•Blood supply of lung includes-
BRONCHIAL CIRCULATION- comprising of bronchial
arteries and veins
PULMONARY CIRCULATION- comprising of
pulmonary arteries and veins
Differences
• Bronchial arteries supplies oxygenated blood
pumped from the left ventricle- systemic circulation
relatively smaller diameter, high pressure
•Pulmonary arteries supplies deoxygenated blood
pumped from the right ventricle . This circulation
relatively larger diameter, low pressure
DEVELOPMENT
•By the completion of 16
th
week intrauterine life, the
preacinar structures of bronchi, pulmonary vessels,
bronchial arteries are developed
•Pulmonary trunk developed from 6
th
primitive
branchial arch
•Vessels developed from mesenchymal tissue
Fetal and neonatal circulation
•Before birth, lungs receive about 10 to 15 percent
of right ventricle output
•In comparison to adult circulation, fetal circulation
has
More vascular resistance
High initial tone
Greater vascular reactivity
Reactive hyperemia
•PGs, endothelins and NO plays an important role in
regulating fetal circulation.
•After first breath there is marked drop in PVR
Due to:
Increased Po2
Expansion of the lungs
Bronchial circulation
•It is a part of systemic circulation
•It contains 1-2 percent of cardiac output
BRONCHIAL ARTERIES
Origin
•The left BA (superior & inferior) usually arise directly from the
thoracic aorta at the level of T5&T6 vertebra
•The origin of the right bronchial artery is variable; in order of
frequency,
it may arise from
• right posterior intercostal artery (usually the 3rd),
• a common trunk shared with the left superior bronchial artery, or
• directly from the aorta.
2 Left bronchial artery
1 Right bronchial artery
Bronchial artery branching pattern
Cauldwell et al - four patterns:
11
Type I
Type II
Type III
Type IV
Cauldwell EW, Siekert RG, Lininger RE, Anson BJ.The bronchial arteries: an
anatomic study of 105 human cadavers. Surg Gynecol Obstet 1948; 86:395–412.
Type I
•Incidence: 40.6%
•Left:2
•Right:1 {intercostobronchial
trunk (ICBT)}
12
Single rt.branch
Lt. 2 br.arties
Sup.left
bronchial
artert
Inf.Left
bronchial
artery.
Right
bronchial
artery
.
Type II
•Incidence: 21.3%
•Left:
1 left Bronchial Artery
•Right: 1intercostobronchial
trunk
13
Single Lft.bron.art
Single.Rt.ICBT
Type III
•Incidence: 20.6%
•Left:2
•Right :2
(1intercostobronchial trunk & 1
Right bronchial artery)
14
Left sup.& Left Inf .bronchial
artery.
Right
ICBT
Right Bronchial
artery
.
Type IV
•Incidence:9.7%
•Left: 1
•Right: 2
(one intercostobronchial trunk
and one bronchial artery)
15
Single Left
artery
Rt.ICBT
Rt.Bron.art.
•Normal BA measure < 1.5 mm in diameter at their
origin and 0.5 mm at their point of entry into a BPS
• BA >2 mm at CT is
most likely abnormal ,
upto 8mm in hypertrophied
Distribution to lung
•The br. A supply blood to the bronchi and connective
tissue of the lungs. They end at the level of the
respiratory bronchioles. They anastomose with the
branches of the pulmonary arteries, and together, they
supply the visceral pleura of the lung
Functions
•It has features of nutrient circulation
•they supply the lungs with oxygenated blood
•It also participates in air conditioning of the inspired
air.
Bronchial veins
•There is typically a single bronchial vein at
each hilum, formed from the superficial bronchial
veins with deep bronchial veins, draining into the
pulmonary veins.
Deep bronchial veins
•The deep bronchial veins form from intrabronchial
venous plexuses. These vein drains either directly
into the left atrium or into thepulmonary vein.
Within the lung there are significant anastmoses
with the intrapulmonary pulmonary veins.
•Superficial bronchial veins
•The superficial bronchial veins consist of a subpleural
venous network which receive tributaries from extra-
pulmonary bronchi, hilar lymph nodes and the vaso
vasorum of the hilar pulmonary vessels and unite to
form a single bronchial vein at each hilum.
•on the right, they drain into the azygos vein. On the left
they drain into the left superior intercostal
vein, accessory hemiazygos vein or left brachiocephalic
vein. At the hilum they communicate with the
pulmonary veins.
