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Pulmonary circulation
The lung is the organ with the highest blood perfusion in the body as total cardiac output
is streaming through the lung. The low driving pressure difference (pressure in right
ventricle minus pressure in left atrium) reveals that Pulmonary Vascular Resistance
(PVR) is much less than total peripheral resistance (TPR) of the systemic circulation (see
the figure). At rest, PVR is 16 times less than TPR.

The intravascular pressures in pulmonary circulation (unlike systemic circulation) are very
low, and therefore, pulmonary blood flow is strongly affected by the hydrostatic (gravity)
forces as well as by perivacular pressures.
Related to perivascular pressures we can differentiate three vascular sections in
pulmonary circulation:
1. Large extra pulmonary vessels that are lying with the heart and cava veins in the
mediastinum. Pressure in medistinum equals pleural pressure (Ppl), which is normally
negative. Therefore, these vessels are pulled outwards by this negative pressure and
remain open. During inspiration the pleural pressure becomes even more negative and
the vessels get dilated which in turn supports the blood flow.
2. The arteries and veins that are bronching together with the bronchial system. These
vessels (like bronchi themselves) are surrounded by the lung tissue with its recoiling
force. The perivascular pressure of these vessels is the same as pleural pressure.
3. The alveolar capillaries that are lying within alveolar walls of neighboring alveoli are
surrounded by alveolar pressure.

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Pulmonary artery balloon catheters (Swan-Ganz ) can be used to measure
pulmonary artery pressure as well as left atrial pressure. Once the catheter
is advanced into the pulmonary artery, the pressure (pulmonary artery) can
be measured before the balloon is inflated. After the balloon is inflated there
is no blood flow and thus the pressure measured at the tip of the catheter
equals the left atrial pressure (wedge pressure). This is used clinically to
diagnose mitral stenosis or congestive heart failure.

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Pulmonary vascular resistance
The low inside pressure (pulmonary blood pressure) and the outside
perivascular pressure (= pleural pressure for most of the lung vessels)
determine the diameter of vessels and, thus PVR in the lung. As mentioned
above PVR is normally very low in comparison to TPR.

Exercise causes cardiac output and thus, lung perfusion to increase by 3 to 6

fold of their levels at rest. The pressure in pulmonary artery, however,
increases much less, maximally by factor 2. Since the driving pressure
difference increases much less than perfusion, the PVR has to be reduced.
Passive and active forces are involved in determination of the PVR.

Passive forces affecting PVR

A decrease in PVR is caused either by widening of already perfused vessels
or by opening of closed vessels (Recruitment). Both of these processes are
passive and occur as cardiac output is increasing during exercise.
Pulmonary blood pressure affects PVR: Increases in intravascular (blood)
pressure in the pulmonary arteries as well as in pulmonary veins stretch the
pulmonary vessels and leads to decreases in PVR.

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Lung volume affects PVR: Increasing lung volume elevates the recoiling
force of the lung which in turn stretches and distends extraalveolar arterial
and venous vessels. Therefore, the resistance of these vessels decreases as
lung volume increases. At the same time, lung inflation also causes
elongation and compression of capillaries within alveolar walls, so-called
alveolar vessels and their resistance increases.
The resistances of both alveolar and extraalveolar vessels are in series and
therefore additive. This leads to lowest total PVR at FRC and to an
increased PVR (decreased flow) with either lung inflation or deflation from
FRC (see figure).

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Active forces affecting PVR
Hypoxic pulmonary vasoconstriction: Hypoxia acts directly on pulmonary
vascular smooth muscle to increase PVR. The smaller pulmonary vessels
constrict when local alveolar PO2 falls. This constriction is augmented if alveolar
PCO2 rises. Hypoxic vasoconstriction is a response to a decrease of PO2 in
alveolar gas, not in the blood, causing hypoxic vasoconstriction only in those
regions that are hypoxic. This regional hypoxic vasoconstriction is beneficial for
the efficiency of gas exchange. When alveolar ventilation is decreased by an
obstructed airway or other injury, local hypoxic vasoconstriction reduces the blood
flow to this hypoxic region and the blood is directed to a region with higher
ventilation. Thus the perfusion of the hypoxic region is adjusted to match its low
ventilation and its gas exchange remains near normal.

