Circulation 8: Special Circulations II Flashcards Preview

FHB I - Cardiac Unit > Circulation 8: Special Circulations II > Flashcards

Flashcards in Circulation 8: Special Circulations II Deck (49):
1

How much resting CO does the brain require?

Although the brain constitutes only 2% of total body weight, it requires about 15 % of the resting cardiac output.

2

Describe the needs of the brain in terms of arterial supply.

Because the brain primarily uses aerobic metabolism of glucose, it needs a relatively large and steady arterial supply of O2 and glucose.

3

What is the most metabolically active tissue in the body? What does this imply about blood flow?

The brain is the most metabolically active tissue in the body. Multiple potential collateral channels exist to supply the high blood flow and metabolism.

The brain contains about 400 miles of capillaries.

4

Describe the brain in regards to lymphatics. What are the implications of this?

The brain lacks lymphatic vessels.

problem w cerebral edema (high altitude hiking) that edema presses on brain. fluid no where to go and no where to take it away.

5

When would you give an alpha receptor antagonist/agonist?

Where are there no alpha receptors?

alpha receptors- vasoconstrictors always. give antagonist to lower bp. give agonist to raise bp. might be given when someone bleeding after car accident to vasoconstrict to bring up bp. coronaries, cerebral and pulmonary have little to no alpha. give agonist wont vasoconstrict those circulations…but you do everything else so you’ll shunt blood to those vital organs.

6

How are cardiac arrhythmias related to the brain?

of all tissues in body brain is least tolerant to ischemia.. loss of 5 sec will lose consciousness…
goes back to cardiac arrhythmias- if CO dropping its not perfusing brain, if go into VF you have about 2 min before irreversible brain damage.

7

What is the circle of Willis?

An anastomotic ring of vessels formed from the two internal carotid arteries (anterior cerebral circulation) and the vertebral-basilar system supplying the hindbrain. The two internal carotid arteries are the major blood supply to the Circle.

Three large paired vessels originate from the circle of Willis: the anterior, posterior, and middle cerebral arteries.

8

Describe the BBB. What is its function?

What forms the BBB?

What can/can't cross the BBB?

Limits the transport of substances from the systemic circulation to the brain parenchyma.

BBB is due to endothelial cell tight junctions, basement membrane, neuroglial processes and metabolic enzymes.

Lipid soluble substances (O2, CO2, ethanol, steroid hormones) and those carried by specific transport systems (glucose and some amino acids) can cross the BBB.

Substances with MW > 500 daltons cannot pass (includes most drugs).

9

Describe 5 main factors affecting cerebral blood flow.

1) Autoregulation
2) Tissue Pressure (Monro-Kellie Doctrine)

3) Metabolism
4) Autonomic Nervous System
5) Cushing’s Response

10

Describe autoregulation as it relates to the brain. Discuss regional blood flow in brain.

maintains a consistent blood flow to the brain (about 55 ml/min/100 g of brain).

However, regional blood flow in the brain is associated with regional neural activity. In other words, flow rates vary dependent upon which part of the brain is active at any given time.

11

What is cerebral perfusion pressure normally?
What happens if it falls/ rises?

Cerebral perfusion pressure (CPP) is normally between 80 - 100 mm Hg.

If CPP falls, there is cerebral vasodilation. If CPP rises, there is cerebral vasoconstriction.

12

Draw a graph comparing mean arterial bp to cerebral blood flow. Draw a normotensive and hypertensive line.

What is the normal range of autoregulation? Describe what happens in a hypertensive state.

Slide 7.

Autoregulation is normally seen between about 70-140 mm Hg. In the hypertensive state the autoregulatory curve is shifted to the right, so that blood flow is not as well maintained at lower mean arterial pressure and blood flow remains normal at higher blood pressures.

range. go too low then wont get constant blood flow or go too high and wont get constant blood flow. hypertensive just like baroreceptors…range does shift if you’re at higher pressure… so you’ll be auto regulated just fine.

13

Describe the tissue pressure in the brain. What are the implications if there is an elevation in intracranial pressure?

Located within a rigid cranium.

levations in intracranial pressure will cause vascular compression resulting in increased resistance to blood flow, i.e. ischemia.

14

How do you determine Cerebral Perfusion Pressure (CPP)?

How can a reduction in CPP occur?

