The
Pulmonary, Skeletal Muscle And Fetal Circulations
As described in Chapter 1, the pulmonary circulation receives the
entire output of the right ventricle. Its high-density capillary network
surrounds the lung alveoli, allowing the O2-poor blood from the
pulmonary arteries to exchange CO2 for O2. The pulmonary
veins return highly oxygenated blood to the left atrium. The pulmonary
circulation contains about 800 mL of blood in recumbent subjects, falling to
about 450 mL during quiet standing.
Mean pulmonary arterial pressure is ∼15 mmHg, and left atrial pressure
is ∼5
mmHg. The right ventricle is able to drive its entire output through the pulmonary circulation utilizing a pressure head
of only 10 mmHg because the resistance of the pulmonary circulation is only 10
- 15% that of the systemic circulation. This arises because the vessels of the
pulmonary microcirculation are short and of relatively wide bore, with little
resting tone. They are also very numerous,
so that their total cross-section is similar to that of the systemic
circulation. The walls of both arteries and veins are thin and distensible, and
contain comparatively little smooth muscle.
The low pressure within the pulmonary circulation means that regional
perfusion of the lungs in the upright position is greatly affected by gravity
(Figure 26a). The extravascular pressure throughout the lungs is similar to the
alveolar pressure (∼0 mmHg). However, the intravascular pressure is low in
the lung apices, which are above the
heart, and high in the lung bases, which are below the heart. Pulmonary vessels
in the lung apices therefore collapse during diastole, causing intermittent
flow. Conversely, vessels in the bases of the lungs are perfused throughout the
cardiac cycle, and are distended. A small increase in pulmonary arterial
pressure during exercise is sufficient to open up apical capillaries, allowing more O2 uptake by the blood.
The low hydrostatic pressure in pulmonary capillaries (mean of 7–10 mmHg)
does not lead to net fluid resorption, because it is balanced by a low
extravascular hydrostatic pressure and an unusually high interstitial plasma
protein oncotic pressure (∼18 mmHg). The lung capillaries
therefore produce a small net flow of lymph, which is drained by an extensive pulmonary lymphatic network.
During left ventricular failure or mitral stenosis, however, the increased left
atrial pressure backs up into the pulmonary circulation, increasing fluid
filtration and leading to pulmonary oedema. Neither the sympathetic
nervous system nor myogenic/metabolic autoregulation have much of a role in
regulating pulmonary vascular resistance or flow. However, the pulmonary
vasculature is well supplied with sympathetic nerves. When stimulated, these
decrease the compliance of the vessels, limiting the pulmonary blood volume so that more blood is available to the
systemic circulation.
The most important mechanism regulating pulmonary vascular tone is hypoxic
pulmonary vasoconstriction (HPV), a process by which pulmonary vessels constrict
in response to alveolar hypoxia. This unique mechanism (systemic
vessels typically dilate to hypoxia) diverts blood away from poorly
ventilated regions of the lungs, thereby maximizing the ventilation –
perfusion ratio. HPV is probably caused mainly by hypoxia-induced release
of Ca2+ from the sarcoplasmic reticulum within the smooth muscle cells of the
pulmonary vasculature.
The skeletal muscles comprise about 50% of body weight, and at rest
receive 15–20% of cardiac output. At rest, skeletal muscle arterioles have a
high basal tone as a result of tonic sympathetic vasoconstriction. At any one
time, most muscle capillaries are not perfused, due to intermittent constriction
of precapillary sphincters (vasomotion).
Because the muscles form such a large tissue mass, their arterioles make
a major contribution to total peripheral resistance (TPR). Sympathetically
mediated alterations in their arteriolar tone therefore have a crucial role in
regulating TPR and blood pressure during operation of the baroreceptor reflex.
The muscles thus serve as a ‘pressure valve’ that can be closed to
increase blood pressure and opened
to lower it.
