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217 Cards in this Set

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Two ways of looking at barometric/atmospheric pressure
1. 1 square of air from earth to space weights 14.7 lbs
2. Air column will push mercury 760 mmHg in vacuum barometer
Atmospheric pressure values
760 mm Hg, 1 atm, 14.7 lb/in^2, 30 in Hg
What alters atmospheric pressure
Drops with elevation
Increases underwater – doubles for each 33 feet.
Partial pressure of gas
Partial pressure of gas = fractional concentration * total barometric pressure
Ambient air fractional concentrations
21% oxygen
79% nitrogen
0.04% CO2 –> Pco2 in air is approximately 0.
Gas dissolved
Solubility coefficient * partial pressure of gas
(Sc * Pgas)
Arterial blood gas
Obtain blood from artery, analyze dissolved gases.
Includes pH, PPO2, PPCO2, and O2 sat
Ways to express amount of gas in solution
1. Gas dissolved (concentration) – mL gas/dl blood
2. Partial pressure – arterial blood gas (ABG) expresses free gas in plasma and does not include Hb bound gas
PO2 and PCO2 in arterial blood
PO2 = 100 mmHg, PCO2 = 40 mmHg
O2 Dissociation curve
Expresses effect of PO2 on percent Hb saturation and oxygen concentration.

As increase PO2, dissolved O2 goes up slightly.
Formula for Hb–bound O2
(Hb concentration in g/dl * 1.4 Oxygen/g Hb) * O2 saturation

First term is maximum O2 concentration
Formula for free O2 in blood
gas dissolved = solubility constant * Pgas
0.003 mL O2/dl blood for every mmHg O2 * PaO2

0.003 mL O2/dl blood is solubility of free oxygen in blood
Total Oxygen concentration
Sum of Hb–bound O2 and free O2 in blood

(Hb concentration in g/dl * 1.4 Oxygen/g Hb) * O2 saturation
0.003 mL O2/dl blood for every mmHg O2 * PaO2

Note that PaO2 impacts both portions (O2 sat and PaO2)
What does partial pressure of gas include?
Includes both Hb–bound and free oxygen.
Can be used to determine % Hb saturation
Dissolved and Hb–bound O2 at very high PaO2
At very high PaO2, dissolved O2 rises more than Hb–bound O2 because Hb is already mostly saturated. Total O2 rises.
Dissolved and Hb–bound O2 at very low PaO2
At very low PO2, dissolved O2 slowly declines and Hb–bound O2 falls off rapidly
PCO2 plasma arterial baseline level
Brain controls PCO2 plasma at 40 mmHg
Forms of CO2 in blood
Free gas in plasma
CO2 dissociation curve
Linear relationship between PCO2 and concentration in plasma that is steeper than O2 dissociation curve.
Why is CO2 dissociation curve steeper than O2 dissociation curve?
1. CO2 is more soluble in plasma than O2
2. Bicarbonate is added CO2 reservoir
3. Hb has more CO2 binding sites than O2 binding sites.
O2 delivery formula
Arterial O2 concentration x Cardiac Output
Mixed venous O2
What is not consumed by tissues
"Mixed" refers to pulmonary artery because different tissues have different consumption.
Mixed venous O2 < arterial O2, because some used up
Mixed venous CO2
Measured as mixed venous partial pressure (PVCO2) or total mixed venous CO2 concentration
Mixed venous CO2 > arterial CO2
Respiratory quotient
Ratio of CO2 production to O2 consumption
VCO2 / VO2

Carbohydrate–rich diet – 1
Lipid–rich diet – 0.7
Normal value – 0.8
Normal values for arterial and venous O2
Arterial PaO2 = 100 mmHg
Total arterial O2 concentration = 20 mL O2/dl

Venous PvO2 = 40 mmHg
Total mixed venous O2 concentration = 15 mL O2/dl
Normal values for arterial and venous CO2
Arterial PCO2 = 40 mmHg
Total arterial CO2 concentration = 48 mL CO2/dl

Venous PvCO2 = 46 mmHg
Total mixed venous CO2 concentration = 52 mL CO2/dl
AV concentration differences for O2 and CO2
Difference between arterial and venous O2 concentration – 5 mL O2/dl
Difference between arterial and venous CO2 concentration – 4 mL CO2/dl

About the same for O2 and CO2
AV Partial Pressure differences for O2 and CO2
Difference between arterial and venous O2 partial pressure – 60 mmHg
Difference between arterial and venous CO2 partial pressure – 6 mmHg
Why is there a big difference between AV partial pressure between O2 and CO2 but not a big difference for AV concentration differences?
CO2 is more soluble than O2 and has dissociation curve has a steeper slope than O2 dissociation curve.

