5. Structures of the Pulmonary System
Gas-exchange airways every bronchus h
own venule and a
– Respiratory bronchioles Every sac has its
cap bed.
– Alveolar ducts
– Alveoli
Epithelial cells
– Type I alveolar cells
Alveolar structure
– Type II alveolar cells
Surfactant
production
5
7. Respiratory Mucosa
Respiratory Mucosa
– Lines the conducting portion of the
respiratory tree
– Lined by a mucous membrane that
contains both epithelium and areolar
tissue
– Structure of the epithelium changes
from the upper to lower respiratory
system
– Upper airway to larger bronchi
Pseudostratifiedciliated columnar
epithelium with large number of goblet
cells and submucosal glands
7
8. Surface View of the Respiratory
Epithelium: Dense Cilia
Hella cilia.
8
12. Respiratory Defense System
Components Innate immunity
– Mucosal membrane
Gobletcells in the epithelial layer
Mucous cells in lamina propria
Cilia
– All work together to sweep mucous and trapped
particles to the oropharynx for expulsion
– Alveolar macrophages important in Addaptie im
clearing foreign material and bacteria
the lower airway
– Irritant receptors - sensitive to noxious
Nose, carina (sneeze, cough) 12
13. Gas Exchange
Alveoli
– Primary gas
exchange unit
Pores of Kohn
– Air passes through
septa from alveolus
to alveolus
Collateral
ventilation and
even air
distribution deep
Only work with
breath.
especially during illness
13
14. Pulmonary and
Bronchial Circulation
Pulmonary circulation has a lower pressure than
systemic circulation (mean = 18 mmHg)
– Only one third of vessels filled with blood at any given
time
– Increased pressure can increase recruitment
– Automatic distribution of blood to area of increased
ventilation.
– Gas Exchange
– delivers nutrients to lung tissues, acts as a reservoir for
the left side of the heart, and filters out clots, air, and
other debris from the circulation.
Bronchial circulation is part of systemic circulation
– Supplies nutrients to conducting airways, nerves, lymph
nodes, large pulmonary vessels, and pleurae
14
16. Pulmonary Circulation
Pulmonary artery
divides and enters
the lung at the
hilus
Each bronchus and
bronchiole has an
accompanying
artery or arteriole
16
17. Pulmonary Circulation
Alveolocapillary membrane
– Formed by shared alveolar and capillary walls
– alveolar epithelium
– alveolar basement membrane
– interstitial space
– capillary basement membrane
17
18. Pulmonary Lymphatic System
Lymph capillaries
keep the lung free
of fluid
– Deep
Begin at the
Terminal
bronchioles, exit at
the hillus. NOT in the
acini.
– Superficial
Pleural membrane -
18
19. Chest Wall and Pleura
Chest wall
– Skin, ribs, and intercostal
muscles, diaphragm
– Thoracic cavity
Pleura
– Serous membrane
– Parietal and visceral
layers
– Pleural space
(cavity)
– Pleural flui
– **they stay
connected!!! 19
20. Main Lung Functions
Gas exchange
– Supply oxygen
– Eliminate CO2 - gaseous form of carbonic acid.
Maintain pH
Eliminate water
Maintain normal body temperature
20
21. Requirements for Ventilation,
Perfusion, and Diffusion
Adequate inspired O2 – (FiO2) (21% at sea level,
rest is nitrogen.)
Ventilation (V) and perfusion(Q) of alveoli
A permeable alveolocapillary membrane
Adequate blood flow
Ability to transport O2 and CO2
Ability of cell to use O2 and eliminate CO2
Dissolved part of GAS is
considered Partial
Pressure.
21
22. Requirements for Ventilation,
Perfusion, and Diffusion
Adequate inspired O2 – (FiO2)
Barometric pressure is 760 at sea level
21% x 760 = partial pressure of O2 at sea level = ~160 mmHg
Barometric pressure is 600 at Salt Lake City
(much lower on Mt. Everest)
21% x 600 = partial pressure of O2 at SLC = ~126 mmHg
Why we give oxygen at high
altitude
22
23. Function of the Pulmonary System
Ventilation
– Mechanical movement of gas or air into
and out of the lungs
– Minute volume
Ventilatory rate multiplied by the volume of
air per breath
– Alveolar ventilation
Movement of air in and out of alveolus
Adequacy determined by arterial blood gas
analysis only!
