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217 Cards in this Set
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- Back
- 3rd side (hint)
Two ways of looking at barometric/atmospheric pressure
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1. 1 square of air from earth to space weights 14.7 lbs
2. Air column will push mercury 760 mmHg in vacuum barometer |
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Atmospheric pressure values
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760 mm Hg, 1 atm, 14.7 lb/in^2, 30 in Hg
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What alters atmospheric pressure
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Drops with elevation
Increases underwater – doubles for each 33 feet. |
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Partial pressure of gas
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Partial pressure of gas = fractional concentration * total barometric pressure
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Ambient air fractional concentrations
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21% oxygen
79% nitrogen 0.04% CO2 –> Pco2 in air is approximately 0. |
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Gas dissolved
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Solubility coefficient * partial pressure of gas
(Sc * Pgas) |
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Arterial blood gas
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Obtain blood from artery, analyze dissolved gases.
Includes pH, PPO2, PPCO2, and O2 sat |
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Ways to express amount of gas in solution
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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 |
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PO2 and PCO2 in arterial blood
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PO2 = 100 mmHg, PCO2 = 40 mmHg
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O2 Dissociation curve
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Expresses effect of PO2 on percent Hb saturation and oxygen concentration.
As increase PO2, dissolved O2 goes up slightly. |
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Formula for Hb–bound O2
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(Hb concentration in g/dl * 1.4 Oxygen/g Hb) * O2 saturation
First term is maximum O2 concentration |
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Formula for free O2 in blood
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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 |
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Total Oxygen concentration
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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) |
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What does partial pressure of gas include?
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Includes both Hb–bound and free oxygen.
Can be used to determine % Hb saturation |
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Dissolved and Hb–bound O2 at very high PaO2
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At very high PaO2, dissolved O2 rises more than Hb–bound O2 because Hb is already mostly saturated. Total O2 rises.
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Dissolved and Hb–bound O2 at very low PaO2
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At very low PO2, dissolved O2 slowly declines and Hb–bound O2 falls off rapidly
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PCO2 plasma arterial baseline level
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Brain controls PCO2 plasma at 40 mmHg
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Forms of CO2 in blood
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Free gas in plasma
Hemoglobin–bound Bicarbonate–bound |
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CO2 dissociation curve
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Linear relationship between PCO2 and concentration in plasma that is steeper than O2 dissociation curve.
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Why is CO2 dissociation curve steeper than O2 dissociation curve?
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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. |
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O2 delivery formula
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Arterial O2 concentration x Cardiac Output
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Mixed venous O2
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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 |
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Mixed venous CO2
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Measured as mixed venous partial pressure (PVCO2) or total mixed venous CO2 concentration
Mixed venous CO2 > arterial CO2 |
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Respiratory quotient
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Ratio of CO2 production to O2 consumption
VCO2 / VO2 Carbohydrate–rich diet – 1 Lipid–rich diet – 0.7 Normal value – 0.8 |
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Normal values for arterial and venous O2
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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 |
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Normal values for arterial and venous CO2
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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 |
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AV concentration differences for O2 and CO2
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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 |
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AV Partial Pressure differences for O2 and CO2
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Difference between arterial and venous O2 partial pressure – 60 mmHg
Difference between arterial and venous CO2 partial pressure – 6 mmHg |
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Why is there a big difference between AV partial pressure between O2 and CO2 but not a big difference for AV concentration differences?
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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. |
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Anemia – Hb levels
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Normal – 15 g/dlAnemic – <13 g/dl
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How does anemia change total arterial oxygen concentration?
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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 |
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PaO2 in anemia
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PaO2 is normal at 100 mmHg
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Total mixed venous O2 concentration in anemia
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Lowered total mixed venous O2 concentration
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Treatment for anemia
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Stop bleeding, transfuse blood if necessary
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How does anemia change saturation curve?
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Must change O2 concentration axis to reflex less Hb. % Hb saturation is unchanged.
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Carbon monoxide
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Odorless, colorless gas that binds Hb 240x more avidly than O2.
Displaces O2 from binding site and prevents O2 binding |
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Effect of CO toxicity on total arterial O2 concentration formula
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Reduces mL O2/g Hb, which is normally 1.4. Thus lowers maximum Hb–bound O.
