CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
211
Severe
Hemorrhage
!
i Inotropy
i Cardiac
Output
i Organ
Blood Flow
V
Blood Flow
i
Arterial
Pressure
Tissue
Hypoxia
i Coronary
Perfusion
Vasodilation
(Sympathetic Escape)
■ FIGURE 9.7 Positive feedback decompensatory mechanisms triggered by severe hypotension. Im pair-
ment of coronary perfusion leads to a loss in cardiac inotropy and an additional decrease in cardiac
output and pressure. Prolonged tissue ischemia (reduced blood flow) and hypoxia caused by hypoten-
sion and sym pathetic vasoconstriction lead to vasodilation (sym pathetic escape), which reduces systemic
vascular resistance and arterial pressure.
conditions), the greater the buildup of vaso-
dilator metabolites. These metabolites even-
tually
override
the
sympathetic-mediated
vasoconstriction (sympathetic escape), and
blood flow begins to increase within the
organ. W hen this sympathetic escape occurs
within major organs of the body (e.g., skeletal
muscle and gastrointestinal tract), systemic
vascular resistance falls. This reduces arterial
pressure and further reduces organ perfusion,
which leads to further vasodilation and hypo-
tension— a positive feedback cycle.
Several other positive feedback cycles can
contribute to irreversible shock:
Prolonged hypotension with accompany-
ing tissue hypoxia results in metabolic
acidosis as organs begin to generate ATP
by anaerobic pathways. Acidosis impairs
cardiac contraction and vascular smooth
muscle contraction, which decreases car-
diac output and systemic vascular resist-
ance, thereby lowering arterial pressure
even more.
Cerebral
ischemia
and
hypoxia
during
severe
hypotension,
although
initially
causing
strong
sympathetic
activation,
eventually results
in
depression
of all
autonomic outflow as the cardiovascular
regulatory
centers
cease
to
function
because of the lack of oxygen. This with-
drawal of sympathetic tone causes arterial
pressure to fall, which further reduces cer-
ebral perfusion.
Reduced organ perfusion during hypoten-
sion
and
intense
sympathetic vasocon-
striction causes increased blood viscosity
within the microcirculation, microvascular
plugging by leukocytes and platelets, and
disseminated
intravascular
coagulation.
Low-flow states within the microcircula-
tion cause red blood cells to adhere to
each other, which increases the viscosity
of the blood. Furthermore, low-flow states
enhance
leukocyte-endothelial
adhe-
sion and platelet-platelet adhesion. This
reduces organ perfusion even more and
can lead to ischemic damage and stimula-
tion of inflammatory processes, which can
further enhance metabolic acidosis and
impair cardiac and vascular function.
In summary, the body responds to hypoten-
sion by activating neurohumoral mechanisms
that serve as negative feedback, compensatory
mechanisms to restore arterial pressure. With
severe hypotension, positive feedback control
mechanisms may become operative. These
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