The Cardiovascular System
The Haematology System O2
CO2
Alveoli of lungs
CO2 O2
Pulmonary
circulation
Systemic
circulation
CO2 O2
Food + O2
CO2 + HO2 + HTP
Tissue cell

9. Ventilation The mechanical process of moving air between the
atmosphere and alveolar sacs
Figure 13.2: Anatomy of the respiratory system.
(a) The respiratory airways. (b) Enlargement of the alveoli (air sacs) at the terminal end of the airways. Most alveoli are clustered in grapelike arrangements at the end of the terminal bronchioles. (Source: Adapted from Cecie Starr and Ralph Taggart, Biology: The Unity and Diversity of Life, 8th ed., Fig a, p Copyright © 1998 Wadsworth.)

10. Air flow down pressure gradient from a region of high pressure to a region of low pressure
The intra-alveolar pressure must become less than atmospheric pressure for air to flow into the lungs during inspiration. How is this achieved?
Before inspiration the intra-alveolar pressure is equivalent to atmospheric pressure
During inspiration the thorax and lungs expand as a result of contraction of inspiratory muscles
But: How the movement of the chest wall expand the lungs as there is no physical connection between the lungs and chest wall?
Ventilation
Boyle’s Law
At any constant temperature the
pressure exerted by a gas varies
inversely with the volume of the gas
as the volume of a gas increases the pressure exerted by the gas decreases

11. Linkage of Lungs to Thorax
Two forces hold the thoracic wall and the lungs in close opposition:
(1) The intrapleural fluid cohesiveness: The water molecules in the intrapleural fluid are attracted to each other and resist being pulled apart. Hence the pleural membranes tend to stick together.
(2) The negative intrapleural pressure: the sub-atmospheric intrapleural pressure create a transmural pressure gradient across the lung wall and across the chest wall. So the lungs are forced to expand outwards while the chest is forced to squeeze inwards.

12. Figure 13.8: Transmural pressure gradient.
Across the lung wall, the intra-alveolar pressure of 760 mm Hg pushes outward, while the intrapleural pressure of 756 mm Hg pushes inward. This 4 mm Hg difference in pressure constitutes a transmural pressure gradient that pushes out on the lungs, stretching them to fill the larger thoracic cavity. Across the thoracic wall, the atmospheric pressure of 760 mm Hg pushes inward, while the intrapleural pressure of 756 mm Hg pushes outward. This 4 mm Hg difference in pressure constitutes a transmural pressure gradient that pushes inward and compresses the thoracic wall.

13. Three Pressures are Important in Ventilation

14. Inspiration is an active process depending on muscle contraction
The volume of the thorax is increased vertically by contraction of the diaphragm (major inspiratory muscle), flattening out its dome shape.
Phrenic nerve from cervical 3,4 and 5
The external intercostal muscle contraction lifts the ribs and moves out the sternum.
The “bucket handle” mechanism.

15. Figure 13.12: Respiratory muscle activity during inspiration and expiration.
(a) Inspiration, during which the diaphragm descends on contraction, increasing the vertical dimension of the thoracic cavity. Contraction of the external intercostal muscles elevates the ribs and subsequently the sternum to enlarge the thoracic cavity from front to back and from side to side.

16. Inspiration is an active process brought about by contraction of inspiratory muscles
The chest wall and lungs stretched
The Increase in the size of the lungs make the intra-alveolar pressure to fall
This is because air molecules become contained in a larger volume (Boyle’s Law)
The air then enters the lungs down its pressure gradient until the intra-alveolar pressure become equal to atmospheric pressure
Inspiration
760
Size of thorax on
contraction of
inspiratory muscles
759
754
Size of lungs as they
are stretched to fill
the expanded thorax

17. Normal expiration is a passive process brought about by relaxation of inspiratory muscles
The chest wall and stretched lungs recoil to their preinspiratory size because of their elastic properties
The recoil of the lungs make the intra-alveolar pressure to rise
This is because air molecules become contained in a smaller volume (Boyle’s Law)
The air then leaves the lungs down its pressure gradient until the intra-alveolar pressure become equal to atmospheric pressure
Expiration
760
Size of thorax on
relaxation of
inspiratory
muscles
761
756
Size of lungs as
they recoil

18. Changes in intra-alveolar and intra-pleural pressures during the respiratory cycle
Inspiration
Expiration
Intra-alveolar
pressure
Atmospheric
pressure
Intrapleural
pressure
Transmural pressure
gradient across the
lung wall
Fig , p. 462

19. Pneumothorax (air in the pleural space) abolishes the transmural pressure gradient
Figure 13.9: Pneumothorax.
(a) Traumatic pneumothorax. A puncture in the chest wall permits air from the atmosphere to flow down its pressure gradient and enter the pleural cavity, abolishing the transmural pressure gradient. (b) Collapsed lung. When the transmural pressure gradient is abolished, the lung collapses to its unstretched size, and the chest wall springs outward. (c) Spontaneous pneumothorax. A hole in the lung wall permits air to move down its pressure gradient and enter the pleural cavity from the lungs, abolishing the transmural pressure gradient. As with traumatic pneumothorax, the lung collapses to its unstretched size.