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O2 dissociation curve for carbon monoxide poisoning
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O2 dissociation curve does not work because PO2 correlation with percent saturation is dramatically changed.
O2 dissociation curve is shifted to the left. |
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Total arterial O2 partial pressure in CO toxicity
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PaO2 = 100 mmHg – unchanged diffusion of O2 into blood
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Ways to measure O2 saturation (especially in CO poisoning)
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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. |
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Treatment of CO toxicity
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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. |
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How does hyperbaric oxygen affect dissolved oxygen?
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Increase FiO2 from 21% to 100%
Increase PB from 1 atm to 3 atm (760 * 3 = 2500 mmHg) Thus increases arterial oxygen |
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Ventilation
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Process of moving air in and out of chest ro provide O2 and remove CO2
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Dead space
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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) |
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Tidal volume
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Amount of air inspired at normal resting breath
VT = VD + VA VT (L/breath) = Dead space component (no exchange) + alveolar component |
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Minute ventilation
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Multiply tidal volume formula by respiratory rate (breaths/min)
Expiratory minute ventilation = dead space ventilation + alveolar ventilation Measured in L/min |
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Normal tidal volume, alveolar volume, minute ventilatoin, alveolar ventilation, and respiratory rate
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VT = 500 mL
VA = 100 mL VE = 5L/min VA = 4L/min Respiratory rate = 10 breaths/min |
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What gas pressure does brain maintain
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Brain mantains PCO2 at around 40 mmHg
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Measuring mean alveolar values
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PAO2/FAO2 and PACO2 and FACO2 are hard to measure. Can't average al alveoli because dead space alveolar–capillary units do not contribute
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What controls mean alveolar O2 and mean alveolar CO2?
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Amount of alveolar ventilation controls mean alveolar O2 and mean alveolar CO2.
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Alveolar ventilation equation
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VCO2 (Tissue CO2 production) = VA (alveolar ventilation) * FACO2 (fractional concentration of CO2)
Modified: 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) |
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Why can PaCO2 substitute for FACO2 in alveolar ventilation equation?
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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. |
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Can PaO2 substitute for FAO2?
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No!
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What happens when change ventilation in alveolar ventilation equation?
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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. |
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Hypercapnea
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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 |
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How does hypoventilation occur?
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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. |
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Mixed expired CO2 (FECO2)
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Fractional concentration of CO2 in entire tidal volume breath. Greater amount of dead space => lower mixed expired CO2 concentration.
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Dead Space Fraction
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VD/VT = 150 mL/500 mL = 0.3, normally
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Bohr Equation of dead space fraction
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VD/VT = (FACO2–FECO2)/FACO2
More dead space = lowered FECO2 If no dead space, FACO2 = FECO2. Not possible. |
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Bohr Equation expressed in pressure
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VD/VT = (FACO2–FECO2)/FACO2 = (PaCO2 – PECO2)/PaCO2
Equate alveolar CO2 to arterial CO2 and change fractional concentration to partial pressure |
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Distribution of ventilation in lungs
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Most of ventilation goes to lower lobes of lung.
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Distribution of profusion in lungs
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Most of profusion goes to lower lungs because of gravity.
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Emphysema
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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) |
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Pulmonary fibrosis
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Excess deposition of matrix in lungs
Stiff, noncompliant lungs |
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Fick's Law of Diffusion
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Vgas = A/t * D * (P1–P2)
D is proportional to solubility/sqrt(MW) |
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Solubility of CO2, O2, and CO
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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
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Partial pressure of gas includes...
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Partial pressure of gas includes only plasma, not Hb–bound gas.
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Change in partial pressure of gases across capillary – figure
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Partial pressure of gases in capillary approach partial pressure of gas in alveolus. Diffusion occurs until partial pressures are equal.
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Change in partial pressure of nitrous oxide across capillary
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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. |
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Change in partial pressure of carbon monoxide across capillary.
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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 |
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Change in partial pressure of oxygen across capillary
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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. |
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Diffusion–limited or perfusion–limited
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Diffusion–limited if end capillary value does not equate to alveolar pressure.
