Lecture 19 - Respiration 2 - Mechanics of Breathing

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    Dr. Christina [email protected]

    PHY2021Mechanics of Breathing

    http://www.google.com.sg/url?sa=i&rct=j&q=old+pictures+paintings+of+respiratory+system&source=images&cd=&cad=rja&docid=8XdAzm7byEcWJM&tbnid=7FuR29Z95rBMTM:&ved=0CAUQjRw&url=http%3A%2F%2Flapetitemort73.blogspot.com%2F2009_03_01_archive.html&ei=Fq42UYStPIGpkwXcp4GwCg&bvm=bv.43287494,d.bmk&psig=AFQjCNH7vAOSQaj7lI6QNH5dLynGrw1ygA&ust=1362623969056948
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    Volume, pressure and airflow changes during respiratory cycle

    Mechanical relationship between lung and chest wall:

    Generation of pressure gradient between atmosphere and alveoli

    Muscles of respiration

    Airway resistance; Stability of alveoli; Pulmonary Surfactant

    Role of lung compliance during breathing

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

    Key Learning Outcomes

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

    Lung Volumes and Capacities

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

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    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

    5. Cellular utilization of O2 & production

    of CO2

    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

    Steps in Ventilation

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    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

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    Boyles law: P1V1=P2V2

    Volumes and pressures are related!

    The pressure of a gas is inversely related to the volume of its container.

    A decrease in thoracic volume leads to an increase in pressure.

    As the chest is a closed container, an increase in thoracic volume will

    lead to a decrease in pressure.

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    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)

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    Lung expansion relies on intrapleural pressure.

    How does increasing and decreasing thoracic

    volume alter lung volume?

    Intrapleural space

    Visceral pleura

    Parietal pleura

    Small changes in this pressure work to couple

    changes in thoracic volume with changes in

    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 chestwall wants to expand. This creates a sub-

    atmospheric intrapleural pressure.

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    Pressure differences involved in ventilation

    Palv

    Intrapleural FluidLung wall

    Chest wall

    Pip

    Atmosphere

    Patm

    Palv < PatmPalv > Patm

    Ptp = Palv - Pip

    Pcw = Pip -Patm

    Patm

    Prs= Palv- Patm

    Opposes inward elastic recoil of the lung

    Opposes out ward elastic recoil of chest wall

    Determines air flow

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    Inspiration as chest wall expands, Pip

    (Boyles law)

    Palv

    Intrapleural Fluid

    Lung wall

    Chest wall

    Pip

    Ptp Pip Lung expands

    Palv Air flows inward

    Ptp = Palv - Pip

    Air flows inward

    Greater than inward elastic recoil force

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    Expiration Decrease firing of phrenic nerve and

    intercostal nerve respiratory muscles

    relax Chest recoils back to originalposition smaller thoracic volume

    Palv

    Intrapleural Fluid

    Lung wall

    Chest wall

    Pip

    Ptp Pip Lung recoils

    Palv Air flows out

    Ptp = Palv - Pip

    Air flows outward

    Lower than inward elastic recoil force

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    Quiet Expiration

    Expiration is due to passive recoil

    During quiet breathing, expiration is passive process

    (no muscle contraction)

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    Stable Balance Between Breaths

    Intrapleural space

    Alveolus

    Chest wall

    Elastic recoil of lung Elastic recoil of chest wall

    Patm= 0mmHg

    Palv = 0mmHg

    Ptp = Palv - Pip= 4mmHg

    Pcw = Pip - Patm= - 4 mmHg

    Pip= - 4mmHg

    Prs= Palv - Patm = 0 mmHg

    No

    Flow

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    Respiratory Cycle & Pressure Changes

    Inspiration Expiration

    2

    - 2

    - 4

    - 6

    0

    0

    0.5

    4 secTime

    Pressuresduringbreathing(m

    mHg)

    Breathvolume(L)

    End of Expiration

    Mid Inspiration

    End Inspiration

    Mid Expiration

    1

    2

    3

    4

    Patm = 0

    Palv = 0

    Nofl

    ow

    Ptp = 4Pip = - 4

    Palv

    Pip

    Ptp

    Airflow

    Patm = 0

    Palv = -1

    Palv - Patm = -1

    Ptp = Patm Pip = 7

    Recoil

    Pip

    = - 6

    Pip

    = - 7

    Recoil

    Patm = 0Noflow

    Palv = 0

    Palv - Patm = 0

    Ptp = Patm Pip = 5

    Pip = - 5

    Recoil

    Ptp = Patm Pip = 6

    Airflow

    Patm = 0

    Palv = 1

    Palv - Patm = 1

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    Deep Breathing

    Inspiration involvescontraction of extramuscles to elevateribs: scalenes,pectoralis minor, &

    sternocleidomastoidmuscles

    Expiration involvescontraction ofinternal intercostals& abdominal muscles

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    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

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    Compliance

    Magnitude of change in lung volumeproduced by a given change in Ptp

    How easily lung expands with pressure

    Major determinants: - Elasticity

    - Surface tension

    Is reduced by factors that cause resistanceto stretching

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    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.

