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Pressure
P~ conc. dissolved gas / solubility
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Tidal Volume (VT)
- V entering/leaving mouth/nose each breath
- 400-500ml
- VT=VD+VA
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FRC- Functional residual capacity
Volune left after normal expiration
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VC- Vital Capacity
max volume exhaled after max inspiration
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RV- Residual Colume
volume after max expiration
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TLC- Total Lung Capacity
total volume at max inspration
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Helium dilution technique
- [He]i x Vsp = [He]f x (Vsp + VL)
- VL= FRC
- Assume all airspaces are vent, so may underestimate FRC.
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Minute Ventilation VdotE or VdotT
VdotT= VT x f
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Efficient breathing
- Increasing VT (deep breaths) increases VA more efficiently than panting (shallow breaths @ high respiratotory rate)
- Through training
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AVE
- VA= (VECO2 / PACO2) x K
- K= 0.863
- Increase rate of CO2 generation-> increases vent to get rid of it
- PACO2 is inversely related to VA. Cuz more vent-> means less PACO2
- PA/a
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AGE
- PAO2= PIO2 - (PA/aCO2/R)
- R= 0.8
- PAO2= 150- (PA/aCO2/0.8)
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Inspiration
diaphram contracts, increasing thorax V->decreasing Ppl! And cause lungs to expand.
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PA and Ppl
- As chest wall expand, Ppl gets MORE neg.
- PA- neg: during insp; pos: during expiration; 0 at end-insp & end-expir (no air flow)
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PA
PTP
- PA: Ppl + Pel
- PTP: PA - Ppl
- -"inside - outside"
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Surface tension
- Collapsing pressure due to water interactions @ gas-liquid interface lining alveoli.
- Collapsing P ~ ST and inv ~ to radius. (small alveoli WOULD collapse)
- Surfactant decreases ST
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Surfactant
- Surfactant decreases ST
- work
- Inc compliance
- minimize leakeage/pulm edema in cap's
- week 24-35
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Resistance
- **R= 8nl / πr4Rtot in series (conducting airways) add them up.
- Rtot in parallel (smaller airways)-> 1/Rtot= 1/R1... (tot R less than indiv.)
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velocity
- v=Q/A
- Q is contant so as A inc, v decreases.
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EEP (Equal Pressure Pt)
- WHERE airway P is = to Ppl (PTP=0)
- At large V: (effort-dep flow) EPP in large airways, protected by cartilage
- At low V: (effort-indep flow) dynamic compression sooner in peripheral airways, can't ovecome with effort. (emphysema problem)
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Bronchodilators/constrictors
- opp of what you'd think. refer to Stull
- P-bronchoconstrictors
- S-bronchodilators
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O2 capacity
- max O2 can be combined with Hb (100% saturation)
- 20.1
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O2 content
- TOTAL O2
- O2 content= (O2 binding capacity x %HB sat) + dissolved O2
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Dissolved O2
- =PO2 x solubility
- =100 x 0.0031
- =0.31
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O2 Sat (SO2)
- percent of Hb binding sites bound by O2
- %SO2= [O2 bound Hb / O2 capacity] x 100
- =[O2 content - O2 dissolved] / O2 capacity] x 100
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VdotO2 (body consumes)
200-250ml/min
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CO
VdotO2 / (CaO2 - CvO2) (contents)
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Zones
- Slinky/wet sponge model: alveoli at top are more open and bigger than base aveoli
- The smaller base alveoli are more compliant so can inc V more than the big apex ones.
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HPV
- Local/Regional
- Generalized HPV: high alt, prolonged hypoxia, COPD, CF
- -Inc PVR->pulm hypertension & edema-> RHF
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Hypoxia & Hypoxemia
Hypoxia- lo O2 in tissue (O2 content)
- Hypoxemia- low PaO2 (chemR respond)
- causes: hypovent, diff impairment, R-to-L shunt, low V/Q, decreased PIO2.
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FEV1- Forced Expiratory Volume
FVC- Forced Vital Capacity
- FEV1- volume of 1st sec of forced expiration
- FVC- max volume exhaled after max inspiration
- FEV1/FVC ratios:
- Obstructive- reduced
- Restrictive- increased/normal
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COPD
- now small airways have lots of R
- Chronic bronhitis- BB, inflammatory edema, V/Q mismathc, cyanotic
Emphysema- PP, V/Q match, NOT cyanotic, barrel chest b/c of increase lung V
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Dorsal respiratory group
- In medulla
- inspiration/rhythm
- Inputs: vagus and glossopharyngeal
- Outputs: phrenic to diaphram
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Ventral respiratory group
- In medulla
- ONLY active with active EXPIRATION (exercise)
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Pneumotaxic center
- upper pons
- Shuts down dorsal (limits insp)
- regulates insp V and rate
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Apneustic center
- lower pons
- prolonged and deep inspirations
- Inhib by pneumotaxic center and vagus
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Central chemoreceptors
- breathing responds to CO2 and H+
- NOT O2
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Peripheral chemoreceptors
- breathing responds to all 3- O2, CO2, H+
- 1. Carotid bodies- glossopharygeal to dorsal
- 2. Aortic - vagus to dorsal
- 3. hypoxic vent response
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hypercapnic vs hypoxic vent repsonse
- more sensitive to hypercapnia.
- both chemoR sensitive to it
- hypoxic response kicks it later after PaO2 drops below 60
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Herring-Bruer response with Stretch R
Irritant R
J R
Chest wall R
- Herring-Bruer response with Stretch R: distention activates stretchR activate pneumotaxic center to protect from overinflation
- Irritant R: smoke, noxious gases cause bronchocnstrictions, coughng, sneezing
- J R: stim when pulm cap's engorgw with blood, cause rapid shallow breathing/dyspnea
- Chest wall R: detect force by resp muscles, cause dysnea
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Cheyene-Stokes breathing
- breaths deeply for short interval, then not at all
- delay in CO2 flow going to brain
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Sleep apnea
- Central sleep apnea- dec central drive to breath
- Obstructive sleep apnea- blockage of airway; weight, pregnancy, age
- Generalized HPV and it's symptoms
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dead space
- VD= VT x [(PaCo2 - ExpiredCO2) / PaCO2]
- VT= VA + VD
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