Respiratory Physiology I by xqo30826

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									Respiratory Physiology I

         Ankit Patel
   Exchange oxygen and carbon dioxide between
    environment and cells of the body
       Oxygen and carbon dioxide are exchanged between
        inspired air and pulmonary capillary blood
   Includes the lungs and series of airways that
    connect lungs to external environment
   Conducting zone (or conducting airways)
       Brings air into and out of lungs
   Respiratory zone
       Lined with alveoli allowing for gas exchange
              Conducting Zone
   Includes the nose, nasopharynx, larynx, trachea,
    bronchi, bronchioles, and terminal bronchioles
   Bring air into and out of respiratory zone
   Warm, humidify, and filter the air before it
    reaches gas exchange region
   Trachea → 2 bronchi → 2 smaller bronchi →
   Lined with mucus-secreting and ciliated cells
    that function to remove inhaled particles
                   Conducting Zone
   Walls contain smooth muscle
   Autonomics nervous system affect airway diameter:
    1.   Sympathetic neurons → β2 receptors → relaxation and
         dilation of airways
            Epinephrine (from adrenal gland) also activates β2 receptors
    2.   Parasympathetic neurons → muscarinic receptors
         →contraction and constriction of airways

        β2-adrenergic agonists (e.g., epinephrine, isoproterenol,
         and albuterol) used to dilate airways in treatment of asthma
               Respiratory Zone
   Includes respiratory bronchioles, alveolar ducts,
    and alveolar sacs (lined with alveoli)
   Alveoli are pouchlike evaginations of the walls
     Each lung has ~300 million alveoli
     Exchange of gases occurs rapidly and efficiently
      across alveoli because walls are thin and have large
      surface area for diffusion
            Pulmonary Blood Flow
   Cardiac output of the right heart
   Right Ventricle → Pulmonary Artery →
    Arterioles → Pulmonary Capillaries (form
    networks around alveoli) → Venules →
    Pulmonary Vein → Left Atrium
   Regulation of pulmonary blood flow is
    accomplished by altering resistance of
    pulmonary arterioles
       Controlled by local factors (mainly O2)
Pulmonary Blood Flow
                     Lung Volumes
       Measured by a spirometer
   Tidal Volume (VT)
       Volume of air that fills both alveoli and airways with a normal
        breath (~500 mL)
   Inspiratory Reserve Volume
       Additional volume inspired above tidal volume (~3000 mL)
   Expiratory Reserve Volume
       Additional volume expired below tidal volume (~1200 mL)
   Residual Volume (RV)
       Volume remaining in lungs after maximal forced expiration
        (~1200 mL)
Lung Volumes
                  Lung Capacities
   Inspiratory Capacity (IC)
       Tidal Volume + Inspiratory Reserve Volume (~3500 mL)
   Functional Residual Capacity (FRC)
       Expiratory Reserve Volume + Residual Volume (~2400 ml)
       Volume remaining in lungs after a normal tidal volume is
        expired (equilibrium volume)
   Vital Capacity (VC)
       Inspiratory Capacity + Expiratory Reserve Volume (~4700 mL)
       Volume that can be expired after maximal inspiration
   Total Lung Capacity (TLC)
       Vital Capacity + Residual Volume (~5900 ml)
Volumes & Capacities
                        Dead Space
   Volume of airways and lungs that does not participate
    in gas exchange
   Anatomic Dead Space (~150 ml)
       Volume of conducting airways because NO alveoli
       TV of 500 ml is inspired, but 500 ml does not reach alveoli
        for gas exchange because portion fills conducting airways
   Physiologic Dead Space
       Anatomic dead space + functional dead space in alveoli
       Functional dead space refers to alveoli that do not participate
        in gas exchange because of mismatch in ventilation and