For O2, small concentration drop associated with very large partial pressure drop. For CO2, same concentration drop associated with smaller partial pressure drop.
Anemia – Hb levels
Normal – 15 g/dlAnemic – <13 g/dl
How does anemia change total arterial oxygen concentration?
Total arterial oxygen concentration = Hb–bound O2 + dissolved O2

Anemia lowers Hb–bound O2 by lowering concentration of Hb (Hb * 1.4 mL O2/g Hb * O2 sat). Thus lowers total arterial oxygen concentration
PaO2 in anemia
PaO2 is normal at 100 mmHg
Total mixed venous O2 concentration in anemia
Lowered total mixed venous O2 concentration
Treatment for anemia
Stop bleeding, transfuse blood if necessary
How does anemia change saturation curve?
Must change O2 concentration axis to reflex less Hb. % Hb saturation is unchanged.
Carbon monoxide
Odorless, colorless gas that binds Hb 240x more avidly than O2.
Displaces O2 from binding site and prevents O2 binding
Effect of CO toxicity on total arterial O2 concentration formula
Reduces mL O2/g Hb, which is normally 1.4. Thus lowers maximum Hb–bound O.
O2 dissociation curve for carbon monoxide poisoning
O2 dissociation curve does not work because PO2 correlation with percent saturation is dramatically changed.
O2 dissociation curve is shifted to the left.
Total arterial O2 partial pressure in CO toxicity
PaO2 = 100 mmHg – unchanged diffusion of O2 into blood
Ways to measure O2 saturation (especially in CO poisoning)
1. Use O2 dissociation curve – extrapolate from PO2. Altered in CO poisoning
2. Finger pulse oximeter – cheap but can't differentiate between O2 and CO
3. Multiwavelength spectrophotometer – only way to assess CO toxicity.
Treatment of CO toxicity
Treat with hyperbaric oxygen to outcompete carbon monoxide for Hb binding sites.
Hyperbaric oxygen reduces half life of Hb–CO from 4–5 hours to 20 minutes.
How does hyperbaric oxygen affect dissolved oxygen?
Increase FiO2 from 21% to 100%
Increase PB from 1 atm to 3 atm (760 * 3 = 2500 mmHg)

Thus increases arterial oxygen
Process of moving air in and out of chest ro provide O2 and remove CO2
Dead space
Area in lungs not exposed to capillary blood. Has ventilation but no perfusion.

Total dead space = anatomic dead space (trachea) + alveolar dead space (parenchyma in lung disease)
Tidal volume
Amount of air inspired at normal resting breath

VT = VD + VA
VT (L/breath) = Dead space component (no exchange) + alveolar component
Minute ventilation
Multiply tidal volume formula by respiratory rate (breaths/min)

Expiratory minute ventilation = dead space ventilation + alveolar ventilation
Measured in L/min
Normal tidal volume, alveolar volume, minute ventilatoin, alveolar ventilation, and respiratory rate
VT = 500 mL
VA = 100 mL
VE = 5L/min
VA = 4L/min
Respiratory rate = 10 breaths/min
What gas pressure does brain maintain
Brain mantains PCO2 at around 40 mmHg
Measuring mean alveolar values
PAO2/FAO2 and PACO2 and FACO2 are hard to measure. Can't average al alveoli because dead space alveolar–capillary units do not contribute
What controls mean alveolar O2 and mean alveolar CO2?
Amount of alveolar ventilation controls mean alveolar O2 and mean alveolar CO2.
Alveolar ventilation equation
VCO2 (Tissue CO2 production) = VA (alveolar ventilation) * FACO2 (fractional concentration of CO2)

PaCO2 (arterial partial pressure of CO2) = (VCO2 (tissue CO2 production)/VA (alveolar ventilation)) * K

