KEY NOTES WK 4 Flashcards
lungs derived from
foregut
lungs in which cavity
pleural cavity
lung buds (respiratory diverticulum) at wk 4 on
ventral wall of foregut
substances that cause development of lung buds
retinoic acid and TBX4 transcription factor
endoderm origin
and splanchnic mesodermal origin
Endodermal Origin: Epithelium of internal lining in larynx, trachea, bronchi, and lungs
- Splanchnic Mesodermal Origin: Cartilaginous, muscular, and connective tissue components of the trachea and lungs
esophageal atresia
Proximal esophagus does not connect with the distal part, creating a blind-ending tube
tracheoesophageal fistula
Connection (fistula) between the trachea and the esophagus
visceral and parietal pleura are formed from what in embryo
mesoderm –> visceral
somatic mesoderm (more outer) –> parietal
4 stages of maturation of lungs in embryo
- psuedoglandular stage (branching –> terminal bronchioles)
- canalicular stage –> divide into respiratory bronchioles into alveolar ducts
- terminal sac (saccular) –> primitive alveoli (terminal sac)
- alveolar period –> mature alveoli get capillary contact (36 wks to 8yoa)
type I vs type II alveolar epithelial cells
type I form blood-air barrier with capillaries around alveolar sacs
type II for surfactant production to reduce surface tension at air-alveolar interface
fetal breathing
aspiration of amniotic fluid for lung development
infant respiratory distress syndrome
not enough surfactant –> high surface tension –> alveolar collapse
larynx orignation
endoderm (internal lining of larynx)
muscles and cartilage from 4th and 6th pharyngeal arches (make thyroid, cricoid and arytenoid cartilage)
nerve for larynx
vagus nerve
visceral and parietal pleura
visceral= attached to lung (inner)
parietal= lines internal thoracic cavity (outer)
== pleural sac
innervation of parietal vs visceral pleua
parietal: general sensory neurons (pain sensitive)
- intercostal nerves for peripheral portion
-phrenic nerves for central portion
visceral: visceral sensory neruons (pain insensitive) via autonomic vagus nerve
visceral and parietal pleura are contagious at the
hilum (at pulmonary ligament)
function of pleura
produce and reabsorb pleural fluid
pleural space
fluid to lubricate gliding breathe movements
surface tension to resist lung collapse
negative pressure (slight less than atmosphere)
chest wall vs lungs elastic recoil
lungs want to go in
chest wall out
= negative intrapleural pressure
pneuomothroax
air in pleural space (breaks coupling btwn visceral and parietal pleura)
equalize atomospheirc and pleural pressure = lung collapse
hemothorax= blood fills pleural space
pleural recesses
areas where lung doesnt fill entire pleural sac in quiet respiration
fluid accumulates here in quiet breathing
lung can expand here in deep inspiration
2 pleural recesses
costodiaphragmatic and costomediastinal
right vs left lung lobe
right has 3 lobes and 2 fissures
left has 2 lobes and 1 fissure and cardiac notch (for heart) and lingula (aka like the middle lobe of right lung)
hilum of the lung
where blood vessel, air passage, lymphatic and nerves enter and leave the lung
connects it to cardio system
2 types of blood supply for lung
- bronchial circulation (get oxygenated blood to bronchial tree)
- pulmonary circulation (deoxygenated blood from heart to lungs and vice versa)
lymphatic drainage of lung
pulmonary and bronchopulmonary (hilar) nodes –> tracheobronchial (carinal) nodes and paratracheal nodes
then into systemic via right lymphatic duct (right lung) and thoracic duct (left lung)
innervation of lungs
PNS and SNS via pulmonary plexus
PNS- vagus nerve = bronchoconstriction and bronchial gland secretion
sympathetic= T1-T4 postganglion sympathetic fibers and cervical sympathetic ganglia
cause bronchodilation and inhibit bronchial gland secretion
SNS controlled by epinephrine
bronchial tree
- Trachea
- Primary bronchi
- Secondary bronchi
- Tertiary bronchi
- Conducting bronchioles
- Terminal bronchioles
- Respiratory bronchioles
- Alveoli
bronchial tree conducting airways (transport and humidify air but not gas exchange)
trachea, primary bronchi, secondary bronchi, and tertiary bronchi.
