Respiratory -Anatomy and Physiology

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  1. Conducting Zone
    • Large airways: nose, pharynx, trachea, bronchi
    • Small airways: bronchioles, terminal bronchioles
    • -cartilage only present in trachea and bronchi
    • -walls of conducting airways contain smooth muscle

    • Functions:
    • -brings air in and out
    • -warms
    • -humidifies
    • -filters

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  2. Conducting zone
    • Extending to end of bronchi:
    • -Cartilage
    • -Goblet cells

    • Extending to end of terminal bronchioles:
    • -Pseudostratified ciliated columnar cells (beat mucus up and out of lungs)
    • -Smooth muscle of airway walls (sparse beyond this point)

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  3. Respiratory Zone
    • Lung parenchyma: Respiratory bronchioles, alveolar ducts, alveoli
    • Function: gas exchange (3L)

    • Histology:
    • -Respiratory bronchioles: cuboidal cells
    • -Alveoli: simple squamous cells
    • -No cilia
    • -Alveolar macrophages clear debris; immune response
  4. Pulmonary Anatomy
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  5. Pneumocytes
    • 1. Pseudstratified ciliated columnar epithelium
    • 2. Type I cells
    • 3. Type II cells
    • 4. Clara cells
  6. Pseudostratified Ciliated Columnar Epithelium
    • -extend to the respiratory bronchioles
    • -goblet cells extend only to bronchi
    • *mucus secreting cells stop before cilia disappear
  7. Type I cells
    • -97% of alveolar surfaces
    • -line the alveoli
    • -thin for optimal gas diffusion
    • Collapsing pressure = P = 2(surface tension)/radius
  8. Type II cells
    • -3%
    • -secrete surfactant (dipalmitoyl phosphatidylcholine)
    • -decreases surface tension
    • -cuboidal cells
    • -clustered

    *precursors to type I cells and other type II cells

    *proliferate during lung damage
  9. Surfactant
    • Complex mix of lecithins
    • most important: dipalmitoylphosphatidylcholine
    • Synthesis begins around 26 weeks gestation
    • Mature levels are not achieved until week 35
  10. Clara Cells
    • -nonciliated, columnar
    • -secretory granules
    • -secrete component of surfactant
    • -degrade toxins
    • -act as reserve cells
  11. Fetal Lung Maturity
    -indicated by a lecithin to sphingomyelin ratio of > 2.0 in amniotic fluid
  12. Gas exchange barrier
    • blood-gas interface is very thin (0.3um)
    • very large surface area
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  13. Gas Exchange Barrier
    Fick's law of diffusion 
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    • Fick's Law of Diffusion
    • -proportional to: the the area, partial pressure difference, solubility of gas
    • -inversely proportional to the thickness, square root of molecular weight
  14. Gross Lung Anatomy
    • R Lung:
    • -3 lobes
    • -more common site for inhaled foreign bodies b/c the R main stem bronchus is wider and more vertical

    • L Lung:
    • -2 lobes and a lingula
    • -make room for heart

    • Vessels and Bronchus Relations:
    • "RALS" Right Anterior Left Superior
    • (pulmonary artery to the bronchus at each lung hilus)
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  15. Foreign Object Aspiration
    • Aspiration while upright:
    • -lower portion of R inferior lobe

    • Aspiration while supine:
    • -superior portion of R inferior lobe
  16. Diaphragm
    • Structures that Perforate the Diaphragm:
    • T8: IVC
    • T10: esophagus, vagus
    • T12: aorta (red), thoracic duct (white), azygous vein (blue)

    "I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12)"

    • "C3, 4, 5 keeps the diaphragm alive"
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  17. Muscles of Respiration
    • Quiet Breathing:
    • -Inspiration: Diaphragm
    • -Expiration: passive

    • Exercise:
    • -InSpiration: external intercostals, Scalene, Sternomastoids
    • -Expiration: rectus abdominus, internal and external obliques, transversus abdominus, internal inter costals
  18. Lung Volumes
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    • Lung Volumes ("LITER"):
    • -IRV
    • -TV
    • -ERV
    • -RV

    • Insipratory Reserve Volume (IRV):
    • -Air that can still be breathed in after normal inspiration

