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    16 Pulmonary Ventsilation CH16 2

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    Brodsky Macedo
    The respiratory system uses pressure changes and muscle contraction to drive breathing. During inspiration, contraction of the diaphragm and external intercostal muscles increases the volume of the thoracic cavity. This causes negative pressure in the pleural space, expanding the lungs and alveoli. During expiration, relaxation of these muscles and contraction of the internal intercostals and abdominal muscles decreases the chest cavity volume and increases alveolar pressure, expelling air. Lung compliance and airway resistance also impact ventilation, with pulmonary surfactant and bronchiole smooth muscle playing important roles. Spirometry measures lung volumes and capacities to evaluate respiratory function.

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    16 Pulmonary Ventsilation CH16 2

    Uploaded by

    Brodsky Macedo
    33 views34 pages
    The respiratory system uses pressure changes and muscle contraction to drive breathing. During inspiration, contraction of the diaphragm and external intercostal muscles increases the volume of the thoracic cavity. This causes negative pressure in the pleural space, expanding the lungs and alveoli. During expiration, relaxation of these muscles and contraction of the internal intercostals and abdominal muscles decreases the chest cavity volume and increases alveolar pressure, expelling air. Lung compliance and airway resistance also impact ventilation, with pulmonary surfactant and bronchiole smooth muscle playing important roles. Spirometry measures lung volumes and capacities to evaluate respiratory function.

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    The respiratory system uses pressure changes and muscle contraction to drive breathing. During inspiration, contraction of the diaphragm and external intercostal muscles increases the volume of the thoracic cavity. This causes negative pressure in the pleural space, expanding the lungs and alveoli. During expiration, relaxation of these muscles and contraction of the internal intercostals and abdominal muscles decreases the chest cavity volume and increases alveolar pressure, expelling air. Lung compliance and airway resistance also impact ventilation, with pulmonary surfactant and bronchiole smooth muscle playing important roles. Spirometry measures lung volumes and capacities to evaluate respiratory function.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    33 views34 pages

    16 Pulmonary Ventsilation CH16 2

    Uploaded by

    Brodsky Macedo
    The respiratory system uses pressure changes and muscle contraction to drive breathing. During inspiration, contraction of the diaphragm and external intercostal muscles increases the volume of the thoracic cavity. This causes negative pressure in the pleural space, expanding the lungs and alveoli. During expiration, relaxation of these muscles and contraction of the internal intercostals and abdominal muscles decreases the chest cavity volume and increases alveolar pressure, expelling air. Lung compliance and airway resistance also impact ventilation, with pulmonary surfactant and bronchiole smooth muscle playing important roles. Spirometry measures lung volumes and capacities to evaluate respiratory function.

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    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 34

    Respiratory System: Breathing Mechanics

    Pressure changes during inspiration and expiration

    The muscles of breathing


    Changes in alveolar volume are generated by the muscles that change
    the volume of the thoracic cavity

    Inspiratory muscles
    Diaphragm:
    contraction pulls the
    diaphragm down
    External intercostals:
    contraction pulls ribs
    up and out
    Together, contraction
    increases the volume
    of the thoracic cavity
    The expanding chest wall pulls against
    the parietal pleura pressure in the
    intrapleural space goes more negative
    and the pleural sac pulls against the lungs, expanding the alveoli

    Expiratory muscles
    During passive expiration:
    No muscle contraction
    Relaxation of the diaphragm
    and external intercostals
    During active expiration:
    Internal intercostals and
    abdominal muscles:
    contraction pulls ribs down and in
    volume of the chest cavity decreases
    volume of the alveoli decreases
    volume down pressure up
    (Boyles law)
    air goes down the pressure gradient

    View of the abdominal surface of the diaphragm


    (looking up) . Unusual skeletal muscle, bone only on one side.

    Flow chart for inspiration

    the difference between


    intrapleural pressure and
    intra-alveolar pressure
    is called
    transpulmonary pressure

    Summary figure for


    pressure changes during
    breathing

    So far weve been focusing on pressure gradients.


