220
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
Ventricular
Failure
Pulmonary Edema
Systemic Edema
■ FIGURE 9.10 Summary of neurohumoral changes associated w ith heart failure. Activation of the sym -
pathetic nervous system, the renin-angiotensin-aldosterone system, and vasopressin cause an increase
in systemic vascular resistance, blood volume, and central venous pressure. Although increased central
venous pressure helps to elevate (+) cardiac output by the Frank-Starling mechanism, it can also lead to
pulmonary and systemic edema. The increased systemic vascular resistance, although helping to elevate
arterial pressure, can depress (-) cardiac output further because of increased afterload. Increased atrial
natriuretic peptide counterregulates the other hormonal systems.
clear what drives the characteristic increase in
sympathetic activity in chronic heart failure,
although humoral changes and cardiac stretch
receptors may be involved, along with barore-
ceptor resetting.
Important humoral changes occur dur-
ing heart failure to help compensate for the
reduction in cardiac output. Arterial hypo-
tension, along with sympathetic activation,
stimulates renin release, leading to the for-
mation of angiotensin II and aldosterone.
Vasopressin (antidiuretic horm one) release
from the posterior pituitary is also stimulated.
Increased
vasopressin
release
seems
para-
doxical because right atrial pressure is often
elevated in heart failure, which should inhibit
the release of vasopressin (see Chapter 6). It
may be that vasopressin release is stimulated
in heart failure by sympathetic activation and
increased angiotensin II. Circulating catecho-
lamines
(norepinephrine
and epinephrine)
are also elevated in heart failure because of
sympathetic stimulation of the adrenals and
spillover of norepinephrine into the circula-
tion from highly activated sympathetic nerves.
These
changes
in
neurohumoral
status
constrict resistance vessels, which causes an
increase in systemic vascular resistance to
help maintain arterial pressure. Venous capac-
itance vessels constrict as well. This increased
venous tone contributes to the increase in
venous pressure. Angiotensin II and aldoster-
one, along with vasopressin, increase blood
volume by increasing renal reabsorption of
sodium and water, which further increases
venous pressure. The increased venous pres-
sure increases cardiac preload and helps to
maintain stroke volume through the Frank-
Starling mechanism.
Increased right atrial
pressure stimulates the synthesis and release
of atrial natriuretic peptide to counterregu-
late
the
renin-angiotensin-aldosterone
sys-
tem. These neurohumoral responses function
as compensatory mechanisms, but they can
aggravate heart failure by increasing ventricu-
lar afterload (which depresses stroke volum e)
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