PHY2021 Mechanics of Breathing

Dr. Christina GY
christina.yap@monash.edu

Key Learning Outcomes

After this lecture and with further reading you will be able to describe:

Mechanical relationship between lung and chest wall:

Generation of pressure gradient between atmosphere and alveoli

Muscles of respiration

Volume, pressure and airflow changes during respiratory cycle Role of lung compliance during breathing
Airway resistance; Stability of alveoli; Pulmonary Surfactant

Lung Volumes and Capacities

A brief review of major respiratory disorders that change the
mechanics of the respiratory system

Essential Reading: Vanders (11th ed) Chapter 13, p 44356

Steps in Ventilation
1. Ventilation: Exchange of air between atmosphere & alveoli by bulk flow

2. Exchange of O2 & CO2 between alveolar air & blood in lung capillaries by diffusion

3. Transport of O2 &CO2 through pulmonary & systemic circulation by bulk flow

4. Exchange of O2 & CO2 between blood in tissue capillaries & cells in tissues by diffusion 5. Cellular utilization of O2 & production of CO2

The respiratory system

Chest is a closed container. Closed at top by muscle & connective tissue. Closed at sides by ribs & muscle Sealed at bottom by diaphragm

Boyles law: P1V1=P2V2

Volumes and pressures are related!
The pressure of a gas is inversely related to the volume of its container.

As the chest is a closed container, an increase in thoracic volume will lead to a decrease in pressure. A decrease in thoracic volume leads to an increase in pressure.

Quiet Inspiration

The diaphragm and external intercostal muscles contract External intercostal muscles elevate the rib cage the sternum moves anteriorly

Diaphragm flattens and moves inferiorly

Volume and Pressure (within the thoracic cavity and the lungs)

Lung expansion relies on intrapleural pressure.

How does increasing and decreasing thoracic volume alter lung volume? The lungs are only attached at the hilus! Lung expansion following increased thoracic volumes is dependent on intrapleural pressure. Consequently, due to elastic recoil of the lung during expiration, lungs collapse away from the chest wall this draws chest wall in! At rest, the lungs want to collapse, but chest wall wants to expand. This creates a subatmospheric intrapleural pressure. Small changes in this pressure work to couple changes in thoracic volume with changes in lung volume!
Visceral pleura

Parietal pleura

Intrapleural space

Pressure differences involved in ventilation

Atmosphere

Patm Palv > Patm Palv < Patm

Ptp

= Palv - Pip

Opposes inward elastic recoil of the lung

Pcw = Palv
Lung wall Intrapleural Fluid Chest wall Pip Prs = Palv- Patm

Pip - Patm

Opposes out ward elastic recoil of chest wall

Patm
Determines air flow

Air flows inward

Inspiration
as chest wall expands, Pip (Boyles law) Pip

Ptp
Palv

Lung expands Air flows inward

Ptp Palv

= Palv - Pip

Greater than inward elastic recoil force

Pip

Lung wall
Intrapleural Fluid

Chest wall

Expiration
Decrease firing of phrenic nerve and intercostal nerve respiratory muscles Air flows outward relax Chest recoils back to original position smaller thoracic volume Pip
Ptp Palv Ptp Lung recoils Air flows out

= Palv - Pip

Lower than inward elastic recoil force

Palv

Pip

Lung wall
Intrapleural Fluid Chest wall

Quiet Expiration

Expiration is due to passive recoil During quiet breathing, expiration is passive process (no muscle contraction)

Stable Balance Between Breaths

Patm = 0mmHg
No Flow

Elastic recoil of lung

Pip = - 4mmHg

Elastic recoil of chest wall

Ptp Alveolus Chest wall

= Palv - Pip = 4mmHg

Pcw = Pip -

Patm = - 4 mmHg

Palv = 0mmHg

Prs = Palv - Patm = 0 mmHg

Intrapleural space

Expiration

Pressures during breathing (mmHg)

