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51 Cards in this Set

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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



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

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)**

what normal factors affect diffusing capacity?

- exercise -> increase


- body position = supine -> increase,


- body size = incr lung vol -> incr D(L)

how does exercise increase lung diffusion capacity?

exercise -> incr CO -> distension of pulmonary capillaries and better ventilation -> better surface area -> incr D(L)

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

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

what pathological factors decrease diffusing capacity?

Pathology ->


- incr thickness


- decr Surface area


- decr capillary volume or weak pulmonary BP

what is the driving force of O2 from alveolar to capillary gas?

P(A)O2 - P(C)O2

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

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

what is diffusion limit?

incomplete equilibration of O2 partial pressure -> difference of P(A)O2 and P(a)O2 = alveolar arterial PO2 difference

why is there a diffusion limit for O2 but not CO2?

CO2 has a 20x higher diffusion capacity

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

how can low D(L) affect diffusion limit?

low D(L) (diffusion capacity of lung) is from decreased surface area or increased thickness

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**

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

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)

what are the only 2 ways the lung can be diffusion limited?

- disease


- high altitude

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

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

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

what two types of forces is pulmonary blood flow strongly affected by?

- hydrostatic (gravity) forces


- perivascular pressures

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

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

describe perfusion throughout the lung

perfusion is greatest at the bottom and low at the top due to the small driving force

how does pulmonary circulation regulation compare with systemic regulation?

Pulmonary = passive forces via transmural pressure differences




systemic = active reg via innervation of arterioles

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)

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

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

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

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

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

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

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**

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

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**

what is the hypocapnic bronchoconstriction reflex?

- hypocapnia -> bronchial smooth muscle contraction -> diverts air from the hypocapnic alveoli

what is the hypoxic vasoconstriction reflex?

- alveoli hypoxia -> vasoconstiction -> match perfusion with ventilation

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

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

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

What happens to the pulmonary vasculature in low P(A)O2 (alveolar hypoxia)

vasoconstriction




via hypoxic vasoconstriction reflex

what happens to bronchioles during low P(A)CO2 (alveolar hypocapnia)?

bronchoconstriction




via hypocapnia bronchoconstriction

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

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

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

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

Why is a right to left shunt dangerous?

lowers the O2 that goes to the tissues

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

What is pleural effusion?

fluid accumulation in the pleural space