Cerebral Perfusion Pressure (CPP) = mean arterial pressure – intracranial venous pressure

Reduction in CPP can result from decrease in mean arterial pressure (e.g. shock) or an increase in intracranial pressure (e.g. tumor, hematoma-bleed out that causes clot that will press on brain, hydrocephalus).

15

If there is a compression what will be compressed first? Where will blood go?

press first on venous side bc venous side has least pressure. as response to decrease in pressure through veins, blood shunted somewhere else. small vessels… so if this tissue pressure decreases blood flow through venous system then that blood in shunted somewhere else and you get less blood flow through this vessel -which means arterials vasodilate and auto-regulate to maintain blood flow

16

Draw a graph that compares cerebral spinal pressure to cerebral blood flow.

(What is normal CSF pressure?)

Describe what happens with an increase in CSF pressure as it approaches arterial pressure.

Slide 9.

An increase in CSF pressure increases vascular resistance and decreases cerebral blood flow initially. Normally, CSF pressure is about 100 mm H2O or about 12 mm Hg. Therefore, CSF and cerebral venous pressure are about the same. As CSF pressure increases, cerebral blood flow decreases initially and metabolically-mediated autoregulation dilates the arterial vascular to maintain cerebral blood flow. However, as CSF pressure increases toward arterial pressure, cerebral blood flow decreases rapidly.

(as CSF pressure increases toward arterial pressure, cerebral blood flow really does decrease. so at normal pressure about 12 mmHg. then cerebral blood flow okay… even if pressure goes up A LOT you are pressing on venous system but arterial portion dilating in response to decrease in blood flow and blood flow remains relatively constant due to auto-regulation. BUT .. when cerebral spinal fluid pressure about 80 (beginning of arterial pressure) see dramatic decrease in blood flow in brain bc can’t compensate for decrease in arterial pressure… decreasing venous pressure compensated by autoregulation. but when pressures go high enough to cut off arterial pressure then brain becomes ischemic.)

17

What is the Monro-Kellie doctrine?

brain volume + cerebral vascular volume + CSF volume = constant

The Monro-Kellie Doctrine states that when the
volume of one compartment increases, there
must be a corresponding and compensatory
decrease in the volume of the other compartments.

For example, an intracranial hemorrhage will cause
an “effective” increase in brain volume, resulting in
a decrease in vascular volume and CSF volume.
The decrease in vascular and CSF volumes results
in an increase in both vascular and CSF pressures.

(decrease in vascular volume will cause increase in pressure ..cut off blood flow)
-increase in CSF pressure cut off blood flow in vascular system and will also crush brain- this increase in CSF if gets high enough

18

What are metabolites?

Which is cerebral blood flow most sensitive to?

CO2, O2, adenosine, K, NO

Cerebral blood flow is very sensitive to arterial PCO2.

metabolites prod. in cerebral blood flow is sensitive to PCO2 (metabolite v sensitive to) sensitive to adenosine too . but particularly to PCO2 which depends on breathing. hyperventilating or hypo. CO2 acts through production of H ions. H ions are acid. become acidic w more CO2 blood acidic get acidosis and as blow off CO2 become alkalotic.

19

Describe the equation for production of H ions.

CO2 acts through the production of H+: CO2 + H2O --- H2CO3 --- HCO3- + H

20

How is blood flow related to pH?

blood flow is inversely related to pH:

decrease in pH causes vasodilation and increase in blood flow

increase in pH causes vasoconstriction and decrease in blood flow

21

How does change in blood pH (metabolic acidosis or alkalosis) affect cerebral blood flow?

Changes in blood pH (e.g. metabolic acidosis or alkalosis) have little effect on cerebral blood flow because H+ cannot easily cross the blood brain barrier.

However changes in blood pH due to changes in CO2 (e.g. respiratory acidosis or alkalosis) can rapidly change cerebral blood flow because CO2 can cross the blood brain barrier.

22

If someone inhaled 7 percent CO2, what would occur?

CO2 lowers pH... (7 % is v high.)
causes vasodilation and can double cerebral blood flow.

23

What effect does hyperventilation have?

Conversely, hyperventilation decreases PCO2 (raises pH) and causes vasoconstriction, decreases blood flow, resulting in dizziness or fainting.

24

How does hyperventilation affect membrane excitability?