Perfusion–limited if end capillary value does equate to alveolar pressure. |
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RBC travel time at rest and exercise
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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. |
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What kind of limitation does thickening of lung lead to?
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PCO2 cannot reach PAO2 = diffusion–limitation. e.g. pulmonary fibrosis
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Alveolar hypoxia
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PAO2 drops from 100 mmmHg –> 50 mmHg
Normal curve is less steep because (P1–P2) is less Takes longer to equate to PO2 |
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Diffusion limitation
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Altering diffusion constants and values can change whether reaches diffusion limitation.
Exercise reduces likelihood of hitting diffusion limitation. |
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Diffusion capacity for carbon monoxide test
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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. |
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Why can't measure O2 for O2 diffusion capacity? Why is CO a good substitute?
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No CO in blood at baseline, so O2 is harder to measure.
If patient can't transfer CO appropriately, also cant transfer O2. |
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Forster Equation for DL
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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. |
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Values in Forster equation
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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. |
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DL depends on three factors:
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1. Amount of surface area present for gas exchange
2. Amount of capillary blood exposed to alveolar gas 3. Amount of Hb present. |
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What reduces diffusion capacity?
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DL is reduced by diseases which reduce functioning of alveolar capillary units.
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Exercise and DLCO
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Exercise increases diffusion capacity because vasodilation increases amount of capillary blood exposed to alveolar gas at a time.
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Effect of raising or lowering O2 tension on DLCO
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100% O2 reduces DLCO because O2 competes with CO for Hb binding sites.
Less CO taken up. |
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Causes of hypoxemia and impaired CO2 gas exchange
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Hypoventilatoin, diffusion limitation, shunt, ventilation–perfusion inequality
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What determines steady state concentrations of mean alveolar values (PAO2/FAO2 or PACO2 or FACO2)?
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Alveolar ventilation
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Equation for partial pressure of gas
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Pxgas = Fxgas * PB, PB = 760 mmHg
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PACO2 formula
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PaCO2 = VCO2/VA * K = PACO2
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Air, alveolar, and arterial PO2
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Ambient air PO2 = 160 mmHg
Alveolar PAO2 = 100 mmHg Arterial PaO2 = 100 mmHg |
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Hypoventilation
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Low alveolar ventilation given PACO2.
Rate of 60 breaths/minute may be normal for PACO2 of 40. |
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Alveolar ventilation equation (PaCO2)
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PaCO2 = VCO2/VA * K
To keep PaCO2 around 40, need around 4L of VA based on amount of CO2 produced. |
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VCO2 – Alveolar gas equation
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VCO2 = VA * FACO2
VCO2 = VA * PACO2/K Assume FICO2 = 0 |
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VO2 – Alveolar gas equation
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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) |
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Alveolar gas equation
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PAO2 = PIO2 – PACO2/R
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PIO2 formula
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PIO2 = FIO2 (PB–PH2O), usually around 150 mmHg
PB = 760 mmHg, PH2O = 47 mmHg |
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FIO2
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21% oxygen in ambient air. More if supplemental
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PB
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Barometric pressure. Varies with altitude, 760 mmHg at sea level.
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PiO2 in trachea
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FiO2 (PB – PH2O)
0.21 (760–47) = 150 |
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R value
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Ratio of CO2 production to O2 consumption
Usually from 0.8 to 1.0 |
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Alveolar ventilation at sea level
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PaO2 = 100 mmHg when PaCO2 = 40 mmHg
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Why is room level PO2 at 160 mmHg while PaO2 is 100 mmHg?
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1. Consuming O2 at tissue level
2. Mixed venous blood coming into alveolar capillary unit is at 40 mmHg. |
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PAO2 when put on supplemental oxygen
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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 |
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PAO2 when hypoventilating (PaCO2 of 80)
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FiO2 = 21%, PaCO2 = 80 mmHg
PAO2 = 0.21 (760–47) – 80/.8 = 50 mmHg |
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Hypoxemia vs hypoxia
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Hypoxemia – Low arterial (blood) partial pressure of O2. Less than 70 mm Hg
Hypoxia – Low air or tissue O2 |
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Overcoming hypercapnea and hypoxemia
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Hypercapnea – Requires mechanical ventilation until underlying disease is addressed.Hypoxemia – usually overcome by giving supplemental oxygen – increase PIO2
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Diffusion limitation and PO2
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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 |
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CO2 diffusion along capillary length
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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). |
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What determines PCO2/PO2 of individual alveolar units?
