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Respiratory - Anatomy and Physiology (Lung Anatomy (Change of Cells from…
Respiratory - Anatomy and Physiology
*Alveolar Cells
type 1 pneumocytes = squamous gas exchange cells
type 2 pneumocytes = cuboidal surfactant cells
Type
Blood BB and Tight Junctions
Notes
:
note that type 2 pneumocytes have the unique ability to proliferate themselves and also be progenitor cells for type 1 pneumocytes
type 1 cells make up 95% of the alveoli, where type 2 are only 5% but they are completely necessary for their progenitation of type 1 cells and for the surfactant they make to stop the alveoli from collapsing
Clinical Case
*Surfactant
made and stored in type 2 pneumocytes of the alveoli
precursor lethicin
--> lecithin sphingomyelin (L:S) ratio > 2
surfactant stored in lamellar bodies of type 2 cells and are released as buds into the alveoli
--> from there they break out into the alveoli and eventually recycled back into the type 2 cells
30 wweeks is magic number for L/S ratio >2
--> premature to this infants at risk for NRDS
--> collapse of alveoli and lungs =
atelectasia
Lung Anatomy
Change of Cells from Trachea --> Bronchi --> bronchioles --> Alveoli
Change of cells as moving towards alveoli
cilia important to move things up
important for cilia below the mucus making cells
--> stop mucus accumulation near alveoli
Notes
:
note that the cilia are the last things to leave as moving distally before the alveoli
--> make sure no mucus or anything ends up in the alveoli
in the alveoli you start to get the type 1 pneumocytes and type 2 pneumocytes
type 1 pneumocytes = 90% = squamous cells = gas exchange
type 2 pneumocytes = surfactant makers = proginators for type 1 pneumos
Clinical Case
*Clinical Anatomy of Lungs
6,8,10, 12 rule for lung markings
Dual *Blood supply to the lungs
both the bronchial arteries (O2 rich) and pulmonary veins (CO2 rich)
--> carry blood to the alveoli
they then anastamose after the alveoli
--> reason for PaO2 drop from alveoli =104 --> 100 in left atrium
note also the thebesian veins drain blood from the lungs directly into the left atriuma dn ventricles
--> another shunt of deoxygenated blood back into the circulation
*Hemoglobin
Haldane Effect (in lungs)
unloading of CO2 and loading of O2
Hb need to deliver H+ protons also to convert bicarb (= primary transporter of CO2)
--> into CO2 and H2O
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
Bronchioles and Resistance
generally decrease exponentially
--> only exception is initially there is a decrease in SA and slight increase in resistance
*Minute Ventilation / Alveolar ventilation
how much air enters the TOTAL respiratory system
--> includes physiological deadspace
Physiological dead space
anatomical + alveolar dead space
High Tidal volumes (with hypoventilation) are better for efficient breathing
rather than hyperventilation = rapid breaths (with low tidal volume)
note you need the high tidal volume to fill the lung and get over the gap of anatomical dead space that is always there of the bronchi
--> this is always 150 of the total 500 that is in the lungs
--> even in a healthy person
*Clinical Symptoms in Respiratory Diseases
dyspnea, SOB, pleuritic chest pain
Notes
:
ONLY the parietal pleura has pain sensation
--> parietal = PAIN
viscera pleura has NO pain sensation
note there are 4 separate parietal pleura in the lungs for all the different surface
the phrenic nerve gives pain sensation to the diaphragm and mediastinal parts
the apices and costal parietal are from the intercostal nerves
*PFTs = Pulmonary Function Tests
COPD PFTs
increase
PFTs and *Aging Lungs
Total lung capacity stays the same throughout your life
calcification of ribs and osteoporosis/increased kyphosis
--> decreased compliance of chest wall
loss of elasticity of lungs
--> increased compliance of lungs
these 2 compliances cancelling each other out
--> leads to the unchanged TLC
elements of both restrictive and obstructive disease
obstructive --> alveoli increase in size = air trapping
restrictive = FEV1 decreases from restrictive compliance of the chest cavity
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
FEV1 decreases starting at age 30
Smoking effect on FEV1 and cessation of smoking
starting at age 30 there is a gradual decline in FEV1
smoking accelerates this
smoking effects are irreversible, but you can slow the progression if you quit
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
*Flow Volume LOOPS
LOOP = means 1 breath tracing of inspiration and expiration
--> gives more detail of a single breath pattern than a normal PFT
slope of FEV1 shows whether COPD vs IPF
--> COPD has a DIP in the slope of FEV1
look at the AMX and MIN of graph for expiration and inspiration
--> IPF is restricted so has a short graph in both max and min
*Home
*ABGs
Arterial Blood Gases
*High Altitude ABGs
hypoxemia due to low pressures of O2
carotid mecahnoreceptors sense low O2
--> central resp hyperventilate
--> expel CO2, still no O2 increase
arespiratory alkylosis
takes 24 hours for renal compensation of bicarb
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
*Gas Exchange in the Lungs and Alveoli
normal O2 arteriole = 100
normal CO2 arteriole = 40
--> note ONLY 45 in veins, not much higher
O2 and CO2 are almost the same on their way back through the veins
--> CO2 is only slightly higher , PCO2 = 45, PO2 = 40
DIffusion vs Perfusion effects on O2 and CO2 in blood
under normal circumstances, alveolar walls have quick enough diffusion so that perfusion is the main limiting factor in gas exchange
during 1/3 trip through the pulmonary veins, the blood already equilibriates
ONLY in 2 cases = exercise and Pulmonary fibrosis/emphysema = when diffusion is the limiting factor
--> alveolar walls too thick in IPF and COPD
--> in exercise blood flow is too fast
CO2 equilibriates 20 times faster than O2
--> even in these 2 states, CO2 is NEVER affect, stays the same
--> when CO2 is equal and O2 is not, = diffusion problem
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
A-a *Gradients
check always in initial Mx for dyspnea and SOB
rule out PE
normal tracheal O2 = 150
normal Alveolar O2 = 104
--> this should match = arterial
--> thus A-a gradient = 0 normally
*Hypoxia Management Map
NORMAL A-a gradient ?
RAISED A-a gradient ?
A-a gradient ?
NORMAL A-a gradient
rules out PE
RAISED A-a gradient
sign of PE
V/Q mismatch
increase in physioloigcal deadspace
Lung Perfusion, ventilation and *V/Q ratio
V/Q ration highest at the apex, lowest at the base
effects are mainly due to gravity on the blood = perfusion = Q
gravity pulling the lungs alveoli downaward and stretching them
--> makes them less compliant and can't expand when air enters
base is lower and thus gravity --> higher V and Q separately
gravity effects blood > lung tissue > air
--> perfusion = Q up more at the base relative to ventilation = air/lung tissue = V
--> V/Q goes down at the base
WOB = *Work of Breathing in normal, restrictive, obstructive patients
people try to breathe where their WOB is minimized
for restrictive lung diseases, they can't take deep breaths since they are restricted
--> restrictive take many, fast and shallow breaths to minimize WOB
obstructive = COPD obstruct the outflow by smaller diameter of bronchioles and lung trapping/turbulence
--> thus to minimize WOB they want take slow, long deep breaths to minimize WOB
Clinical Cases
Clinical Case
Notes
:
note that
Clinical Case