    Two other factors also affect pulmonary ventilation:
    1) Lung compliance
    2) Airway resistance

    1) Lung compliance
    Refers to the amount of increase in lung volume for a given amount of work
    High compliance is good
    Lung compliance depends on:
    1) the elasticity of the lungs
    remember that the lungs are spring loaded to pull inward
    affected by lung tissue thickness
    (thickening results from tissue damage
    eg tobacco toxins)
    2) the surface tension of the fluid lining
    the alveoli
    the surface of the epithelial cells is
    covered by a thin layer of water
    (keeps the cells from drying out)
    problem: water molecules tend to
    pull together (form droplets)
    pulling them apart requires work
    solution: type II epithelial cells
    secrete a substance that reduces
    surface tension pulmonary surfactant

    pulmonary surfactant forms a film on the inner surface of the alveoli

    Pulmonary surfactant is comprised of


    phospholipids and lipids (predominantly
    cholesterol - Chol) and surfactant
    associated proteins.
    The components are synthesized within
    type II epithelial cells.
    Stored in secretory vesicles termed
    lamellar bodies (LB).
    The lamellar bodies are exocytosed into the
    liquid lining of the lung (the hypophase)
    where the lipids assemble to create the
    surfactant film at the air-liquid interface.

    Low amounts of surfactant can cause alveolar collapse


    Surfactant is formed relatively late in fetal life; thus premature infants
    are at risk for respiratory distress

    (Same principle
    behind blowing
    bubbles with
    soapy water)

    So far weve been focusing on pressure gradients.


    Two other factors also affect pulmonary ventilation:
    1) Lung compliance
    2) Airway resistance

    2) Airway resistance
    Refers to resistance in the entire airway system
    (like total peripheral resistance in the cardiovascular system)
    Usually resistance is low
    Resistance depends mostly on the cross-sectional area of the pathway
    Does the cross-sectional area of the airway
    increase or decrease from the big larynx to the
    the teeny tiny bronchioles?
    A big factor is contraction of the smooth muscle
    in the walls of the bronchioles
    (remember, the bronchioles lack cartilage,
    but they are ringed by smooth muscle)

    Factors affecting contraction of smooth


    muscle in the walls of the bronchioles
    Neural and hormonal signals
    Sympathetic inputs relaxation
    (Beta 2 adrenergic receptors) see next fig
    Parasympathetic inputs constriction
    (muscarinic ACh receptors)
    Local chemicals
    Histamine constriction of smooth muscle
    and increased release of mucus
    (both increase resistance) see next next
    High levels of CO2 relaxation

    Beta 2 and Alpha receptors in muscle around arterioles


    Alpha receptors in arteriole muscle promote vasoconstriction
    (like norepinephrine from sympathetic inputs)
    Beta 2 receptors in arteriole muscle promote vasodilation
    (opposite effect to the same hormone !)
    ** Overall effect depends on (1) proportion of alpha and beta receptors
    and (2) concentration of epinephrine.
    Arteriole smooth muscle in skeletal muscle has
    a high proportion of Beta 2 (epinephrine dilates)
    So, high concentrations of epinephrine bring
    more blood to skeletal muscles.
    Gut arteriole muscle has a high proportion
    of Alpha receptors (epinephrine constricts)
    good for fight or flight
    blood pressure goes up,
    AND blood available to the
    muscles that need it in an emergency

    Histomine has opposite effects in arterioles and bronchioles


    Bee sting allergy:
    toxin triggers release of histamine (vasodilator)
    Histamine release is normal in injury
    effects are local
    But too much and
    histamine gets into the circulation

    Measurement of lung volumes and capacities


    A spirometer is used to measure volumes of inspired and expired air
    Used to
    diagnose disorders
    to measure severity of disorders
    to measure effectiveness
    of different treatments