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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 |
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Dead–space
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High V/Q ratio – high perfusion, low perfusion
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Shunt
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Low V/Q ratio – low ventilation, high perfusion
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Low V/Q ratio is caused by:
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Alveoli filled with infection, water, protein, collagen
Alveolar collapse Mucus plugging or edema at small airways In presence of maintained capillary blood flow |
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High V/Q ratio is caused by:
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Capillary obstruction from vascular disease or blood clots
In presence of maintained ventilation to alveolus (or increased ventilation with normal perfusion) |
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What does end capillary blood resemble in low and high V/Q?
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Low V/Q – resembled mixed venous blood
High V/Q – resembles inspired air V/Q of 1 – normal arterial values (100, 40) |
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Normal O2 and CO2 values in arteries
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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 |
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Normal O2 and CO2 in inspired air
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PIO2 = 150 mmHg
PICO2 = 0 mmHg |
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V/Q Ratio Equation
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Used to calculate individual alveolar capillary unit values with differing VQ ratios
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Graph for V/Q ratio equation
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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. |
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Main concern of high V/Q ratio
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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 |
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Describing V/Q ratio with PO2/PCO2 curve
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Increasing V/Q ratio – PO2 increases and PCO2 decreases.
Decreasing V/Q ratio – PO2 decreases and PCO2 increases. |
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PE in left lung – initial changes in VE, VD, VA
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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 |
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In PE, what happens to blood going to affected lung?
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Redirected to other lung
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PE in left lung – compensation
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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. |
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Mild increases in minute ventilation to overcome dead space ventilation
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Not a problem – keep VA normal to keep PaCO2 normal and then keep PaO2 normal.
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Severe increases in minute ventilation to overcome dead space ventilation
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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. |
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How can hypoventilation occur?
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1) Low total VE – narcotic overdose, excessive work of breathing (COPD, asthma)
2) Low VA because of increased dead space (high minute ventilation) |
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What does end capillary blood look like for low V/Q ratio?
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Mixed venous blood
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Causes of low V/Q
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Alveoli villed with infection, pus, water, protein, collagen
Mucus plugging or edema of small airways With maintained capillary blood |
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Normal concentration of O2 in mixed venous and arterial blood
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Comes in at 15 mL O2/dl, exits at 20 ml O2/dl
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Low V/Q ratio in right upper lobe – effect on right lung
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Right – Mixed venous blood comes in at 15 mL O2/dl, exits at 16 mL O2/dl
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Low V/Q ratio in right upper lobe – effect on left lung
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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 |
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Left atrium O2 concentration when low V/Q of right upper lung (with left lung compensation)
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Left atrium O2 concentration is low (18 mL )2/dl blood). PaO2 = 50 mmHg.
Cannot maintain PaO2. |
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Treatment of hypoxemia in low V/Q
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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. |
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Normal mixed venous and arterial CO2 concentrations
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Mixed venous blood comes in at 52 mg/dl, exits at 48.
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Pneumonia in right upper lobe, effect on right lobe mixed venous and arterial CO2
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Right lung – mixed venous comes in at 52 mg, exits at 51 mg/dl
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Pneumonia in right upper lobe, compensation effect on left lobe mixed venous and arterial CO2
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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 |
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Pneumonia in right upper lobe, effect on concentration of CO2 and PCO2 in left atrium
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Normal 48 mL CO2/dl blood
PaCO2 = 40 mmHg |
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Low V/Q with compensation – effect on arterial O2 and CO2 levels
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Systemic arterial hypoxemia but normocapnea
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Treatment of low V/Q pneumonia in right upper lobe
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Ventilation and antibiotics
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Shunt
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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. |
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A–a gradient
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Used to assess patient's oxygenation.
