Chapter 4: Blood Flow and Metabolism Flashcards

1
Q

Where do the pulmonary ateries branch off into the capillary bed?

A

pulmonary arteries accompany airways to the terminal bronchioles and then branch off to supply pulmonary capillaries

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2
Q

What are the systolic, diastolic and mean pressures of the pulmonary artery?

A
  • 25, 8, and 15 mm Hg, respectively
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3
Q

what makes up the pressure gradient for pulmonary capillary perfusion?

A

pulmonary arterial mean pressure (15 mm Hg) minus left atrial pressure (5 mm Hg)
Pressure gradient of only 10 mm Hg

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4
Q

Fill in the pressures in the blanks

A
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5
Q

What is the transmural presure of the pulmonary capillaries?

A

pressure difference between the inside and outside of the capillaries
i.e., outside effective presssure is the alveolar pressure –> if alveolar pressure rises and is above capillary pressure –> capillaries collapse

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6
Q

explain how the transmural pressure of pulmonary arteries and veins differs from the capillaries?

A

when lungs expand the large vessels are pulled open by radial traction - less pressure around the vessels during increased lung volume/alveolar pressure

capillaries - with increased lung volume - transmural pressure decreases –> collapse

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7
Q

Explain how three different sizes of pulmonary vessels undergo different pressur influence from their surrounding structures

A

alveolar vessels - capillaries which caliber is determined by the surrounding alveolar pressure
extra-alveolar vessels- arteries and veins running through the lung parenchyma, their caliber is determined by the the radial pull
very large vessels near the hilum - outside of the lung substance - intrapleural pressure exposure

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8
Q

What is the equation for vascular resistance?

A

Vascular resistance = (input pressure - output pressure) / blood flow

blood flow is the same as systemic circulation but pressure gradient is small (see above, 10 mm Hg), so vascular resistance must be very small

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9
Q

How does pulmonary vascular resistance respond to an increase in pulmonary arterial or venous pressure?
What are the two mechanisms responsible for this process?

A

pulmonary vascular resistance will decrease
mechanisms:
1. Recruitment: at normal condition some pulmonary capillaries are either closed or open with no blood flow - as pressure increases they conduct blood - increased surface area –> decreases resistance
2. Distension: increased pressure widens individual capillary segments - increases their caliber - possible due to thin capillary membranes

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10
Q

How does lung volume affect the caliber of extra-alveolar vessels?

A

increased lung volume –> expands/pulls open the vessels - low vascular resistance
collapsed lungs –> elastic tissue and smooth muscles pull vessels together –> increased vascular resistance
* if the lungs are completely collapsed - smooth muscle is very strong - pulmonary artery pressure must be raised significantly to allow blood flow - critical opening pressure

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11
Q

What is the critical opening pressure?

A

the air pressure needed to allow blood flow through the extra-alveolar vessels

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12
Q

Name 4 susbtances that can cause smooth muscle contraction and increase pulmonary vascular resistance

A
  • serotonin
  • histamine
  • norepinephrine
  • endothelin
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13
Q

Name 5 substances that can relax smooth muscles in the pulmonary circulation and decrease vascular resistance

A
  • acetylcholine
  • Ca-channel blockers
  • Phosphodiesterase-5 inhibitors
  • nitric oxide
  • prostacyclin (PGI2)
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14
Q

Explain with this graph why pulmonary vascular resistance is the lowest at normal lung volumes

A

At low lung volumes, the extra-alveolar vessels collapse due to their elastic/smooth muscle wall
At high lung volumes the alveolar vessels will be compressed/collapse

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15
Q

How can you measure pulmonary blood flow?

A
  • Fick’s principle
  • indicator or thermo dilution techniques
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16
Q

What is the Fick’s principle?

A

states that the O2 consumption/min measured with mouth-piece (VO2) is equal to the O2 taken up by the lungs per minute (Q x (CaO2 = CvO2)
so, VO2 = Q x (CaO2 - CvO2)
so, Q = VO2 / (CaO2 - CvO2)

Q is blood passing through lungs per minute

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17
Q

In the upright lung, how does blood flow change?

A

blood flow is the highest in the most dependet/lowst region and decreases almost linearly from bottom to top

18
Q

What force explains blood flow differences between lung levels?

A

gravity affects hydrostatic pressure - e.g., if the top of the lung is 30 cm above the bottom, there will be about 30 cm H2O or 23 mm Hg difference in hydrostatic pressure iwthin the blood vessels –> large difference for the low-pressure pulmonary circulation

19
Q

Describe Zone 1 of lung blood flow

A

Within Zone 1, the pulmonary arterial pressure is so low, it falls below the alveolar pressure –> capillaries collapse and now blood flow occurs
* Zone 1 is not present under normal physiologic conditions

20
Q

Describe Zone 2 of lung blood flow

A

In Zone 2, the pulmonary arterial pressure is above alveolar pressure, but the pulmonary venous pressure is lower than alveolar pressure&raquo_space; venous pressure has no influence on blood flow, which is now depndent on the gradient between arterial and alveolar pressure
called:
* starling resistor effect
* sluice effect
* waterfall effect

21
Q

Describe Zone 3 of lung blood flow

A

Venous pressure now exceeds alveolar pressure&raquo_space; blood flow depends on arterial to venous pressure gradients

21
Q

Why does zone 3 have the most blood flow?

