pulmonary circulation
Functional Organization
• The pulmonary arteries branch like that of airways so that each
airway branch and arterial branch runs parallel to each other.
Pulmonary capillaries are large in diameter and have multiple
anastomoses.
• The arrangement of capillaries is such that each alveolus is
surrounded by a capillary basket.
• A branch of pulmonary artery divides further to form arterioles that
in turn form extensive capillary lattice around a single alveolus, which
drains into a branch of pulmonary veins.
• The pulmonary blood vessels with blood in them constitute about
40% of the total weight of the lungs.
Arrangement of blood supply to alveoli
Functions of Pulmonary Circulation
• 1. Gas exchange
• 2. Serves as a filter: Pulmonary vessels filter thrombi and emboli that
originate from venous compartment and right side of the heart.
• 3. Metabolic functions
• 4. Serves as a blood reservoir: About 500 mL of circulating blood is
present in the pulmonary circulation.
Special Features of Pulmonary Circulation
• 1. The pulmonary circulation is a low-pressure (mean pulmonary arterial
pressure is 15 mm Hg), and low resistance system.
• 2. The pulmonary artery and its branches have thin walls. There is less smooth
muscle in the walls of pulmonary arteries. Due to their thin walls and paucity
of smooth muscles, pulmonary arteries are more compliant.
• 3. The pulmonary arterioles are also thin-walled and contain less smooth
muscle. Therefore, the ability to constrict is less than thick-walled, muscular
arterioles of systemic circulation.
• 4. The pulmonary veins are also thin-walled and highly compliant.
• 5. The arrangement of pulmonary capillaries is different. The capillaries form
lattice in the alveolar wall so that blood flows as a thin sheet.
• 6. Change in pulmonary venous and left atrial pressures profoundly
affects gas exchange. The pulmonary wedge pressure indirectly
measures these pressures.
• 7. Pulmonary vascular resistance: Pulmonary vascular resistance is
very low, which is about one-tenth that of systemic vascular
resistance.
• 8. A unique feature of the pulmonary circulation is that the
pulmonary vascular resistance (PVR) falls with increased pulmonary
arterial pressure as occurs in increased cardiac output.
Physiological Significance of Low PVR
• The decrease in pulmonary vascular resistance with increased cardiac output
has three beneficial effects.
• a. The decreased resistance decreases the velocity especially when the flow
rate is high. This provides adequate time for pulmonary capillary blood to take
up oxygen and dispose of carbon dioxide.
• b. The capillary distension that decreases resistance increases the capillary
surface area, which facilitates diffusion of gases along the alveolar-capillary
membrane.
• c. A high capillary pressure can cause pulmonary edema, and impair gas
exchange. For example, during vigorous exercise cardiac output increases
enormously that increases blood flow and pressure in pulmonary circulation.
However, the decrease in pulmonary vascularresistance decreases the load on
the right ventricle and lowers the capillary pressure that prevents pulmonary
edema.
Pulmonary Blood Flow
• There is approximately 500 mL of blood present in pulmonary circulation at
any given time, which is about 10% of the total circulating blood volume.
• The distribution of 500 mL of blood is as follows:
• In pulmonary arteries : 150 mL
• In pulmonary veins : 270 mL
• In pulmonary capillaries : 80 mL
Distribution of Pulmonary Blood Flow
• In upright posture, blood flow increases from apex to the base of the lungs.
This difference (the lowest blood flow at apex and highest blood flow at base)
is due to the effect of gravity
Factors Affecting Pulmonary Blood Flow
• Factors that affect pulmonary blood flow are:
• 1. Pulmonary vascular resistance
• 2. Gravity
• 3. Alveolar pressure
• 4. Arterial to venous pressure gradient
Pulmonary Vascular Resistance
• 1. Lung Volumes
• Pulmonary vascular resistance is lowest at functional residual capacity and
increases at both higher and lower lung volumes.
• 2. Hormones
• Serotonin, norepinephrine, histamine, thromboxane A2, and leukotrienes are
potent vasoconstrictors. They increase pulmonary vascular resistance,
particularly at low lung volumes when the vessels are already compressed.
Adenosine, acetylcholine, prostacyclin (PG-I2), and isoproterenol relax smooth
muscle of blood vessel and decrease pulmonary vascular resistance.
