Pulm review Flashcards
Development stages
from lung bud (distal divirticulum)
Every Pulmonologist Can See Alveoli.
Embryonic stage, Pseudoglandular, Canalicular, Saccular, Alveolar
Embryonic stage
Embryonic stage (wk4-7): lung bud-> trachea-> bronchial buds-> main stem bronchi-> secondary Lobar bronchi-> tertiary (segmental bronchi)
Bronchi have hyaline cartilage
Broncioles have no cartilage, Terminal–> respiratory
Alveoli (capillaries and gas exchange
If theresa mistake–> transesophageal fistula
Pseudoglandular stage
Wk 5-17
Lung resembles gland, endodermal tubules–> terminal bronchioles surrounded by capillaries
Respiratory bronchioles and alveoli are NOT present, not compatible with life
Fetal respiration- fetus breathes in utero takes up amnion–>stimulates lung development and growth of respiratory muscles, important to growth in pseudoglandular phase
Oligohydroamnios- pulmonary hypoplasia, potters sequence, fetal kidney abnormalities
Canalicular phase
wk 16-25, terminal bronchioles divide–> respiratory bronchioles–> alveolar ducts
Respiration capable at the end of the canalicular phase airway diameter increases, pneumocytes start to develop
Type 1 are for respiration
Type 2 secrete surfactant to lower the surface tesnsion and keeps the alveoli open
Saccular phase
phase wk 26 to birth terminal sacs (primitive alveoli) form, capillaries multiply to prep for gas exchange
Alveolar period
Week36 to 8 years old
At birth, only 1/3 of alveoli are present , following birth theres an increase in the number of respiratory bronchioles and alveoli
Alveolarization and airspaces subdivide, new walls form septa
Bronchopulmonary dysplasia
premature babies need surfactant and O2 with mechanincal ventilation (they dont have surfactant and stong enough muscles to breath)
Ventilation and O2 can cause toxicity, alveolarization doesnt progress normally but during childhood they can do better
Pulmonary hypoplasia
oligohydramnios (potters sequence). congenital diaphragmatic hernia- defective formation of pleuroperitoneal membrane (leads to a hole in diaphragm, abdominal organs herniate into chest –> pulmonary hypoplasia Fatal
Broncho genic cysts
abnormal budding of foregut and dilitation of terminal/ terminal large, discrete, round fluid filled destension CXR asymptomatic
usually in mediastinum, contain clear fluid –> air when infected No communication of lungs, columnar ciliated
Pulmonary vascular resistance in utero is high, hypoxemia–> vasoconstriction at birth PVR goes down
Upper respiriatory tract and lower respiratory tract
Upper: nasal cavity, pharynx and larynx
Lower: trachea, brocni and lungs
Conducting zone
NO GAS EXCHANGE, large airways: nose, pharynx, trachea and bronchi
Filters, warms humidifies the air, anatomic dead space
cartilage and goblet cells–> bronchi, pseudostratified ciliary epithelium–> terminal bronchioles “mucociliary escalator”–> cuboid cells
Smooth muscles: sympthetic activation (beta 2) activation–> bronchodilation
Parasympathetic activation M3 –> bronchoconstriction
Respiratory zone
GAS EXCHANGE, respiratory bronchioles, alveolar ducts and alveoli
CUBOID in bronchioles–> simple squamous in alveoli
NO cilia, Alveolar macrophages clear debris and immune response
Difference between bronchi and bronchioles
Bronchi has cartilage: left and right primary, secondary/tertiary aka lobar or segental,
Bronchioles have NO cartilage: loular /large, terminal respiratory feed alveoli
Airway cells
- Goblet cells: secrete mucus (moslty glycoproteins and water) protects against particles and infections
- Ciliated epithelial cells: beating cilia moves mucus to epiglotis, so you can swallow it
- Club cells in bronchioles: non ciliated epithelial cells, secrete protective proteins, detoxify P450
- Trachea and bronchi cells: ciliated pseudostratified columnar cells and GOBLET cells
- Bronchiole cells: epithelium transitions to ciliated simple squamous cuboidal epithelial, and club cells
Resistance to air flow
UPPER airways (nose, mouth, pharynx): 50% Airway resistance LOWER airways- highest in medium bronchi (turbulent flow); lowest in terminal bronchioles- slow turbulent flow
ALVEOLI histology
small sacs, separated by septa, simple squamous Pneumocytes, gas exchange, surrounded by capillaries
Type 1 pneumocytes- vast majority of cells in alveoli, thin for gas exchange
Type 2 pneumocytes- produce surfactant, proliferate to form other cell types, key for regeneration after injury
Alveolar Macrophages- phagocytose foreign material, release cytokines and proteases
Surfactant when you exhale, alveoli shrink and want to collapse–> atelectasis, decreases efficiency for gas exchange. Surfactant prevents collapse: mix of lecithins–> DipalmitolPTcholine
Neonatal respiratory distress syndrome
Fetal lung maturity: lungs mature when adequate surfactant is present 35 WEEKS
Lecithin-sphingomyein L:S ratio both are 1:1 until 35 weeks, when the ratio is >2:1 its considered mature