23
24. Principles underlying Ventilation
Air
flows from an area of higher
pressure to an area of lower pressure
Visceralpleura that lines the outside
of the lung remains in contact with
parietal pleura that lines the chest
cavity
24
25. Principles underlying Ventilation
Enlargement of the chest cavity by
muscle contractions will affect
pressure changes
When the diaphragm contracts, the
lung cavity volume increases and the
pressure decreases and air enters
since the lung pressure is lower than
atmospheric pressure Quiet breathing =
DIAPHRAM.
25
26. Ventilation Principles Recoil
CHest wa
Lung wan
Elastic recoil: tendency of lungs to return to
resting state after inspiration is responsible for
passive exhalation
Compliance: measure of chest wall and lung
distensibility: reciprocal of elastic recoil
Airway Resistance: determined by the length, Compli
recoil.
radius, and cross sectional of the airway and the
density, viscosity, and velocity of the gas
Work of breathing is determined by the
muscular effort required for breathing. Increased
work of breathing will increase markedly the
oxygen needs and metabolic demands
1/2 - 2/3 resistance t
air is in the nose.
26
27. Pulmonary volumes
Volume Relationships
– Resting Tidal Volume Vt: amount of
air you move in and out of your lungs in
one respiratory cycle (500 ml)
– Forced Vital Capacity: maximum
amount of air you can move in and out
of your lungs during one respiratory
cycle
sum of tidal volume and inspiratory and
expiratory reserves
27
28. Pulmonary volumes
Volume Relationships
– Expiratory Reserve: amount of air
you can voluntarily expel after you
completed normal quiet respiratory
cycle
– Residual Volume: amount of air left
after maximum expiration - dead space
left over: conducting part, prevent
collapse.
28
29. Pulmonary Volumes
Volume Relationships
– Inspiratory reserve: amount of air
you can inhale over and above a quiet
respiratory cycle
– Functional residual capacity: (FRC)
is the amount of air remaining in your
lungs after you have completed a quiet
resting cycle; expiratory reserve
volume + residual volume.
29
31. Lung Volumes and Capacities
Based on Age, Gender, Height
Dead space: oropharynx to division
16 of bronchioles
– volume about equal to ideal body weight
Tidalvolume VT (per breath)
400-800 ml
IRV 3000 ml additional air that could
be inhaled
31
32. Lung Volumes and Capacities
Based on Age, Gender, Height
ERV 1000 ml remaining air
– Can be forcefully expired after normal
expiration FEV1 - athma and emphysema.
– Why abdominal thrusts work; expel VT
plus ERV
Forced vital capacity (theoretical)
– VT + IRV + ERV ~4500-5000 ml
Residual volume constant ~1200 ml
– Air remaining in alveoli
32
33. Example using Formulas
Minute ventilation (or volume/min)
– RR x VT
– RR 16, VT 500
– 16 x 500 = 8000 ml/min
Effective
minute volume (happening
down at alvioli): RR x (VT -DS)
– 100 lb, RR 16, VT 500 ml
– 16 (500-100) = 6400 ml/min
33
34. Control of Ventilation
ANS - automatic.
– Stimulates smooth muscle
Airway lumen diameter
– Sympathetic - muscle relaxation
– Parasympathetic – muscle contraction
Main controller under normal conditions
Bronchial smooth muscle tone
– Depends on equilibrium
Equal stimulation of contraction & relaxation
– Constriction occurs with irritant receptor
stimulation (epithelium)
Inspired air irritants (pollen, toxic vapors)
Endogenous substances – inflammatory
chemical mediators such as histamine,
prostaglandins
Drugs
34
35. Control of Ventilation
Chemoreceptors
– Central receptors
Reflects PaCO2
Stimulated by H+ in cerebrospinal fluid (pH)
– CO2 diffuses into CSF until equilibrium is reached
– Combines with H2O = H2CO3
– H2CO3 dissociates into H+ + HCO3- (↓
– Peripheral receptors
Aortic arch and carotid bodies
Primarily stimulated by hypoxemia (PaO2)
– Also sensitive to changes in PaCO2 and pH
Sends efferent signals to DRG (Dorsal respiratory group).