20. Elastic connective tissue in the lungs
What causes the lungs to recoil during expiration? (i.e. what gives the lungs their elastic behaviour)
Elastic connective tissue in the lungs
The whole structure bounces back into shape
But even more important is the alveolar surface tension

21. What is alveolar surface tension?
Attraction between water molecules at liquid air interface
In the alveoli this produces a force which resists the stretching of the lungs
If the alveoli were lined with water alone the surface tension would be too strong so the alveoli would collapse

22. Surfactant Reduces the Alveolar Surface Tension
According to the law of LaPlace: the smaller alveoli (with smaller radius - r) have a higher tendency to collapse
Pulmonary surfactant is a complex mixture of lipids and proteins secreted by type II alveoli
It lowers alveolar surface tension by interspersing between the water molecules lining the alveoli
Surfactant lowers the surface tension of smaller alveoli more than that of large alveoli
This prevent the smaller alveoli from collapsing and emptying their air contents into the larger alveoli
Surfactant Reduces the Alveolar Surface Tension
Surfactant prevent this happening
If we regard the alveoli as spherical bubles, then:
P = inward directed collapsing pressure
T = Surface Tension
r = radius of the buble
(LaPlace’s Law)

23. Respiratory Distress Syndrome of the New Born
Developing fetal lungs are unable to synthesize surfactant until late in pregnancy
Premature babies may not have enough pulmonary surfactant
This causes respiratory distress syndrome of the new born
The baby makes very strenuous inspiratory efforts in an attempt to overcome the high surface tension and inflate the lungs.

24. Another factor which helps keep the alveoli open is: The Alveolar Interdependence
Figure 13.17: Alveolar interdependence.
(a) When an alveolus (in pink) in a group of interconnected alveoli starts to collapse, the surrounding alveoli are stretched by the collapsing alveolus. (b) As the neighboring alveoli recoil in resistance to being stretched, they pull outward on the collapsing alveolus. This expanding force pulls the collapsing alveolus open.
If an alveolus start to collapse the surrounding alveoli are
stretched and then recoil exerting expanding forces in the
collapsing alveolus to open it

26. Figure 13.11: Anatomy of the respiratory muscles.
Fig , p. 459

27. Lung Volumes and Capacities
See Practical Class and Online Tutorial

28. Predicted normal values vary with age, height, gender,..
Figure 13.18: Variations in lung volume.
(b) Normal spirogram of a healthy young adult male. (The residual volume cannot be measured with a spirometer but must be determined by another means.)
Predicted normal values vary with age, height, gender,..

29. Lung Volumes and Capacities
Description
Average Value
Tidal volume (TV)
Volume of air entering or leaving lungs during a single breath
500 ml
Inspiratory reserve volume (IRV)
Extra volume of air that can be maximally inspired over and above the typical resting tidal volume
3000 ml
Inspiratory capacity (IC)
Maximum volume of air that can be inspired at the end of a normal quiet expiration (IC =IRV + TV)
3500 ml
Expiratory reserve volume (ERV)
Extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume
1000 ml
Residual volume (RV)
Minimum volume of air remaining in the lungs even after a maximal expiration
1200 ml

30. Lung Volumes and Capacities
Description
Average Value
Functional residual capacity (FRC)
Volume of air in lungs at end of normal passive expiration (FRC = ERV + RV)
2200 ml
Vital capacity (VC)
Maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV)
4500 ml
Total lung capacity (TLC)
Maximum volume of air that the lungs can hold (TLC = VC + RV)
5700 ml
Forced expiratory volume in one second (FEV1): Dynamic volume
Volume of air that can be expired during the first second of expiration in an FVC (Forced Vital Capacity) determination
FEV1% = FEV1/FVC ratio
Normal >75%

31. Spirometry for Dynamic Lung Volumes
Volume time curve - allow you to determine:
FVC = Forced Vital Capacity (maximum volume that can be forcibly
Expelled from the lungs following a maximum inspiration)
FEV1 = Forced Expiratory volume in one second
FEV1% = FEV1/FVC ratio

32. Normal
Obstructive Lung Disease

35. Airway Resistance F: Flow P: Pressure R: Resistance
Resistance to flow in the airway normally is very low and therefore air moves with a small pressure gradient
Primary determinant of airway resistance is the radius of the conducting airway
Parasympathetic stimulation causes bronchoconstriction
Sympathetic stimulation causes bronchodilatation
Disease states (e.g. COPD or asthma) can cause significant resistance to airflow
Expiration is more difficult than inspiration

36. Dynamic Airway Compression
During inspiration the airways are pulled open by the expanding thorax. Therefore in cases of increased airway resistance expiration tends to be more difficult.
The transairway pressure tends to compress airways during active expiration -
pleural pressure rises during expiration (increases airway resistance)
If no obstruction: the increased airway resistance causes an increase in
airway pressure upstream. This helps open the airways (i.e. reduce the
compressive transairway pressure)
Transairway Pressure = Airway Pressure – Pleural pressure
If there is an obstruction (e.g. COPD), the driving pressure between the alveolus and airway is lost over the obstructed segment. This causes a fall in airway pressure along the airways resulting in airway compression by the transairway pressure during active expiration.

37. Peak Flow Meter Gives an estimate of peak flow rate
The peak flow rate assess airway function
The test is useful in patients with obstructive lung disease (e.g. asthma and COPD)
It is measured by the patient giving a short sharp below into the peak flow meter
The average of three attempts is usually taken
The peak flow rate in normal adults vary with age and height
You will practice taking the peak flow rate in the Clinical Skills Centre
Peak Flow Meter

38. Compliance During inspiration the lungs are stretched
Compliance is measure of effort that has to go into stretching or distending the lungs
Volume change per unit of pressure change across the lungs
The less compliant the lungs are, the more work is required to produce a given degree of inflation
Decreased by factors such as pulmonary fibrosis

39. Work of Breathing
Normally requires 3% of total energy expenditure for quiet breathing
Lungs normally operate at about “half full”
Work of breathing is increased in the following situations
When pulmonary compliance is decreased
When airway resistance is increased
When elastic recoil is decreased
When there is a need for increased ventilation