-tying back to membrane excitability- hyperventilation will change PCO2, change pH and change binding of Ca to tissues. changes Na permeability. can increase excitability. hyperventilation actually lowers free Ca and increase membrane excitability- adds to anxiety. hyper-excited. increase fainting and dizziness.

25

If a patient had high intracranial pressure (cerebral edema) due to head injury, would you want to induce hyperventilation or hypoventilation? Why?

Patients with high intracranial pressures (cerebral edema) due to head injury are artificially ventilated at high rates (hyperventilation) to lower arterial PCO2 levels. Low PCO2 results in vasoconstriction, which decreases cerebral blood flow. The decrease in cerebral blood flow decreases vascular volume and hence decreases edema formation and intracranial pressure. Thus, there is a trade off between decreased cerebral blood flow and decreased extravascular pressure. This trade off involves the Monro-Kellie doctrine.

26

What has a stronger effect on the brain: decreases in PO2 or CO2?

Decreases in PO2 may cause cerebral vasodilation but the effects are less than changes in CO2.

27

What is the basis for MRI tool?

the oxygenation/deoxygenation state of hemoglobin in cerebral capillaries and veins provides the basis of a useful tool for studying localized brain function called functional magnetic resonance imaging (fMRI).

The magnetic resonance (MR) signal of blood is slightly different depending on the level of oxygenation. The fMRI signal is thus determined by the balance of deoxygenated to oxygenated hemoglobin in blood, which in turn is a function of local arterial autoregulation or vasodilation. This allows determination in unanesthetized patients of the brain’s metabolic activity during different tasks, i.e. speech, movement, reading, etc.

have people read or do diff tasks and see diff parts of brain light up due to vasodilation- more O getting in to diff regions.

28

What metabolites are vasodilators?

Describe mechanisms.

adenosine, K, NO

NO- same as usual. relaxes vascular smooth muscle via cGMP. ultimately though it decreases phosphorylation of myosin light chain kinase, and causes realization.

adenosine is main player in terms of vasodilation. NO is endothelial mechanism that is secondary. more endothelial mechanism than metabolic…

Adenosine is a metabolite (breakdown of ATP) that is produced in response to ischemia, hypoxia, hypotension, electrical stimulation of the brain, and seizures. Any intervention that either reduces O2 supply or increases O2 demand results in rapid (within 5 seconds) formation of adenosine. Adenosine remains elevated throughout the period of O2 imbalance. Adenosine acts on purinergic receptors on vascular smooth muscle cells to activate ATP-sensitive K+ current causing hyperpolarization, which turns off Ca2+ current, and lowers intracellular Ca2+. Adenosine also may release NO from endothelial cells to relax vascular smooth muscle.

Nitric oxide (NO) is released from cerebral endothelium, neurons, and glial cells in response to various stimuli, causing relaxation (vasodilation) of vascular smooth muscle. Neuronally derived NO may mediate local increases in cerebral blood flow during increases in cerebral metabolism. Increases in cerebral blood flow during hypercapnia also may be dependent on NO production. Constitutively produced NO influences basal cerebral vascular tone. NO relaxes vascular smooth muscle via increases in cGMP and protein kinase G (PKG) activities to increase phosphorylation of myosin light chain kinase (MLCK) and ultimately decrease phosphorylation of myosin light chain.

29

How does K work in cerebral circulation? How does this differ from its function in the heart?

K stimulates Na/K ATP-ase pump which will hyperbolize membrane and cause relaxation as well. totally diff. than in heart.

K+ ions released from repolarizing, active nerves. Extracellular K+ concentrations increase in response to electrical stimulation of the brain and during seizures. Small increases in extracellular K+ cause vascular smooth muscle cells to hyperpolarize and thereby relax (vasodilate) presumably by stimulating the electrogenic Na+/K+-ATPase pump and increasing membrane conductance to K+. Astrocytes take up K+ released from neurons and help maintain stable extracellular [K+] in brain.

30

Describe autonomic nervous control.

How will the baroreceptor reflex/response affect cerebral circulation?

Parasympathetic: A division of the facial nerve carries parasympathetic innervation to some cerebral vessels, causing moderate vasodilation.

Sympathetic: Exerts minimal vasoconstriction to increase cerebral vascular resistance. Therefore, baroreceptor reflex stimulation of sympathetic nerve activity has little effect on cerebral vascular resistance.