K accounts for change from FACO2 to VCO2
Also note that FACO2 (alveolar) changed to PaCO2 (arterial)
Why can PaCO2 substitute for FACO2 in alveolar ventilation equation?
Equal because:
1) CO2 dissociation curve is linear and steep so constant relationship between partial pressure and total CO2 concentratoin.
2) CO2 is very soluble – unlikely to be diffusion limited.
Can PaO2 substitute for FAO2?
What happens when change ventilation in alveolar ventilation equation?
If VCO2 is constant at around 200 mL/min and brain regulates FACO2 at 40 mmHg, then:
If decreaes ventilation, PaCO2 goes up (hypercapnea)
If increase ventilation, PaCO2 go down.
High PaCO2
60–70 mmHg is moderately high and 100 mmHg is very high
Causes drowsiness, unconsciousness, respiratory arrest
Metabolic acidemia
Tolerated worse than hypoxia
How does hypoventilation occur?
1 Total minute ventilation is low (so alveolar ventilation is low). Due to depressed respiratory center in brainstem and narcotics or excessive work of breathing (asthma, COPD)
2. Low alveolar ventilation because of increased dead space ventilation with normal minute ventilation.
Mixed expired CO2 (FECO2)
Fractional concentration of CO2 in entire tidal volume breath. Greater amount of dead space => lower mixed expired CO2 concentration.
Dead Space Fraction
VD/VT = 150 mL/500 mL = 0.3, normally
Bohr Equation of dead space fraction
More dead space = lowered FECO2
If no dead space, FACO2 = FECO2. Not possible.
Bohr Equation expressed in pressure

Equate alveolar CO2 to arterial CO2 and change fractional concentration to partial pressure
Distribution of ventilation in lungs
Most of ventilation goes to lower lobes of lung.
Distribution of profusion in lungs
Most of profusion goes to lower lungs because of gravity.
Destruction of normal matrix in lungs –> compliant lungs
Almost exclusively caused by smoking
Detected 95% by radiography. Large conglomerate air spaces with small amount of surrounding capillary flow (high ventilation, low profusion)
Pulmonary fibrosis
Excess deposition of matrix in lungs
Stiff, noncompliant lungs
Fick's Law of Diffusion
Vgas = A/t * D * (P1–P2)
D is proportional to solubility/sqrt(MW)
Solubility of CO2, O2, and CO
CO2 is 25 times more soluble than O2. CO is about as soluble as O2. Solubility is directly related to Vgas by D, diffusion constant
Partial pressure of gas includes...
Partial pressure of gas includes only plasma, not Hb–bound gas.
Change in partial pressure of gases across capillary – figure
Partial pressure of gases in capillary approach partial pressure of gas in alveolus. Diffusion occurs until partial pressures are equal.
Change in partial pressure of nitrous oxide across capillary
Initial concentration of 0 mmHg in capillary.
Inspire N2O into alveolar space. Diffuses across alveolar capillary membrane –> gas as plasma (PcN2O). No combination with Hb.
Because no H binding, PcN2O rises rapidly until equates with PAN2O – no further flow.
Perfusion–limited – only way to add more PCN2O is to move more air into alveolus.
Change in partial pressure of carbon monoxide across capillary.
Inspire CO into alveolar space. Diffuse across alveolar capillary membrane –> transiently xists as free gas –> almost all binds to Hb
PCCO never rises very much and never equates to PACO.
Transfer of CO is diffusion limited – because PCCO isn't close to PACO, can increase PCCO by Fick's law properties
Change in partial pressure of oxygen across capillary
Inspire O2 into alveolar space (PAO2). Begins at given mixed venous pressure of O2 and diffuses across alveolar capillary membrane –> exists both as free gas and Hb–bound.
Normal circumstances – PCO2 rises fairly rapidly until it reaches PAO2. Perfusion–limited because can only increase PAO2 by bringing more air in.
Disease conditions – PCO2 does not equate to PAO2 – governed by factors of diffusion so diffusion–limited.
Diffusion–limited or perfusion–limited
Diffusion–limited if end capillary value does not equate to alveolar pressure.
Perfusion–limited if end capillary value does equate to alveolar pressure.
RBC travel time at rest and exercise
At rest, PO2 in capillary reaches PAO2 after 1/3 of capillary.
In exercise, travel time reduced from 3/4 sec to 1/4 second. PCO2 no longer reaches PaO2 – diffusion–limited.
What kind of limitation does thickening of lung lead to?
PCO2 cannot reach PAO2 = diffusion–limitation. e.g. pulmonary fibrosis
Alveolar hypoxia
PAO2 drops from 100 mmmHg –> 50 mmHg
Normal curve is less steep because (P1–P2) is less
Takes longer to equate to PO2
Diffusion limitation
Altering diffusion constants and values can change whether reaches diffusion limitation.
Exercise reduces likelihood of hitting diffusion limitation.
Diffusion capacity for carbon monoxide test
Patient inhales small amount of CO, holds breath, then exhales.
Measures amount of CO that moved to capillary, calculated by measuring how much CO is exhaled.
Why can't measure O2 for O2 diffusion capacity? Why is CO a good substitute?
No CO in blood at baseline, so O2 is harder to measure.
If patient can't transfer CO appropriately, also cant transfer O2.
Forster Equation for DL
1/DL = 1/DM + 1/(theta – Vc)
Reciprocals because D is a conductance – can add resistance but not conductance in series.
1/DM reflects diffusion process itself.
1/(THETA*Vc) reflects time for O2 or CO2 to react with Hb.
Values in Forster equation
DL: Diffusion capacity of lungs
DM: True diffusing capacity of membrane separating alveolus from blood.
Theta – Affinity of Hb for CO
VC – Total mL of blood in capillaries exposed to arterial gas on one time.
DL depends on three factors:
1. Amount of surface area present for gas exchange
2. Amount of capillary blood exposed to alveolar gas
3. Amount of Hb present.
What reduces diffusion capacity?
DL is reduced by diseases which reduce functioning of alveolar capillary units.
Exercise and DLCO
Exercise increases diffusion capacity because vasodilation increases amount of capillary blood exposed to alveolar gas at a time.
Effect of raising or lowering O2 tension on DLCO
100% O2 reduces DLCO because O2 competes with CO for Hb binding sites.

