Pulmonary Circulation And Anatomical Right-To-Left
Shunts.
Pulmonary circulation compared with the systemic circulation (Fig.
13a)
The pulmonary circulation is in series with the systemic
circulation, and pulmonary blood flow nearly equals aortic blood flow. Pulmonary
vascular resistance is only about one-sixth of systemic resistance, and the
thin-walled right ventricle needs only to generate a mean pulmonary artery
pressure of about 15 mmHg to drive the cardiac output through the lungs.
Systemic pressures are higher (Fig. 13a), dropping steeply across the main
resistance vessel, the arteriole, to give a capillary flow which is usually
non-pulsatile. Pulmonary vascular resistance is more evenly distributed in the
microcirculation and pulmonary capillary flow remains pulsatile.
Local systemic resistance and blood flow are controlled by sympathetic
nerves, metabolites and other substances acting on arterioles. Both sympathetic
and parasympathetic nerves innervate pulmonary vessels, but their influence is weak in most circumstances.
Systemic arterioles dilate in response to hypoxia, increasing flow and hence
oxygen delivery to hypoxic tissues. In contrast, hypoxic pulmonary vasoconstriction
occurs in the pulmonary circulation. This response, which is accentuated by
high Pco2, improves gas exchange by diverting blood from
underventilated to well-ventilated regions (Chapter 14). The response is
unhelpful in the presence of global lung hypoxia, at altitude or in respiratory
failure, where it may contribute to the development of pulmonary hypertension
and right-sided heart failure.
Systemic vascular beds (especially the renal and cerebral) respond to
changes in perfusion pressure by constricting or dilating to hold blood flow
fairly constant. This autoregulation does not occur in the pulmonary
circulation. As cardiac output increases in exercise, pulmonary vascular
resistance falls, as vessels are recruited and distended and the rise in
pulmonary arterial pressure is small. The pulmonary circulation acts as a blood
reservoir and the volume it contains varies, being about 450 mL when upright
and 800 mL when lying down. Inspiration also increases pulmonary vascular
volume.
Fluid balance across capillaries is determined by hydrostatic and oncotic
pressures (the Starling forces; see The Cardiovascular System at a
Glance) across capillary walls. Capillary oncotic pressure opposes
filtration and is about 27
mmHg in both circulations. Although hydrostatic pressure is low in the
pulmonary capillaries ( 10 mmHg), net filtratio of fluid occurs in pulmonary
capillaries as it does in systemic capillaries. Other factors favouring filtration
are interstitial oncotic pressure, which is relatively high in the lungs
(about 18 mmHg) and interstitial hydrostatic pressure, which is negative
(about 4 mmHg). Pulmonary oedema occurs when these forces are altered to
increase net filtration above the rate that can be cleared by the pulmonary lymphatics.
For example, it may occur when pulmonary capillary pressure is increased in mitral
stenosis and left ventricular failure. Inspiratory crepitations (crackles)
on auscultation in these conditions are probably caused by popping open of
airways in lungs stiffened by congestion with blood. They are most obvious at
the bases, where hydrostatic pressure is highest. Pulmonary congestion and
oedema (and hence breathlessness in these conditions) are worsened by the
increase in pulmonary blood volume lying down.
Anatomical or true right-to-left shunts Ideally, all venous blood
emerging from tissues would return to the right side of the heart to be pumped
through the gas-exchanging lung. In fact, part of the blood draining the bronchial
circulation joins the pulmonary vein. This part results in deoxygenated
blood from the airways contaminating blood returning from alveoli (Fig. 13a).
In addition, a small amount of the coronary venous blood drains directly into
the left ventricular cavity via the venae cordis minimae (Thebesian veins).
These additions of deoxygenated (right-sided) blood to oxygenated (left-sided)
blood are known as anatomical right-to-left shunts. In healthy people,
they are equivalent to 2% or less of the cardiac output, but they explain why
arterial Po2 is less than alveolar Po2 even
though pulmonary capillary blood equilibrates with alveolar gas.
In disease, right-to-left shunting of blood may be much larger. Atelectasis
(airless lung) or consolidation in pneumonia will result in
pulmonary arterial blood supplying the affected region failing to undergo gas
exchange. Right-to-left shunts are also the cause of reduced arterial
oxygenation in cyanotic congenital heart disease such as tetralogy of
Fallot. Atrial or ventricular septal defects do not usually cause impaired
gas exchange and cyanosis, as the higher left-sided pressures give rise to left-to-right
shunts in which some oxygenated blood is pumped again through the lungs. If
a large left-to-right shunt remains untreated, eventually the excessive
pulmonary blood flow leads to pulmonary hypertension. As right ventricular
pressure increases, the shunt through the atrial or ventricular septal defect
may then reverse to give a right-to-left shunt and cyanosis (Eisenmenger's
syndrome).
Effect of right-to-left shunts on arterial blood gases
In the right-to-left shunt, shown schematically in Fig. 13b, 20% of blood
fails to pass through functioning alveoli and its O2 and CO2
contents remain at mixed venous levels of 150 and 520 mL/L, respectively.
Eighty per cent of the blood undergoes normal gas exchange, emerging with
normal O2 and CO2 contents of 200 and 480 mL/L,
respectively. The initial effect on arterial gas contents is calculated from a
weighted average of the contents in these two bloodstreams. This gives an
arterial O2 content 10 mL/L below normal and CO2 content
8 mL/L above normal. From the f at part of the oxygen dissociation curve, it
can be seen that the resulting arterial Po2 is about 9 kPa
(68 mmHg) compared with the normal 13 kPa (97 mmHg). The much steeper CO2
dissociation curve means the rise in Pco2 is small, from the
normal value of 5.3 kPa (40 mmHg) to about 5.5 kPa (41 mmHg).
If the respiratory system is otherwise normal, the reduced Pao2
and increased Paco2 simulate ventilation via the
chemoreceptors and the CO2 washed-out of the functioning areas
restores arterial CO2 content and Paco2
to normal. In contrast, increased ventilation has little effect on arterial
oxygen content and Po2, as blood draining the ventilated
areas of the lung was already saturated. If hypoxia is severe, the stimulation
in ventilation is often great enough to reduce Paco2
below normal. Typically, in a right-to-left shunt, there is a low Pao2
with a normal or low Paco2.