            Normally, Anatomic = Physiologic Dead Space
               Ventilation Rate
   Volume of air moved into and out of lungs per
    unit time
   Minute ventilation = total rate of air movement
    into and out of lungs
   Alveolar ventilation = corrects for physiologic
    dead space
        Forced Expiratory Volumes
   Vital Capacity = volume expired following maximal
   Forced Vital Capacity (FVC) = volume forcibly
    expired after maximal inspiration
       FEV1 = Volume forcibly expired in the 1st second
       FEV2 = Cumulative volume expired in 2 seconds
       FEV3 = Cumulative volume expired in 3 seconds
   FVC and FEV1 are useful indices of lung disease
   FEV1/FVC can be used to differentiate among diseases
               FEV & Lung Disease
   Normal Person:
       FEV1/FVC is ~0.8 (80% of vital capacity can be forcibly
        expired in 1st second)
   Obstructive Lung Disease (Asthma):
       FVC and FEV1 are decreased, but FEV1 is decreased more
        than FVC
       FEV1/FVC is decreased
   Restrictive Lung Disease (Fibrosis):
       FVC and FEV1 are decreased, but FEV1 is decreased less than
       FEV1/FVC is actually increased
FEV & Lung Disease
           Mechanics of Breathing
   Inspiration
       Diaphragm contracts → abdominal contents pushed
        downward and ribs are lifted upward and outward
       Produces ↑ intrathoracic volume → ↓ intrathoracic pressure
        and initiates flow of air into the lungs
   Expiration
       Normally a passive process as diaphragm relaxes
       Air is driven out of lungs by reverse pressure gradient
        between lungs and the atmosphere
       Abdominal muscles can assist during exercise or disease
Mechanics of Breathing
Mechanics of Breathing
           Compliance & Pressure
   Distensibility of a system
       Measure of how volume changes as a result of a pressure
   Compliance of lungs and chest wall is inversely correlated
    with elastance
   Transmural pressure is pressure across a structure
       Transpulmonary pressure is difference between intra-alveolar
        pressure and intrapleural pressure
       Lung pressures always referred to atmospheric pressure,
        which is called "zero"
           Compliance of Lungs
   Sequence of inflation followed by deflation
    produces a pressure-volume loop
   Slope of pressure-volume loop is compliance
    of lung
     Pressure outside lung made more negative → lung
      inflates and volume increases until alveoli are filled
      and become stiffer and less compliant
     Pressure outside lungs less negative → lung volume
      to decrease during expiration
Compliance of Lung
         Compliance of Chest Wall
    Negative Intrapleural Pressure created by 2 opposing
     elastic forces:
    1.   Lungs tend to collapse
    2.   Chest Wall tends to spring out
    Therefore, negative intrapleural pressure prevents
     lungs from collapsing and chest wall from springing
    Pneumothorax (introducing air into intrapleural space)
     causes intrapleural pressure to become equal to
     atmospheric pressure (intrapleural pressure = 0)
        No longer negative intrapleural pressure so:
            Lungs collapse and chest wall springs out
Compliance of Chest Wall
            Changes in Compliance
   Emphysema (increased lung compliance)
       Associated with loss of elastic fibers in lungs
       At FRC, tendency of lungs to collapse is less than tendency of chest wall
        to expand
       To reestablish balance, volume must be added to the lungs to increase
        their collapsing force
       Thus, combined lung and chest-wall system seeks new higher FRC
   Fibrosis (decreased lung compliance)
       Associated with stiffening of lung tissues
       At FRC, tendency of lungs to collapse is greater than tendency of chest
        wall to expand
       To reestablish balance, the lung and chest-wall system will seek a new
        lower FRC
        Surface Tension of Alveoli
   Alveoli are lined with film of fluid
   Surface Tension
     Attractive forces between adjacent molecules of
      liquid are stronger than attractive forces between
      molecules of liquid and molecules of gas
     As molecules of liquid are drawn together by
      attractive forces, surface area becomes smaller
     Surface tension generates a pressure that tends to
      collapse alveolus:
                             P = 2T/r
         Surface Tension of Alveoli
                          P = 2T/r