trachea cartilage and muscle
c shaped rings of hyaline cartilage
tracheal muscle
where does trachea bifurcate into primary bronchi
carina
nasal cavity
humidify with seromucous glands
goblet cells and mucus to trap inhaled particles
IgA to inactivate microorganism
vibrissae (hairs) to filter particulate matter
olfactory neurons for odoriferous substances
respiratory epithelium
ciliated cells
goblet cells (with mucin)
brush cells (microbial for chemosensory receptors)
small granule cells
basal cells
parts of pharynx
nasopharynx
oropharynx
laryngopharynx
larynx catilage
hyaline cartilage (ie..thyroid, cricoid) and smaller elastic cartilage (i.e. epiglottis)
epiglottis function
at top of larynx to prevent swallowed food or fluid from entering air passage
trachea
c shape hyaline cartilage with trachealis muscle
bronchi into bronchioles cartilage and muscle
primary bronchi: full circle of catilage, lots of mucus and glands
bronchioles: lose caritilage, get muscle and MALT, are ciliated to clear debris
–> lack mucosal glands
terminal bronchioles cells and function
club cells secrete surfactant, AMPs, cytokines
chemosensory brush cells
stem cells
alveoli
cells and fibers
site of gas exchange
type I pneuomcytes (desmosomes and tight junctions)
type II penurmocytes (have lipids, phospholipids, proteins and make surfactant)
dust cells to phagocytose erythrocytes from damaged capillaries
elastic fibers to expand and contract
reticular fibers to prevent collapse
rich capillary network
ventilation via Boyles law
pressure and volume inversei
inspiration
dripahram contract and flattens down (increase volume)
contract external intercostal muscle (lift ribs and sternum anterior)
pressure decreases (negative pressure) Create vacuum and pull air into lung
quiet expiration
passive; inspiratory muscles relax, diaphragm ascends, rib cage descends, elastic lung tissue recoils
force expiration
contract expiratory muscles (external and internal oblique, transverse and rectus abdomens)
increase intra-abdominal pressure, ab organs forced against dipgram and raise it
depress rib cage
accessory muscles for inspiration and experiation
inspire; SCM, scalene, external intercostal
expire: internal intercostal, rectus abdominis
ventilation vs external and internal respiration
ventillaiton= move air in and out of lungs
external respiration= gas exchange in lungs
internal respiration= gas exchange in tissue
forces of ventrilation
inspiration: diagram, external intercsotals
expiration: passive and elastic recoil in normal breath but forced expiration is ab muscles and internal intercostals
Boyles law drives ventilation
pressure and volume inverse
tidal volume
Volume of air inspired or expired with each normal
breath
inspiratory reserve volume
Extra volume of air that can be inspired over and
above normal tidal volume
expiratory reserve volume
Extra amount of air that can be expired by forceful
expiration after the end of normal tidal expiration
residual volume
Volume of air remaining in the lungs after the
most forceful expiration
inspiratory capacity
– Tidal volume + inspiratory reserve volume
– Amount of air a person can breath beginning at the normal expiratory level and distending lungs to maximum amount
functional residual capacity
– Expiratory reserve volume + residual volume
– Amount of air that remains in the lungs at the end of normal expiration
vital capacity
– Inspiratory reserve volume + tidal volume + expiratory reserve volume
– Maximum amount of air a person can expel from the lungs after first filling the lungs to their maximum extent and then expiring to maximum extent
total lung capacity
– Vital capacity + residual volume
– Maximum volume to which the lungs can be expanded with the greatest possible inspiratory effect
cant measure____ in spirometry so use _____ to measure FRC
residual volume, functional residual capacity and total lung capacity
helium dilution or plethysmography
anatomic vs physiologic vs alveolar dead space
anatomic: volume of space of respiratory system (i.e. conducting airways) but doesnt include alveoli where gas exchange occurs
alveolar dead space: if alveolar are ventilated but not perfused (lack blood)
physiologcial dead space: sum of anatomic and alveolar (should be ~ equal to anatomic if healthy)
dead space is inhaled air that doest reach gas exhange areas (ventilation occurs but no gas exhange)
minute respiratory volumne
amount of air inhaled or exhaled per minute
= tidal volume x respiratory rate
~6L/min
rate of alveolar ventilation per minute
total volume of new air entering gas exhchange area per min
= resp rate x amount of breath that enters alveoli (tidal volume- dead space volume
negative pleural pressure via
lung (in) and chest wall (out) elastic recoil in opposite directions
airflow resistance effects expiratory time
expiration longer than inspiration
lung/ alveoli want to recoil inwards and collapse becasue
compliance
i.e. expand lots with little pressure difference, also means the forces causing collapse aren’t that large
what affects lung compliance
elasticity and surface tension o lungs
surface tension
pull liquid molecules together (liquid wants to hydrogen bond and interact with each other) at the air-liquid interface
liquid wants to minimize contact with air
type II alveolar cells make ____ and use proteins A and D as _____ and proteins B and C as _____
surfactant
A and D for opsonins (bind pathogens ~ immune)
B and C for even distribution of surfactant
lung compliance curve
at higher pressure lung is stiffer and harder to expand (decrease compliance)
S shaped
hysteresis
difference in inflation and deflation curves (for compliance)
surfactant interact more with lung when inflating and less when deflating and elastic recoil too
surfactant decreases work of breathing by incrasing
pulmonary compliance
done via decrasing inward recoil of lung caused by surface tension
very low lung volumes
airways close because intrapleural pressure exceed atmospheric pressure
resistnace changes with lung volume
at low lung volumes airways are smaller and compressed ; so higher restiance (lower conductance) ]
high volumes, airways are open and lower resistance
2 sites of major airway resistnace
bronchi and bronchioles
bc small diameter
COPD causing increased resistnace in small airways
COPD breathe at higher ____ volumes
higher functional residual capacity/ residual volumes
higher volume to open airways arnd decrase resistance
breathe out and gas velocity increases and so does linear pressure, but less pressure pushing out on wall (Bernoulli)
keep airways open by moving faster and less pressure on walls
velocity increases when
expiration and when airway diameter decreases
Bernoulli principle
Bernoulli’s Principle states that in a steady, incompressible fluid flow, velocity and pressure are inversely related: high velocity → low pressure and low velocity → high pressure.