A–a = PAO2 – PaO2 Remember: PAO2 = PIO2 – PACO2/R In healthy lungs, no A–a gradient |
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Elevated A–a gradient
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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. |
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V/Q ratio changes as descend lung
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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. |
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Muscle movements of inspiration
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Contract diaphragm and expand chest wall
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Mechanical movements of expiration
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Normally passive, can forcefully exhale
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Diaphragm innervation
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Phrenic nerve (C3–5) – injury impairs breathing
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Tidal volume
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Volume of one inspiration/expiration
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Total lung capacity
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Volume of active breath in and out
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Residual volume
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Residual volume left after complete exhalation
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Functional residual capacity
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Volume remaining at end of normal tidal volume exhalation.
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Lung recoil pressure
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Inwards (towards lower volume)
Because of intrinsic properties – elastin, fibronectin, collagen and surface tension |
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Chest wall recoil pressure
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Outwards (higher volume) except at very high volumes
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Pleural space and fluid
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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 |
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Subatmospheric intrapleural pressure
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<760 mmHg because inward lung recoil and outward chest wall recoil.
Verify by puncturing chest wall – air follows pressure gradient into chest |
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Pneumothorax
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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. |
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Figure of Lung capacity vs airway pressure
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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. |
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Figure of lung capacity vs airway pressure – summation of chest wall and lung and FRC
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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.
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Intrapleural pressure during breath
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Inspiration – intrapleural pressure becomes more subatmospheric
Expiration – passively returns to resting subatmospheric pressure |
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Emphysema and gas exchange
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Emphysema destroys ECM. Leads to high V/Q ratio.
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Fibrosis and gas exchange
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Fibrosis has excess ECM deposition. Some areas of low V/Q and others of high V/Q
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Pressure–volume curve of lung
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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) |
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Compliance
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Measures distensibility
dV/dP |
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Elastance
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1/Compliance
Measures ability to return to original position |
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Compliance in fibrosis and emphysema
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Emphysema – high compliance – small pressure to generate same volume
Fibrosis – low compliance – larger pressure to generate same volume |
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Model of elastic recoil
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Elastic recoil causes lung to recoil to lower volume and tethers small airways open (preventing collapse) when springs are stretched during inspiration
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Alteration of recoil during emphysema
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Emphysema – decreased elastic recoil (overly compliant) – reduced tethering of small airways = increased tendency for airway collapse
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Alteration of recoil during fibrosis
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Fibrosis – larger inward recoil of lung (low compliance) and increased tethering of airways, preventing small airway collapse. But requires more energy to distend lungs.
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Surface tension
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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 |
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Surfactant
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Phospholipid secreted by type 2 alveolar cells into alveolar space linings
Lowers surface tension of fluid lining alveolus |
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Surface tension and compliance – saline experiment
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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. |
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Infant respiratory distress syndrome (RDS)
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Developmental deficiency in surfactant
More surface tension = lower compliance. PV curve similar to fibrosis. Treat with exogenous surfactant replacement |
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Law of Laplace and alveoli
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Law of Laplace – P = 4T/r
As alveolus gets smaller, greater recoil pressure (P) inwards. Thus, small alveoli have greater tendency to collapse |
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Surfactant and small alveoli
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Surfactant has lower surface tension at lower surface area.
Stabilizes small alveoli from Law of Laplace effects, preventing collapse. |
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Hysteresis in saline and air–filled lungs
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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. |
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Why is ventilation higher in lower lobes than upper?
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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. |
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What does pressure differnce over tube depend on?
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Rate and pattern of flow
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Ohms Law
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Resistance = P1–P2/Flow
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Pulmonary Vascular Resistance equation (Ohm's Law)
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(MPAP–Left Atrial (Wedge) Pressure)/CO
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Pouiseuille's Law
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R=8nl/PIr^4
Resistance is proportional to length and viscosity and inversely proportional to radius^4 |
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Turbulent flow
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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 |
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Heliox
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Gas mixture of helium and oxygen. Helium is less dense than oxgen so lowers resistance
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Airway resistance varies with lung volume
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Airway resistance decreases with increase in lung volume (because of increase in radius)
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Chief site of airway resistance
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Large airways (larynx and trachea) because have lowest overall cross–sectional area.
