Pulm Circulation I Flashcards
2 functions of pulm circulation in lung
1) gas exchange
2) water-solute balance
what do disruptions to normal function of pulm circulation manifest as?
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)
what are components of pulm circulation starting at pulm trunk
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
what is in common amongst pulm trunk, pulm arteries, and extra-alveolar arteries
importance?
elastic = important for absorbing pulsatile pressure from heart
what are the muscular arteries of pulm circulation
why?
alveolar arteries
constrict and dilate to regulate blood flow (smooth muscle contracts in response to alveolar hypoxia)
how does smooth muscle respond to alveolar hypoxia?
what is this caused?
what happens to blood?
smooth muscle contracts
called hypoxic pulm vasoconstriction (HPV)
diverts blood from hypoxic areas of lung
pulm vasculature is highly ____
what does that imply?
compliant
–> low resistance, high volume for gas exchange
what is mean pulm artery pressure criterion for pulmonary HTN
what is normal mPAP
25/10
normal = 15-18
how does pulm vasculature maintain high compliance
incr CO, incr distensability of perfused vessels and recruiting previously unperfused vessels
recruitment = parallel (more vessels, decr total resistance)
how does gravity affect variation in blood pressure and blood flow in lung when standing
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
equation for PAP
PAP = CO x PVR + LAP
ways to incr PAP
1) usu incr pulm vascular reisstance
2) incr LA pressure
3) incr CO (rarely)
if pulm HTN due to pre-capillary what does that mean?
PCWP value?
pulm arterial hypertension (PAH)
incr pulm vascular resistance thru lung
PCWP
if pulm HTN due to post-capillary what does that mean?
PCWP value?
pulm venous hypertension (PVH)
incr LA pressure
PCWP
hemodynamic definition of PAH
+ mean PAP > 25
+ PCWP/LVEDP 3 Wood’s unit
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what are the “west zones” of the lung
3 vertical regions organized by
1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure
how do
1) pulm arterial pressure
2) pulm venous pressure
3) alveolar pressure
vary in west zones of lung
alveolar pressure = constant
arterial and venous pressure vary due to gravity
the zones are ___ not anatomic so …
physiologic
so change in position, change orientation with respect to apex and base
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what is relationship of 3 pressure in zone 1 (apex)
PAlveolar > Parterial > Pvenous
since PA > Pa, arterial microvasculature compressed, minimal blood flow
what is relationship of 3 pressures in zone 2 (middle)
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
what is determinant of driving force for flow in zone 2
difference btwn arterial and alveolar pressure
what is relationship of 3 pressures in zone 3 (base)?
Parterial > Pvenous > PAlveolar
greatest flow
driving force = difference btwn arterial and venous pressure
continuous flow from arteries across alveoli into venous
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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»_space;> Pi
Πmv > Πi
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under normal conditions what is relationship of
hydrostatic and oncotic inside vessel vs. out
hydrostatic > oncotic
so fluid out of vessel
what is equation for net filtration
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
in healthy vessels, what is relationship btwn hydrostatic and oncotic pressure and how does that affect fluid transport?
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
Lung mechanism of preventing pulmonary edema
1) Decr interstitial oncotic pressure
1) fluid enters interstitial space, decr interstitial oncotic pressure
2) counteracts incr hydrostatic P in vessel
Lung mechanism of preventing pulmonary edema
2) incr interstitial hydrostatic P
1) fluid in interstitium incr hydrostat P
2) opposes filtration from vessels –> promotes flow from interstitial space into lymphatics
Lung mechanism of preventing pulmonary edema
3) incr plasma oncotic P
1) loss of fluid from vessel incr oncotic P
2) opposes filtration
Lung mechanism of preventing pulmonary edema
4) lymphatic reserve system
1) lymphatics have reserve to accomodate edema
2) lymph flow incr 15x to maintain balance
hydrostatic cardiogenic
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
noncardiogenic (incr permeability)
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
ARDS
- Bilateral Alveolar Infiltrates! 2. PaO2/FiO2
Difference between cardiac vs noncardiac pulm edema
Clinical setting
CHF = cardiogenic