Mid Expiration

Palv
0 -2

Patm
No flow

Palv = 1 Ptp = Patm Pip = 6 Recoil Pip = - 5 =0

Palv - Patm = 0

Air flow

Inspiration

Respiratory Cycle & Pressure Changes

Patm = 0 Palv - Patm = 1

Patm = 0
No flow

Ptp Pip

Palv = 0 Ptp = Patm Pip = 7 Recoil

Palv = 0
-4 Ptp = 4 Pip = - 4 Patm = 0

-6 Breath volume (L) 0.5 0 4 sec Time

Air flow

End of Expiration

Pip = - 7

Palv - Patm = -1

End Inspiration

Palv = -1 Recoil Pip = - 6

Ptp = Patm Pip = 5

Mid Inspiration

Deep Breathing
Inspiration involves

contraction of extra muscles to elevate ribs: scalenes, pectoralis minor, & sternocleidomastoid muscles
Expiration involves contraction of internal intercostals & abdominal muscles

Physical Aspects of Ventilation

Ventilation results from pressure differences induced by changes in lung volumes

Air moves from higher to lower pressure

Compliance, elasticity, & surface tension

of lungs influence ease of ventilation

Compliance
Magnitude of change in lung volume

produced by a given change in Ptp

How easily lung expands with pressure Major determinants: - Elasticity

- Surface tension
Is reduced by factors that cause resistance

to stretching

Elasticity
Tendency to return to initial size after distension

Due to high content of elastin proteins

Elastic tension increases during inspiration &

is reduced by recoil during expiration

Elastic Recoil
- return to the original dimension driven by the elastic tension generated during stretching.

Surface tension
Surface tension (& elasticity) are forces that promote alveolar
collapse & resist stretching

Surface tension of H2O tends to collapse alveoli (attractive forces

between liquid molecules is greater than forces between liquid and gas molecules)

Smaller alveoli tend to collapse more than larger ones Law of Laplace relationship between pressure (P), surface tension
(T), and the radius (r) of an alveolus : P = 2T/r
Pressure needed to 2x Surface tension = keep a sphere shape radius

Pulmonary surfactant
Produced by alveoli type II cells Function: - reduce surface tension during expiration - consequently increasing the lung compliance (decreasing the work of breathing). - Prevents alveoli from collapse - Preventing fluid accumulation in the alveoli - host defense mechanism against infection
and inflammation

Alveolar wall H2O molecules Surfactant

Surface tension & surfactant

Surfactant reduces surface tension Surfactant production starts in late gestation Secreted by type II alveolar cells Surfactant (a mixture of phospholipids & proteins) Diplamitoyl phosphatidyl choline (DPPC) Hydrophobic tail, hydrophillic head

Role of surfactant in hysteresis

Surfactant molecules pushed out of film allowing alveolus to decrease easily Alveolus starting to decrease in size but surfactant molecules prevent this.

Hysteresis

Surface tension forces overcome by surface film pressure (prevent collapse) Surface tension forces overcome by surface film pressure (prevent collapse)

More surfactant molecules produced. Alveolus expands easily

surfactant water alveolus

Alveolus expands. Not enough surfactant molecules to totally resist surface tension forces. - Difficult to expand

Airway resistance - effect of radius on airflow

Factors affecting airway radii (resistance): - physical - Trans pulmonary pressure (Ptp) - elastic connective fibers - Intrapleural pressure (Pip) - neuro-endocrine influence the airway smooth muscle - epinephrine - relaxes smooth muscles - leukotrines - contract smooth muscles
constant x length radius 4 = doubles the resistance

Ohms and Poiseuilles Laws combined: Resistance = Double the length

Halve airway radius = 16 xs increase in resistance (e.g. asthma)

Airway resistance (RAW)

Raw > in medium-sized bronchi, not small bronchioles The medium-sized bronchi (over 2mm) around the 7th generation have the highest resistance This is because the small airways are so numerous and, existing in parallel, have a large total crosssectional area Example cross-sectional areas Trachea = 2.5cm2 Terminal bronchioles = 240cm2

Importantly, the low resistance of the small airways makes them a silent zone on auscultation
Early obstructive (emphysema) disease affects these vessels first, but is hard to detect.