Less CO taken up.
Causes of hypoxemia and impaired CO2 gas exchange
Hypoventilatoin, diffusion limitation, shunt, ventilation–perfusion inequality
What determines steady state concentrations of mean alveolar values (PAO2/FAO2 or PACO2 or FACO2)?
Alveolar ventilation
Equation for partial pressure of gas
Pxgas = Fxgas * PB, PB = 760 mmHg
PACO2 formula
PaCO2 = VCO2/VA * K = PACO2
Air, alveolar, and arterial PO2
Ambient air PO2 = 160 mmHg
Alveolar PAO2 = 100 mmHg
Arterial PaO2 = 100 mmHg
Low alveolar ventilation given PACO2.
Rate of 60 breaths/minute may be normal for PACO2 of 40.
Alveolar ventilation equation (PaCO2)
PaCO2 = VCO2/VA * K
To keep PaCO2 around 40, need around 4L of VA based on amount of CO2 produced.
VCO2 – Alveolar gas equation

Assume FICO2 = 0
VO2 – Alveolar gas equation
VO2 = VA * (FIO2 – FAO2)
VO2 = VA * (PIO2 – PAO2)/K

Need two fractional concentratoins because present in both air and blood (as oppose to CO2, which is only present in blood)
Alveolar gas equation
PIO2 formula
PIO2 = FIO2 (PB–PH2O), usually around 150 mmHg
PB = 760 mmHg, PH2O = 47 mmHg
21% oxygen in ambient air. More if supplemental
Barometric pressure. Varies with altitude, 760 mmHg at sea level.
PiO2 in trachea
FiO2 (PB – PH2O)
0.21 (760–47) = 150
R value
Ratio of CO2 production to O2 consumption
Usually from 0.8 to 1.0
Alveolar ventilation at sea level
PaO2 = 100 mmHg when PaCO2 = 40 mmHg
Why is room level PO2 at 160 mmHg while PaO2 is 100 mmHg?
1. Consuming O2 at tissue level
2. Mixed venous blood coming into alveolar capillary unit is at 40 mmHg.
PAO2 when put on supplemental oxygen
FiO2 = 100%
PAO2 = 1.0 (760–47) – 40/0.8 = 650 mmHg

No change in alveolar ventilation (40/0.8), changing concentration of inspired gas
PAO2 when hypoventilating (PaCO2 of 80)
FiO2 = 21%, PaCO2 = 80 mmHg
PAO2 = 0.21 (760–47) – 80/.8 = 50 mmHg
Hypoxemia vs hypoxia
Hypoxemia – Low arterial (blood) partial pressure of O2. Less than 70 mm Hg
Hypoxia – Low air or tissue O2
Overcoming hypercapnea and hypoxemia
Hypercapnea – Requires mechanical ventilation until underlying disease is addressed.Hypoxemia – usually overcome by giving supplemental oxygen – increase PIO2
Diffusion limitation and PO2
Normal conditions – PO2 quickly equates to alveolar value
Mildly abnormal conditions – equates less quickly
Grossly abnormal conditions – may not equate with alveolar value = diffusion abnormality

Exercise shortens time to 0.25s from 0.75 s – adds diffusion limitation in mildly abnormal conditions
CO2 diffusion along capillary length
CO2 is very soluble. By 1/3 of capillary, equates to PACO2
Rarely diffusion limited (diffusion limitation occurs when end capillary and alveolar pressures do not equate).
What determines PCO2/PO2 of individual alveolar units?
1. Composition of inspired gas (FIO2)
2. Composition of mixed venous blood (PVO2)
3. Ventilation–perfusion ratio
4. Slopes and positions of O2/CO2 dissociation curves
High V/Q ratio – high perfusion, low perfusion
Low V/Q ratio – low ventilation, high perfusion
Low V/Q ratio is caused by:
Alveoli filled with infection, water, protein, collagen
Alveolar collapse
Mucus plugging or edema at small airways

