Lecture Respiratory System Part II

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julianne.elizabeth
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Lecture Respiratory System Part II
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2012-10-25 01:01:59
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LCCC II respiratory system pressure volumes capacities
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for exam II John Loughman
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  1. What are the two phases of pulmonary ventilation?
    Inspiration: gases flow into lungs

    Expiration: gases flow out of lungs
  2. Why is atmospheric pressure important for breathing?
    Patm is the pressure exerted by the air surrounding the body

    Patm=760 mm Hg at sea level or 1 Patm

    *respiratory pressures are described relative to Patm

    • Negative respiratory pressure is less than 1Patm
    • Positive respiratory pressure is more than 1Patm
    • Zero  respiratory pressure is 1 Patm
  3. What is intrapulmonary pressure (Ppul)?
    Also called intra-alveolar pressure

    • Pressure in the alveoli
    • fluctuates with breathing

    *Ppul always eventually equalizes with Patm
  4. What is intrapleural pressure (Pip)?
    • Pressure in the plural cavity
    • fluctuates with breathing

    • *always a negative pressure (< Patm and < Ppul)
    • ~4mm Hg below Ppul
  5. Why is intrapleural pressure always negative?
    • Two inward forces always promote lung collapse:
    • 1. elastic recoil of lungs decrease its size
    • 2. surface tension on the alveolar reduce its size

    • One outward force tends to enlarge the lungs:
    • 1. elasticity of the chest wall pulls the thorax outward

    *the key is that the close proximity of the pleura holds it together and keeps it negative, like water holding 2 slides together
  6. What is the relationship between Ppul and Pip?
    If Pip=Ppul then the lungs collapse (Atelectasis)

    • Ppul-Pip= TRANSPULMONARY PRESSURE
    • -keeps the airways open
    • -the greater the Ptrans, the larger the lungs
  7. What causes Atelectasis?
    Plugged bronciholes --> collapse of alveoli

    wound that admits air into the pulmonary cavity (pneumothorax)
  8. What is pulmonary ventilation dependent upon?
    Inspiration and Expiration are mechanical processes that depend on the volume changes in the thoracic cavity

    • Volume change leads to pressure change
    • Pressure change leads to gas flow in order to equalize pressure
  9. What is Boyle's Law?
    The relationship between the pressure and volume of gas at a constant temperature

  10. Describe the process of inhilation
    An Active process

    • 1. Inspiratory muscles contract (diaphram descends, rib cage rises)
    • 2. Thoracic cavity volume increases
    • 3. Lungs are stretched; intrapulmonary volume increases.
    • 4. Intrapulmonary pressure drops to -1mm Hg
    • 5. Air (gases) flow into lungs down its pressure gradient until intrapulmonary pressure is 0 (equal to atmospheric pressure)
  11. Describe the process of Expiration
    Quiet Expiration is normally a passive process

    • 1. Inspiratory muscles relax (diaphram rises, rib cage descends due to recoil of costal cartilages)
    • 2. Thoracic cavity volume decreases
    • 3. Elastic recoil passively, intrapulmonary volume decreases.
    • 4. Intrapulmonary pressure rises to +1 mm Hg
    • 5. Air (gases) flow out of the lungs down the pressure gradient until the intrapulmonary pressure is at 0 (Atmospheric pressure)

    • *forced expiration is an active process: it uses the abdominal and internal intercostal muscles
  12. Describe how pressure changes throughout pulmonary ventilation
  13. What are the physical factors influencing pulmonary ventilation?
    • Inspiratory muscles consume energy to overcome 3 factors that hunder air passage
    • 1. airway resistance
    • 2. alveolar surface tension
    • 3. lung compliance
  14. What is airway resistance?
    Friction (drag) is the major nonelastic source of resistance to gas flow


    -->the relationship between flow, pressure, and resistance

    DeltaP is the pressure gradient between Ppul and Pip (2 mmHg or less during normal quiet breathing)

    small changes to P lead to large changes in F

    gas flows inversley with resistance
  15. Why is airway resistance typically insignificant?
    • 1. large airway diameters in the first part of the conducting zone
    • 2. Progressive branching of airways as they get smaller, increasing the total cross-sectional area

    The greatest resistance is at the medium sized bronci and resistance disappears at the terminal bronchioles when diffusion drives gas movement

  16. What happens when airway resistance increases?
    Breathing movements become more strenuous

    • Severely constricting or obstruction of bronchioles can:
    • 1. prevent life sustaining ventilation
    • 2. occur during acute asthma attacks and stop ventilation

    Epinephrine dialates bronchioles and reduces R
  17. What are the respiratory volumes?
    TV (Tidal Volume): air in and out of lungs during normal quiet breathing-->500ml

    IRV (Inspiratory Reserve Volume): amount of air that can be forced during inspiration -->2100-3200ml

