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Physiology > Pulmonary Diffusion and Pulmonary Circulation > Flashcards

Pulmonary Diffusion and Pulmonary Circulation Flashcards

1
Q

how does steady state alveolar air for CO2 and O2 compare to steady state venous blood and arterial blood pressure?

A 
PAO2 = 100 mmHg
PaO2 = 95 mmHg
PvO2 = 40 mmHg
PACO2 = 40 mmHg
PaCO2 = 40 mmHg
Pv = 46 mmHg
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2
Q

Henry’s Law of Solubility

-what does alpha mean?

A

Ci = alphai * Pi where C = gas concentration in solution, alpha = solubility coefficient, and P = partial pressure of i

  • this is only when liquid and gas phase are in equilibrium at a given temperature
  • liquid pressure only from dissolved gases
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3
Q

Rick’s Law of Diffusion

-what do D and Dl mean?

A

gas flow = (area/thickness) * D * (P1 - P2) where D = diffusion coefficient

  • single most important is P gradient
  • since Dl = (DA)/T, flow = Dl * (P1 - P2) where Dl = diffusion capacity of the lung
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4
Q

how does D relate to solubility and molecular weight?

A

diffusion coefficient = solubility / (square root MW)

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5
Q

is there hypoxemia and hypercapnea in hypoventilation and diffusion problems?

A

there is hypoxemia in both (O2 = 78 mmHg), but hypercapnea only in hypoventilation (CO2 = 55); diffusion problems have CO2 = 35 b/c CO2 is 20X more diffusable than O2

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6
Q

what is the regular transit time through a pulmonary capillary?

A

0.75 - 1.2 seconds, since t = V/Q = 75 mL / 100 mL/sec

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7
Q

how is the diffusion of O2, N2O, and CO along length of pulmonary capillary?

A

N2O has higher perfusion than O2, but both are quickly equilibrized within 0.1 sec
-transfer of N2O and O2 is perfusion-limited (more gas flow = more transfer)
CO has very low partial pressure and perfusion, b/c transfer is diffusion-limited
-doesn’t reach equilibrium even after 0.75 seconds b/c affinity for Hb is 210 X that of O2

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8
Q

what happens if diffusion of O2 is abnormal?

A

O2 will not reach equilibrium until after the full 0.75 seconds of flow through capillaries

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9
Q

CO2 diffusion along pulmonary capillary

A

it seems like the inverse of O2 (b/c diffusing out of body)

  • it equilibriates quickly through fibrotic tissue and fluids present in pulmonary edema
  • slowed down by CO2 chemical reactions
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10
Q

what happens to PO2 during exercise-induced hypoxemia?

A

transit time is reduced to 0.25 seconds, since flow can increase 3x
-a normal person would still equilibrate capillary blood with alveolar gas, but if there is a diffusion problem, they would get hypoxemia during exercise (longer to equilibrate)

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11
Q

what happens to PO2 and DlCO at high altitudes?

A

inspiratory hypoxia and vasoconstriction reduces DlCO and slows the rate of equilibration

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12
Q

what is relation of pressure gradient (between alveolar and capillaries) and equilibration time?

A

the smaller the difference, the shorter time to equilibrate

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13
Q

what happens if you increase the BP in the pulmonary artery?

A

there is edema, which increases the thickness of the lung, which decreases flow and rate of diffusion, taking longer to equilibrate

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14
Q

equations to measure diffusion capacity

A

flow of gas in blood (comparable to diffusion capacity) = inspiratory flow - expiratory flow
-usually assume inspiratory flow = expiratory flow

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15
Q

how does DlO2 compare to DlCO?

A

DlO2 = 1.23 DlCO

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16
Q

how does body position influence DlCO?

A

DlCO is greater when supine than upright, b/c when you lie down, there is more blood to the lung

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17
Q

how does exercise influence DlCO?

