CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
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pulmonary vasculature, leading to pulmonary
edema. The increase in end-diastolic volume,
however, is not as great as the increase in end-
systolic volume. Therefore, the net effect is a
decrease in stroke volume (decreased width
of the pressure-volume loop). Because stroke
volume decreases and end-diastolic volume
increases, a substantial reduction in ejec-
tion fraction occurs. Ejection fraction (stroke
volume divided by end-diastolic volume) is
normally >55%, but it can fall below 20% in
severe systolic failure.
The second type of heart failure is diastolic
failure, which is caused by impaired ventricu-
lar filling. Diastolic failure can be caused by
either decreased ventricular compliance (e.g.,
as occurs with ventricular hypertrophy; see
Chapter 4) or impaired relaxation (decreased
lusitropy; see Chapter 3). Ventricular hyper-
trophy most commonly is caused by chronic,
uncontrolled hypertension, w hich results in
a thickening of the ventricular wall as new
sarcomeres are added in parallel to exist-
ing
sarcomeres.
The
hypertrophy
enables
the heart to contract more forcefully against
the higher pressure in the aorta and helps
to normalize wall stress (see Equation 4-2).
Therefore, a hypertrophied heart may exhibit
a leftward shift in the end-systolic pressure-
volume relationship (not shown in Fig. 9.9,
panel B). Other causes of diastolic failure
include hypertrophic cardiomyopathy, a dis-
ease resulting from a genetic defect that alters
myocardial
structure.
Normal
age-related
changes to cardiac structure can make the
ventricle less compliant, leading to impaired
ventricular filling in the elderly population.
Reduced ventricular compliance, whether
of anatomic or physiologic origin, shifts the
ventricular
end-diastolic
pressure-volume
relationship (i.e., passive filling curve) up
and to the left (Fig. 9.9, panel B). This results
in less ventricular
filling
(decreased
end-
diastolic volume) and a greater end-diastolic
pressure. Stroke volume, therefore, decreases.
Depending upon the relative change in stroke
volume and end-diastolic volume, ejection
fraction may or may not change. For this rea-
son, reduced ejection fraction is useful only as
an indicator of systolic failure.
Increased ventricular end-diastolic pres-
sure, which can exceed 30 mm Hg in left
ventricular failure, can have serious clinical
consequences because left atrial
and pul-
monary capillary pressures rise. Pulmonary
edema can occur when the left ventricular
end-diastolic pressure exceeds 20 mm Hg. If
the right ventricle is in diastolic failure, the
increase in end-diastolic pressure is reflected
back into
the
right atrium
and
systemic
venous vasculature. This can lead to periph-
eral edema and abdominal ascites.
It is not uncommon in chronic heart fail-
ure to have a combination of both systolic
and diastolic dysfunction to varying degrees
(Fig. 9.9, panel C). With both systolic and
diastolic dysfunction, the slope of the end-
systolic
pressure-volume
relationship
is
decreased, and the slope of the passive fill-
ing curve is increased. This causes a dramatic
reduction in stroke volume because end-sys-
tolic volume is increased and end-diastolic
volume is decreased. This combination of
systolic and diastolic dysfunction can lead to
high end-diastolic pressures that can cause
pulmonary congestion and edema.
Systemic Compensatory
Mechanisms in Heart Failure
Heart failure, whether systolic or diastolic in
nature, leads to a reduction in stroke volume
and cardiac output. In the absence of compen-
satory mechanisms, a fall in cardiac output
has two effects on pressure: decreased arterial
pressure and increased central venous pressure
(see Fig. 5.18). These changes activate neuro-
humoral mechanisms that attempt to restore
cardiac output and arterial pressure (Fig. 9.10).
In response to an acute reduction in car-
diac output and arterial pressure, decreased
firing of arterial baroreceptors activates the
sympathetic adrenergic nerves to the heart
and
vasculature.
The
baroreceptor
reflex
responds mainly to acute changes in arterial
pressure and therefore cannot be responsible
for maintaining the increased sympathetic
drive when hypotension accompanies chronic
heart failure. In addition, not all patients in
chronic heart failure are hypotensive. It is not
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