VENOUS DRAINAGE
•The bronchial circulation proliferates beyond the
limits in the following conditions:
Pulmonary atresia
bronchiectasis
lung abscess
lung cancer
•In chronic MS, Haemoptysis occurs from bronchial
veins
Pulmonary circulationPulmonary circulation
PULMONARY CIRCULATION
Pulmonary artery
Arises from the infundibulum of the right ventricle
at pulmonary valve and runs posteriorly slightly
upwards and divide below the aortic arch in to right
and left
Right pulmonary artery runs laterally under aortic
arch and posterior to ascending aorta and superior
venacava before dividing at the hilum into upper,
middle and lower branches ,to supply upper, middle
and lower lobes respectively
•Left pulmonary artery runs laterally, upwards and
posteriorly,anterior to descending aorta and
connected to ligamentum arteriosum.
•It divides into upper and lower branches; they
supply upper and lower lobes
•Sub divides in a variable pattern on both sides
•Counting from peripheral small arteries to the main
pulmonary trunk, there are 17 orders of branching
on both sides.
•Pulmonary arteries breaking up to pulmonary
capillaries that form network around the alveolus.
•Media of the vessels consists of elastic fibrils(5 or
6layers) with smooth muscle fibers, collagen and
mucopolysaccharide ground substance.
Pulmonary artery
distribution
Alveolar wall
Lung capillaries
Lung capillaries
Alveolus
Pulmonary veins
•Four in number two on each side
They commence in a capillary network upon the
walls of the air sacs, where they are continuous
with capillary ramifications of the pulmonary artery
and joining together form a single trunk for each
lobule
•On right side two in number - because middle lobe
vein joined with upper lobe vein
•On left side two in number
•These four veins perforate the fibrous layer of the
pericardium and opens separately in to upper and
back of the left atrium
•Pulmonary artery—de-oxygenated
•Pulmonary veins—only veins which carry oxygenated
blood
Functions of the pulmonary
circulation
•Respiratory and non-respiratory
•Respiratory- gas exchange
•Non-respiratory
•Blood filter
•Blood reservoir
•Metabolic
•Nutrient
Gas exchange
The pulmonary artery branches rapidly give rise to
nearly 300 million capillaries
Gas exchange between alveolar gases and blood
occur within the lung capillaries by simple diffusion.
Oxygen diffuses from the alveolus to pulmonary
capillary blood, ,Co2 diffuses in the reverse
direction, as determined by their concentration
gradient
Blood filter
•Micro vessels are so numerous, that effectively
serves as a filter to entrap the foreign materials
present in the blood
•This filter mechanism prevent entry of potentially
harmful particles in to systemic circulation
•Entrapped materials can be removed by enzymatic
process, macrophages or absorption into lymphatic
system
Reservoir of blood for left ventricle
•Pulmonary circulation is very compliant and
accommodate about 500 ml of blood in an adult
•This can serve as a reservoir for left ventricle
particularly during times when output exceeds venous
return
•The cardiac output can increase rapidly by drawing
upon pulmonary blood volume without depending on
instantaneous increase in venous return
Metabolic function of the pulmonary
circulation
•Uptake or metabolic conversion of vasoactive
substances into circulation done by endothelial
cells.
•Conversion of Angiotensin I to angiotensin II
Neurohumoral function of lung
Angiotensinogen
ANGIOTENSIN I
ANGIOTENSIN II
RENIN
CONVERTING
ENZYME
PERIPHERAL
VASOCONSTRICTION
ALDOSTERONE
SECRETION
INCREASED BLOOD PRESSURE
Pulmonary vascular resistance
•Normal pulmonary circulation is a low resistance, high
compliant vascular bed
•Calculated by using
• R=P.PA-P.LA/QT
•Normal value of R for pulmonary circulation is 0.1 mm
hg/L/min
In humans residing at high altitude, will have high PVR,
because muscular media of the small pulmonary arteries
and arterioles becomes thicker.
Pulmonary vascular pressures
•Pulmonary pressure drop along the length of
pulmonary vascular tree
•Since pulmonary capillary pressure can’t be
measured directly, they are generally estimated to
be intermediate between the mean pulmonary
arterial and pulmonary wedge pressures
•Pulmonary capillary flow recorded by using
Body plethysmograph
Nitrous oxide method
Average pul. Art. Pressure is about 10-12 mm Hg(1/8 th
of systemic circulation)
During systole 20-30 mm of Hg
diastole 5 to 10mm of Hg
Ageing associated with slight increase in pulmonary
arterial pressure
LEFT ATRIAL AND PULMONARY WEDGE
PRESSURE
•In intact, unanaesthetized humans, the mean left
atrial pressure is about 5 to 10 mm Hg.