Global hypoxia is however considered a disadvantage. Patients with generalized

alveolar hypoxia due to lung disease or low PIO2 (high altitude) may develop
pulmonary hypertension and eventually right heart failure. At high altitude, some
normal individuals develop high altitude pulmonary edema (HAPE), possibly
because of a greater hypoxic vasoconstriction response that causes pulmonary
hypertension (see figure).

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Hypoxia is believed to inhibit a K+ channel in the membrane of smooth muscle cells of
pulmonary vessels. This inhibition of K+ channel depolarizes the cell membrane and
opens the voltage gated Ca++ channels, through which Ca++ enters the cells and causes
contraction. Hypoxia also leads to the release of endothelin-1 from the endothelial cells
causing contraction of smooth muscles.
This effect of hypoxia in pulmonary circulation is opposite to what is seen in the systemic
circulation where low oxygen produces vasodilatation that is mediated through an ATP
dependent K+ channel (Hypoxia opens this channel and produces hyperpolarization of
the cells). In the systemic circulation, hypoxia also causes endothelium to release nitric
oxide (NO) which dilates the vessels.
Pulmonary vascular resistance can also be affected by a number of vaso-active
substances like histamine, serotonin, angiotensin II, prostaglandins and nitric oxide (NO).
In a healthy person, all these substances may modify PVR, but are not involved in the
process of hypoxic vasoconstriction. NO is however, clinically used in pulmonary failure
(ARDS) to reduce PVR and improve gas exchange.

Autonomic control is not important in pulmonary circulation

Although sympathetic and parasympathetic nerves are present in the lungs, the
autonomic nervous system exerts little or no control over pulmonary circulation in
humans. However, pulmonary vascular resistance is altered by vasoactive drugs; e.g.,
beta 2 agonists, used to treat asthma, cause bronchodilatation.

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In this example, alveolar ventilation and blood perfusion are heterogeneously
distributed over two lung regions. Alveolar region 1 receives high a ventilation and a
low perfusion, whereas alveolar region 2 receives a low ventilation and a high
perfusion. As a result region 1 becomes hypocapnic and hyperoxic, whereas region 2
becomes hypoxic and hypercapnic. Hypocapnia in region 1 causes bronchial smooth
muscles of this region to contract (hypocapnic bronchoconstriction), which produces a
partial diversion of ventilation from region 1 to region 2. On the other hand the
hypoxia in region 2 causes a vasoconstriction, which converts the blood flow from
region 2 to region 1. These two mechanisms jointly reduce the extent of the
ventilation/perfusion mismatch and improve the effectiveness of the gas exchange
between the alveolar gas and pulmonary blood.

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Distribution of blood flow in the lung.
The gravity force causes blood pressure to be lower at the top than at the
lower areas of lungs (see figure). In an upright body position some lung
regions close to the peak may have capillary blood pressures lower than
alveolar pressure (PA). These capillaries will be compressed by PA and will
not be perfused with blood (zone I). On the other hand capillaries at the base
of the lung, where both pulmonary artery pressure and pulmonary venous
pressure are higher than PA, will be permanently perfused (zone 3). In the
middle zone (zone II), where PA is lower than arterial but higher than venous
pressure, the capillary will be slightly compressed at a point towards end of
the capillary, and remains perfused at a lower range. Therefore, the perfusion
of the lung is unequally distributed particularly in the upright position. The
perfusion increases from the peak to the base of the lung. This regional
unequal distribution of blood flow affects the efficiency of the pulmonary gas
exchange (more later).The increase in pulmonary artery pressure during
exercise minimizes zone I and reduces the inequality of distribution.

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Normal Anatomical Shunts
Bronchial circulation: Bronchial artery blood is oxygenated blood that
supplies the supporting tissues of the lungs, including the connective tissue,
septa, and large and small bronchi. The bronchial venous blood
(deoxygenated blood) drains into the pulmonary veins and enters the left
atrium, producing a shunt of deoxygenated into oxygenated blood.
Coronary circulation: Coronary venous blood (deoxygenated blood)
partially enters the left atrium and left ventricle via Thebesian veins (venae
cordis minimae) and is the second normal source of venous admixture or
shunt. These shunts are only about 1 to 2 per cent of the total cardiac output
and contribute about equally with VA/Q mismatch for the normal alveolar-
arterial PO2 difference of 3-10 mm Hg. The human fetus has additional
normal shunts; i.e., the foramen ovale and the ductus arteriosis.