    ERV (Expiratory Reserve Volume): amount of air that can be forced during expiration --> 1000-1200ml

    RV (Residual Volume): amount left in lungs after forced expiration (keeps alveoli open) --> 1200ml

  18. What are the Respiratory capacities?
    IC (inspiratory capacity): TV+IRV = IC

    FRC (functional residual capacity): RV+ERV=FRC

    VC (Vital Capacity): TV+IRV+ERV=VC

    • TLC (Total lung capacity): RV+VC=TLC
  19. What is dead space?
    Some inspired air never contributes to gas exchange

    Anatomical dead space: volume of the conducting zone (~150ml)

    Alveolar dead space: alveoli that cease to act in gas exchange due to collapse or obstruction

    Total dead space: sum of both anatomical and alveolar dead space volumes
  20. What is a spirometer?
    intrument used to measure respiratory volumes and capacities

    • Spirometry can distinguish between:
    • 1. obstructive pulmonary disease--> increased airway resistance like bronchitis (increases in TLC, FRC, RV)
    • 2. restrictive disorders-->reduction in the TLC, VC, FRC, and RV  due to structural or function lung changes such as fibrosis or TB
  21. What are minute ventilation, FVC, and FEV?
    these are pulmonary function tests

    Minute ventilation: total amount of gas flow into or ou fo the respiratory tract in one minute (normal is about 12 breaths a minute)

    FVC (forced vital capacity): gas forcibly expelled after taking a deep breath

    FEV (forced expiratory volume): the amount of gas expelled during specific time intervels of FVC

    FEV1: what is expelled in the 1st second, normally about 80% of lungs volume
  22. What is the Alveolar Ventilation Rate (AVR)?
    flow of gases in or out of alveoli in a certain amount of time

    AVR= minute ventilation x (TV-dead space)

    dead space is constant. rapid, shallow breathing decreases the AVR

    AVR is normally 4200ml/min
  23. Name some non-respiratory air movments
    most are a result of a reflex action

    cough, sneeze, crying, laughing, hiccups, and yawns
  24. What is Dalton's Law?
    Total pressure exerted by a mixture of gases is the sum of the pressured exerted by each gas

    • the partial pressure of each gas is directly proportional to its percentage in the mixure
  25. What is Henry's Law?
    When a mixture of gases is in contact with a liquid, each gas will dissolve in the liquis in proprtion to its partial pressure

    At equilibrium, the partial pressure in both phases with be equal

    • The amount of gas that will dissove in a liquid also depends upon soluability
    • -CO2 is 20x more soluble in water than O2
    • -Very litte N2 dissolves in water
  26. What influences the composition of Alveolar Gas?
    • It contains more CO2 and water vapor than atmospheric are
    • -gas exchange in lungs
    • -humidification of air
    • -mixing of alveolar gases that occur with each breath

  27. What is external respiration and what is it influenced by?
    The exchange of O2 and CO2 across the respiratory membrane (lung to blood)

    • Influenced by:
    • 1. partial pressure gradients and gas solubilities
    • 2. ventilation-perfusion coupling
    • 3. structural characteristics of the respiratory system
  28. How does the partial pressure and gas solubility of O2 affect external respiration?
    • partial pressure gradient for O2 in the lungs is steep
    • -venous blood= 40mm Hg
    • -alveolar PO2 = 104 mm Hg
    • *reaches equilibrium of 104 mm Hg in about .25 seconds, abouit 1/3 the time a red blood cell is in the pulmonary capillary
  29. How does the partial pressure and gas solubility of CO2 affect external respiration?
    • partial pressure gradient for CO2 is less steep than O2 in the lungs
    • -venous blood Pco2 = 45 mm Hg
    • -Alveolar Pco2 = 40 mm Hg

    • **BUT CO2 is 20x more soluable in plasma than O2, therefore it diffuses in equal amount with oxygen
  30. What is ventilation-perfusion coupling?
    • ventilation: amount of gas reaching the alveoli
    • perfusion: blood flow reaching the alveoli
    • *ventilation and perfusion must be matched (coupled) for efficient gas exchange

    • Changes in Po2 in the alveoli cause changes in the diameters of the arterioles
    • -where alveolar O2 is high, arterioles dialate
    • -where alveolar O2 is low, arterioles constrict

    • Changes in Pco2 in the alveoli cause changes in the diameters of the bronchioles
    • -where alveolar CO2 is high, bronchioles dialate
    • -where alveolar CO2 is low, bronchioles constrict
  31. What is internal respiration and how does the partial pressure gradient affect it?
    internal respiration is the capillary exchange of gases in the body tissue though blood