In presence of maintained capillary blood flow
High V/Q ratio is caused by:
Capillary obstruction from vascular disease or blood clots

In presence of maintained ventilation to alveolus
(or increased ventilation with normal perfusion)
What does end capillary blood resemble in low and high V/Q?
Low V/Q – resembled mixed venous blood
High V/Q – resembles inspired air
V/Q of 1 – normal arterial values (100, 40)
Normal O2 and CO2 values in arteries
PaO2 = 100 mmHg, 20 mL O2/dl
PvO2 = 40 mmHg, 15 mL O2/dl

PaCO2 = 40 mmHg, 48 mL O2/dl
PvCO2 = 46 mmHg, 52 mL CO2/dl
Normal O2 and CO2 in inspired air
PIO2 = 150 mmHg
PICO2 = 0 mmHg
V/Q Ratio Equation
Used to calculate individual alveolar capillary unit values with differing VQ ratios
Graph for V/Q ratio equation
PO2 ranges from 40–150 mmHg with 100 mmHg at V/Q of 1
PCO2 ranges from 46–0 mmHg with 40 mmHg at V/Q of 1
O2 concentration runs with PO2 but plateaus when Hb is fully saturated.
Main concern of high V/Q ratio
Blood readily exchanges gas but small amount of blood so little contribution to blood gas. Concern is that it increases dead space ventilation, lowering alveolar ventilation.

VE = VA + VD
Describing V/Q ratio with PO2/PCO2 curve
Increasing V/Q ratio – PO2 increases and PCO2 decreases.
Decreasing V/Q ratio – PO2 decreases and PCO2 increases.
PE in left lung – initial changes in VE, VD, VA
No change in VE (5 L/min)
VA – 2L/min in right lung, 0 L/min in left lung
VD – 0.5L/min in left lung, 2.5 L/min in left lung

VA drops to half (4 –> 2), so PCO2 rises 2x by equation PaCO2 = VCO2/VA * K
In PE, what happens to blood going to affected lung?
Redirected to other lung
PE in left lung – compensation
Increase total minute ventilation to maintain alveolar ventilation
Increase Ve to 9 L/min
VA = 4L/min in right lung, 0 L/min in left lung
VD = 0.5 L/min in right lung, 4.5 L/min in left lung

Maintained VA so PACO2 does not drop.
Mild increases in minute ventilation to overcome dead space ventilation
Not a problem – keep VA normal to keep PaCO2 normal and then keep PaO2 normal.
Severe increases in minute ventilation to overcome dead space ventilation
May be ok
Or may not be able to – inability to maintain VE –> respiratory muscle failure
VE falls, followed by decrease in VA because increase in VD.
Decrease in VA causes hypercapnea and hypoxemia.
How can hypoventilation occur?
1) Low total VE – narcotic overdose, excessive work of breathing (COPD, asthma)
2) Low VA because of increased dead space (high minute ventilation)
What does end capillary blood look like for low V/Q ratio?
Mixed venous blood
Causes of low V/Q
Alveoli villed with infection, pus, water, protein, collagen
Mucus plugging or edema of small airways
With maintained capillary blood
Normal concentration of O2 in mixed venous and arterial blood
Comes in at 15 mL O2/dl, exits at 20 ml O2/dl
Low V/Q ratio in right upper lobe – effect on right lung
Right – Mixed venous blood comes in at 15 mL O2/dl, exits at 16 mL O2/dl
Low V/Q ratio in right upper lobe – effect on left lung
Breathe faster to create high V/Q in left lung (increased ventilation)
Mixed venous blood comes in at 15, leaves at 20.5
PO2 is higher but small change in oxygen concentration because of flattening of O2 dissociation curve
Left atrium O2 concentration when low V/Q of right upper lung (with left lung compensation)
Left atrium O2 concentration is low (18 mL )2/dl blood). PaO2 = 50 mmHg.

