CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
221
and increasing venous pressures and cardiac
preload to the point at which pulmonary or
systemic congestion and edema occur. The
volume and afterload increases also increase
oxygen demand by the heart, which can fur-
ther exacerbate ventricular failure over time.
Exercise Limitations Imposed
by Heart Failure
Heart
failure
can
severely
limit
exercise
capacity. In early or mild stages of heart fail-
ure, cardiac output and arterial pressure may
be normal at rest because of compensatory
mechanisms. W hen the person in heart fail-
ure begins to perform physical work, how-
ever, the maximal workload is reduced, and
he or she experiences fatigue and dyspnea at
less than normal maximal workloads.
A comparison of exercise responses in a
normal person and in a heart failure patient is
shown in Table 9-4. In this example, the degree
of heart failure is moderate to severe. At rest,
the person with congestive heart failure (CHF)
has reduced cardiac output (decreased 29%)
caused by a 38% decrease in stroke volume.
Mean arterial pressure is slightly decreased,
and resting heart rate is elevated. Whole-body
oxygen consumption is normal at rest, but the
reduced cardiac output results in an increase in
the arterial-venous oxygen difference as more
oxygen is extracted from the blood because
organ blood flow is reduced. At a maximally
tolerated exercise workload, the CHF patient
can increase cardiac output by only 50%, com-
pared to a 221% increase in the normal person.
The reduced cardiac output is a consequence
of the inability of the left ventricle to augment
stroke volume as well as a lower maximal heart
rate (exercise intolerance limits the heart rate
increase). The CHF patient has a significant
reduction in arterial pressure during exercise
in contrast to the normal person’s increase in
arterial pressure. Arterial pressure falls because
the increase in cardiac output is not sufficient
to maintain arterial pressure as the systemic
vascular resistance falls during exercise. The
maximal whole-body oxygen consumption is
greatly reduced in the CHF patient because
reduced perfusion of the active muscles lim-
its oxygen delivery and therefore the oxygen
consumption of the muscles. The CHF patient
experiences substantial fatigue and dyspnea
during exertion, which limits the patient’s abil-
ity to sustain the physical activity.
Some of the neurohumoral compensatory
mechanisms that operate to maintain resting
cardiac output in heart failure contribute to
limiting exercise capacity. The chronic increase
in sympathetic activity to the heart down-
regulates P1-adrenoceptors, which reduces the
heart’s chronotropic and inotropic responses
to acute sympathetic activation during exer-
cise.
Increased
sympathetic
activity
(and
possibly circulating vasoconstrictors) to the
skeletal muscle vasculature limits the degree
of vasodilation during muscle contraction.
This limits oxygen delivery to the working
TABLE 9-4
COMPARISON OF CARDIOVASCULAR FUNCTION IN A NORMAL PERSON
AND A PATIENT WITH MODERATE-TO-SEVERE CHF AT REST AND AT
MAXIMAL (MAX) EXERCISE
C o (L /M in )
H r (B e a ts /
M in )
S v (M l)
M ap (M m H g )
V o 2 (M l O 2/M in )
C a O 2-C v O 2 (M l
O 2/1 0 0 M l)
N orm al
(R est)
5.6
70
80
95
220
4.0
N orm al
(M ax)
18.0
170
106
120
2 5 00
13.9
CHF (R est)
4.0
80
50
90
220
5.5
CHF (M ax)
6.0
120
50
85
780
13.0
CO, cardiac output; HR, heart rate
SV, stroke volume; MAP, mean arterial pressure; VO., w hole-body oxygen consumption;
CaO2-C vO 2, arterial-venous oxygen difference. VO. is calculated from the product of CO and CaO2-C vO 2, after the units for
CO are converted to m L/m in and the units fo r CaO
2
-C vO
2
are converted to mL O
2
/m L blood.
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