NRDS: is a surfactant deficiency, increased surface tension–> alveolar collapse–> atelectasis, ground glass look, hypoxemia an increased CO2 due to poor ventilation, poorly responsive to O2 (lungs are collapsed, intrapulmonary shunting- no gas exchange)
Risk factors: prematurity, maternal diabetes (high insulin decrease surfactant) C section (decreases cortisol, decreases surfactant)
Complications: bronchopulmonary dysplasia (O2 toxicity, no alveolarization) patent ductus arteriosus– hypoxia keeps shunt open, Retinopathy of prematurity (O2 –> free radicals, neovascularization in retina, retinal detachment –> blindness
Treatments: BETAMETHASONE (Corticosteroid given to mom), direct surfactant administration
Foreign body aspiration
Commonly with peanuts and kids, Right lung is more common. Site of aspiration is the RIGHT lung (wide, less of angle, more verticle), right 60%, in main bronchus, sometimes in right lower lobe, Left 23% main bronchus small number in left lower,
Adequacy of effort and diffusing capability of membrane
Adequacy of effort- the volume of inspired air should be >90% of the largest Vital capacity
Diffusing capacity of membrane: volume of gas that diffuses per minute per mmHg 21 ml/min/mmHg norm
Lung volumes: Tidal volume Inspiratory volume Expiratory volume Residual volume Total lung capacity Inspiratory capacity Vital capacity Functional residual capacity
Capacity= is multiple volume
Tidal volume: air that moves into lung with each quiet inspiration 500 mL
Inspiratory volume: air that’s still breathed in after tidal inspiration
Expiratory volume: air thats expired out after tidal expiration
Residual volume: air after maximum expiration (expiratory volume) cant be measured by spirometry
Total Lung capacity: all air in lungs at maximum inspiration, Inspiratory reserve volume+ Tidal volume + expiratory volume + residual volume
Inspiratory capacity: air that can be inspired after tidal expiration, IRV + TV
Vital capacity: air that can be expired after maximum inspiration
Functional residual capacity: residual volume after quiet expiration (RV + ERV) volume when system is relaxed
Lung pressures
atmospheric pressure, alveolar pressure, intrapleural pressure, transpulmonary pressure
atmospheric pressure: 760 mmHg
Alveolar pressure (PA) pressure in the alveoli
Intrapleural pressure: pressure in pleural space
Transpulmonary pressure: Alveolar pressure-intrapulmonary pressure (need it to keep alveoli OPEN): Negative during normal quiet breathing, alveoli and lungs tend to collapse in on themselves, pull inward /recoild and need an outward force to keep the walls open. Chest wall tends to expand, creates a NEGATIVE pressure in pleural space–> you need to suck the alveoli open
PNEUMOTHORAX: TPP=PA-Pp in pneumothorax Pp goes from -5 to 0 the lung collapses in on itself
AIRFLOW and pressure changes (Quiet Breathing)
Inhalation: intrapleural pressure becomes more negative, alveolar pressure becomes negative airflows into the lungs
Exhalation: intrapleural pressure becomes less negative, alveolar pressure becomes positive, airflow out of lungs
Lung compliance
Decreased compliance issues, increased lung compliance issues
for a given pressure how much volume changes
Compliance: small amount of diaphragm effort, generates small pressure change across lungs, large volume change, easy to move air in and out
= change of Volume/ change of pressure
A non compliant lung: large amount of diaphragm effort to get a big pressure change across lung and only a small amount of volume change, harder to move air in/out-> decreases Functional reserve capacity
Decreased lung compliance: decrease FRC: Pneumonia, pulmonary edema, pulmonary fibrosis
Increased lung compliance: increased FRC: Emphysema (floppy lungs), Aging, surfactant
Emphysema
floppy chest, Increased FRC/lung compliance, increased volume in chest–> Barrel chest
Forced exhalation
when pleural pressure becomes positive, compresses airway pressure on alveoli-> positive pressure in airway pushes air out–> air flows from airways
Equal pressure point
why forced exhalation does not cause collapse/atelectasis
Pleural pressure= airway pressure, beyond the point the airway would collapse, but at that point there is cartilage preventing it from collapsing
Diseased lungs: equal pressure point, moves toward alveoli. Obstruction (bronchitis) more pressure drop, tmphysema leads to a loss of elastic recoli, collapses
COPD
Slow exhalation, prevents large rise in pleural pressure, forceful exhaaltion would increase pleural pressure, pursed lips–> increased airway and alveolar pressure, prevents collapse
Hemoglobin
Dissolved o2 equation
O2 transport- Dissolved O2 (determined by Henry’s law: PaO2 x solubility= Dissolved o2
Very small amount (2%) of total blood O2)
Bound O2= hemoglobin 98%, positive cooperativity
Right Curve shift: unloading of O2, releases R=Release,
Things that rise metabolic activity (increased CO2, decreased pH, increased temp, increased 23BPG_
Left curve shift: Latches on the O2, low metabolic activity, decreased CO2, increased pH, decreased temp and decreased 23BPG