In general, neural control of the cerebral vascular is relatively weak. Local metabolic activity of brain cells exerts primary control of vasomotor activity in the brain.

31

What is Cushing response?
Graph cerebral spinal pressure against mean arterial pressure.

How will an elevation of intracranial pressure affect cerebral perfusion?

What will result? How will this affect autonomic control? How is bp affected? Will systemic arterial bp be high or low?
What will elevation of intracranial pressure affect heart rate?


Slide 16
An elevation of intracranial pressure causes a decreased cerebral perfusion.
The cerebral ischemia causes stimulation of vasomotor centers in the medulla that increase sympathetic nerve activity.
The increase in sympathetic nerve activity elevates systemic blood pressure (may help to maintain cerebral blood flow).
Therefore, head trauma patient may exhibit very high systemic arterial blood pressure.
The elevation of intracranial pressure also activates parasympathetic nerve activity which decreases heart rate.

32

When is the only time you may get a decrease in cerebral perfusion?

is if cerebral pressure exceeds arterial pressure (if exceeds venous you get autoregulation; its only when you exceed arterial pressure that you get ischemia)

33

If someone came in after a car accident with a bp of 200mmHg/150 what would this indicate?

What would be another physiological manifestation in this case?

means prob cerebral ischema- first indication of Cushing response. other indication is elevation of intracranial pressure activates para. which decreases HR. unusual to see bp going up and HR down..not due to baroreceptors. not due to bp increasing baroreceptor response and causing decrease in HR. no its a direct stimulation of ischemia to parasym. NS. thats why prob depolarizing symp. and para. neurons.
hallmark of cushing response-increase in bp, decrease in HR.

as cerebral spinal pressure goes up, doesn't have repose till 150mmHg which is mean arterial bp in brain. when compress those arteries then you see cushing response. -is medical emergency- got to reduce activity in brain.

34

Describe the pulmonary and systemic "bronchial" circulation of the lungs.

What is the function of the pulmonary circulation?

Mammalian lungs have both a pulmonary and a systemic (“bronchial”) circulation.

Pulmonary circulation receives 100% of the total cardiac output and the bronchial circulation receives less than 1% of the total cardiac output.

The pulmonary circulation functions to transfer gas between the blood and the alveolar air, and to modify the chemicals in the blood as it passes through the lungs to the left heart.

35

Describe pulmonary circulation. (pressure, resistance, flow, pressure gradient)

What is unique about pulmonary arteries?

Pulmonary circulation is a low pressure, low resistance, high flow system with a mean pressure gradient of about 6 mm Hg
(mean pulmonary arterial pressure (14 mm Hg) – mean left atrial pressure (8 mm Hg)).

Pulmonary arteries are 7 times more compliant than systemic arteries due to their minimal smooth muscle.

36

Describe pulmonary capillaries when distended.

Describe how capillaries in pulmonary circulation differ from those is systemic circulation.

Pulmonary capillaries form a network in the alveolar walls that is continuous throughout the lungs. When distended, they are so numerous that blood flows as an unbroken sheet (sheet flow) between the air spaces.

In contrast to the capillaries in the systemic circulation, capillaries in the pulmonary circulation have a major influence on vascular resistance, representing about 40% of the resistance. reason is bc they are located in alveolar walls for this gas exchange. alveolar wall distends during inspiration, relaxes during expiration. changes resistance in capillaries.

systemic circulation where capillaries don’t offer any resistance to flow bc theres so many of them. most of resistance in system is pre capillary sphincters and arterioles.

37

Describe the max. systolic pressure in the pulmonary artery.

What if LA pressure goes up? What will happen? (What causes LA pressure to go up?)

max. systolic pressure is 25. that is RV pressure. (peak. diastolic is around 10. pulse pressure in pul. arteries is about 25/10. peak is same as RV pressure. and diastolic around 10. mean around 14. driving force from pulmonary artery to L side of heart is about 6 mmHg or 8. relatively low.

implication? if LA pressure goes up, doesn't take a lot to reduce blood flow through lung and increase capillary hydrostatic pressure in pul. system bc pressure backs up. increase in LA? LV pump disfunction. LV heart failure backs pressure into LA and that easily increases pressure in pul. system. mitral stenosis. get pul. edema. low pressures v easily influenced by LV pump function.