A

increased blood to lung will increase blood flow and DlCO

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18
Q

how do lung diseases and dysfunction influence DlCO?

A

they decrease it

  • loss of lung tissue from surgery will decrease area
  • mismatch of ventilation to perfusion (such as airway obstruction, shut, alveolar dead space that increase thickness)
  • pulmonary HTN with edema
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19
Q

differences between pulmonary and systemic circulations

A
  • pulmonary is only vascular bed to receive entire CO, w/ low pressure
  • lung volume changes during breathing affects pulmonary vascular resistance
  • ischemic damage is rare in lung due to multiple supplies of O2
  • minimal basal tone in pulmonary vessels (passive distension w/ increased P or Q w/o significant autoregulation)
  • hypoxic vasoconstriction in lung
20
Q

what are 3 O2 supplies to lung?

A
  • bronchial circulation
  • pulmonary circulation
  • alveolar gas O2 supply
21
Q

pulmonary circulation and pressures

A

pulmonary circulation is smaller than systemic circulation (thus “lesser” circulation)

  • pulmonary BP are lower b/c pulmonary vascular resistance is 10x lower than TPR
  • afterload of RV is less than LV, so right heart does less work than left
22
Q

where is pulse pressure largest?

A

in the left ventricle

23
Q

anatomic shunts

A

normal, left to left that’s 1-2% of CO (up to 20% if obstruction)

  • bronchial circulation starts at the base of the aorta, perfuses large airways, vessels, and nerves, then drains into bronchial vein and then pulmonary vein, thus bypassing the lungs
  • responsible for the slight drop from 100 mmHg in alveoli to 95 mmHg in aorta
24
Q

what do lymphatic vessels return excess fluid to? what are they regulated by?

A

returns it to circulation via caudal mediastinal lymph node and thoracic duct

  • regulated by intrinsic propulsion, mechanical pumping during breathing, and sympathetic activity
  • -intrinsic propulsion can generate up to 20 mmHg if flow occluded
25
Q

physiological shunt

A

sum of normal anatomic shunt (left to left) plus any pathological intrapulmonary right to left shut that occurs when airways are blocked, resulting in hypoxemia

26
Q

pathologic shunt

A

right to left shunting of blood

  • causes hypoxemia w/o hypercapnea
  • if Qs = Qt, that means all blood is shunted, and there’s no O2ation
27
Q

features of pulmonary vessels

  • wall thickness
  • what kind of vessels they are
  • what capillaries are surrounded by
A
  • pulmonary arteries and veins are both thin-walled and highly distensible
  • graduation of muscularity from muscular to partially muscular to nonmuscular with no distinct arterioles, and can be gas-exchanging (less than 1 mm) or non-exchanging (all larger)
  • capillaries are surrounded by alveolar air, so external pressure is alveolar pressure that oscillates during breathing
  • alveolar and extra-alveolar vessels have different mechanical properties, and are affected differently by changes in lung volume, but don’t differ anatomically
  • changes in lung volume during breathing also affect pulmonary vascular resistance
28
Q

pulmonary blood pressure along vasculature

-what is average PBP, and what values make it pulmonary HTN or pulmonary edema

A

PBP is low, and dissipates gradually along vasculature

  • PBP is 11-12 mmHg, compared to 93 mmHg of aorta
  • over 20 mmHg is pulmonary HTN
  • over 25 mmHg is pulmonary edema, resulting in diffusion problem b/c hydrostatic pressure is higher, forcing filtration
29
Q

how is pulmonary arterial pressure measured?

A

a cardiac catheter called Swan Ganz is inserted in jugular, brachial, or femoral vein and advanced into pulmonary artery

30
Q

what is pressure (LA)?

A

pulmonary wedge pressure obtained when catheter in pulmonary vasculature is inflated to occlude flow downstream

31
Q

how does CO relate to pulmonary vascular resistance?

A

CO = (P1 - P2) / PVR = (P PA - P LA) / PVR
so
PVR = (P PA - P LA) / CO

32
Q

are changes in PVR passive or active?

