Blood Flow and Metabolism.pptx

1. Blood Flow and
Metabolism
IRMA RAHAYU
C185192002

2. The Lungs
and The
Pulmonary
Circuit

3. Pressure within Pulmonary
Blood Vessels
• Very low due to large surface area
and low resistance
• Not much smooth muscle in the
arteries or veins
• Reverse the flow and almost no
difference
Comparison of pressures (mmHg) in
the pulmonary and systemic
circulations. Hydrostatic differences
modify these.

4. Pressure around
Pulmonary Blood Vessels
Alveolar and Extra-Alveolar vessels
• Alveolar vessels are exposed to
alveolar pressure and are
compressed if this increases
• Extra-alveolar vessels are
exposed to a pressure less than
alveolar and are pulled open by
the radial traction of the
surrounding parenchyma
Effect of lung volume on pulmonary vascular
resistance when the transmural pressure of the
capillaries is held constant. At low lung volumes,
resistance is high because the extra-alveolar
vessels become narrow. At high volumes, the
capillaries are stretched and their caliber is
reduced. Note that the resistance is least at normal
breathing volumes.

5. Pressure around Pulmonary Blood Vessels
“Alveolar” and “extra-alveolar” vessels . The first are
remainly the capillaries and are exposed to alveolar
pressure. The second are pulled open by
the radial traction of the surrounding lung
parenchyma and the effective pressure around them
is therefore lower than alveolar pressure.
Section of lung showing many alveoli and an extra-alveolar
vessel (in this case, a small vein) with its perivascular
sheath.

6. Alteration in
FRC
Above FRC
• As lung volume increases above the
FRC, the pulmonary vessels outside
the alveoli are distended and their
resistance falls.
• On the other hand, the septal
capillaries in the alveolar walls are
stretched so that their diameters are
reduced.
• The net effect is an increase in overall
pulmonary vascular resistance since
the narrowing of septal capillaries is
the dominant effect.

7. Alteration
in FRC
Below FRC
• As lung volume decreases below the FRC,
the pulmonary vessels outside the alveoli
tend to collapse as their walls are no longer
being stretched by the surrounding lung
tissue, leading to an increase in their
resistance.
• The reduction in alveolar size leads to a
reduction in the stretched of their walls.
• Although the resistance of the capillaries
decreases, the overall effect is an increase
in pulmonary vascular resistance since the
increase in the extra-alveolar vessels is the
dominant effect.

8. Pulmonary
Vascular
Resistance
• PVR = (input pressure-
output pressure)/blood
flow
• PVR = (Ps-Pd)/CO
Fall in pulmonary vascular re s is tance as the pulmonary
arterial or venous pressure is ra is ed. When the a rte ria l
pressure was changed, the venous pressure was held
constant at 12 cm water, and when the venous pressure was
changed, the arterial pressure was held at 37 cm water.
(Data rom an excised animal lung preparation.)

9. Very Low Resistance
is Due To
Vascular
Changes
As pressure rises
resistance tends to fall in
the lung due to
Recruitment of
more capillaries
Distension of the
blood vessels due to
increasing pressure
Mostly seen at high
pulmonary vascular
pressures
Recruitment (opening of previously closed vessels)
and distension (increase in caliber of vessels).
These are the two mechanisms for the decrease in
pulmonary vascular resistance that occurs as
vascular pressures are raised.

10. Very Low Resistance
is Due to
Lung Volume
 Large lung Volumes increase
PVR by increasing capillary
resistance
 High resistance at low lung
volumes
• Critical opening pressure
Effect of lung volume on pulmonary
vascular resistance when the transmural
pressure of the capillaries is held
constant. At low lung volumes, resistance
is high because the extra-alveolar vessels
become narrow. At high volumes, the
capillaries are stretched and their caliber
is reduced.

11. Measurement
of Pulmonary
Blood Flow
• Fick principle
• VO2 = Q (CaO2-CvO2)
• Cardiac Output 𝐶𝑂 =
 Blood oxygen carrying capacity = Hb
(gm%)x1.34 (mL O2/gm of Hb)x10 = mL
O2/L blood
 Oxygen content of venous or arterial blood
= oxygen carrying capacity X % of
saturation
 Peripheral artery oxygen content =
pulmonary venous content (if no
intracardiac shunt is present)
𝑂2 𝐶𝑜𝑛𝑠𝑢𝑚𝑝𝑡𝑖𝑜𝑛 (𝑚𝐿/𝑚𝑖𝑛)
𝑃𝑢𝑙𝑚𝑜𝑛𝑎𝑟𝑦 𝑣𝑒𝑛𝑜𝑢𝑠 𝑂2 𝑐𝑜𝑛𝑡𝑒𝑛𝑡
𝑚𝐿
𝐿
− 𝑝𝑢𝑙𝑚𝑜𝑛𝑎𝑟𝑦 𝑎𝑟𝑡𝑒𝑟𝑦 𝑂2 𝑐𝑜𝑛𝑡𝑒𝑛𝑡 (𝑚𝐿/𝐿)
= L/min

12. Distribution of
Blood Flow
 Change based on:
• Posture
• Exercise
 Zones of West:
• Zone I
o PA>Pa>Pv
• Zone II
o Pa>PA>Pv
• Zone III
o Pa>Pv>PA
Measurement of the distribution of blood flow in the upright
human lung, using radioactive xenon. The dissolved xenon
is evolved into alveolar gas from the pulmonary capillaries.
The units of blood flow are such that if flow were uniform,
all values would be 100. Note the small flow at the apex.

