CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
205
than the maximal heart rate of a 20-year-old
person. Increasing age also reduces maximal
stroke volume because of impaired ventricu-
lar filling (decreased ventricular compliance)
and reduced inotropic responsiveness to sym-
pathetic stimulation. Together, these changes
reduce maximal cardiac output substantially.
Older individuals have reduced skeletal mus-
cle mass as well as decreased maximal muscle
blood flow per unit weight of muscle. A reduc-
tion in vasodilatory capacity of resistance ves-
sels in skeletal muscle in older persons may be
related to reduced endothelial production or
bioavailability of nitric oxide and altered vascu-
lar smooth muscle responsiveness to metabolic
vasodilators. Although increasing age inevita-
bly limits exercise capacity, exercise habits and
general health can significantly influence the
decline in maximal cardiac output with age.
Gender influences cardiovascular responses
to exercise. Generally, males can reach and
sustain significantly higher workloads and
maximal
oxygen
consumptions
than
can
females. Maximal cardiac outputs are about
25% less in females, although the maximal
heart rates are similar. This difference is partly
owing to increased skeletal muscle mass and
to increased cardiac mass in males.
Finally, cardiac disease can significantly
limit exercise capacity. As described later in this
chapter, diseases that impair cardiac function
(e.g., heart failure) can limit the ability of the
heart to increase cardiac output during physi-
cal activity. Arrhythmias, such as atrial fibril-
lation or AV nodal block, can reduce exercise
capacity by decreasing maximal cardiac output.
MATERNAL CHANGES IN
CARDIOVASCULAR FUNCTION
DURING PREGNANCY
Pregnancy causes significant changes in the
cardiovascular system (Fig. 9.3). Increased
uterine mass and the developing fetus require
large amounts of blood flow. To supply this
flow,
cardiac output increases by 30%
to
50% during the first and second trimesters
and then plateaus during the third trimes-
ter. In the first half of the pregnancy, the
cardiac output is primarily increased through
Trimester
Trimester
Trimester
■ FIGURE 9.3 Changes in maternal hem ody-
namics during pregnancy. Early in the course of
pregnancy, cardiac output (CO) increases because
stroke volume (SV) increases owing to an increase
in blood volume; systemic vascular resistance
(SVR)
and mean arterial pressure
(MAP)
decrease.
Heart rate
(HR)
gradually increases throughout
pregnancy; SV declines as HR increases.
increases in stroke volume. By the third tri-
mester, however, stroke volume may be only
slightly elevated. At this stage of pregnancy,
the increased cardiac output is sustained by
an elevated heart rate, which may increase by
10 to 20 beats/min.
Cardiac output increases because blood
volume (and therefore ventricular preload)
increases dramatically during pregnancy. By
week 6, blood volume may be increased by
10%. By the end of the third trimester, blood
volume may be increased by 50%. The increase
in blood volume is brought about by estrogen-
mediated activation of the renin-angiotensin-
aldosterone system, which increases sodium
and water retention by the kidneys.
Although cardiac output is elevated, mean
arterial pressure generally falls owing to a
disproportionate decrease in systemic vascu-
lar resistance. The fall in systemic vascular
resistance may be caused in part by hormonal
changes that dilate resistance vessels; however,
the major factor contributing to the reduced
resistance is the development of low-resistance
uterine circulation, particularly in the later
stages of pregnancy. Diastolic pressure falls
more than systolic pressure because of reduced
systemic vascular resistance, so there is an
increase in pulse pressure. Increased pulse
pressure results from the increase in stroke
volume during the first and second trimesters.
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