• 3. Oxygen tension
• Low oxygen tension increases pulmonary vascular resistance by causing
vasoconstriction
• Effects of Gravity
• Gravity significantly affects pulmonary blood flow. Due to effect of
gravity, in upright posture pulmonary blood flow increases from apex
to base of the lungs
• Effects of Alveolar Pressure
• Alveolar pressure depends on lung volumes. Alteration in alveolar
pressure due to change in lung volume changes pulmonary blood
flow.
• Arterio-venous Pressure Gradient
• The difference between the pressure at arterial and venous
compartment of pulmonary circulation determines the rate of blood
flow. Arterial to venous pressure gradient is affected by alveolar
pressure.
Regulation of Pulmonary Blood Flow
• Pulmonary blood flow is regulated by active and passive factors.
• Active Factors
• Active factors are neural, hormonal and chemical.
• Neural Regulation
• Though the pulmonary circulation is richly innervated with sympathetic
nerves, pulmonary vessel diameter is virtually unaffected by autonomic
nerves in normal conditions.
• 1. This is because the resting sympathetic tone of pulmonary circulation is
almost absent.
• 2. However, sympathetic stimulation causes mild vasoconstriction and
parasympathetic stimulation causes mild vasodilation.
• Hormonal Regulation
• 1. Major vasoconstrictors in pulmonary bed are serotonin, norepinephrine,
endothelin, angiotensin, thromboxane A2, and leukotrienes . They decrease
pulmonary blood flow.
• 2. Vasodilators that increase blood flow are adenosine, acetylcholine, prostacyclin
(PG-I2), bradykinin and nitric oxide.
• 3. Chemical Regulation
• Hypoxemia or alveolar hypoxia causes vasoconstriction of small pulmonary arteries.
In contrast, hypoxia in systemic circulation and other parts of the body produces
vasodilation.The exact mechanism of this unique phenomenon of hypoxia-induced
pulmonary vasoconstriction is not known. It is proposed that hypoxia directly causes
contraction of pulmonary vascular smooth muscles.
• The probable mechanism is that hypoxia inhibits K+ channels that depolarize the
muscle cells. This opens the voltage-gated Ca++ channels. Influx of Ca++ causes
vasoconstriction. The hypoxia-induced vasoconstriction is accentuated by high
carbon dioxide and low blood pH.
• Passive Factors
• Passive factors that regulate pulmonary blood flow are cardiac
output, gravity and lung volumes. Increase in cardiac output increases
pulmonary blood flow.
Filtration Across Pulmonary Capillaries
• 1. Hydrostatic and osmotic pressure gradients
• The hydrostatic pressure in pulmonary capillaries is low, which is about 8 to 10 mm Hg.
As it is significantly less than the oncotic pressure, which is 25 mm Hg, this favors the net
absorption of fluid from interstitial space into capillary blood.
• 2. Role of alveolar surface tension
• Alveolar surface tension favors filtration and counteracts the advantage of low
hydrostatic pressure. The net result is that a small quantity of fluid fluxes out of the
capillaries into the interstitial space. This small amount of excess fluid circulates from
the interstitium into the perivascular and peribronchial spaces and then from there
passes into the lymphatic channels.
• 3. Role of lymphatics
• The lymphatic system is extensive and well-developed in lungs. The lymphatics are
mainly located near the terminal bronchioles, which is favorable for them to drain
excess fluid from peribronchial space.
Pulmonary Edema
• Pulmonary edema develops when excess of free fluid accumulates in
interstitial spaces and alveoli Pulmonary edema is caused by following
mechanisms:
• 1. Increased capillary hydrostatic pressure: This is the commonest cause of
pulmonary edema. Most frequently it results from an abnormally high
pulmonary venous pressure as occurs in mitral stenosis or left heart failure.
• 2. Increased alveolar surface tension: High surface tension lowers interstitial
hydrostatic pressure that favors filtration. Decreased surfactant synthesis
increases the surface tension and causes pulmonary edema as occurs in ARDS.
• 3. Decreased oncotic pressure: Plasma colloid osmotic pressure decreases in
hypoproteinemia as occurs in starvation.
• 4. Increased capillary permeability: This is a major cause of
pulmonary edema. Increased capillary permeability occurs with
pulmonary vascular injury as occurs in:
• Oxidant damage, e.g. oxygen therapy, ozone toxicity
• − Inflammatory reactions, e.g. by the action of endo_x0002_toxins
• − Neurogenic shock, e.g. head injury is a major cause
• of pulmonary edema.