    Expired reserve volume:


    the extra you can squeeze out
    when you really try
    ~1000 ml
    Residual volume:
    the volume left after squeezing
    out all you can
    measured by taking a breath of helium
    and measuring how much helium
    comes back out (some mixes w/ residual)

    normal breath

    maximum
    expiration

    maximum
    inspiration

    normal breath

    Inspired reserve volume:


    the extra you can squeeze in
    when you really try
    ~3000 ml

    normal breath

    Tidal volume:
    the volume in and out during
    a normal breath
    ~500 ml

    normal breath

    Volumes for normal and maximum inspirations & expirations

    Lung capacities are calculated from the volume measures


    Inspiratory capacity: the maximum volume you can get in after a normal expiration
    tidal vol + inspiratory reserve vol = 500 + 3000 = 3500 ml
    Vital capacity: the maximum volume you can get out after maximum inspiration
    tidal vol + inspiratory reserve vol + expiratory reserve vol = 500 + 3000 + 1000 = 4500
    Functional residual capacity: the volume remaining after a regular expiration
    expiratory reserve vol + residual vol = 2200 ml
    Total lung capacity: the total volume you can get in, 5700 ml

    Two additional measures are used to distinguish obstructive pulmonary disease (eg
    emphysema, chronic bronchitis) - narrowing or blockage of the airways from restrictive pulmonary disease (eg thoracic tumors, pulmonary fibrosis [scarring
    of the lungs]) - decrease in the elasticity of the lungs

    Forced vital capacity: the maximum volume you can get out as fast and as forcefully
    as possible after maximum inspiration
    Forced expiratory volume: the percentage of the FVC you can get out in the
    first 1 second

    You can measure


    Forced expiratory volume and
    Forced vital capacity (maximum volume you can get out)
    flow-volume loop
    take the deepest breath you can,
    then exhale into the sensor
    as hard as possible,
    for as long as possible

    You can measure


    Forced expiratory volume (first 1 second) and
    Forced vital capacity (maximum volume you can get out)

    Normal

    FEV1andFVCarecalculatedfrom
    theflowvolumecurves

    Obstructivelungdisease
    (emphysema)

    FEVisreduceddisproportionately
    morethantheFVCresultinginan
    FEV/FVCratiolessthan7080%.

    Restrictivelungdisease
    (pulmonaryfibrosis)

    BoththeFEVandFVCare
    reducedproportionately.

    Emphysema (a.k.a. chronic obstructive pulmonary disease)


    From exposure to toxins (e.g. tobacco smoke)
    Progressive destruction of alveoli and the surrounding tissue that supports the
    alveoli. With more advanced disease, large air cysts develop where normal lung
    tissue used to be. Air is trapped in the lungs due to lack of supportive tissue which
    decreases oxygenation.

    Bronchitis
    Bronchitis is the inflammation of the bronchi.
    It generally follows a viral respiratory infection (can also be caused by
    tobacco smoke). Symptoms include; coughing, shortness of breath,
    wheezing and fatigue.
    Sometimes it can lead to pneumonia.

    Pneumonia
    Alveolar inflammation and abnormal alveolar filling with fluid
    Can result from a variety of causes, including infection with bacteria,
    viruses, fungi, or parasites, and chemical or physical injury to the lungs.
    Treatment depends on the cause.

    asbestos fiber

    Pulmonary fibrosis
    excess fibrous connective tissue (scarring of the lungs)
    Many causes including tuberculosis and asbestos

    Not all of the air reaching the alveoli is fresh air


    The volume of fresh air reaching the alveoli each minute is called
    Alveolar ventilation
    Remember that the conducting zone is
    considered dead space as far as gas
    exchange is concerned
    At the end of expiration there is about
    150 ml of stale air in the conducting
    zone
    The next inspiration pushes the stale air
    into the alveoli ahead of the fresh air
    So, the amount of fresh air inspired is more
    than the amount reaching the alveoli
    Fresh air inspired per minute
    = 500ml x 12 breaths/min = 6000ml/min
    Fresh air reaching alveoli per minute
    = (500ml-150ml) x 12 breaths/min = 4200ml/min

    Increases in alveolar ventilation (eg during exercise)


    involves increasing tidal volume, or respiration rate,
    or both
    Increasing tidal volume is more efficient

    same tidal vol.


    double
    respiration
    rate

    double tidal vol.


    same respiration
    rate

    Why?

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