In the lungs, airflow velocity increases in narrower airways, causing a decrease in airway pressure, which can contribute to airway resistance in diseases like asthma.
increase velocity, decrease pressure outwards on walls
emphysema
destruction of alveolar walls and loss of elastic recoil in lungs
air trapping, reduced gas exhange
emphysema is a loss of
elastin, less elastic pull to keep small airways open
increased velocity
collapse walls
hard to exhale
destruction of alveolar walls, loss of elastic recoil, and air trapping
daltons law
partial pressure of each gases summed up
(gases in alveoli: CO2, O2, water vapour, N2)
pulmonary artery vs aorta blood
pulmonary is low in 02 and high in co2
aorta is high in O2
PO2 highest when leaving lungs
PCO2 highest when entering lungs
gas exhange at pulmonary capillary [blood- gas interface]
O2 and CO2 move across alveolar capillary membrane via diffusion
respiratory membrane (between alveoli and capillary) contains
layer of surfactant etccc
Factors affecting rate of gas diffusion through respiratory membrane
- thickness of membrane
- surface area of membrane
- diffusion coefficient of gas
- partial pressure difference (and concentration) between 2 sides of membrane
what increases thickness of respiratory membraen
edema
lung fibrosis
what decreases surface area of respiratory membrane
emphysema
diffusion across respiratory membrane follows
Ficks law (thickness, partial pressure difference, area, diffusion constant)
exercise impact on oxygenation
During exercise, the time available for oxygenation in the pulmonary capillaries decreases due to increased cardiac output (CO) and faster blood flow through the lungs
lung diffusing capacity
total volume of O2 taken up per minute
2 components of lung diffusing capacity
- diffusion process itself
- time taken for O2 (or CO2) to react with hemoglobin
Hb dissociation curve
S shaped
When one O₂ molecule binds to Hb, it increases the affinity for additional O₂ molecules.
Conversely, when one O₂ molecule is released, Hb is more likely to release more O₂.
factors that shift Hb curve to the right/ increase p50 making it promote oxygen unloading so that tissues get more oxygen (i.e. in hypoxia, fever, exercise)
increased CO2, acidity, temperateure , 2,3 (DPG) red cells
anemia and CO (carbon monoxide) impact on oxygenation
anemia lower O2 content in blood by lowering Hb
CO poisoning reduces CaO2 and shifts curve left
3 forms of carbon dioxide transport in blood
- bicarbonate (mainly)
- dissolved
- carbamino-hemoglobin in the red cell
carbon dioxide association curve for hemoglobin
quite linear
Haldane effect
When oxygen binds hemoglobin. Kicks off carbon dioxide promoting its release (in the lungs)
Oxygenated Hb releases CO₂, while deoxygenated Hb binds CO₂ more easily.
✔ Tissues: Deoxygenated Hb enhances CO₂ uptake.
✔ Lungs: Oxygenation promotes CO₂ unloading and exhalation.
✔ Works opposite to the Bohr Effect, optimizing gas exchange in both lungs and tissues.
bohr vs Haldane effect
Bohr effect: COs promotes release of O2 in the tissues —> help Hb release O2 and give to tissues
haldane effect: O2 promotes CO2 rlease in the lungs —> helps Hb unload CO2 for gas exhange