38

How is pulmonary resistance decreased?

Explain.

Pulmonary resistance decreases as flow and pressure increase (as during exercise) due to recruitment (opening) of new vessels.

parallel networks of capillaries in tissues. in lung when capillaries open up in exercise it reduces resistance to pulmonary blood flow more and get more blood flow. most due to increase in flow and pressure… they just pop open. there is NO mechanism also-increase flow through pul. system, NO releases and increases flow
-most is just pop open bc of pressure.

39

Describe alveolar vessels and extra-alveolar vessels.

Alveolar vessels – microvessels located within the alveolar walls.

Extra-alveolar vessels – larger arterial and venous vessels which are not in the alveolar walls.

40

Describe what happens in alveolar and extra-alveolar vessels during inspiration/expiration.

How are alveolar microvessels affected?
What is overall effect?
What about in deep inspiration?

Inspiration
Negative intrapleural pressure tends to distend extra-alveolar vessels, causing a slight decrease in resistance.
Inflation of alveoli compress and elongate alveolar microvessels, causing a slight increase in resistance.

(during high volumes-breathe in, more air into alveolars and wall stretches, thins out, compresses capillaries in alveolar wall. at same time the negative pressure during inspiration expands the extra-alveolar arterioles and venules. trade off between resistance which is going up in alveolar wall and decrease in extra-alvelolar vessels)
Net effect of inspiration is slight increase or no change in pulmonary peripheral resistance.


During deep inspiration, the above changes in alveolar and extra-alveolar vessels causes transient pooling of blood in pulmonary circulation.

Expiration
Opposite changes occur resulting in a slight decrease or no net change in pulmonary peripheral resistance. expiration - shown on L, low volumes, make alveolar sac smaller so it opens up the capillaries and it compresses the extra-alveolar vessels-resistance higher. reciprocal relationship between alveolar and extra-alveolar


arterioles are outside and lead to capillaries that are inside the wall. then blood flow out of capillaries and goes to venules that are outside wall. changes resistance through vessels during inspiration and expiration.

41

Graph vital capacity (RV, FRC, TLC) against pulmonary vascular resistance.

Slide 20.

on ordinant is pul. vascular resistance. blood flow through lung. . its going up from top to bottom. down here are diff states of lung, FRC is lung when you’re not breathing. sitting quietly. TLC total lung capacity. enormous large deep breath. fill lung w air. RV is residual capacity…certain amount of volume left in lung no matter how hard you expire. don't collapse lung when have forced expiration
FRC to R is inspiration. to L is forced expiration
what happening? showing that if you start at FRC where in equilibrium not breathing and breathe in to R. alveolar vessels get compressed and resistance goes up. extra alveolar at same time distend and resistance goes down.
expiration - alveolar vessels dilate, resistance down. extra-a constrict and resistance goes up.

normal breathing-tidal volume. normally 500 ml of air. start at FRC only go up little to R and little to L. showing that total resistance to blood flow under normal conditions is not a lot of change. pretty flat.

during strong inspiration like when exercising could get up to here- so most of increase in resistance is due to compression of alveolar vessels. inspiration, total resistance follows alveolar constriction. those capillaries influence blood flow when take deep inspiration- capillaries in alveolar wall are more important. during forced expiration, total resistance following extra-al. compression and resistance goes up. from FRC if have strong inspiration total resistance goes up and forced expiration total resistance goes up.. but normal conditions tidal volume prob doesn’t change a whole lot. got to do w inverse rel. between two diff vessels. influences blood flow in lung.

42

Describe hydrostatic pressure in the lung.

In the upright person are intravascular pressures higher at bottom or at top of lung? What about blood flow?

Gravity and anatomy also influence the distribution of pulmonary blood flow.

In the upright person, intravascular pressures are higher at the bottom than at the top of the lung due to gravitational force.

Blood flow is least at the top and greatest at the bottom of the lung

43

What is intravascular pressure at top and bottom of lung? How do you calculate?

here is 16 mmHg (mean pul. artery pressure into pul. artery) at top of lung bc of gravity pulling blood down have to subtract 11mHg. (distance equiv. to 11mmHg). at bottom of lung, hydrostatic column of fluid will increase… now get 27. at bottom of lung hydrostatic pressure about 27. at top 5.