    • Tidal Volume (TV):
    • -Air that moves into lungs with each normal inspiration
    • -typically 500 mL

    • Expiratory Reserve Volume (ERV):
    • -Air that can still be breathed out after normal expiration

    • Residual Volume (RV):
    • -Air in lung after maximal expiration
    • -CANNOT be measured on spirometry
  19. Lung Capacities
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    **Capacities are the sum of two or more volumes

    • Lung Capacities:
    • -IC
    • -FRC
    • -VC
    • -TLC

    • Inspiratory Capacity (IC):
    • = IRV + TV

    • Functional Residual Capacity (FRC):
    • = RV + ERV
    • -volume in lungs after normal expiration

    • Vital Capacity (VC):
    • = TV + IRV + ERV
    • -Maximum volume of gas that can be expired after a normal inspiration

    • Total Lung Capacity (TLC):
    • = IRV + TV + ERV + RV
    • -Volume of gas present in lungs after a maximal inspiration
  20. Determination of Physiologic Dead Space
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    • VD (physiologic dead space):
    • =anatomic dead space of conduction airways + functional dead space in alveoli
    • -apex of healthy lung is the largest contributor of functional dead space
    • -functional dead space = volume of inspired air that does not take part in gas exchange

    • VT  (Tidal Volume)
    • PaCO2 = arterial PCO2

    PECO2 = expired air PCO2

    "Taco, Paco, PEco, Paco" (Orders of variables in equation)
  21. Lung and Chest Wall Physics
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    • Natural Tendency:
    • -lungs to collapse inward
    • -chest wall to spring outward
    • *elastic properties of both chest wall and lungs determine their combined volume

    • At FRC:
    • -the inward pull of the lung is balanced outward pull of chest wall
    • -system pressure = atmospheric
    • -airway and alveolar pressure are 0
    • -intrapleural pressure is negative (prevents pneumothorax)
  22. Compliance
    -change in lung volume for a given change in pressure

    • -pulmonary fibrosis
    • -pneumonia
    • -pulmonary edema

    • -emphysema
    • -normal aging
  23. Hemoglobin
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    • Composed of 4 polypeptide subunits (2 alpha, 2 beta)

    • Exists in 2 forms:
    • 1. T (taut) form:
    • -low affinity for O2
    • 2. R (relaxed) form:
    • -high affinity for O2 (300x)
    • -Hb exhibits positive cooperativity and negative allostery

    "Taut in Tissues, Relaxed in Respiratory"

    • Shift from relaxed to taut form:
    • -INCREASED: Cl-, H+, CO2, 2,3-BPG, temperature
    • -shifts O2 dissociation curve to right
    • -leads to increased O2 unloading

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    • HbF:
    • -2a2g
    • -lower affinity for 2,3-BPG than adult Hb
    • -thus has a higher affinity for O2
  24. Hemoglobin Modifications
    Lead to tissue hypoxia from decreased O2 saturation an decreased O2 content

    • Carboxyhemoglobin:
    • -Hb bound to CO in place of O2
    • -Causes decreased O2 binding capacity
    • -Left shift in the O2-Hb dissociation curve
    • --> decreased O2 unloading in tissues
    • *CO has 200x greater affinity than O2 for Hb

    • Methemoglobin:
    • -oxidized form of hemoglobin (ferric, Fe3+)
    • -normal Hb has reduced iron (ferrous, Fe2+)
    • -does not bind O2 as readily
    • -has increased affinity for CN-
    • -use nitrates to oxidize methemoglobin, which binds CN-, allowing cytochrome oxidase to function
    • -Thiosulfate (binds CN --> thiocynate --> renal secretion)

    "Methemoglobinemia can be treated with methylene blue"

    *nitrates cause poisoning by oxidizing Fe2+ to Fe3+
  25. Oxygen-Hemoglobin Dissociation Curve
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    • Positive Cooperativity:
    • -tetrameric Hb can bind 4 oxygen molecules
    • -affinity increases for each subsequent oxygen molecule bound
    • -curve has sigmoidal shape

    *Myoglobin is monomeric, lacks positive cooperativity and curve lacks sigmoidal shape

