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51 Cards in this Set
- Front
- Back
how is diffusion rate calculated? |
diffusion rate = V(gas) = D(L)*(P1-P2) diffusion capacity = D(L) = d*a*A/T d = diffusion coef a = solubility A = surface area T = thickness (P1-P2) = driving force |
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how does the lung diffusion capacity for CO2 compare with diffusion capacity for O2? why is this difference important? |
CO2 lung diffusion capacity is 20x larger than O2 - diseases may affect O2 but not CO2 gas exchange |
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how can diffusion capacity for O2 be calculated? what are some problems and how are they solved? |
D(L)O2 = (uptake O2)/(P(A)O2 - P(C)O2) P(A)O2 = alveolar PO2 - P(C)O2 = capillary PO2, is hard to calculate because it changes P while PcCO = 0 is constant **D(L)CO is found instead and then converted to D(L)O2 (only different by a constant factor)** |
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what normal factors affect diffusing capacity? |
- exercise -> increase - body position = supine -> increase, - body size = incr lung vol -> incr D(L) |
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how does exercise increase lung diffusion capacity? |
exercise -> incr CO -> distension of pulmonary capillaries and better ventilation -> better surface area -> incr D(L) |
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how can exercise hurt diffusing capacity? who does this occur in? |
the incr CO -> decrese in trasit time (the time that diffusion can occur -> incomplete transfer of O2 (diffusion limit) - occur in elite athletes |
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how does body affect diffusing capacity? Why? |
supine -> higher diffusing capacity **supine position -> incr capillary volume and more even distribution of blood flow -> incr in gas exchange surface area |
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what pathological factors decrease diffusing capacity? |
Pathology -> - incr thickness - decr Surface area - decr capillary volume or weak pulmonary BP |
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what is the driving force of O2 from alveolar to capillary gas? |
P(A)O2 - P(C)O2 |
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how does driving force of O2 relate to the length of the capillary? |
the driving force is constantly decreasing along the length of the capillary due to strong diffusion at the beginning -> more PO2 in capillary -> weaker driving force downstream |
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how does transit time compare to time to equilibration between gas and blood? why? |
transit time ~ 1sec equilibration is 1/4 to 1/3 transit time - due to diffusion capacity being so high |
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what is diffusion limit? |
incomplete equilibration of O2 partial pressure -> difference of P(A)O2 and P(a)O2 = alveolar arterial PO2 difference |
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why is there a diffusion limit for O2 but not CO2? |
CO2 has a 20x higher diffusion capacity |
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how can exercise -> diffusion limitation of O2 |
**only in elite athletes or **when not at sea level CO increases much more than pulmonary capilaries increase -> shorten transit time through the lungs -> no equilibration -> arterial hypoxemia |
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how can low D(L) affect diffusion limit? |
low D(L) (diffusion capacity of lung) is from decreased surface area or increased thickness |
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how does low alveolar PO2 (hypoxia) affect diffusion limit? Why? |
decreases when severe hypoxia or mild+exercise **does not show with mild hypoxia - less driving force limits the rate of diffusion **in severe hypoxic lung O2 dissociation curve is steep -> a large amount of O2 can enter blood with only small increase in PO2 -> does not reach equilibrium with lung** |
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how is gas exchange limited if there is no diffusion limitation? |
Perfusion limited - can not load more O2 in the blood, but the transport of blood can affect how much O2 can get to the body |
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what is perfusion limitation? |
Limit of transport of O2 from the lungs to the tissue (transport rate of blood) **only way increase uptake is if there is increased blood flow (perfusion) |
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what are the only 2 ways the lung can be diffusion limited? |
- disease - high altitude |
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How is N2O limited? Why? |
perfusion limited - Nitrous oxide is highly soluble in blood -> rapidly taken up by the capillary blood -> PNO in blood euilibrates with PNO in alveoli -> no diffusion limit |
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how is CO limited? Why? |
diffusion limited - the CO that enters the blood is quickly mopped up by Hemoglobin -> low PCO in the blood -> high difference in the P(A) and P(C) of CO - only can increase uptake by increase diffusion |
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how does PVR compare to TPR? why? |
PVR = pulmonary vascular resistance PVR is less than TPR (16x less) due to the low driving pressure difference |
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what two types of forces is pulmonary blood flow strongly affected by? |
- hydrostatic (gravity) forces - perivascular pressures |
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what three vascular sections are associated with perivascular pressures? what do these vessel pressures equal? |
- large extra pulmonary vessels - lie with the heart and cava veins Pressure = Ppl = negative -> they remain open - arteries and veins - branching with bronchial system, pressure = Ppl = neg -> remain open - alveolar capillaries - lie within alveolar walls, are surrounded by alveolar pressure |
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How does thoracic pressure affect pulmonary circulation vs systemic circulation? |
- pulmonary = drastic changes in blood flow - systemic = minimal if any blood flow change **due to pulmonary circ. has much lower pressure compared to the higher pressure in systemic |
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describe perfusion throughout the lung |