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    Surface tension (& elasticity) are forces that promote alveolar

    collapse & resist stretching

    Surface tension of H2O tends to collapse alveoli (attractive forcesbetween 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

    Surface tension

    Pressure needed to

    keep a sphere shape=

    2x Surface tension

    radius

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    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

    Surfactant

    H2O molecules

    Alveolar wall

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    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

    R l f f t t i h t i

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    Role of surfactant in hysteresis

    Hysteresis

    Surface tension forces

    overcome by surface film

    pressure (prevent collapse)

    Surface tension forces

    overcome by surface film

    pressure

    (prevent collapse)

    Alveolus expands.

    Not enough surfactant

    molecules to totally resist

    surface tension forces.- Difficult to expand

    More surfactant molecules

    produced.

    Alveolus expands easily

    Alveolus starting to decrease in

    size but surfactant moleculesprevent this.

    Surfactant molecules pushed

    out of film allowing alveolusto decrease easily

    surfactant

    water

    alveolus

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    Resistance =

    Airway resistance - effect of radius on airflow

    radius 4

    constant x lengthOhms and Poiseuilles Laws combined:

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

    Double the length = doubles the resistance

    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

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    Airway resistance (RAW)

    Raw > in medium-sized

    bronchi, not small bronchioles

    Example cross-sectional areas

    Trachea = 2.5cm

    2

    Terminal bronchioles = 240cm2

    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 cross-

    sectional area

    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.

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    Measuring lung function

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    Measurement of Lung volumes and capacities

    Spirometer - for measuring lung volumes & capacities

    - also inspiratory and expiratory flow rates

    Spirogram

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    Spirogram

    Measure changes in lung volumeduring breathing.

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

    Cannot measure the absolute gas volumein the lungs

    - need Helium dilution or plethysmography.

    Lung volumes - related to gender, height, weight, age.

    - also affected by lung diseases.

    Tid l V l ( i t b thi )

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    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)

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    Tidal volume

    500ml

    LUNG VOLUMES

    Inspiratory

    reserve

    volume

    Expiratory reservevolume

    Residua

    l

    Volume

    (1.2L)

    Dead space

    (airways)

    Lung volumes and capacities

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    Lung volumes and capacities

    Expiratory Reserve Volume (ERV)

    Amount of expired air during forced expiration after quiet breathingResidual Volume (RV)

    Amount of air remain in lungs after maximal expiration

    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

    Vital Capacity (VC)

    Total amount of air that is maximally expired after maximum inspiration

    = IRV + TV + ERV

    Lung Volumes & Capacitiescontinue

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    Lung Volumes & Capacities

    Inspiratory Capacity (IC)

    Total amount of air that is maximally inspired after normal expiration

    IC = IRV + TVFunctional 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 byspirometer

    RV & FRC is measurable

    by N2 wash-out technique

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    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 DeadSpace Volume)

    Maximum voluntary ventilation

    = maximum minute ventilation

    (i.e maximum breathing effort)

    Depends on muscular effort and airway resistance

    Ob t ti l di

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    Obstructive lung disease1- 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.

    N E

    Lung volumes and work of breathing

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    Lung volumes and work of breathing

    Diseases/conditions

    affecting themRESTRICTIVE

    Pulmonary fibrosis, chest

    burns, diaphragm in obesity

    and pregnancy, muscleweakness

    OBSTRUCTIVE

    Asthma, COPD,

    Bronchiectasis, bronchitis,

    tumours

    Work aspects of breathing

    Work to expand the chest

    FEV1 is severely decreased:

    FEV1/FVC = < 80%

    FEV1 and FVC are decreased. But:

    FEV1/FVC = about 80% (normal)Airway resistance

    - Work to move air into the lungs

    S i t Fl l

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    Spirometry: Flow-volume curves

    Respiratory Physiology. John West. Chapter 10; page 160

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    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 & Physiology7th Ed

    (chapter 22)