Measuring lung function

Measurement of Lung volumes and capacities

Spirometer - for measuring lung volumes & capacities

- also inspiratory and expiratory flow rates

Spirogram

Measure changes in lung volume during breathing.

Can also be used to measure flow rates (L/sec) - inspiratory or expiratory.

Cannot measure the absolute gas volume in the lungs - need Helium dilution or plethysmography. Lung volumes - related to gender, height, weight, age. - also affected by lung diseases.

Tidal Volume (quiet breathing)

Each breath is ~500 ml - Most of this reaches the alveoli In each breath, ~350 ml reaches the alveoli and ~150 ml stays in the airways (ie. dead space).

Anatomical dead space is the air

in conducting airways (~150 ml). At end of normal expiration, there

~2.5 L in the Lungs:

ie. they are never empty. (values are for typical young adult male)

LUNG VOLUMES
Dead space (airways)
Residua l Volume 500ml (1.2L)

Expiratory reserve volume

Tidal volume

Inspiratory reserve volume

Lung volumes and capacities

Tidal Volume (TV) Amount of air that goes in/out of lungs for each inspiration/expiration Inspiratory Reserve Volume (IRV) Amount of inspired air more than TV during maximal inspiration Expiratory Reserve Volume (ERV) Amount of expired air during forced expiration after quiet breathing Residual Volume (RV) Amount of air remain in lungs after maximal expiration Vital Capacity (VC) Total amount of air that is maximally expired after maximum inspiration = IRV + TV + ERV

continue

Lung Volumes & Capacities

Inspiratory Capacity (IC)

Total amount of air that is maximally inspired after normal expiration

IC = IRV + TV Functional Residual Capacity (FRC) Total amount of residual air in the lungs after normal expiration FRC = ERV + RV Total Lung Capacity (TLC)

Total amount of air in the lungs after maximal inspiration

TLC = IRV + TV + ERV + RV RV & FRC cannot be measured by spirometer RV & FRC is measurable by N2 wash-out technique

Pulmonary Ventilation
Minute ventilation Volume of air breathed per minute (litres/min)
MV = Tidal Volume (mL/breath) x Respiratory rate (breaths /min)

eg: 12 breaths/min x 500 ml = 6 litres/min

Alveolar minute ventilation = breath/min x (TV Dead Space Volume)

Maximum voluntary ventilation = maximum minute ventilation (i.e maximum breathing effort) Depends on muscular effort and airway resistance

Obstructive lung disease

1- Asthma.
Chronic inflammation of airways and hypersensitivity to allergens. Increased tone of airway smooth muscle and excessive mucus secretion .

2- Chronic bronchitis.
Increase in mucus secretion and inflammation of airway walls .

3- Emphysema.
Destruction of alveolar walls reduce the

radial traction of airways and therefore

the airway resistance is abnormally high

Obstructive lung diseases - airway resistance is abnormally increased.

Lung volumes and work of breathing

Work aspects of breathing
Work to expand the chest

Diseases/conditions affecting them

RESTRICTIVE Pulmonary fibrosis, chest burns, diaphragm in obesity and pregnancy, muscle weakness
FEV1 and FVC are decreased. But: FEV1/FVC = about 80% (normal)

Airway resistance - Work to move air into the lungs

OBSTRUCTIVE Asthma, COPD, Bronchiectasis, bronchitis, tumours FEV1 is severely decreased: FEV1/FVC = < 80%

Spirometry: Flow-volume curves

Respiratory Physiology. John West. Chapter 10; page 160

Reading...

Recommended reading

Vanders (chapter 13) p443-56 Silverton (chapter 17) p 568-574, p 578-589

Other very very useful information...!

Ward JPT Respiratory System at a Glance (chapters 1-3, 20) Marieb & Hoehn Human Anatomy & Physiology 7th Ed
(chapter 22)