A

changes in PVR are mostly passive
-pulmonary blood volume is about 200-300 mL, and can increase 2-3x during exercise, but compliance of vessels is high so pressure doesn’t increase much

33
Q

what is the relationship between radius, resistance and pressure if vasodilate?

A

increased radius will decrease resistance and increase pressure
-this means that vessels don’t contract under constant pressure

34
Q

how do alveolar and extra-alveolar blood vessels respond to decreased intrapleural pressure during inspiration?

A
  • alveolar blood vessels are stretched and become narrower as capillaries increase in length, which increases resistance, due to changes in capillary pressure relative to alveolar pressure
  • extra-alveolar blood vessels expand due to the more negative intrapleural pressure
35
Q

when can alveolar vessels collapse completely?

A

if pressure outside (alveolar pressure) exceeds capillary pressure

  • flow will stop
  • larger vessels never collapse b/c protected by surrounding parenchyma
36
Q

what is lung volume’s relationship to PVR?

A

the lung has an optimum volume that minimizes PVR

  • alveolar and extra-alveolar vessels are in series, so resistances are additive
  • thus, PVR is at a minimum at FRC (equilibrium position of system)
  • long volume changes during breathing, which affects PVR (PVR is highest at RV and TLC extremes)
37
Q

what are “corner vessels”?

A

small vessels in alveolar septum that are capillaries at junctional “corners” of alveoli
-when the lung inflates, they expand to lower resistance as extra-alveolar vessels that never close

38
Q

what does gravity have to do with blood flow?

A

blood flow is 6X greater at the base of lung than at the apex, due to gravity and passive distension

  • pressure outside capillaries is constant throughout lung, but inside it increases from top to bottom b/c hydrostatic pressure is exerted by intrapleural pressure
  • thus, at base there is high transmural pressure and capillaries are wide open, more distended, lower resistance, and increased blood flow
39
Q

what is the three zone model for pulmonary blood flow

A

capillaries become more distended as you go down, increasing flow

  1. usually not present in healthy lung (capillaries collapse and flow stops, so ventilated but not perfused, b/c top lung pressure falls below alveolar pressure); alveolar > arterial > venous pressure
  2. flow depends on alveolar pressure (hydrostatic pressure increases and intravascular pressure exceeds alveolar pressure causing recruitment and opening of capillaries w/ increased blood flow); arterial > alveolar > venous pressure
  3. flow increases due to gravity and passive distension (capillaries become wide open, and flow determined by difference in P pa - P pv; driving pressure constant, but resistance decreases and flow increases); arterial > venous > alveolar
40
Q

what clinical problems can cause increased capillary permeability?

A
  • adult respiratory distress syndrome (ARDS)
  • O2 toxicity (via ROS)
  • inhaled or circulating toxins
41
Q

what clinical problems can cause increased capillary hydrostatic pressure?

A
  • increased left atrial pressure from LV infarction or mitral stenosis (will lead to pulmonary edema)
  • overadministration of intravenous fluids
42
Q

what clinical problems can cause decreased interstitial hydrostatic pressure

A

too rapid evacuation of pneumothorax or hemothorax

43
Q

what clinical problems can cause decreased colloid osmotic pressure

A
  • protein starvation
  • dilution of blood proteins by intravenous solutions
  • renal problems causing urinary protein loss
44
Q

what clinical problems can cause insufficient pulmonary lymphatic drainage?

A
  • tumors

- interstitial fibrosing diseases

45
Q

how is the O2 and CO2 concentration in the right to left pathologic shunt? can these problems be solved with O2-enriched gas?

A

a small change in O2 content will decrease PO2 very much (steep slope), but not so much in CO2 (flatter slope)
-no, unlike with diffusion problems, breathing gas enriched with O2 will not help patients with these abnormal shunts

Physiology (60 decks)

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