13. Explanation of the uneven
distribution of blood flow in
the lung, based on the
pressures affecting the
capillaries.

14. Two Starling resistors, each
consisting of a thin rubber tube
inside a container. When chamber
pressure exceeds downstream
pressure as in A, flow is
independent of downstream
pressure. However, when
downstream pressure exceeds
chamber pressure as in B, flow is
determined by the upstream-
downstream difference.

15. Zones of West
Zone I
• Alveolar pressure is greater
than both local pulmonary
arterial and venous
pressure
• Vessel are compressed
and there is no flow
• Palv>Pa>Ppv

16. Zones of West
Zone II
• Pulmonary arterial pressure is greater than alveolar
pressure.
• The alveolar pressure is greater than the venous
pressure. However, so that the downstream pressure is
alveolar pressure.
• This situation is termed a “vascular waterfall”: the flow is
independt of the eventual venous pressure and
depends only on the difference between pulmonary
arterial pressure and alveolar pressure.
• Pa>Palv>Ppv

17. Zones of West
Zone III
• Pulmonary arterial pressure is greater
than venous pressure and alveolar
pressure.
• The venous pressure is greater than the
alveolar pressure so that flow depends
on the arterio-venous pressure
difference.
• Pa>Pv>Palv

18. Why are Clinically?
• Affect PA catheter readings
• Ventilator management
Overventilation can affect PVR
Alteration in FRC may affect the PVR

19. Dead
Space
and
Shunt
• Alveolar Dead Space
 Ventilation without perfusion
 V/Q1/O = ∞
• Shunt
 No ventilation with perfusion
 V/Q0/1 = 0

20. Active Control of Circulation
• Hypoxic pulmonary vasoconstriction
 Does not depend on CNS
 Dependent on the PAO2 concentration not the PaO2 concentration
 Increase the PAO2 the greater the perfusion to that area
 Alveolar hypoxia constricts small pulmonary arteries
 Probable a direct effect of the low PAO2 on vascular smooth muscle
 Critical at birth in the transition from placental to air breathing
 Direct blood flow away from poorly ventilated areas of the diseased lung in the
adult

21. Effect of
reducing
alveolar PO2
on pulmonary
blood flow

22. Hypoxic Pulmonary
Vasoconstriction
• Alveolar hypoxia constricts small pulmonary arteries.
• Probably a direct effect of the flow PO2 on vascular smooth
muscle.
• Its release is critical at birth in the transition from placental to
air breathing.
• Directs blood flow away from poorly ventilated areas of the
diseased lung in the adult.

23. Water Balance in
The Lung
• Too much volume leads
to leakage into:
Interstitium
Alveoli
Much more serious
Two possible paths or fluid that moves out of the
pulmonary capillaries. Fluid that enters the
interstitium initially finds its way into the perivascular
space (1). Later, fluid may cross the alveolar wall
(2).

24. Other
Function
of The
Lung
Reservoir
• When you suddenly lie down after standing, quite a bit
of venous blood formerly in the legs drains to the right
atrium.
• The right ventricle pumps the extra blood into the lung,
but not all of it immediately moves to the left ventricle, i.
e. some of it is “stored” in the lung.
• This prevents cardiac output from increasing
excessively as one goes from an upright to a lying-
down position.
• On the other hand, when one goes from a lying-down to
an upright position (and blood now pools in the legs),
the “stored” blood in the lung now flows into the left
atrium helping to maintain cardiac output long enough
for baroreceptor reflexes to initiate other compensatory
mechanisms.

25. Metabolic
Functions of
The Lung
 Arachidonic acid metabolites
o Prostaglandins E2 and F2
o Leukotrienes
Two pathways of arachidonic acid
metabolism. The leukotrienes are
generated by the lipoxygenase
pathway, whereas the prostaglandins
and thromboxane A2 come from the
cyclooxygenase pathway.

26. Fate of
Substances
in The
Pulmonary
Circulation

27. Metabolic Functions
of The Lung
 The type-2 alveolar cells make
pulmonary surfactant.
• Pulmonary surfactant is essential
for normal compliance of the lung.
 Converting enzyme
• Converts inactive angiotensin I to
active angiotensin II.
• Converts active bradykinin to an
inactive metabolite.

28. Metabolic
Functions
of The
Lung
 The lung makes immunoglobulin A
• Provides a defense mechanism against
pulmonary infection.
 The upper airways secrete mucus
• Essential for removal of inhaled
particles.
 The lung removes serotonin from the
blood
• Serotonin may be transferred to
platelets.
 The lung can partially remove and
inactive
• Norepinephrine
• Epinephrine

29. Metabolic Functions of The Lung
 Prostaglandin E2 is produced by the lung of the fetus
• Serves as a smooth muscle relaxant keeping the ductus
arteriosus open during fetal life
• Elevation of pulmonary and systemic PO2 which occurs when the
newborn child begins to breath causes contraction of the smooth
muscle of the ductus arteriosus causing the ductus to close
• If the ductus fails to close, inhibitors of prostaglandin synthesis
(Indomethacin) can be administrated to facilitate closure of the
ductus.