With rhythmic exercise, compression of blood vessels during the
contraction phase causes the blood flow to become intermittent. However,
increased muscle metabolism causes the generation of vasodilating factors;
these factors cause an enormous increase in blood flow during the relaxation
phase, especially to the white or phasic fibres involved in movement. With
maximal exercise, the skeletal muscles receive 80–90% of cardiac output.
Vasodilating factors include K+ ions, CO2
and hyperosmolarity. In working muscle their effects completely override
sympathetic vasoconstriction, while arterioles in non-working muscle remain
sympathetically constricted so that their blood flow does not increase.
Sustained compression of blood vessels during static (isometric)
muscle contractions causes an occlusion of flow that rapidly results in muscle
fatigue.
A diagram of the fetal circulation is shown in Figure 26b. The fetus
receives O2 and nutrients from, and discharges CO2 and
metabolic waste products into, the maternal circulation. This exchange occurs in the placenta, a thick spongy
pancake-shaped structure lying between
the fetus and the uterine wall. The placenta is composed of a space containing
maternal blood, which is packed with fetal villi, branching tree-like
structures containing fetal arteries, capillaries and veins. They receive the
fetal blood from branches of the two umbilical arteries, and drain back
into the fetus via the umbilical vein. Gas and nutrient exchange occurs
between the fetal capillaries in the villi and the maternal blood surrounding
and bathing the villi. The fetal circulation differs from that of adults in
that the right and left ventricles pump the blood in parallel rather than in
series. This arrangement allows the heart and head to receive more highly
oxygenated blood, and is made possible by three structural shunts unique
to the fetus: the ductus venosus, the foramen ovale and the ductus arteriosus (highlighted in
Figure 26b).
Blood leaving the placenta (1) via the umbilical vein is 80%
saturated with O2. About half of this flows into the fetal liver.
The rest is diverted into the inferior vena cava via the ductus venosus (2),
mixing with poorly oxygenated venous blood returning from the fetus’ lower
body. When the resulting relatively oxygen-rich mixture (about 67% saturated)
enters the right atrium, most of it does not pass into the right ventricle as
it would in the adult, but is directed into the left atrium via the foramen
ovale, an opening between the fetal atria (3). Blood then flows into
the left ventricle, and is pumped into the ascending aorta, from which it
perfuses the head, the coronary circulation and the arms (4). Venous
blood from these areas re-enters the heart via the superior vena cava. This
blood, now about 35% saturated with O2, mixes with the fraction of
blood from the inferior vena cava not entering the foramen ovale (5),
and flows into the right ventricle, which pumps it into the pulmonary artery.
Instead of then entering the lungs, as it would in the adult, about 90% of the
blood leaving the right ventricle is diverted into the descending aorta through
the ductus arteriosus (6). This occurs because pressure in the
pulmonary circulation is higher than that in the systemic circulation, as a
result of pulmonary vasoconstriction and the collapsed state of the lungs.
About 60% of blood entering the descending aorta then flows back to the
placenta for oxygenation (7). The rest, now 58% saturated with O2,
supplies the fetus’ trunk and legs (8).
Circulatory Changes At Birth
Two events at birth quickly cause the fetal circulation to assume a
quasi-adult pattern. First, the pulmonary vascular pressure falls well below
the systemic pressure because of the initiation of breath- ing and the
resulting pulmonary vasodilatation. Together with constriction of the ductus
arteriosus caused by increased blood O2 levels, this reversal of the
pulmonary – systemic pressure gradient, which is aided by the loss of the low-resistance
placental circulation, abolishes the blood flow from the pulmonary artery into
the aorta within 30 min after delivery.
Second, tying off the umbilical cord stops venous return from the
placenta, abruptly lowering inferior vena caval pressure. Together with the
fall in pulmonary resistance, this lowers right atrial pressure, causing within
hours functional closure of the foramen ovale. The ductus venosus also closes
with the abolition of venous return from the placenta.
Although these fetal circulatory shunts are functionally closed
soon after birth, complete structural closure only occurs after several
months. In 20% of adults, the structural closure of the foramen ovale remains
incomplete, although this is of no haemodynamic consequence.