44

Where in the lungs would you first hear pulmonary edema? Why?

so where do u first hear pulmonary edema? hear at base of lung bc hydrostatic pressure much larger and easier for hydrostatic pressure to overcome in abnormal conditions oncotic pressure and cause edema formation. fills w edema from bottom to top. why they feel better when lie down bc effect of gravity it gone.

45

What is the vascular "waterfall" effect? Draw diagram.

Slide 22.

In an upright person, height divides the pulmonary vascular system and blood flow into 3 “zones”.

Zones of perfusion are determined by the relationship between arterial and venous to alveolar pressures.

amount of water going over waterfall does not dep. on height of waterfall. idea that amount of blood crossing pul. system not related nec. to pressure gradient between arterial and venous side. has to do w alveolar. upright person bc of this hydrostatic pressure on lung. height divides pul. system into 3 zones. rel. between pressure in vascular system and pressure exerted by alveolus on capillaries.

46

Describe the hydrostatic pressure in Zone 3

bc bottom of lung has highest hydrostatic pressure (arterial and venous pressures quite high bc of hydrostatic column of fluid) pul. arterial pressure and pul. venous pressure both exceed alveolar pressure during inspiration. means blood flow through base of lung is basically normal blood flow-det. by pressure gradient between arterial and venous side and alveolar has little effect on blood flow at base of lung. bc hydrostatic pressure in vascular space are much larger than alveolar pressures generated by inspiration (air coming to alveolar sac) so plenty of blood flow down at base of lung. as go toward upper part of zone 3 (less blood flow bc hydrostatic pressure column less as u go up so now alveolar pressure has influence

Zone 3 – Both the arterial and venous pressures exceed the alveolar pressure and therefore flow depends on the arterial-venous pressure gradient.

47

Describe the pressures in the Zone 2 and the effect on flow.

see that in middle section.-pulmonary artery pressure still highest but alveolar pressure can be sign. higher than venous pressure. so every time inspire bc of expansion of alveolar sac and compression of cap. the resistance goes up. now blood flow not just det. by diff between arterial and venous pressure which it normally is. now alveolar pressure has influence on blood flow. as go higher and higher up lung, less blood flow bc hydrostatic force is less and alveolar force more significant in impeding blood flow or increasing resistance. during inspiration compresses capillaries and reduces blood flow. resistance. up lung less blood flow during inspiration

Zone 2 – Alveolar pressure exceeds venous pressure but does not exceed arterial pressure. Therefore, capillaries are partially collapsed and flow depends on the pressure difference between arterial and alveolar pressure, and is independent of venous pressure. Under normal conditions, zone 2 comprises the upper third of the lung.

normal blood flow is diff between arterial and venous pressures but alveolar pressures can modulate … under normal conditions zone 2 comprises upper 3rd of lung. zone 2 there throughout zone 1.
flow dep. on AV pressure gradients which is normal.
how much O in relation to how much blood flow-changes in abnormal conditions.
.

48

Describe what happens in expiration and in zone 1.

during inspiration compresses capillaries and reduces blood flow. resistance. up lung less blood flow during inspiration. during expiration too bc ..increasing resistance during inspiration and during expiration. large increase in either, reduce resistance of blood flow through zone 2 either by compressing alveolar wall vessels or extra-alveolar vessels. resistance of blood flow through lung is influenced by alveolar pressures. det. blood flow as u go up. at top, alveolar pressures higher than arterial or venous so in theory no blood flow. not really what happens. that is what could potentially happen.

Zone 1 – Alveolar pressure exceeds both arterial and venous pressures. Therefore, capillaries collapse, preventing blood flow. Zone 1 does NOT exist under normal conditions. However, if arterial pressure decreases (hypotension) or alveolar pressure increases (positive pressure mechanical ventilation) zone 1 can be achieved.

49

What two conditions might you see a Zone 1?

if arterial pressure decreases (hypotension) or alveolar pressure increases (positive pressure mechanical ventilation) zone 1 can be achieved.

under normal conditions adequate blood flow. but if bp drops not perfusing heart but also not getting flow to part of heart. alveolar pressure increase can result from positive pressure mechanical ventilator- chaining from negative pressure breather (expand thorax and suck air in through neg. pressure) to positive pressure- forcing air into lung. can compress alveolar vessels and increase resistance and reduce oxygenation and CO2 transfer. can occur in abnormal conditions.