Page 224 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Pulmonary Hypertension
The mean pulmonary artery pressure moved more distally, thus increasing the vas-
(P ¯ PA ≈ 15 mmHg = 2 kPa) is determined by three cular cross-sectional area. Pressure may also
variables, namely pulmonary vascular resis- be reduced by thrombolysis or possibly by di-
tance (PVR), cardiac output, and left atrial minished vasoconstriction. Embolism may re-
pressure (P LA = ca. 5 mmHg = 0.7 kPa). sult in pulmonary infarction, especially when
According to Ohm’s law ∆P = PVR · CO. medium-sized vessels are obstructed and at
the same time the blood supply to the bron-
As ∆P = P ¯ PA – P LA , chial arteries is reduced (e.g., in pulmonary ve-
P ¯ = PVR · CO + P LA . nous congestion or systemic hypotension).
PA
However, massive pulmonary embolism may
Pulmonary hypertension (PHT) develops when also lead to acute right heart failure (→ A, bot-
tom right), so that flow into the left ventricle
one (or several) of the above variables is raised
Heart and Circulation exercise it is above 32 mmHg (see pulmonary a decrease in systemic blood pressure and to
so much that at rest P ¯
PA is over 20 mmHg; on
and thus its output falls. This in turn leads to
circulatory
shock
consequences
edema, p. 80). In principle, PHT can have three
and
its
causes (→ A):
(→ p. 230).
! PVR rise, so-called obstructive PHT, caused,
Among the causes of chronic PHT are:
for example, by pulmonary embolism or em-
a Lung disease (asthma, emphysema, chronic
bronchitis or fibrosis, together accounting
of the resulting hypoxemia and its conse-
for > 90% of chronic cor pulmonale cases);
quences (pulmonary hypoxic vasoconstriction,
7 physema. PVR may further increase because b Chronic thromboembolism and systemic
increased hematocrit). vascular disease;
! P LA rise, so-called passive PHT, for example, c Extrapulmonary causes of abnormal pul-
in mitral stenosis (→ A, upper right and p.194). monary function (thoracic deformity, neu-
! Cardiac output increase, except in left-to- romuscular disease, etc.);
right shunt (→ p. 204). A rise in cardiac output d Removal of lung tissue (tuberculosis, tu-
alone will lead to (hyperkinetic) PHT only in ex- mors);
treme cases, because the pulmonary vascula- e Chronic altitude hypoxia with hypoxic con-
ture is very distensible and additional blood striction that can also, to an extent, be in-
vessels can be recruited. A rise in cardiac out- volved in causes a–c;
put (fever, hyperthyroidism, physical exertion) f Idiopathic primary PHT of unknown etiol-
can, however, aggravate an existing PHT due to ogy.
other reasons. Causes b and e lead to precapillary PHT; cause a
Acute PHT almost always results from a re- usually to capillary PHT. In all these disorders
duction in the cross-sectional area of the vas- the resistance in the pulmonary circulation is
cular bed (of at least 50%, because of the high chronically elevated, due to either exclusion
vascular distensibility), as by pulmonary em- of large segments of the lung, or generalized
bolism, i.e., migration of thrombi or (rarely) vascular obstruction. The consequence of
other emboli from their site of origin into the chronic PHT is right ventricular hypertrophy
pulmonary arteries (→ A, top and p. 240). If (chronic cor pulmonale; → A, bottom left) and
embolism arises, it is likely that additional ultimately right ventricular failure (→ A, bot-
(hypoxic?) vasoconstriction will develop, tom right). In contrast to a–f, the cause of pas-
which will then reduce the vascular cross-sec- sive PHT is primarily not in the lung but in the
tional area even more. Sudden vascular ob- left heart (postcapillary PHT). Thus, almost all
struction causes acute cor pulmonale (acute patients with mitral valve disease (→ p.196ff.)
right heart load). In acute PHT the right or left heart failure (→ p. 224ff.) develop PHT.
ventricular systolic pressure can rise to over
60 mmHg (8 kPa), but may become normal
214 again within 30–60 minutes in certain cir-
cumstances, for example, if the thrombus has
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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