CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
209
Blood Loss
I
■ FIGURE 9.6 Activation of humoral mechanisms following acute blood loss (hemorrhage). Decreased
arterial pressure activates the sym pathetic nervous system (baroreceptor reflex), which stimulates cat-
echolamine release
(Epi,
epinephrine;
NE,
norepinephrine) from the adrenal medulla. This increases cardiac
output
(CO)
and systemic vascular resistance
(SVR),
which elevates (+) arterial pressure. Renin release
is stim ulated by the enhanced sym pathetic activity, increased circulating catecholamines, and hypoten-
sion; this leads to the form ation of angiotensin II and aldosterone. Vasopressin release from the posterior
pituitary is stim ulated by angiotensin II, reduced atrial pressure (not shown), and increased sym pathetic
activity (not shown). These hormones act together to increase blood volume through their renal actions
(sodium and water retention), which elevates arterial pressure. Angiotensin II and vasopressin also elevate
arterial pressure by increasing SVR. These changes in systemic vascular resistance, blood volume, and
cardiac output thereby help to restore the arterial pressure.
water
excretion
gradually
increases
blood
volume over several hours and days.
Enhanced sympathetic activity stimulates
the adrenal medulla to release catecholamines
(epinephrine
and
norepinephrine).
This
causes cardiac stimulation (P^adrenoceptor
mediated)
and peripheral
vasoconstriction
(a -adrenoceptor mediated), and contributes
to the release of renin by the kidneys through
renal P-adrenoceptors.
Other mechanisms besides the barorecep-
tor reflex and hormones have a compensa-
tory role in hemorrhagic hypotension. Severe
hypotension can lead to activation of chem-
oreceptors (see Chapter 6). Low perfusion
pressures and reduced organ blood flow cause
increased production of lactic acid as organs
are required to switch over to anaerobic glyco-
lysis for the production of ATP. Acidosis stim-
ulates peripheral and central chemoreceptors,
leading to increased sympathetic activity to
the systemic vasculature. Stagnant hypoxia
in the carotid body chemoreceptors, which
results from reduced carotid body blood flow,
stimulates chemoreceptor firing. If cerebral
perfusion becomes impaired and the brain
becomes
ischemic,
intense
sympathetic-
mediated vasoconstriction of the systemic
vasculature will result.
Reduced
arterial
and venous pressures,
coupled
with
a
decrease
in
the
post-to-
precapillary resistance ratio, decreases capil-
lary hydrostatic pressures (see Chapter 8).
This leads to enhanced capillary fluid reab-
sorption. This mechanism can result in up to
1 L/h of fluid being reabsorbed back into the
intravascular compartment, which can lead
to a significant increase in blood volume and
arterial pressure after a few hours. Although
capillary fluid reabsorption increases intra-
vascular volume and serves to increase arte-
rial pressure, it also leads to a reduction in
hematocrit and dilution of plasma proteins
until new blood cells and plasma proteins
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