    • Right Curve Shift:
    • -decrease affinity of Hb for O2
    • -facilitates unloading of O2 to tissue
    • **increase in all factors (except pH) causes a shift to RIGHT

    • "Right Shift: C-BEAT"
    • -CO2
    • -BPG (2,3 BPG)
    • -Exercise
    • -Acid/Altitude
    • -Temperature

    • Fetal Hb has a higher affinity for O2 than than adult Hb --> dissociation curve is shifted LEFT
  26. Pulmonary Circulation
    • Pulmonary Vascular Pressure:
    • -normally very low (mean = 15, vs systemic mean = 100)

    • Pulmonary Vascular Resistance:
    • -normally very small
    • High Compliance

    • Hypoxic vasoconstriction
    • -decrease in PAO2 causes vasoconstriction
    • -shifts blood away from poorly ventilated areas of lung

    • Distribution of Blood Flow:
    • -decreased at apex (in upright position) due to hydrostatic pressure differences
  27. Diffusion vs. Perfusion Limitation
    • Perfusion Limited:
    • -transfer of gas is limited by the amount of perfusion
    • -EG: CO2, N2O, O2 (NORMAL HEALTH)
    • -under typical resting conditions capillary PO2 reaches that of alveolar gas when the RBC is 1/3 of the way along the capillary (normally RBC is in the capillary for 0.75s)
    • -Gas equilibrates early along the length of the capillary
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    • Diffusion Limited:
    • -depends on the diffusion properties of the blood-gas barrier, no the amount of blood available
    • -gas does not equilibrate by the time blood reaches the end of the capillary
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  28. O2: Diffusion vs Perfusion limitation
    Under normal resting conditions the capillary PO2 reaches that of the alveolar gas when the red cell is one third of the way along the capillary --> perfusion limited

    If the blood-gas barrier thickens or during exercise (when the blood spends less time in the capillaries) the blood PO2 does not reach the alveolar value by the end of the capillary --> diffusion limitation

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  29. Pulmonary hypertension
    normal vs abnormal pressures
    • Normal pulmonary artery pressure = 10-14mmHg
    • PTH > 25mmHg or >35mmHg during exercise

    • Etiology:
    • -arteriosclerosis
    • -medial hypertrophy
    • -intimal fibrosis of pulmonary arteries
  30. Pulmonary hypertension
    Primary vs secondary
    • Primary:
    • -inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation)
    • -poor prognosis

    • Secondary:
    • -COPD
    • -Mitral steonosis
    • -recurrent thromboemboli
    • -autoimmune disease
    • -left-to-right shunt
    • -sleep apnea
    • -living at high altitude

    Course: severe respiratory distress → cyanosis and RVH → death from decompensated cor pulmonale
  31. Pulmonary Vascular Resistance
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    • PL atrium = pulmonary wedge pressure
    • n=viscosity
    • l=vessel length
    • r=vessel radius

    • -decreases on exercise b/c of recruitment and distention of capillaries
    • -increases at high and low lung volumes
    • -increases with hypoxia

    *PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation
  32. Oxygen Content of Blood
    O2 content = (O2 binding capacity x % saturation) + dissolved O2

    • -Normally 1g of Hb can bind 1.34 mL O2
    • -Normally 15g/dL Hb in blood
    • (Cyanosis when Hb < 5g/dL)

    -O2 binding capacity = 20.1 mL O2/dL

    O2 content of arterial blood decreases as Hb falls, but O2 saturation and arterial PO2 do NOT

    O2 Delivery to tissues = CO x O2 content of blood
  33. Alveolar Gas Equation
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    • PAO2: Alveolar PO2
    • PIO2: PO2 in inspired air
    • PaCO2: arterial PCO2
    • R: respiratory quotient (CO2 produced/O2 consumed)
    • A-a gradient: PAO2 - PaO2 = 10-15 mmHg

    • Increase A-a gradient may occur in hypoxemia:
    • -shunting
    • -V/Q mismatch
    • -fibrosis (impairs diffusion)
  34. Oxygen Deprivation
    • 1. Hypoxemia (decreased PaO2)
    • a) Normal A-a gradient
    •      -high altitude
    •      -hypoventilation
    • b) increased A-a gradient
    •      -V/Q mismatch
    •      -diffusion limitation
    •      -R to L shunt

