210
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
are
synthesized.
The
reduced
hematocrit
decreases the oxygen-carrying capacity of the
blood. Eventually, dilution of plasma proteins
decreases plasma oncotic pressure sufficiently
to limit the amount of fluid reabsorption.
Most
of
the
compensatory
responses
described above occur regardless of the cause
of hypotension; however, the ability of the
heart and vasculature to respond to a specific
compensatory mechanism may differ depend-
ing upon the cause of the hypotension. For
example, if hypotension is caused by cardio-
genic shock (a form of acute heart failure) sec-
ondary to a myocardial infarction, the heart
will not be able to respond to sympathetic
stimulation in the same manner as would a
normal heart. As another example, vascu-
lar responsiveness to sympathetic-mediated
vasoconstriction is significantly impaired in a
person in septic shock. Finally, drugs that a
person is taking for hypertension (e.g., beta-
blockers, alpha-blockers, ACE inhibitors) can
interfere with neurohumoral compensatory
responses to hypotension.
CASE 9-2
A patient who is being aggressively
treated for severe hypertension with
a diuretic, an angiotensin-converting
enzyme (ACE) inhibitor, and a
calcium channel blocker is in a serious
automobile accident that causes
significant intra-abdominal bleeding.
How might these drugs affect the
compensatory mechanisms that are
activated following hemorrhage? How
might this alter the course of this
patient’s recovery?
Decompensatory Mechanisms
Following Severe and Prolonged
Hypotension
Severe, prolonged hypotension can lead to
irreversible shock and death. This occurs
when normal compensatory mechanisms (and
additional medical resuscitation) are unable
to restore arterial pressure to adequate levels
in a timely manner. For example, if 40% of a
person’s blood volume is lost by hemorrhage,
arterial pressure may begin to recover as com-
pensatory mechanisms are activated; how-
ever, the recovery may last only an hour or
two before arterial pressure once again falls,
causing death despite heroic interventions.
This secondary fall in arterial pressure
results from the activation of decompensatory
mechanisms. These decompensatory mecha-
nisms are positive feedback cycles, in con-
trast to the negative feedback control offered
by compensatory mechanisms. A negative
feedback mechanism attempts to restore a
controlled variable (in this case arterial pres-
sure) to its normal value, whereas a positive
feedback mechanism causes the controlled
variable to move even farther away from its
control point.
In the case of severe hemorrhagic shock
and some other forms of hypotensive shock
(e.g., cardiogenic and septic shock), several
potential positive feedback mechanisms can
lead to irreversible shock and death. These
mechanisms include cardiac depression, sym-
pathetic escape, metabolic acidosis, cerebral
ischemia, rheological factors, and systemic
inflammatory responses.
Figure 9.7 illustrates how cardiac depres-
sion and sympathetic escape can lead to
decompensation in severe hemorrhage.
If
mean arterial pressure falls below 60 mm Hg,
coronary blood flow is insufficient to sup-
port the metabolic demands of the heart
because this pressure is below the coro-
nary autoregulatory range (see Chapter 7).
Reduced coronary blood flow causes myocar-
dial hypoxia, which impairs cardiac contrac-
tions (reduces inotropy). When this occurs,
stroke volume and cardiac output decrease,
causing additional decreases in arterial pres-
sure and coronary perfusion—a positive feed-
back cycle. Also shown in Figure 9.7 is the
effect of hypotension on organ blood flow.
Hypotension decreases organ blood flow by
decreasing perfusion pressure and through
baroreceptor-mediated
sympathetic
activa-
tion that constricts resistance vessels. This
reduced flow causes tissue hypoxia. The more
hypoxic a tissue becomes and the longer it
remains hypoxic (especially under low flow
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