– Increase respiratory rate and depth
Major stimulus to ventilation in chronic hypoventilation
– Central chemoreceptors become insensitive
– Renal compensation with HCO3 diffusion into CSF 35
36. Ventilation
Neurochemical
control
– Respiratory center
Dorsal respiratory group - sets
basic rythm.
Ventral respiratory group - deep
breath, quicker expiration.
Pneumotaxic center
Modulators
Apneustic center
36
38. Overview: Mechanics of Breathing
Mechanical aspects of inspiration and
expiration
– Major and accessory muscles
– Elastic properties
Lungs
Chest wall
– Resistance of airflow
Conducting airways
38
39. Mechanics of Breathing
Major and
accessory muscles
– Major muscles of
inspiration
Diaphragm inhale
External intercostals
– Accessory muscles
of inspiration
Sternocleidomastoid
exhale
and scalene muscles
– Accessory muscles
of expiration
Abdominal and
internal intercostal 39
40. Mechanics of Breathing
Alveolar surface tension
– Function of surfactant
Elastic properties of lung and chest
wall
– Elastic recoil
– Compliance
Airway resistance (normally low)
– Airway size; smaller
– Gas velocity (Poiseuille’s law)
R = ∆P/F,
40
42. Laplace’s Law
The smaller a sphere’s radius (alveoli) the
greater the surface tension and the more
difficult (work) to expand the alveoli
P = 2t/r
– P = pressure inside a sphere (alveoli)
– t = surface tension
– r = radius of a sphere
Surfactant reduces fluid surface tension
lining the alveoli and decreases tendency
to collapse, preventing atelectasis
– Also keeps fluid out of alveoli
– Participates in host defense against pathogens
42
43. Compliance
A measure of lung and chest wall
distensibility or “stiffness”
― volume of air moved
― force to move the
air
Low: increased work of inspiration
– Stiff lungs
High: increased work of expiration
– Baggy lungs
43
44. Measurement of Gas Pressure
Barometric pressure
– Partial pressure
Partial pressure of water vapor
44
46. Gas Transport – Four Steps
Oxygen Carbon Dioxide
– Ventilation of the – Diffusion of CO2 out
lungs of cells and into
– Diffusion of oxygen systemic capillaries
obviuse
from the alveoli into – Perfusion of the
the capillary blood pulmonary capillary
– Perfusion of bed by venous
systemic capillaries blood
with oxygenated – Diffusion of CO2
blood from the lungs into
– Diffusion of oxygen the alveoli
from systemic – Removal of CO2
capillaries into the from the lung by
cells ventilation 46
47. Distribution of Ventilation and Perfusion
Gravity and alveolar pressure
Ventilation-perfusion ratio
– Normal V/Q = 0.8 - perfusion is just a
little hier!
47
48. Gas Transport: O2
Oxygen transport
– Diffusion across alveolocapillary membrane
Large total surface area
Very thin
High concentration gradient
– Determinants of arterial oxygenation
Hemoglobin concentration (15g/dl)
SaO2 (97% on RA at sea level)
PaO2 (100 mm Hg)
48
49. Gas Transport: O2
Oxygen Transport
– Transported by combination with Hgb
(19.7 ml/dl) or dissolved in plasma
(0.3 ml/dl)
– Diffusion across the alveolar membrane
Amount of oxygen in the alveolus depends
upon the amount of oxygen in the inspired
air as well as the amount of physiologic
dead space
Oxygen diffuses across the membrane and
binds with Hgb
49
51. Gas Transport: O2
Oxygen Transport
– Hgb binds with oxygen and forms
oxyhemoglobin
– Hgb binding with oxygen in the lungs is
called Hgb saturation (SaO2); Oxygen
release from Hgb occurs in the tissues
and is called Hgb desaturation
– Can plot this process on a graph called
the oxyhemoglobin dissociation
curve
51
53. Oxyhemoglobin Association and
Dissociation
Oxygen Transport
– Factors that change the association
between oxygen and Hgb
Decreased affinity of Hgb for oxygen will be
depicted as a shift to the right of the
oxyhemoglobin dissociation curve
– Acidosis Increased DPG
– Increased PCO2
– Elevated temperature or hyperthermia
Increasedaffinity of Hgb for Oxygen will be
depicted as a shift to the left of the
oxyhemoglobin dissociation curve
– Alkalosis Hypothermia
– Decreased PCO2 Decreased DPG
53
54. Oxyhemoglobin Association and
Dissociation
BOHR EFFECT:
– Increased PaCO2 and H+
Result of cellular metabolism
shift to the right with less affinity of Hgb for
O2 and can be given up at the tissue level
easier
– Decreased PaCO2
Result of gas moving from blood to alveoli
shift to the left: increased affinity of Hgb for
O2 which promotes association in the lungs
54
55. Effects of pH and Temperature
on Hemoglobin Saturation
55
56. Gas Transport: CO2
Carbon dioxide transport
– Dissolved in plasma
– Bicarbonate - 90%!!!
