CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
207
vasoconstriction may be impaired, which can
result in a fall in arterial pressure when the
person stands up (orthostatic hypotension)
and when the person exercises.
Hypotension can also occur when cardiac
output is reduced by a decrease in either heart
rate or stroke volume. Ventricular rate can be
reduced by sinus bradycardia, which may
be caused by excessive vagal activation of the
SA node. A vasovagal reflex can lower heart
rate and arterial pressure sufficiently to cause
syncope (see Chapter 6). Second- and third-
degree AV nodal blockade (see Chapter 2)
reduce ventricular rate. Ventricular fibrilla-
tion prevents coordinated ventricular beats so
the effective ventricular rate is zero.
Stroke volume can be reduced by decreases
in
either
inotropy
or
ventricular
filling
(preload) (see Chapter 4). Reduced inotropy
occurs during heart failure (systolic failure)
or when autonomic dysfunction decreases
sympathetic outflow to the heart. A sudden
loss of mechanical efficacy by the heart, as
occurs following acute ischemic damage (e.g.,
myocardial infarction), is a frequent cause of
cardiogenic shock. Decreased preload can
be caused by several conditions: (1) hypov-
olemia, which results from blood loss (hem-
orrhage) or dehydration; (2) a redistribution
of blood volume, as occurs when a person
stands
up
(orthostatic
hypotension;
see
Chapter 5); (3) reduced venous return, which
can result from compression of the vena cava
(e.g., supine hypotensive syndrome during
pregnancy); and (4) tachyarrhythmias, such
as atrial fibrillation and ventricular tachycar-
dia, which reduce ventricular filling.
Compensatory Mechanisms
during Hypotension
When hypotension occurs, the body attempts to
restore arterial pressure by activating neurohu-
moral compensatory mechanisms (see Chap-
ter 6). Initial, short-term mechanisms involve
baroreceptor reflex activation of sympathetic
nerves, which constrict systemic vascular beds
and stimulate the heart. More slowly activated,
long-term compensatory mechanisms include
the renin-angiotensin-aldosterone system and
vasopressin. These hormone systems serve to
increase blood volume and reinforce the vaso-
constriction caused by increased sympathetic
activity. Neurohumoral compensatory mecha-
nisms increase arterial pressure and thereby
help to maintain normal cerebral and coronary
perfusion at the expense of reduced blood flow
to less essential organs. The following dis-
cussion specifically addresses compensatory
mechanisms in hypotension caused by hemor-
rhage-induced hypovolemia.
The fall in blood volume during hemor-
rhage reduces central venous pressure, which
reduces cardiac filling and stroke volume
through the Frank-Starling mechanism. The
fall in cardiac output causes the arterial pres-
sure fall. The baroreceptor reflex is the first
compensatory mechanism to become acti-
vated in response to blood loss (Fig. 9.5).
This reflex occurs within seconds of a fall in
arterial pressure. As described in Chapter 6,
a reduction in mean arterial pressure and
arterial pulse pressure decreases the firing
of arterial baroreceptors. This activates the
sympathetic
nervous
system
and
inhibits
vagal influences to the heart, thereby increas-
ing heart rate and inotropy. It is important to
note that cardiac stimulation alone does not
lead to a significant increase in cardiac out-
put. For cardiac output to increase, some
mechanism
must
increase
central
venous
pressure and therefore filling pressure for the
ventricles. This is accomplished, at least ini-
tially following hemorrhage, by an increase in
venous tone produced by sympathetic stimu-
lation of the venous capacitance vessels. The
partially
restored
central
venous
pressure
increases stroke volume through the Frank-
Starling mechanism. The increased preload,
coupled with cardiac stimulation, attenuates
the decline in cardiac output. The partially
compensated cardiac output along with sys-
temic
vasoconstriction
causes
the
arterial
pressure to increase toward its normal value.
Although
the
baroreceptor
reflex
can
respond quickly to a fall in arterial pressure
and provide initial compensation, the long-
term recovery of cardiovascular homeostasis
requires activation of hormonal compensatory
mechanisms to restore blood volume through
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