    • Partial pressure and diffusion gradiient are reversed compared to external respiration
    • -Po2 in tissue is alweays lower than systemic arterial blood
    • -Po2 of venous blood is 40mm Hg and Co2 is 45 mm Hg
  32. How is O2 transported in the blood?
    • 3 ways:
    • -1.5% dissolved in plasma
    • -98.5% loosely bound to each Fe of Hb in RBCs
    • (4 O2 per Hb)
  33. Explain the loading and unloading of O2 with Hemoglobin
    • Oxyhemoglobin (HbO2): Hb-O2 combo
    • Reduced Hemoglobin (deoxyhemoglobin)(HHb): hemoglobin that has released it O2


    • Loading and unloading is faciliated by change in shape of Hb
    • -As O2 binds, Hb affnity for O2 increases
    • -As O2 is released, Hb affinity for O2 decreses
    • (like a following the leader style thing)

    *Hb is fully saturated with 4 O2 or partially saturated with 1-3 O2
  34. What influences the rate of O2 loading and unloading on Hb?
    • Po2
    • Temperature
    • Blood pH
    • Pco2
    • Concentration of BPG
  35. How does Po2 influence Hb saturation?
    • The oxygen-hemoglobin dissociation curve
    • Hb saturation plotted against Po2 is not linear, but S-shaped
    • shows how binding and release of O2 is influence by the Po2

    • In arterial blood (away from heart):
    • -Po2 = 100 mm Hg
    • -Contains 20 ml O2 per 100 ml blood (20% vol)
    • -Hb is 98% saturated
    • *any further increases in Po2 (ex. breathing deeply) produce minimal increases in O2 binding

    • In venous blood (towards heart):
    • -Po2 = 40 mm Hg
    • -contains 15% vol O2
    • -Hb is 75% saturdated

    • *Hb is almost completely saturated at Po2 of 70 mm Hg
    • *further increases in Po2 produce minimal increase in O2 binding
    • *O2 loading and delivery to tissues adequate when Po2 is below normal levels
    • *only 20-25% of O2 is unloaded during on systemic circulation (Rest in venous blood called venous reserve)

    • If O2 levels in tissues drop:
    • -more O2 dissociated from Hb and is used in cells
    • -respiratory rate or cardiac output need not increase
  36. How do increases in temperture, H+, Pco2, and BPG influence Hb saturation?
    Modify structure of Hb and decrease its affinity for O2

    Occur in systemic capillaries

    enhance O2 unloading

    • shift the O2 Hb dissociation curve to the right (decreases shift to the left)
  37. What increases the unloading of O2 from Hb?
    • As cells metabolize glucose...
    • -Pco2 and H+ increase in concentration in capillary blood
    • -this declining pH weakens (acidosis) the Hb-O2 bond (BOHR EFFECT) as the O2 is unloaded where it is most needed.
    • -Heat production then increases which directly and indirectly decreases Hb affinity for O2
  38. What is Hypoxia?
    The inadequate delivery of O2 to tissues

    caused by: too few RBCs

    • -Anemichypoxia: abnormal or too little Hb
    • -Ischemic/Stagnant hypoxia: blocked circulation
    • -Histoxic hypoxia: metabolic poisons
    • -Hypoxemic hypoxia: pulmonary diseases
    • -Carbon monoxide which displaces O2 from Hb
  39. How is CO2 transported in the blood?
    • 3 Ways:
    • - 7-10% dissolved in plasma
    • -20% chemically bound to globin of Hb (Carbinohemoglobin)
    • -70% as bicarbonate ions (HCO3-) in plasma
  40. How is CO2 exchanged in the blood?
    CO2 combines with water to form carbonic acid (H2CO3) which quickly dissociated into hydrogen and bicarbonate ions


    Most of this occurs in RBCs where carbonic anhydrase reversibly and rapidly catalyzes the reaction

    • In pulmonary capillaries:
    • -HCO3- quickly moces into the RBCs and binds with H+ to form H2CO3
    • -H2CO3 is split by carbonic anhydrase into CO2 and water
    • -CO2 diffuses into teh alveoli

    • In systemic Capillaries:
    • -HCO3- quickly diffuses from RBCs to plasma
    • -the chloride shift occurs: outruse of HCO3- from the RBCs is balance as Cl- moves in from the plasma
  41. What is the haldane effect?
    The amount of CO2 transported if affected by the Po2

    The lower the Po2 and Hb satururation with O2 the more Co2 can be carried in the blood

    • As more CO2 enters the blood at the tissues...
    • -more O2 dissociated from Hb (bohr effect)
    • -as HbO2 releases O2, it more readily forms bonds with Co2 to form carbinohemoglobin
  42. How does CO2 influence blood pH?
    HCO3- in plsma is the alkaline reserve of the carbonic acid-bicarbonate buffer system

    If H+ concentration in the blood rises, excess H+ is removed by combining with HCO3-