A

due to the increase of vascular transmural pressure –> capillaries will be distended

this is because capillaries lie between arterial and venous vessels which now have a higher pressure (lying lower with higher hydrostatic pressure), but alveolar pressure remains constant –> capillaries will distent more

22
Q

What determines hypoxic pulmonary vasoconstriction

A

PO2 of alveolar gas - not the pulmoanry arterial PO2

23
Q

Describe the nonlinear stimulus-response curve of hypoxic pulmonary vascular constriction

A

with changes at higher PAO2 around 100 mm Hg, only little vasoconstriction occurs
PAO2 < 70 mm Hg, marked vasoconstriction occurs
severely low PAO2 may almost abolish blood flow

24
Q

What is the major trigger for smooth muscle contraction?

A

increase is cytoplasmic calcium ion concentration

25
Q

Explain how nitric oxide is synthesized and how it excerts effects on smooth muscle tone

A

shear forces –> trigger Ca influx –> Ca combines with eNOS –> eNOS produces NO from L-arginine, NADPH, and O2

NO –> activates soluble guanylate cyclase –> synthesis of cGMP (guanosine 3,5-cyclic monophosphate) from GTP –> cGMP inhibits Ca channels –> prevents the cytoplasmic Ca cc rise –> causes myosin light chain dephosphorylation, decoupling –> smooth muscle relaxation –> promotes vasodilation

26
Q

Name 2 potent vasoconstrictors released by pulmonary vascular endothelial cells

A

endothelin-1 (ET-1)
thromboxane A2 (TXA2)

27
Q

Explain how pulmonary vascular tone changes at birth

A

fetal pulmonary vascular resistance is high - partially from hypoxic vasoconstriction
only 15% CO goes through the fetal lungs
firth breahts –> alveolar oxygen cc drastically increases –> releaxation of smooth muscles –> pulmonary blood flow increases drastically

28
Q

How does acidemia affect pulmonary vascular tone?

A

causes vasocosntriction - especially when alveolar hypoxia is present

attenuated by hypothermia

29
Q

Write the Starling’s equation and explain it’s components

A

net fluid out = K [(Pc - Pi) - o (Onc c - Onc i)]
* K - filtration coefficient
* Pc and Pi - capillary and interstitial hydrostatic pressure
* Onc c and Onc i - capillary and interstitially colloid osmotic/oncotic pressure
* Ohm - refleciton coefficient - measure of effectiveness of the capillary wall preventing passage of proteins across it

30
Q

Whatis a normal capillary coilloid osmotic pressuure?

A

25-28 mm Hg

31
Q

is the net pressure of the starling equation in or outward?

A

outward - small volume will exit the capillaries

32
Q

how is the small net outflow from capillaries into the pulmonary interstitium removed?

A

fluid leaking into the pulmonary interstitium tracks through the interstitial space –> to the perivascular and peribronchial space –> taken up by lymphatics there –> transported to the hilar lymph nodes

33
Q

Where does early pulmonary edema accumulate?

A

within the perivascular and peribronchial spaces - i.e., interstitial edema

34
Q

Where does fluid start to accumulate in advanced stages of pulmonary edema?

A

within the alveoli
suspected to occur because maximum drainage rate through interstitial space is exceeded –> moves past alveolar epithelium into alveolar space

35
Q

How is alveolar fluid removed?

A

actively pumped out by sodium-potassium-ATPase pumps in epithelial cells

35
Q

What substance is activated by passage through the pulmonary circulation?

A

Angiotensin I is ativated to Angiotensin II by ACE

the only known example of biological acitvation by passage through lungs

35
Q

Name 4 subtances that are removed when passing through the lungs

A
  • serotonin - almost completely removed
  • norepinephrine - up to 30% removed
  • prostaglandins E2 and F2alpha - almost completely removed
  • leukotrienes - almsot completely removed
36
Q

How is serotonin removed in the lungs, in what disease process does this matter?

A

not degraded but taken up and stored - e.g., in platelets and other cells - will be released during anaphylaxis

37
Q

Name 6 substances that are not affected by the circulation through the lungs

A
  • angiotensin II
  • vasopressin
  • histamine
  • dopamine
  • epinephrine
  • prostaglandins A1 and A2
38
Q

Where in the lungs are arachidonic acid metabolites produced?

A

pulmonary macrophages

39
Q

what is the unit for vascular resistance?

A

mm Hg/L/min

mm Hg/mL/min