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Spr2015_Week5 > Pulm Circulation I > Flashcards

Pulm Circulation I Flashcards

1
Q

2 functions of pulm circulation in lung

A

1) gas exchange

2) water-solute balance

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2
Q

what do disruptions to normal function of pulm circulation manifest as?

A

1) abnormal gas exchange (hypoxemia = low O2 or hypercapnea = high CO2)
2) abnormal incr in fluid (pulm edema can’t exchange gas)
3) incr in pulm vasc resistance (pulm HTN with decr CO, heart failure)

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3
Q

what are components of pulm circulation starting at pulm trunk

A

1) pulm trunk off RV
2) main pulm arteries and lobar branches
3) intra-pulm arteries, arterioles, capillaries, venules
4) large pulm veins return to LA

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4
Q

what is in common amongst pulm trunk, pulm arteries, and extra-alveolar arteries

importance?

A

elastic = important for absorbing pulsatile pressure from heart

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5
Q

what are the muscular arteries of pulm circulation

why?

A

alveolar arteries

constrict and dilate to regulate blood flow (smooth muscle contracts in response to alveolar hypoxia)

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6
Q

how does smooth muscle respond to alveolar hypoxia?

what is this caused?

what happens to blood?

A

smooth muscle contracts

called hypoxic pulm vasoconstriction (HPV)

diverts blood from hypoxic areas of lung

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7
Q

pulm vasculature is highly ____

what does that imply?

A

compliant

–> low resistance, high volume for gas exchange

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8
Q

what is mean pulm artery pressure criterion for pulmonary HTN

what is normal mPAP

A

25/10

normal = 15-18

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9
Q

how does pulm vasculature maintain high compliance

A

incr CO, incr distensability of perfused vessels and recruiting previously unperfused vessels

recruitment = parallel (more vessels, decr total resistance)

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10
Q

how does gravity affect variation in blood pressure and blood flow in lung when standing

A

divides into 3 zones when standing

1) base of lung = greatest BP, constant flow
2) middle = middle BP, intermittent flow
3) apex = low BP, little to no flow

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11
Q

equation for PAP

A

PAP = CO x PVR + LAP

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12
Q

ways to incr PAP

A

1) usu incr pulm vascular reisstance
2) incr LA pressure
3) incr CO (rarely)

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13
Q

if pulm HTN due to pre-capillary what does that mean?

PCWP value?

A

pulm arterial hypertension (PAH)
incr pulm vascular resistance thru lung

PCWP

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14
Q

if pulm HTN due to post-capillary what does that mean?

PCWP value?

A

pulm venous hypertension (PVH)
incr LA pressure

PCWP

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15
Q

hemodynamic definition of PAH

A

+ mean PAP > 25

+ PCWP/LVEDP 3 Wood’s unit

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16
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17
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18
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19
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20
Q

what are the “west zones” of the lung

A

3 vertical regions organized by

1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure

21
Q

how do

1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure

vary in west zones of lung

A

alveolar pressure = constant

arterial and venous pressure vary due to gravity

22
Q

the zones are ___ not anatomic so …

A

physiologic

so change in position, change orientation with respect to apex and base

23
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25
Q

what is relationship of 3 pressure in zone 1 (apex)

A

PAlveolar > Parterial > Pvenous

since PA > Pa, arterial microvasculature compressed, minimal blood flow

26
Q

what is relationship of 3 pressures in zone 2 (middle)

A

Parterial > PAlveolar > Pvenous

since Pa > PA, greater flow than zone 1

flow limited because PA > Pv so driving force for flow = difference btwn arterial and alveolar pressure

27
Q

what is determinant of driving force for flow in zone 2

A

difference btwn arterial and alveolar pressure

28
Q

what is relationship of 3 pressures in zone 3 (base)?

A

Parterial > Pvenous > PAlveolar

greatest flow
driving force = difference btwn arterial and venous pressure

continuous flow from arteries across alveoli into venous

29
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30
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31
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32
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33
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34
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35
Q

net pressure from capillaries into interstitium

with oncotic pressure, you have albumin inside blood and capillaries are strong so pull fluid back into capillaries

normally slight net flow out of capillaries into interstitium (hydrostatic > oncotic)

normally Pmv&raquo_space;> Pi
Πmv > Πi

A

a

36
Q

under normal conditions what is relationship of

hydrostatic and oncotic inside vessel vs. out

A

hydrostatic > oncotic

so fluid out of vessel

37
Q

what is equation for net filtration

A

Qf = Kf [(Pmv-Pi) – σ(Πmv -Πi)]

Qf = fluid filtration rate

Kf = filtration coefficient, dependent on leakiness of vessel (higher=leakier)

Pmv/i = vascular and interstitial hydrostatic pressure

σ= osmotic reflection coefficient
(0=unrestricted passage of protein; 1=no passage of protein)

Πmv/I = vascular and interstitial oncotic pressure

38
Q

in healthy vessels, what is relationship btwn hydrostatic and oncotic pressure and how does that affect fluid transport?

A

hydrostatic > oncotic

fluid moves from vessels into interstitium

fluid can be reabsorbed by capillaries and venules or taken up into lymphatics

NOT ENTER ALVEOLAR SPACES

39
Q

Lung mechanism of preventing pulmonary edema

1) Decr interstitial oncotic pressure

A

1) fluid enters interstitial space, decr interstitial oncotic pressure
2) counteracts incr hydrostatic P in vessel

40
Q

Lung mechanism of preventing pulmonary edema

2) incr interstitial hydrostatic P

A

1) fluid in interstitium incr hydrostat P

2) opposes filtration from vessels –> promotes flow from interstitial space into lymphatics

41
Q

Lung mechanism of preventing pulmonary edema

3) incr plasma oncotic P

A

1) loss of fluid from vessel incr oncotic P

2) opposes filtration

42
Q

Lung mechanism of preventing pulmonary edema

4) lymphatic reserve system

A

1) lymphatics have reserve to accomodate edema

2) lymph flow incr 15x to maintain balance

43
Q

hydrostatic cardiogenic

A

incr pulm capillary wedge pressure

incr vascular pressure (Pmv)

pushing fluid out of capillaries into interstitium
and lymphatics are full so fluid from interstitium then enters into alveolus

interlobular septa (lymphatics) enlarge and acinus fills with fluid

44
Q

noncardiogenic (incr permeability)

A

integrity of vessels is destroyed/decr
albumin and proteins that normally incr oncotic pressure in pulm vessels is lost so now no more oncotic pressure pulling fluid back in and now net flow of fluid out of vessels

– Proteins leave the vasculature! – πmv goes down!
– πi goes up!
– Ø effectively goes down (proteins can cross easily)!

shift in curve up and to the left so now for same presusre in vessel, incr rate of edema formation

45
Q

ARDS

A
  1. Bilateral Alveolar Infiltrates! 2. PaO2/FiO2
46
Q

Difference between cardiac vs noncardiac pulm edema

A

Clinical setting

CHF = cardiogenic

Spr2015_Week5 (19 decks)

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