40,000 small areas and 1 trachea/larynx. |
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Reynold's number
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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. |
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Gas density and Reynold's number
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Gas density increases with atmospheric pressure and molecular weight (i.e. Nitrogen vs Helium)
Increases Reynold's number –> turbulent flow |
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Intraalveolar and intrapleural pressure at FRC
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No flow.
Atmospheric intraalveolar pressure Subatmospheric intrapleural pressure |
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Intraalveolar and intrapleural pressure during inspiration
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Slightly subatmospheric intraalveolar pressure
Further subatmospheric intrapleural pressure |
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End–inspiration intraalveolar and intrapleural pressure
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Atmospheric intraalveolar pressure
Minimal subatmospheric intrapleural pressure |
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Intraalveolar and intrapleural pressure during normal passive expiration
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Slightly atmospheric intraavlveolar pressure
Subatmospheric intrapleural pressure returns to rest subatmospheric pressure |
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Intraalveolar and intrapleural pressure during forced expiration
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Intraalveolar pressure rises substantially above atmospheric
Intrapleural pressure also rises substantially above atmospheric Both rise to same degree, depending on degree of muscular effort |
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Airway collapse during forced expiration
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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. |
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Determining factor for airway collapse during forced expiration
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Difference between alveolar and pleural pressure
Depends on elastance of lung |
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Effect of emphysema and fibrosis on likelihood of airway collapse during forced expiration
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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 |
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FEV1
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Amount of volume can exhale in 1 second
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FEV1/VC
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FEV1/VC is usually 75%. Limited by airway collapse.
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FEV1/VC in emphysema
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FEV1/VC is around 40% in emphysema – more likely to collapse so exhale less before collapse occurs.
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FEV1/VC in fibrosis
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FEV1/VC is around 90% in fibrosis – less likely to collapse so exhale more before collapse occurs.
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Is flow generally effort–dependent or independent in forced expiration?
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Generally effort–independent because effort doesn't change difference between pleural and alveolar pressure.
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Is flow effort–dependent at beginning of forced expiration?
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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. |
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Importance of hypercapnea
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Indicates critical illness – represents failure to regulate PCO2.
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Is hypoxemia critical?
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Hypoxemia is abnormal but not as reflective as emergency.Hypoxemia does not trigger response until it reaches 50 mmHg.
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Pulmonary circulation pressures
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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. |
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Measuring pulmonary artery pressures
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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 |
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Compliance of pulmonary vasculature
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Highly compliant with little smooth muscle – little work required
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Pulmonray Vascular Resistance equation
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Pulmonary Vascular Resistance = (MPAP – Left Atrium Pressure)/Cardiac Output
Expressed in Wood units. Normal value is < 3 |
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PVR response to increase in vascular pressure or flow
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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 |
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Alveolar and extraalveolar vessels and associated forces
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Capillaries are alveolar vessels – exposed to alveolar forces
Arterioles are extraalveolar vessels – exposed to recoil forces |
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Effect of lung volume on PVR
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Low volumes – extraalveolar vessels are small – high PVR
High volumes (TLC) – capillaries are stretched – increased PVR Lowest point is at middle volume (FRC) |
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Starling resistor effect
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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 |
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West Zone 1
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Top of lung
PA > Pa > Pv No flow because alveolar pressure is too high |
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West Zone 2
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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. |
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West Zone 3
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Bottom of lung
Pa > Pv > Pa Alveolar pressure is irrelevant. Flow determined by afferent–to–efferent pressure drop |
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Central controllers of ventilation
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Brainstem (automatic, involuntary)
Cerebral cortex (voluntary |
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Central controllers locations
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Medulla – intrinsic, automatic rhythm of ventilation
Lower and upper pons |
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What are three things chemoreceptors change?
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PaCO2 – depressed by age, sleep, narcotics
pH – goes along with PaCO2 PaO2 – doesn't change ventilation until below 50 mmHg |
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Central chemoreceptors location
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Ventral surface of medulla
Surrounded by ECF and CSF |
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What do central chemoreceptors sense?
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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 |
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Peripheral chemoreceptors
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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 |
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