– Carbamino compounds (Hb)
Haldane effect
– O2 effect on CO2 transport
Lungs – oxygen binds to Hgb
Tissues – oxygen dissociates from Hgb
56
57. Summary of Gas Transport:
CO2
Mostly binds to Hb.
Buffers.
Travels in the blood as 57
bicarb.
58. Control of Pulmonary Circulation
Hypoxic pulmonary vasoconstriction
– Caused by low alveolar PO2
– Blood is shunted to other, well-ventilated
portions of the lungs
Better ventilation and perfusion matching
If alveolar hypoxia affects all segments of lungs, the
vasoconstriction can result in pulmonary
hypertension
– Reversible if not chronic
Acidemia also causes pulmonary artery
constriction
Other biochemical factors affect vessel
caliber
– Histamine, prostaglandins, endothelin, 58
serotonin, nitric oxide, bradykinin
Larynx is what devides Upper from Lower. \nBronchial circ vs Pulmonary circ.\nPulm ART carry deoxygenated.\nBronchial circ capillaries add mixture, some dump into pulm vein. \nRight lobe is wider, Left lobe is longers. \n
Larynx - false and true chords. PHARYNX make the sound of the voice. \n
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redundant\n
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Pseudostrativied - every cell touches the basement membrane. \n
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Single lobule - good illustration. \nSee: blood, nerve, lymph (not all the way down!) requires Macrophage migrations. \n
ONly 1/3 of vessels are being perfused at any time. Protects lungs agains pulm htn in the case of increased CO. \nActs like a pressure valve. \n
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Basement membranes fuse. \n
Pluged = Pulmonary edema\n
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Accessory muscles - SCM and scalenes --> direct chest out!\n
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Know this.\n
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Slow down. \nUsually breath 1L less than we could. \n
Usually involuntare. \nBronchial smooth muscle tone a balance of ANS:\nSympathetic fibers innervate lumen of bronchial tubes --> relaxation.\nParasym, cholinergic --> Contraction. \nbeta blockers with asthma, need to be careful of HTN ptnt has Asthma\n
Take home:\nChronic hypovent - central lose sensitivity to pCO2, get “reset”, so peripheral get more important. \nCOPD - drive to breath by peripheral. THerefore, too much O2 stops drive to breath.\nTheory - bicarb reabsorbed from kidneys, goes into CSF and prevents sensitivity to H+. \n
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Figure out receptors\n
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Surface tension happens on any gas, water interface. \nSurfactant - lipid protein, breaks molecules that cause ST.\n
Great Picture.\nMuscle contraction wins. \n
NOT in the objectives.\n\nSurfactant - might be antioxident, attract M0.\n\n
Compliance = stiff lungs. That’s it!\n
Pp - % of that gas in the air. \nWater vapor has nothing to do with Pressue, temp only. \n\n
Note average values of 02, CO2, and N. \nCO2 IS 20 X MORE SOLUBLE than O2, gradient isn’t strong, but the solubility helps it move. \n
Bhor effect - in the lungs, co2 leaves Hb, makes more affinity to load O2.\nHaldan effect - in the tissues. \n
Orthopnea,\nParoxysmal nocturnal dyspnea.\n
Diffusion taks .25 sec.\nCells in lungs for .75 sec. \n
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Control of hypoxia - pulmonary art constrict to got to perfused part of the lung. \n
X-ray: air trapping, consolidation, nodules. \n\nage: loss of recoil, stiffen chest wall, alt gas exchange. \nGreater risk of respiratory risk from medications, have lower tolerance from exercise. \n