Cannot maintain PaO2.
Treatment of hypoxemia in low V/Q
Supplemental O2 – nasal prongs or mask
Increases FiO2 from 0.21 to 0.5 or 1.0 so PiO2 increases (PiO2 = Pb*FiO2)
Increases PaO2 mainly of affected lung because hemoglobin already saturated in normal lung.
V/Q and PO2 curve shifts left so at given V/Q ratio, PO2 increases.
Normal mixed venous and arterial CO2 concentrations
Mixed venous blood comes in at 52 mg/dl, exits at 48.
Pneumonia in right upper lobe, effect on right lobe mixed venous and arterial CO2
Right lung – mixed venous comes in at 52 mg, exits at 51 mg/dl
Pneumonia in right upper lobe, compensation effect on left lobe mixed venous and arterial CO2
Hyperventilation increases V/Q in left lung.
Mixed venous comes in at 52 mg, exits at 45 mg/dl.
Because linear relationship between partial pressure and concentration for CO2, lowering pressure does lower concentration
Pneumonia in right upper lobe, effect on concentration of CO2 and PCO2 in left atrium
Normal 48 mL CO2/dl blood
PaCO2 = 40 mmHg
Low V/Q with compensation – effect on arterial O2 and CO2 levels
Systemic arterial hypoxemia but normocapnea
Treatment of low V/Q pneumonia in right upper lobe
Ventilation and antibiotics
Extremely low V/Q of 0
End capillary gas concentrations = mixed venous concentrations.
Cannot overcome O2 changes with supplemental O2 – does not reach lobe. Ventilation can't offset global hypoxemia but can offset CO2 – same as low V/Q.
A–a gradient
Used to assess patient's oxygenation.
A–a = PAO2 – PaO2

Remember: PAO2 = PIO2 – PACO2/R
In healthy lungs, no A–a gradient
Elevated A–a gradient
Not caused by hypoventilation – mean alveolar O2 (PAO2) causes reduction in PaO2.
Occurs with:
Diffusion abnormality – PaO2 does not reach PAO2
Or mostly low V/Q or shunt mismatch – low ventilation reduces PaO2 compared to PAO2 (where there is a PAO2) because PAO2 depends on PIo2 which is normal.
V/Q ratio changes as descend lung
Top of lung has higher V/Q ratio than bottom of lungs
As descend, ventilation increases at slower rate than does blood flow (gravity). So, V/Q goes down as you go down lung.
Muscle movements of inspiration
Contract diaphragm and expand chest wall
Mechanical movements of expiration
Normally passive, can forcefully exhale
Diaphragm innervation
Phrenic nerve (C3–5) – injury impairs breathing
Tidal volume
Volume of one inspiration/expiration
Total lung capacity
Volume of active breath in and out
Residual volume
Residual volume left after complete exhalation
Functional residual capacity
Volume remaining at end of normal tidal volume exhalation.
Lung recoil pressure
Inwards (towards lower volume)
Because of intrinsic properties – elastin, fibronectin, collagen and surface tension
Chest wall recoil pressure
Outwards (higher volume) except at very high volumes
Pleural space and fluid
Pleural space = potential space between visceral and parietal pleura
Small amount of pleural fluid in this space (radiographically undetectable) mechanically couples lungs and chest wall.
Pleural fluid transmits force of diaphragm and inspiratory muscle to lungs
Subatmospheric intrapleural pressure
<760 mmHg because inward lung recoil and outward chest wall recoil.
Verify by puncturing chest wall – air follows pressure gradient into chest
Uncouples lung and chest wall
Lung recoils to smaller volume and chest wall to larger volume
Can occur due to puncturing of either lung or chest wall.
Figure of Lung capacity vs airway pressure
Middle line – relaxation pressure of 0.
Lung is on right – wants to recoil inwards (so manometer reads positive airway pressure). Increase in volume increases inwards recoil force.

