CHAPTER 8 • EXCHANGE FUNCTION OF THE MICROCIRCULATION
189
hydrostatic
pressure,
tissue
(interstitial)
hydrostatic
pressure,
capillary
(plasma)
oncotic
pressure,
and
tissue
(interstitial)
oncotic pressure (Fig. 8.7). These physical
forces are sometimes referred to as Starling
forces in honor of Ernest Starling who pro-
posed in 1896 that these forces govern cap-
illary fluid exchange.
The net hydrostatic
pressure driving fluid out of the capillary
(filtration) is the hydrostatic pressure inside
the capillary minus the interstitial hydrostatic
pressure (Pc - P.). The net oncotic pressure
drawing fluid into the capillary (reabsorption)
is the capillary plasma oncotic pressure minus
the interstitial oncotic pressure (nc - n.).
CAPILLARY HYDROSTATIC PRESSURE
Capillary hydrostatic pressure
(PC)
drives
fluid out of the capillary, and it is highest at
the arteriolar end of the capillary and lowest
at the venular end. Depending on the organ,
the pressure may drop along the length of the
capillary (axial or longitudinal pressure gradi-
ent) by 15 to 30 mm Hg owing to capillary
resistance. Because of this pressure gradient
along the capillary length, filtration is favored
NDF = (Pc- P ) -a(Tlc-ni)
Filtration:
NDF > 0
Reabsorption:
NDF < 0
■ FIGURE 8.7 Net driving force for fluid move-
ment across capillaries. Hydrostatic and oncotic
pressures w ithin the capillary (Pc, pc) and the tis-
sue interstitium
(P, p)
determ ine the net driving
force
(NDF)
for fluid movement out of the capil-
lary (filtration) or into the capillary (reabsorption).
The hydrostatic pressure difference favors filtra-
tion
(redarrow )
because Pc is greater than Pi. The
oncotic pressure difference favors reabsorption
(black arrow)
because nc is greater than ni. The
oncotic pressure difference is m ultiplied by the
reflection coefficient (a), a factor that represents
the perm eability of the capillary to the proteins
responsible for generating the oncotic pressure.
at the arteriolar end of the capillary where
capillary hydrostatic pressure is greatest.
The average capillary hydrostatic pressure
is determined by arterial and venous pres-
sures (PA
and PV), and by the ratio of post-to-
precapillary resistances (RV
/RA). An increase
in either arterial or venous pressure increases
capillary pressure; however, the effects of ele-
vations in venous pressure are m uch greater
than
those
of an
equivalent elevation in
arterial pressure. The reason for this is that
postcapillary resistance is m uch lower than
precapillary resistance. In most organs, the
postcapillary resistance is only 10% to 20%
of the precapillary resistance; therefore, RV
/ RA
ranges from 0.1 to 0.2. If we assume that
RV/ Ra = 0.2, the following relationship (Equa-
tion 8-3) can be derived:
0.2 Pa + Pv
1.2
The above equation assumes that PC
repre-
sents a point between two series resistances—
an arterial or precapillary resistance (RA) and
a venous or postcapillary resistance (RV). It
also assumes that the flow that enters the cap-
illary and exits the capillary is the same (i.e.,
there is conservation of flow). Therefore, on
the precapillary side, flow into the capillary
can be expressed as: F
= (PA
- Pc)/RA. On the
postcapillary, the flow out of the capillary can
be expressed as: Fout = (Pc - PV)/R V Assum-
ing that F
equals F
, solving for P results in
Equation 8-3.
Equation 8-3 shows that increasing venous
pressure by 20 mm Hg increases mean capil-
lary pressure by 16.7 mm Hg when RV
/ RA
=
0.2. In contrast, increasing arterial pressure
by 20 mm Hg increases mean capillary pres-
sure by only 3.3 mm Hg. The reason for this
difference is that the high precapillary resist-
ance blunts the
effects
of increased arte-
rial pressure on the downstream capillaries.
Therefore,
mean capillary
hydrostatic pres-
sure is more strongly influenced by changes in
venous pressure than by changes in arterial pres-
sure
.
This has significant clinical implication.
Conditions
that
increase
venous
pressure
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