perfusion is greatest at the bottom and low at the top due to the small driving force |
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how does pulmonary circulation regulation compare with systemic regulation? |
Pulmonary = passive forces via transmural pressure differences systemic = active reg via innervation of arterioles |
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how does Cardiac output regulate PVR? Why? |
as CO increases -> decrease in PVR - increase CO -> recuitment (opening of closed vessels) and distension (widening of open blood vessels due to an increase in arterial pressure) |
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what is distension? What is recruitment? |
- distension = widening of vessels caused by an increase in internal vessel pressure (increase in diameter -> decrease in resistance - recruitment = opening closed blood vessels |
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how does pulmonary BP affect PVR? why? |
increase in pulmonary BP -> decrease in PVR - due to increase in vessel pressure -> increase in vessel diameter -> decrease in resistence |
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how does lung volume affect PVR? Why? |
increaseing volume to FRC -> decrease in PVR increasing above FRC -> increase in PVR **FRC = lowest PVR in pulmonary circulation** due to summation of the effect of extraalveolar and alveolar vessels |
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what are extraalveolar vessels and how do they contribute to PVR when lung volume increases? |
- extraalveolar vessels = arteries/veins between the alveoli - as volume increases the recoli of the alveoli stretches these open -> dilation -> decrease in PVR |
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what are alveolar vessels and how do they contribute to PVR when lung volume increases? |
Alveolar vessels are the capillaries within the alveolar walls - when alveoli expand -> alveolar vessels collapse -> increase in resistance |
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What is HAPE? what is its mechanism? |
HAPE =High altitude pulmonary edema - generalized hypoxia in the alveoli (ex: from high altitude or lung disease) -> constriction of the blood vessels around alveoli -> increase in BP -> edema |
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what is hypoxic pulmonary vasoconstriction? what is it responding to? |
when an alveoli or region in the lung is hypoxic -> smooth muscle constriction of the vessels in the area of hypoxic alveoli -> divert blood to are where alveoli are normoxic **perfusion matches the gas exchange** **is response to low PO2 in the ALVEOLAR gas ** **NOT PO2 in the blood** |
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What is the mechanism of hypoxic pulmonary vasoconstriction? |
- hypoxia -> inhib K+ channel in the mem of sm muscles -> depolarization -> open Ca++ channels -> contraction - hypoxia ->endothelin-1 -> contraction of smooth mucsles |
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what is the importance of the symp and parasymp nerves in the lungs? |
- has little or no control over pulmonary circulation **can be targeted clinically change pulmaonary vascular resistance, and can change bronchodilation/constriction** |
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what is the hypocapnic bronchoconstriction reflex? |
- hypocapnia -> bronchial smooth muscle contraction -> diverts air from the hypocapnic alveoli |
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what is the hypoxic vasoconstriction reflex? |
- alveoli hypoxia -> vasoconstiction -> match perfusion with ventilation |
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describe the bronchial circulation. what is special about it? |
- bronchial artery blood is Oxygenated and used for on lung tissue - bronchial venous blood then drains into the pulmonary vein -> LA -> shunt of deoxy blood to oxy blood |
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describe coronary circulation. What is special about this? |
coronary venous blood partially enters the left atrium and left ventricle via Thebesian veins = shunt of oxy and deoxy blood |
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how much of the CO is in shunts? what is the effect of having these shunts? |
- 1-2% of CO is in the shunts - contribute equally to the V(A)/Q mismatch for normal arterial PO2 difference of 3-10mmHg |
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What happens to the pulmonary vasculature in low P(A)O2 (alveolar hypoxia) |
vasoconstriction via hypoxic vasoconstriction reflex |
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what happens to bronchioles during low P(A)CO2 (alveolar hypocapnia)? |
bronchoconstriction via hypocapnia bronchoconstriction |
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How does a low D(L) caused bby increase thickness or decreased surface area present itself at rest? when does the presentation change? |
can cause a diffusion limitation but at rest will appear normal - exercise will unmask due to a reduction in transit time |
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how is diffusion capacity for CO2 affected by a diseased lung such as pulmonary edema? Why? |
unchanged - the diffusion capacity is so high it remains unaffected |
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what is the combine effects of extralveolar and alveolar vessels on PVR? Why? |
- at FRC the PVR is the lowest - inflation or deflation above or below FRC -> PVR increase -> decrease in flow - extraalveolar and alveolar vessels are in series so their effects are added |
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Why is a left to right shunt dangerous? how is a left to right shunt detected? |
- increase pulm artery pressure - may cause hypoxia by increasing perfusion -> lower V/Q ratio - higher than normal O2 in RA |
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Why is a right to left shunt dangerous? |
lowers the O2 that goes to the tissues |
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what is ARDS? what is it caused by and what does it result in? |
ARDS = acute respiratory distress syndrome caused by decrease in surfactants AND increase in capillary permeability -> pulmonary edema |
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What is pleural effusion? |
fluid accumulation in the pleural space |