CHAPTER 8 ■
EXCHANGE FUNCTION OF THE MICROCIRCULATION
193
PROBLEM 8-2
Given that Pc = 22 mm Hg, Pi = -3 mm
Hg, tic = 26 mm Hg, jt, = 6 mm Hg, and
a
= 0.9, answer the following questions:
a) What is the net driving force for
transcapillary fluid exchange?
b) Is filtration or reabsorption occurring?
c) If the product of KF
and A is doubled,
what will happen to the net rate of
fluid movement across the capillary,
assuming that the net driving force
does not change?
EDEMA FORMATION
When the fluid volume within the intersti-
tial compartment increases because filtration
exceeds the rate of capillary reabsorption plus
lymphatic flow, the interstitial compartment
increases in volume, leading to tissue swelling
(i.e., edema). As already discussed, the change
in interstitial pressure that results from an
increase in interstitial volume depends on the
compliance of the interstitial compartment.
Edema can damage organs and, in some
cases, cause death.
For example, cerebral
edema following brain trauma can lead to cel-
lular death because the increased interstitial
pressure damages neurons and causes tissue
ischemia by compressing blood vessels. Even
in tissues that are relatively compliant, such as
skin and skeletal muscle, severe edema can lead
to tissue necrosis. Pulmonary edema can be life
threatening because gas exchange is impaired.
Table 8-1 lists some of the many causes of
edema. Every cause of edema can be related to
one or more of the following:
Increased capillary hydrostatic pressure
Increased capillary permeability
Decreased plasma oncotic pressure
Lymphatic obstruction
The most common cause of edema is elevated
capillary pressure, such as occurs during heart
failure or venous obstruction. Both conditions
increase venous pressure, which is transmit-
ted hack to the capillaries, causing an increase
in fluid filtration. Localized edema in tissues is
commonly caused by injury or inflammation
TABLE 8-1
CAUSES OF EDEMA
Increased Capillary Pressure
Increased venous pressure
- Heart failure
- Increased blood volume
- Venous obstruction (thrombosis or
compression)
- Incompetent venous valves
- Gravity
Increased arterial pressure
- Hypertension
Decreased arterial resistance
- Vasodilation (physiologic or
pharmacologic)
Increased Capillary Permeability
Vascular damage (e.g., burns, trauma)
Inflammation
Decreased Plasma Oncotic Pressure
Reduced plasma proteins
(e.g., malnutrition, burns, liver dysfunction)
Lymphatic Blockage (Lymphedema)
Tissue injury
Inflammation of lymphatics
Lymphatic invasion by parasites
(e.g., filariasis)
(e.g., sprained ankle, bee sting), which causes
the release of local paracrine substances (e.g.,
histamine, bradykinin, and leukotrienes) that
increase capillary and venular permeability.
Some of these substances (e.g., histamine)
also increase capillary pressure by dilating
arterioles and constricting venules.
The treatment for edema involves modify-
ing one or more of the physical factors that
regulates fluid movement. For example, in
pulmonary or systemic edema secondary to
heart failure, diuretics are given to the patient
to reduce blood volume and venous pressure,
thereby reducing capillary hydrostatic pres-
sure. A patient suffering from ankle edema
following an injury will be instructed to keep
that foot elevated whenever possible to dimin-
ish the effects of gravity on capillary pressure
and to use a tight-fitting elastic stocking or
bandage around the ankle to increase tissue
hydrostatic pressure (which opposes filtra-
tion). Drugs (e.g., corticosteroids, antihis-
tamines) are sometimes used to block the
release or action of paracrine substances that
increase
capillary
permeability
following
tissue injury or inflammation.
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