•It is measured by advancing a cardiac catheter
through the right side of the heart and pulmonary
arterial tree until it impacts in a small precapillary
vessel
Pulmonary blood volume
•It is about 10 percent of total systemic circulation
•Measured by using indicator dilution principle
•70 kg human male contains approximately 400-500
ml
•This value is useful for
1.Determination of the mechanical behavior of lung.
2.Provides preload for the left ventricle, acts as a
reservoir
3.As a supply of Hb for alveolar-capillary gas exchange
4.As a source of water and macromolecules that
engage in alveolar-capillary exchange
5.As a potential mechanism for increasing pulmonary
capillary pressures and promoting pulmonary edema.
Pulmonary blood volume Increases in
-IV infusion
-immersing the body in water
-by inflation of an antigravity suit
-by negative pressure breathing
-systemic vasoconstriction
-lying down position
•Decreases
-when person stands
- After a large venesection
-during positive-pressure breathing
-valsalva maneuver
-systemic vasodilatation
Pulmonary
vasomotor
control
•The initial vascular tone of pulmonary
circulation is attributed to balance between
vasodilation and vasoconstriction caused by
various mediators.
•Vasodialtion caused by prostacyclins, nitric
oxide
•Constriction by endothelins..
Under normal conditions
hypoxia
Role of nerves in pulmonary
vasomotor control
•Sympathetic innervation to pulmonary circulation
includes
alpha adrenergic receptors -predominate-(eg:NE)-
constrictor
beta adrenergic receptors-(eg:isoproterenol)-
dilator
•Cholinergic activity does not appear to be implicated
Acute hypoxia
•Pressor effect of acute hypoxia on the pulmonary
circulation was given by Euler and Liljestrand
•This pressor effect redirects blood flow to better
ventilated portion
•Acute hypoxia increases pulmonary arterial
pressure, does not affect left atrial pressure, and
little increase in cardiac output
•The pressor effect starts within seconds, generally
reaches peak by 3 min, and attenuates gradually as
hypoxia continues
•Acidosis augments pressor response
•This effect Is predominantly at pre-capillary level
(i.e.: small muscular art. and arterioles)
Chronic hypoxia
•Ex. High altitude
•It causes remodeling of small pulmonary arteries and
arterioles leading to high PVR,due to muscular media
thickening.
•Acute hypercapnia
-Little response is seen if the pH is maintained
at near normal level
Acidosis causes pulmonary vasoconstriction, where
as alkalosis causes vasodilatation.
other vasoactive
substances
•Vasodilators
Ach
Bradykinin
Isoprenaline
•Vasoconstrictors
Catecholamine
Angiotensin II
Histamine
Serotonin
Effect of gravity
•In upright lung blood flow increases steadily from
top to bottom
Gravity determines highest
blood flow at lung base
0 cm
End expiration
+10
cm
-10
cm
Pa >Ppa >Ppv
(cmH2O)
Ppa >Pa >Ppv
Ppa > Ppv >Pa
Palv = 0
HEMOPTYSIS
COMMON CAUSES:
•Tuberculosis ( active or inactive)
•Bronchiectasis (including cystic fibrosis)
•Bronchogenic Carcinoma
•Mycetoma ( aspergillloma /Fungal ball)
•Lung abcess
•Mitral stenosis
•Pulmonary Contusion or trauma
Tuberculosis
MECHANISMS
•Active tubercular pneumonitis- bronchiolar erosion
•Rupture of Rasmussen’s aneurysm (pulmonary. artery)
•Healed calcified lymphnode - eroding through
bronchial arteries into airway (expectoration of
broncholith)
BRONCHIECTASIS
•Pathologically it is destruction of the cartilaginous
support of bronchial wall and bronchial dilatation
owing to parenchymal retraction from alveolar
fibrosis
ANATOMICAL CHANGES:
•Bronchial artery hypertrophy
•Expansion of peribronchial & sub mucosal
bronchiolar arteriolar plexus
•Augmentation of anastomoses with the pulmonary
arterial bed
MYCETOMA
MECHANISMS:
•Mechanical trauma of the vascular granulation
tissue by the movement of the fungal ball in the
cavity
•Vascular injury from aspergillus associated
endotoxin
•Aspergillus related proteolytic activity
•Vascular damage from a type 3 hypersensitivity
reaction
Abnormal pulmonary
vascular
communications
Systemic artery-pulmonary
vascular communications
•May be congenital or acquired
•Acquired is most common
•Haemodynamically presents as left to right shunt
between coronary,intercostal or internal
mammary and pulmonary circulation
•There will be continuous murmur over the site of
communication
•It maybe a complication of intrathoracic
neoplasm or chronic inflammatory conditions.
