Pulmonary Diffusion and Pulmonary Circulation Flashcards
how does steady state alveolar air for CO2 and O2 compare to steady state venous blood and arterial blood pressure?
PAO2 = 100 mmHg PaO2 = 95 mmHg PvO2 = 40 mmHg
PACO2 = 40 mmHg PaCO2 = 40 mmHg Pv = 46 mmHg
Henry’s Law of Solubility
-what does alpha mean?
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
Rick’s Law of Diffusion
-what do D and Dl mean?
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
how does D relate to solubility and molecular weight?
diffusion coefficient = solubility / (square root MW)
is there hypoxemia and hypercapnea in hypoventilation and diffusion problems?
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
what is the regular transit time through a pulmonary capillary?
0.75 - 1.2 seconds, since t = V/Q = 75 mL / 100 mL/sec
how is the diffusion of O2, N2O, and CO along length of pulmonary capillary?
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
what happens if diffusion of O2 is abnormal?
O2 will not reach equilibrium until after the full 0.75 seconds of flow through capillaries
CO2 diffusion along pulmonary capillary
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
what happens to PO2 during exercise-induced hypoxemia?
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)
what happens to PO2 and DlCO at high altitudes?
inspiratory hypoxia and vasoconstriction reduces DlCO and slows the rate of equilibration
what is relation of pressure gradient (between alveolar and capillaries) and equilibration time?
the smaller the difference, the shorter time to equilibrate
what happens if you increase the BP in the pulmonary artery?
there is edema, which increases the thickness of the lung, which decreases flow and rate of diffusion, taking longer to equilibrate
equations to measure diffusion capacity
flow of gas in blood (comparable to diffusion capacity) = inspiratory flow - expiratory flow
-usually assume inspiratory flow = expiratory flow
how does DlO2 compare to DlCO?
DlO2 = 1.23 DlCO
how does body position influence DlCO?
DlCO is greater when supine than upright, b/c when you lie down, there is more blood to the lung
how does exercise influence DlCO?
increased blood to lung will increase blood flow and DlCO
how do lung diseases and dysfunction influence DlCO?
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
differences between pulmonary and systemic circulations
- 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
what are 3 O2 supplies to lung?
- bronchial circulation
- pulmonary circulation
- alveolar gas O2 supply
pulmonary circulation and pressures
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
where is pulse pressure largest?
in the left ventricle
anatomic shunts
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
what do lymphatic vessels return excess fluid to? what are they regulated by?
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
physiological shunt
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
pathologic shunt
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
features of pulmonary vessels
- wall thickness
- what kind of vessels they are
- what capillaries are surrounded by
- 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
pulmonary blood pressure along vasculature
-what is average PBP, and what values make it pulmonary HTN or pulmonary edema
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
how is pulmonary arterial pressure measured?
a cardiac catheter called Swan Ganz is inserted in jugular, brachial, or femoral vein and advanced into pulmonary artery
what is pressure (LA)?
pulmonary wedge pressure obtained when catheter in pulmonary vasculature is inflated to occlude flow downstream
how does CO relate to pulmonary vascular resistance?
CO = (P1 - P2) / PVR = (P PA - P LA) / PVR
so
PVR = (P PA - P LA) / CO
are changes in PVR passive or active?
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
what is the relationship between radius, resistance and pressure if vasodilate?
increased radius will decrease resistance and increase pressure
-this means that vessels don’t contract under constant pressure
how do alveolar and extra-alveolar blood vessels respond to decreased intrapleural pressure during inspiration?
- 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
when can alveolar vessels collapse completely?
if pressure outside (alveolar pressure) exceeds capillary pressure
- flow will stop
- larger vessels never collapse b/c protected by surrounding parenchyma
what is lung volume’s relationship to PVR?
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)
what are “corner vessels”?
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
what does gravity have to do with blood flow?
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
what is the three zone model for pulmonary blood flow
capillaries become more distended as you go down, increasing flow
- 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
- 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
- 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
what clinical problems can cause increased capillary permeability?
- adult respiratory distress syndrome (ARDS)
- O2 toxicity (via ROS)
- inhaled or circulating toxins
what clinical problems can cause increased capillary hydrostatic pressure?
- increased left atrial pressure from LV infarction or mitral stenosis (will lead to pulmonary edema)
- overadministration of intravenous fluids
what clinical problems can cause decreased interstitial hydrostatic pressure
too rapid evacuation of pneumothorax or hemothorax
what clinical problems can cause decreased colloid osmotic pressure
- protein starvation
- dilution of blood proteins by intravenous solutions
- renal problems causing urinary protein loss
what clinical problems can cause insufficient pulmonary lymphatic drainage?
- tumors
- interstitial fibrosing diseases
how is the O2 and CO2 concentration in the right to left pathologic shunt? can these problems be solved with O2-enriched gas?
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