Chest wall is on left – wants to recoil outwards (so manometer reads negative airway pressure) – except at high pressures, at which wants to recoil inwards.
Figure of lung capacity vs airway pressure – summation of chest wall and lung and FRC
Summation line crosses airway pressure of 0 at functional residual capacity (FRC) – this is the volume at which lung inward recoil force equals chest outward recoil force.
Intrapleural pressure during breath
Inspiration – intrapleural pressure becomes more subatmospheric
Expiration – passively returns to resting subatmospheric pressure
Emphysema and gas exchange
Emphysema destroys ECM. Leads to high V/Q ratio.
Fibrosis and gas exchange
Fibrosis has excess ECM deposition. Some areas of low V/Q and others of high V/Q
Pressure–volume curve of lung
Inspiration – intrapleural pressure becomes more negative and volume increases.
Curve is steep at first – small change in pressure needed for large change in volume (high compliance)
Curve eventually flattens – more pressure needed to change volume (less compliant)
Measures distensibility
Measures ability to return to original position
Compliance in fibrosis and emphysema
Emphysema – high compliance – small pressure to generate same volume
Fibrosis – low compliance – larger pressure to generate same volume
Model of elastic recoil
Elastic recoil causes lung to recoil to lower volume and tethers small airways open (preventing collapse) when springs are stretched during inspiration
Alteration of recoil during emphysema
Emphysema – decreased elastic recoil (overly compliant) – reduced tethering of small airways = increased tendency for airway collapse
Alteration of recoil during fibrosis
Fibrosis – larger inward recoil of lung (low compliance) and increased tethering of airways, preventing small airway collapse. But requires more energy to distend lungs.
Surface tension
Partly responsible for compliance.
Forces acting along 1 cm line on surface of liquid at gas–liquid interface
Cohesion between water is stronger than adhesion to air
Acts on small amount of liquid lining alveolus to make liquid surface area and alveolus volume as small as possible
Phospholipid secreted by type 2 alveolar cells into alveolar space linings
Lowers surface tension of fluid lining alveolus
Surface tension and compliance – saline experiment
If fully fill lung with saline, surface tension forces are obliterated. Leads to steeper PV curve (greater compliance), similar to emphysema..

Demonstrates that surface tension reduces compliance.
Infant respiratory distress syndrome (RDS)
Developmental deficiency in surfactant
More surface tension = lower compliance. PV curve similar to fibrosis.
Treat with exogenous surfactant replacement
Law of Laplace and alveoli
Law of Laplace – P = 4T/r
As alveolus gets smaller, greater recoil pressure (P) inwards. Thus, small alveoli have greater tendency to collapse
Surfactant and small alveoli
Surfactant has lower surface tension at lower surface area.
Stabilizes small alveoli from Law of Laplace effects, preventing collapse.
Hysteresis in saline and air–filled lungs
Time lag in 2 associated events.
Air filled lung surface tension –> hysteriesis
Saline –> no surface tension forces –> no hysteresis

Surface tension forces are responsible for hysteresis.
Why is ventilation higher in lower lobes than upper?
Upper portion has more recoil forces inward than bottom because of gravity.

Upper lobe alveoli are higher on PV curve = larger volume at rest but less change in volume with inspiration because less compliant.
Basal alveoli are lower on PV curve – lower resting volume but more compliant, so greater change in V with inspiration.
What does pressure differnce over tube depend on?
Rate and pattern of flow
Ohms Law
Resistance = P1–P2/Flow
Pulmonary Vascular Resistance equation (Ohm's Law)
(MPAP–Left Atrial (Wedge) Pressure)/CO
Pouiseuille's Law

Resistance is proportional to length and viscosity and inversely proportional to radius^4
Turbulent flow
Nonlinear pressure–flow relationship
Pressure is proportional to (flow rate)^2
Generally, higher airway resistance because larger drop in pressure
Increase in gas density increases resistance
Gas mixture of helium and oxygen. Helium is less dense than oxgen so lowers resistance
Airway resistance varies with lung volume
Airway resistance decreases with increase in lung volume (because of increase in radius)
Chief site of airway resistance
Large airways (larynx and trachea) because have lowest overall cross–sectional area.
40,000 small areas and 1 trachea/larynx.
Reynold's number
Determines whether flow is laminar or turbulent.
Re = 2rvd/n
Velocity, density, radius are positively correlated and viscosity is negatively correlated with turbulent flow.
Reynolds > 2000 indicates turbulent flow.
Gas density and Reynold's number
Gas density increases with atmospheric pressure and molecular weight (i.e. Nitrogen vs Helium)
Increases Reynold's number –> turbulent flow
Intraalveolar and intrapleural pressure at FRC
No flow.
Atmospheric intraalveolar pressure
Subatmospheric intrapleural pressure
Intraalveolar and intrapleural pressure during inspiration
Slightly subatmospheric intraalveolar pressure
Further subatmospheric intrapleural pressure
End–inspiration intraalveolar and intrapleural pressure
Atmospheric intraalveolar pressure
Minimal subatmospheric intrapleural pressure
Intraalveolar and intrapleural pressure during normal passive expiration
Slightly atmospheric intraavlveolar pressure
Subatmospheric intrapleural pressure returns to rest subatmospheric pressure
Intraalveolar and intrapleural pressure during forced expiration
Intraalveolar pressure rises substantially above atmospheric
Intrapleural pressure also rises substantially above atmospheric
Both rise to same degree, depending on degree of muscular effort
Airway collapse during forced expiration
Airway pressure drops from alveolus to mouth. At some point, airway pressure drops below pleural pressure and airway collapse.
Pressure behind collapse causes airway to open. Pressure drop causes it to close again. Called a starling resistor.
Determining factor for airway collapse during forced expiration
Difference between alveolar and pleural pressure
Depends on elastance of lung
Effect of emphysema and fibrosis on likelihood of airway collapse during forced expiration
Emphysema – decreased elasticity/inward recoil. Less subatmospheric intrapleural pressure –> lesser difference between pressure –> greater tendency to collapse