Systemic artery–pulmonary artery shunt
Congenital Pulmonary
Arteriovenous Malformation
(PAVM)
•AKA pulmonary a-v fistulae = pulmonary a-v aneurysm =
cavernous angiomas of the lung
•Defined as abnormal vascular communications between
pulmonary arteries and veins that lead veno-arterial shunting
There is a close association b/w PAVM and hereditary
hemorrhagic telangiectasia (osler weber rendu syndrome),an
autosomal dominant condition in 50-60% of cases and
the reverse in 5-15% cases
It has been shown that a gene located on
chr 9q3 is strongly associated with the presence of
two conditions
•Divided into simple or complex
•Simple PAVMs consist of segmental artery joining
thin-walled aneurysmal sac drained by single vein
(majority of cases)
•Complex PAVMs involves arterial supply from 2
different segmental arteries (only small percentage)
•Can have multiple lesions(20-30%),
•bilateral disease(10%)
•More than half found in lower lung fields
•Sizes vary typically 1-5 cm and can exceed 10cm
•Most commonly found in lower lobes adjacent to visceral
pleura
•Presenting features:
dyspnea and epistaxis
Cyanosis and clubbing
Extra cardiac murmur
•Treatment is by excision
ANOMALOUS SYSTEMIC
PULMONARY PERFUSION
•Usually from descending thoracic aorta, also from
ascending aorta, innominate, subclavian etc
•Asymptomatic but may present with recurrent hemoptysis
in some cases
CXR shows normal or increased vascular markings in the
vicinity of anomalous vessels
Aortograhy is diagnostic
Treatment consists of surgical ligation, embolisation or
even lung resection to control hemoptysis.
ANOMALOUS ORIGIN OF
LEFT PULMONARY ARTERY
•The left pulmonary artery arises in anomalous fashion
from right pulmonary artery
•To reach left lung, it loops around right main bronchus
like a sling and runs b/w trachea and esophagus to
enter left hilum with consequent dyspnoea and
dysphagia
ANOMALOUS PULMONARY VENOUS
DRAINAGE
As a result of persistant communication b/w
embryonic system of cardinal veins and pulmonary
venous plexus, pulmonary veins drain systemically into
ivc.
PULMONARY ARTERY
STENOSIS
•Charaterised by coarctation of pulmonary arteries with
poststenotic dilatation
BAUM and his colleagues divided the patients into two
groups
TYPE1: Main pulmonary artery affected; associated with
CVS anomalies
TYPE2: Peripheral branch involved
CXR may show poststenotic dilatation of affected
pulmonary artery branches, oligemia and signs of PAH or
cor pulmonale
Diagnosis confirmed by pulmonary angiography
ABSENT UNILATERAL
PULMONARY ARTERY
•Failure of development of either right or left side of primitive
sixth branchial arch so that no communication exists b/w
main pulmonary artery trunk and the lung on affected side,
which receives its blood supply systemically most frequently
bronchial vessels.
Usually associated with CHD
Associated with pulmonary artery hypertension
Diagnosis by CXR, VP-scan, pulmonary arteriography
Treatment usually not possible, although reconstructive
anastomotic surgery and recanalisation possible
in some.
SINGLE LEFT PULMONARY
ARTERY
ABSENCE OF MAIN PULMONARY ARTERY
The pulmonary artery trunk may be completely absent
as a result of agenesis of primitive sixth branchial arch
or of developmental failure of septum dividing truncus
arteriosus
L-R shunt exists, the lungs being supplied by
bronchial or other systemic aberrant vessels
Poor prognosis, most patients being stillborn or
dying in infancy with pulmonary hypertension.
Pulmonary hypertension
•Mean pulmonary artery pressure >25mm Hg
at rest or >30 mm Hg with exercise
•Anatomical changes
Intimal atheromas
Medial hypertrophy
Remodeling of muscular arteries
Pulmonary
thromboembolism
•The condition in which blood clot (thrombus or multiple
thrombi) migrate from the systemic circulation to
pulmonary vasculature.
•Most of the clots arise from “ deep veins” of lower &
upper extremity
•Increases right vent. overload - RHF
•Increase in intrapulm. shunting , V/Q mismatch
•Pulm. infarct in 20% of cases in patients with cardiac or
pulmonary disease