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Abnormal anatomical shunts:
Congenital or pathological conditions, such as pulmonary arteriovenous
fistulas produce shunts in which venous blood is added to arterial blood (right
to left, or R → L shunts).

Intracardiac defects may produce R → L or L → R shunts depending on the

pressures of the two connected chambers. A right to left shunt is harmful by
adding deoxygenated blood to arterialized blood and lowering the oxygen of
blood going to tissues. A left to right shunt is harmful by increasing
pulmonary artery pressure and possibly causing hypoxemia by increasing
perfusion and lowering V/Q ratios in the lung. Left to right shunt is detected
by a finding of abnormally high oxygen saturation in the right atrium or

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Fluid Exchange in Pulmonary Capillaries
The Starling forces you learned about for systemic capillaries are qualitatively the same in the pulmonary circulation, but two additional forces are important in the
lungs: alveolar pressure and surface tension. Pulmonary edema (excess fluid in the interstitial space or alveoli) can result from increased capillary permeability or
from increased hydrostatic pressure or decreased colloid osmotic pressure in the capillary. Increased surface tension in the alveoli (surfactant deficiency) would
also cause edema.

Pulmonary Edema has multiple Causes

1) Increased hydrostatic pressure. Mitral stenosis and congestive heart failure result in increased left atrial and pulmonary capillary hydrostatic pressure. The
lymphatic system of the lung has a high capacity to remove excess filtered fluid (“lymphatic reserve”), so that edema start to form after left atrial pressure is
elevated to above 20 mm Hg. This type of edema is called “cardiogenic edema”.

2) Increased permeability. Damage to capillary and alveolar endothelium allows plasma proteins to leak into the interstitial space and alveoli. Water then
moves into the interstitial space and alveoli by osmosis. Inflammation and heroin overdose are two examples of factors causing this type of edema. This type of
edema is called “non-cardiogenic edema”.

3) High surface tension. If surfactant is reduced, surface tension will increase leading to fluid movement into the interstitial space and alveoli. Acute respiratory
distress syndrome (ARDS) is associated with both an increase capillary permeability and decreased surfactant. Both factors result in pulmonary edema.

4) Decreased plasma protein. Decreased colloid osmotic pressure can also result in pulmonary (as well as systemic; e.g., ascites) edema. (Examples:
starvation, liver disease, hemodilution ).

5) Impaired lymphatic drainage or increased central venous pressure. In the lung, if the lymphatic vessels are blocked or lymph drainage flow back to the
central veins is impeded by high central venous pressure, edema will result (examples; cancer, heart failure).

6) High altitude pulmonary edema. Global hypoxia as observed by pulmonary diseases like COPD or at high altitude leads to pulmonary hypertension. In
COPD, hypertension often leads to right heart failure (Cor Pulmonale). A small percentage of normal subjects at high altitude develop pulmonary edema (HAPE)
but the mechanism is not clear. Lung fluid collected from HAPE patients has elevated protein levels indicating a non-cardiogenic cause (inflammatory response).

7) Drowning. Freshwater and saltwater drowning both fills the lungs with water (unless the victim has a laryngospasm). Freshwater rapidly enters the pulmonary
circulation and causes hemodilution that results in a decreased plasma osmolarity. The red blood cells rupture and release potassium, which in turn leads to death
by ventricular fibrillation and asphyxiation. Salt water is hypertonic and leads to water loss from blood into lungs. Death is occurring by asphyxiation.

Pleural Effusion
Pleural effusion is edema of the pleural space. At FRC, pressure in pleural space is negative (about – 4 mm Hg), due to tendency of lungs to collapse and chest
wall to spring out. However, pleural space between visceral and parietal pleura is filled with a tiny layer of fluid. The amount of the fluid is regulated by capillaries
located on surfaces of both visceral- and parietal pleura. Fluid accumulation in this space is called Pleural effusion. X-ray shows blunting of the costophrenic
angle (where ribs meet diaphragm) by pleural effusion. The base of the lung is always more susceptible to edema because of the higher hydrostatic pressure at
the base.

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