Fibrosis – increased elasticity/inward recoil. Greater subatmospheric intrapleural pressure –> greater difference between pressures –> lesser tendency to collapse
Amount of volume can exhale in 1 second
FEV1/VC is usually 75%. Limited by airway collapse.
FEV1/VC in emphysema
FEV1/VC is around 40% in emphysema – more likely to collapse so exhale less before collapse occurs.
FEV1/VC in fibrosis
FEV1/VC is around 90% in fibrosis – less likely to collapse so exhale more before collapse occurs.
Is flow generally effort–dependent or independent in forced expiration?
Generally effort–independent because effort doesn't change difference between pleural and alveolar pressure.
Is flow effort–dependent at beginning of forced expiration?
No – greater effort results in more flow at beginning of forced expiration.
Because at high volumes, airways are so distended that they will not collapse even if tendency to collapse.
Importance of hypercapnea
Indicates critical illness – represents failure to regulate PCO2.
Is hypoxemia critical?
Hypoxemia is abnormal but not as reflective as emergency.Hypoxemia does not trigger response until it reaches 50 mmHg.

Pulmonary circulation pressures
Pulmonary circulation is low pressure
Pulmonary artery has pressure of 25/10 instead of 120/80. MPAP is 15.
Increased MAP of 30–50 under pulmonary hypertension.
Measuring pulmonary artery pressures
Use pulmonary artery catheter
Insert in any vein, access vena cavae, thread into right atrium and then pulmonary artery and wedge into small arteriole.
Balloon catheter – inflated and carried by cardiac output
Compliance of pulmonary vasculature
Highly compliant with little smooth muscle – little work required
Pulmonray Vascular Resistance equation
Pulmonary Vascular Resistance = (MPAP – Left Atrium Pressure)/Cardiac Output
Expressed in Wood units. Normal value is < 3
PVR response to increase in vascular pressure or flow
Falls because of intrinsic changes in response to increase in pressure/flow – (a) Recruitment (opening of closed capillaries) and (b) Distension of open capillaries
Counterintuitive – by PVR = Pressure/CO, PVR should rise when pressure rises
Alveolar and extraalveolar vessels and associated forces
Capillaries are alveolar vessels – exposed to alveolar forces
Arterioles are extraalveolar vessels – exposed to recoil forces
Effect of lung volume on PVR
Low volumes – extraalveolar vessels are small – high PVR
High volumes (TLC) – capillaries are stretched – increased PVR

Lowest point is at middle volume (FRC)
Starling resistor effect
Water can flow through 2 pathways
A – if chamber pressure exceeds downstream pressure, flow is independent of downstream pressure
B – if downstream pressure exceeds flow pressure, flow depends on upstream to downstream difference
West Zone 1
Top of lung
PA > Pa > Pv
No flow because alveolar pressure is too high
West Zone 2
Middle of lung
Waterfall or starling effect
Pa > PA > Pv
PA is close to Pa – vessel collapses, increaseing Pa, reopening vessel which then collapses again.
West Zone 3
Bottom of lung
Pa > Pv > Pa
Alveolar pressure is irrelevant. Flow determined by afferent–to–efferent pressure drop
Central controllers of ventilation
Brainstem (automatic, involuntary)
Cerebral cortex (voluntary
Central controllers locations
Medulla – intrinsic, automatic rhythm of ventilation
Lower and upper pons
What are three things chemoreceptors change?
PaCO2 – depressed by age, sleep, narcotics
pH – goes along with PaCO2
PaO2 – doesn't change ventilation until below 50 mmHg
Central chemoreceptors location
Ventral surface of medulla
Surrounded by ECF and CSF
What do central chemoreceptors sense?
Responds to [H+] – increase stimulates ventilation, decrease inhibits ventilation

Rise in [H+] occurs when CO2 is high and diffuses into brain, converted by carbonicc anhydrase
Peripheral chemoreceptors
Located at carotid body bifurcation and aortic arch
Respond to all three but less important than central:

1. Decrease in PaO2 – completely responsibly for hypoxia response
2. Decrease in pH
3. Increase in pCO2