   Large alveolus has low collapsing pressure
   Small alveolus has high collapsing pressure
       However, alveoli need to be small to increase total
        surface area for gas exchange
   Fundamental conflict is solved by Surfactant
   Mixture of phospholipids that line alveoli and
    reduce their surface tension
     Reduces collapsing pressure for a given radius
     Intermolecular forces between surfactant molecules
      break up the attracting forces between liquid
      molecules lining the alveoli
   Surfactant also increases lung compliance
       Reduces work of expanding the lungs during
         Case 7: Chief Complaint
   Within an hour of being born, a 2 week
    premature baby starts breathing very rapidly and
   Skin appears cyanotic
              Case 7: Test Results
   Pulse 160 (normal 140) and Respiratory Rate 70
    (normal 50)
   Arterial CO2 is elevated and arterial O2 is
       pH is low
                     Case 7: Diagnosis
   Baby has Neonatal Respiratory Distress Syndrome
       Lungs lack surfactant
            Premature infants are less likely to have surfactant present
       Small alveoli have ↑ surface tension and ↑ pressures causing
        them to collapse (atelectasis)
       Collapsed alveoli are not ventilated and cannot participate in
        gas exchange
            Consequently, hypoxemia (low oxygen within blood) and respiratory
             acidosis develop (elevated CO2, decreased pH)
       ↓ lung compliance → ↑ work of inflating lungs during
             Case 7: Treatment
   Baby is placed under continuous positive airway
    pressure (splint airways open) and surfactant is
   Respiratory rate returns to normal as does
    arterial blood gas values
   1 week later baby is discharged home with
    Airflow, Pressure, & Resistance
                           Q = ΔP/R
   Q = airflow (ml/min or L/min)
   ΔP = pressure gradient (mm Hg or cm H2O)
   R = airway resistance (cm H2O/L/sec)

   Between breaths, alveolar pressure = atmospheric
       No pressure gradient, no driving force, and no airflow
   During inspiration, alveolar pressure < atmospheric
    pressure (b/c increase lung volume)
       Pressure gradient drives airflow into lungs
              Airway Resistance
                   R = 8 η l/π r4
   R = resistance
   η = viscosity of inspired air
   l = length of the airway
   r = radius of the airway

   Medium-sized bronchi are sites of highest
    airway resistance
     Changes in Airway Resistance
    Change airway diameter to alter resistance and
        Smooth muscle in walls of conducting airways is innervated
         by autonomic nerve fibers:
1.   Parasympathetic stimulation → constriction of
     bronchial smooth muscle → ↓ airway diameter → ↑
     resistance to airflow
2.   Sympathetic stimulation → relaxation of bronchial
     smooth muscle via β2 receptors → ↑ airway diameter
     → ↓ resistance to airflow
        β2 agonists such as epinephrine used for treating asthma
                 Breathing Cycle
   3 Phases:
       rest, inspiration, and expiration

   Transmural pressure = airway or alveolar
    pressure - intrapleural pressure
     + transmural pressure is an expanding pressure on
      the lung
     - transmural pressure is a collapsing pressure on the
               Breathing Cycle: Rest
   Alveolar pressure = atmospheric
    pressure = 0
       No airflow because no pressure
   Intrapleural pressure is negative
       Opposing forces of lungs trying to
        collapse and chest wall trying to expand
        create a negative pressure
   Transmural pressure across the
    lungs and airways at rest is +5 cm
    H2O which means these structures
    will be open
   Volume present in lungs =
    equilibrium volume = FRC
         Breathing Cycle: Inspiration
    Diaphragm contracts → ↑
     thorax volume → ↓ lung
    Airway and alveolar pressure
     become negative
         Pressure gradient drives airflow
          into lungs
    Intrapleural pressure
     becomes even more negative
    1.    ↑ lung volume → ↑ elastic recoil of
          lungs → pull more forcefully
          against intrapleural space
    2.    Airway and alveolar pressures
          become negative as ↑ thorax
        Breathing Cycle: Expiration
   Expiration is passive process
   Alveolar pressure becomes
       Elastic forces of lungs compress the
        greater volume of air in the alveoli
       Alveolar pressure > atmospheric
        pressure so air flows out of lungs
        and volume returns to FRC
   Intrapleural pressure returns to
    resting value of 5 cm H2O
       As ↓ lung volume, ↓ elastic recoil of
        Forced Expiration: Normal
   Expiratory muscles make lung
    and airway pressures very positive
   Expiratory muscles raise
    intrapleural pressure
   Will lungs/airways collapse under
    positive intrapleural pressure?
       No, because transmural pressure
        remains positive
   Expiration is rapid and forceful
    because pressure gradient
    between alveoli and atmosphere is
    much greater than normal
         Forced Expiration: COPD
   ↑ Lung Compliance because ↓
    elastic fibers
   ↑ Intrapleural pressure to same
    value as in normal
   ↓ Alveolar pressure and airway
    pressure because lungs have ↓
    elastic recoil
   Negative transmural pressure
    across large airways
       Airways collapse → ↑ resistance to
        airflow and expiration is difficult
   Persons with COPD expire
    slowly with pursed lips → ↑
    airway pressure → prevents
    negative transmural pressure →
    prevents collapse

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