    • 2. Hypoxia (decreased O2 delivery to tissues)
    •      -decreased CO
    •      -hypoxemia
    •      -anemia
    •      -CO poisoning

    • 3. Ischemia (loss of blood flow)
    •      -impeded arterial flow
    •      -reduced venous drainage
  35. Lung Zones
    • Zone 1:
    • -top of lung
    • -Pa < PA
    • -capillaries are squashed --> no flow
    • =alveolar dead space
    • *doesn't occur under conditions
    • *may be present after severe hemorrhage, or if PA increases (positive pressure ventilation)
    • -V/Q = 3 (wasted ventilation)

    • Zone 2:
    • -Pa > PA > Pv
    • -blood flow determined by difference between arterial and alveolar pressures (rather than normal arterial-venous pressure difference)

    • Zone 3:
    • -Pa > Pv > PA
    • -flow determined in the usual way by arterial-venous pressure difference
    • -V/Q = 0.6 (wasted perfusion)

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  36. Lung zones
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  37. V/Q Mismatch
    Ideally ventilation is matched to perfusion (V/Q = 1)

    • V/Q mismatch seen in the normal lung:
    • -apex V/Q = 3 (wasted ventilation)
    • -base V/Q = 0.6 (wasted perfusion)

    **both ventilation and perfusion are greater at the base of the lung than at the apex

    With exercise (increased CO) there is vasodilation of apical capillaries --> V/Q approaches 1

    • V/Q --> 0 = airway obstruction
    • -shunt
    • -100% O2 doesn't improve PO2

    • V/Q --> infinity = blood flow obstruction
    • -physiologic dead space
    • -100% O2 should improve PO2 (if < 100% dead space)
  38. CO2 Transport
    • CO2 Transported in 3 Forms:
    • 1. Bicarbonate (90%)
    • 2. Carbaminohemoglobin or HbCO2 (5%)
    •      -CO2 bound to Hb (not heme)
    •      -favors taut (O2 unloaded)
    • 3. Dissolved CO2 (5%)

    • Bicarbonate in Blood:
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    • -the first reaction occurs slow in the blood but fast in the RBC b/c of the presence of carbonic anhydrase
    • -HCO3- readily diffuses out of the cell but H+ doesn't
    • -this is balanced by Chloride shift into the cell

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  39. CO2 transport
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  40. Haldane Effect
    • -In the lungs, oxygenation of Hb promotes dissociation of H+ from Hb
    • -this shifts the equilibrium toward CO2 formation
    • -therefore CO2 is released from RBCs
    • -"deoxygenation of blood increases its ability to carry CO2"

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  41. Bohr effect
    • -in peripheral tissue increased H+ from tissue metabolism shifts curve to the right, unloading O2
    • -"increased PCO2 shifts the oxygen dissociation curve to the right and is mostly due to its action on the H+ concentration"
  42. Response to High Altitude
    • Acute:
    • -increase in ventilation (Resp. Alkalosis)
    • -decrease in PO2 and PCO2

    • Chronic:
    • -increase in ventilation (Resp. Alkalosis)
    • -increase epo --> increase Hct and Hb
    • -increase 2,3 BPG (binds Hb so it can release more O2)
    • -Cellular changes (increased mitochondria)
    • -increase renal excretion of bicarb to compensate for respiratory alkalosis
    • --> can augment with acetazolamide
    • -chronic hypoxic pulmonary vasoconstriction --> RVH
  43. Response to Exercise
    • -increased CO2 production
    • -increased O2 consumption
    • -increased ventilation rate to meet O2 demand
    • -V/Q ratio from apex to base becomes more uniform
    • -increased pulmonary blood flow (due to increased CO)
    • -decreased pH during strenuous exercise (secondary to lactic acidosis)
    • -No change in PaO2 and PaCO2
    • -Increase in venous CO2 content and decrease in venous O2 content
Card Set:
Respiratory -Anatomy and Physiology
2013-04-01 05:03:04

Respiratory anatomy and physiology
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