    If H+ concentration in the blood drops, H2C03 dissociated releasing H+


    • Changes in the respiratory rate can also alter the blood pH
    • -example: slow shallow breathing allows CO2 to accumulate in the lungs causing pH to drop
    • -As a result, changing ventilation can be used to adjust pH when it is disturbed by metabolic factors (deep breathing with flush out CO2)
  43. What are the medullary respiratory centers and what to they do?
    • 1. Dorsal Respiratory group (DRG)
    • -near the root CN IX
    • -integrates input from peripheal stretch and chemoceptors
    • (relays the messages to the VRG)

    • 2. Ventral Respiratory group (VRG)
    • -rhythm generating and integrative center
    • -sets eupnea (12-15 breaths/minute)

    Inspiratory neurons excite inspiratory muscles via the phrenic and intercostal nerves

    • Expiratory neurons simply inhibit the inspiratory neurons
  44. What are the pontine respiratory centers and what do they do?
    They influence and modify the activity of the VRG

    Smooth out transition between inspiration and expiration
  45. What is the most widely held hypothesis for the genesis of respiratory rhythm?
    Reciprocal inhibition of two cets of interconnected neuronal netowkds in the medulla sets the rhythm
  46. How are depth and rate of breathing determined?
    Depth: how activily the respiratory center stimulates the respiratory muscles

    Rate: how long the respiratory center is active

    • Influence of CO2:
    • -If Pco2 levels rise (hypercapnia), CO2 accumulates in the brain
    • -H+ stimulates the central chemoceptors of the brain stem
    • -Chemoceptors synapse with the respiratory regulatory centers, increasing the depth and rate of breathing
    • *Rising CO2 levels are the most powerful respiratory stimulant

    • Hyperventilation: increased depth and rate of breathing that exceeds the body's need to remove CO2
    • -causes hypocapnia
    • -may cause cerebral vasocronstriction that occurs when Pco2 is abnormally low

    Apnea: period of breathing ceccation tha toccurs when Pco2 is abnormally low

    • Influence of Po2
    • -peripheal chemoceptors in the aortic and carotid bodies are O2 sensors
    • -when excited, they cause the respiratory centers to increase ventilation
    • -substantial drops in Po2 (to 60 mm Hg) must occur in order to stimulate increased ventilation

    • Influence of the arterial pH
    • -decreased pH may reflect CO2 retention, accumulation of lactid acid, excess keton bodies in those with diabetes
    • -respiratory sustem contraols will attempt to raise the pH by increasing the respiratory rate and depth
  47. What is the influence of the higher brain centers on respiration?
    • Hypothalamic controls act through the limbic system to modify the rate and depth of respiration for emotion of pain
    • ex: breath holding that occurs during anger or gasping with pain

    a rise in body temp acts to increase respiratory rate

    cortical controls are direct signals from the cerebral motor cortex that bypass medullary cords-->voluntary control like breath holding
  48. What are pulmonary irritant reflexes?
    Receptors in the bronchioles respond to irritants

    promote reflexive constriction of air passages

    receptors in te larger airways mediate the cough and sneeze reflexes
  49. What is the hering-breuer reflex?
    • stretch receptors in the plurae and airways are stimulated by lung inflation
    • -inhibitory signals to the medullary respiratory centers end inhalation and allow expiration to occur
    • -acts more as a protective response to stop over stretching of lungs
  50. What adjustments does exercise cause in respiration?
    Adjustments are geared to both the intestity and the duration of the work out

    Hyperpnea: increase in ventilation (10-20 fold) in response to metabolic needs

    Pco2, Po2, and pH remain suprisingly constant during respiration

    • 3 neural factors cause increase in ventilation at start
    • 1. Psychological stimuli-anticipation of work out
    • 2. Simultaneous cortical motor activiation of skeletal muscles and respiratory centers
    • 3. exictatory impulses reaching respiratory center from propricenters in moving muscles, tendons, and joints

    • When exercise ends:
    • -ventilation declines suddenly as the three neural factors shut off
  51. What adjustments does high altitude cause in respiration?
    • Quick travel to altitudes above 8000ft may produce symptoms of Acute Mountain Sickness (AMS)
    • -heaches, shortness of breath, nausea, and dizziness
    • -in severe cases, lethal cerebral and pulmonary edema

    • Acclimization: respiratoy and hematopoietic adjustments to altitude
    • -chemoreceptors become more responsive to Pco2, Po2 declines
    • -substantial deline in Po2 directly stimulates peripheal chemoreceptors
    • -result: minute ventilation increases and stabilizes in a few days to 2-3L/min higher than at sea level

    decline in blood O2 stimulates the kidneys to accelerate production of EPO, RBC numbers increase slowly to provide long term compensation

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