C h a p t e r 1 8
Disorders of Blood Flow and Blood Pressure
437
Etiology.
Prolonged standing and increased intra-
abdominal pressure are important contributing fac-
tors in the development of primary varicose veins.
71–75
Because there are no valves in the inferior vena cava
or common iliac veins, blood in the abdominal veins
must be supported by the valves located in the exter-
nal iliac or femoral veins. When intra-abdominal pres-
sure increases, as it does during pregnancy, or when
the valves in these two veins are absent or defective,
the stress on the saphenofemoral junction is increased.
The high incidence of varicose veins in women who
have been pregnant also suggests a hormonal effect
on venous smooth muscle contributing to venous dila-
tion and valvular incompetence. Lifting also increases
intra-abdominal pressure and decreases flow of blood
through the abdominal veins. Occupations that require
repeated heavy lifting predispose to development of
varicose veins.
Prolonged exposure to increased pressure causes the
venous valves to become incompetent so they no longer
close properly. When this happens, the reflux of blood
causes further venous enlargement, pulling the valve
leaflet apart and causing more valvular incompetence
in sections of adjacent distal veins. Another consider-
ation in the development of varicose veins is the fact
that the superficial veins have only subcutaneous fat and
superficial fascia for support, whereas the deep venous
channels are supported by muscle, bone, and connec-
tive tissue. Obesity reduces the support provided by
the superficial fascia and tissues, increasing the risk for
development of varicose veins.
Clinical Manifestations.
The signs and symptoms
associated with primary varicose veins vary. Most
women with superficial varicose veins complain of
their unsightly appearance. In many cases, aching in
the lower extremities and edema, especially after long
periods of standing, may occur. The edema usually sub-
sides at night when the legs are elevated. When the com-
municating veins are incompetent, symptoms are more
common.
Iliofemoral vein
Great saphenous
vein
Incompetency of
great saphenous
vein
Intact communicating
veins
Incompetency of
communicating
veins
Small saphenous
vein
Incompetency of
small saphenous
vein
A
B
FIGURE 18-17.
Superficial and deep venous channels of the leg.
(A)
Normal venous structures and
flow patterns.
(B)
Varicosities in the superficial venous system are the result of incompetent valves
in the communicating veins.The arrows in both views indicate the direction of blood flow. (Modified
from Abramson DI. Vascular Disorders of the Extremities, 2nd ed. NewYork, NY: Harper & Row; 1974.)
To heart
To heart
Vein
Valve
closed
Contracted
skeletal
muscles
Valve
open
Relaxed
skeletal
muscles
FIGURE 18-18.
The skeletal muscle pumps and their function
in promoting blood flow in the deep and superficial calf vessels
of the leg.
