Page 234 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Heart Failure
Heart failure (HF) is the state of reduced myo- creased heart rate and peripheral vasocon-
cardial performance, and mainly affects the striction (see below; → B). If chronic volume
left ventricle (LV). Its most common causes load develops, the dilated ventricle reacts
(→ A) are coronary heart disease (→ p. 218ff.) with hypertrophy to compensate, i.e., with an
and hypertension (→ p. 208ff.), but nearly all increased wall thickness (d). However, r re-
other forms of cardiac disease (valvar defects, mains elevated (eccentric hypertrophy; → A1),
cardiomyopathies; → A) as well as some extra- and this form of HF usually has a less favorable
cardiac diseases can result in HF. Right ventric- course than one with concentric hypertrophy
ular failure can occur with right heart defects (see below). If the underlying condition (e.g.,
and shunts (→ p. 202ff.), and particularly with valvar defect) is not removed early, HF gets
pulmonary hypertension (→ p. 214). However, worse relatively rapidly because of the result-
ing myocardial remodeling (see below). Stiffen-
the right ventricle may also be affected sec-
Heart and Circulation (mitral stenosis, left HF). is involved in this development. Because of its
ing of the ventricle, caused by the hypertrophy,
ondarily by abnormalities in the left ventricle
steeper compliance (= lusitropic = relaxation)
In principle a distinction is made between
curve (→ A3, R becomes R′), it has a dimin-
HF due to reduced systolic ejection (systolic or
ished enddiastolic volume and thus a small
forward failure), resulting from either an in-
stroke volume (backward HF; see also A5, or-
creased volume load, myocardial disease, an
the dilated ventricular wall gives way even
filling of the heart, and HF in which diastolic
more (dilation with myocardial restructuring)
filling is impaired (diastolic or backward fail-
7 increased pressure load, or impaired diastolic ange arrows). A vicious circle arises, in that
ure), for example as a result of greater ventric- and r rises steeply. This decompensation is
ular wall stiffness. In forward HF the stroke characterized by a life-threatening fall in
volume, and thus cardiac output, can no longer stroke volume despite an enormously elevated
adequately meet the organism’s requirements. enddiastolic volume (→ A5, red arrows).
In backward HF this can be counteracted only HF caused by myocardial disease. In coro-
by increasing the diastolic filling pressure. nary heart disease (ischemia; → p. 218) and
Usually HF only becomes manifest initially on after myocardial infarction (→ p. 220) the load
severe physical work (when maximal O 2 uptake on the uninvolved myocardium increases, i.e.,
and maximal cardiac output is decreased, but forward HF develops due to diminished con-
otherwise without symptoms; stage I of the tractility. This is reflected by a shift of the con-
NYHA [New York Heart Association] classifica- tractility (C) curve of the ventricular work dia-
tion). However, symptoms later develop pro- gram (→ A2, C becomes C′). The endsystolic
gressively, at first only on ordinary physical ac- volume and, to a lesser extent, the EDV also
tivity, later even at rest (NYHA stages II–IV). rises, while stroke volume falls (→ A2, SV be-
HF caused by volume load. Aortic and mitral comes SV′; see also A5, lilac arrows). Hypertro-
regurgitation, for example, are characterized phy of the remaining myocardium, a stiff myo-
by the regurgitant volume (→ p.196 and 200) cardial scar as well as the diminished effect of
that is added to the effective stroke volume. ATP on actin–myosin separation in the
The enddiastolic volume, and therefore the ra- ischemic myocardium will lead to additional
dius (r) of the left ventricle, are increased so backward HF. Finally, a compliant infarct scar
that, according to Laplace’s law (→ A), the wall may bulge outward during systole (dyskinesia;
tension (T), i.e., the force that has to be gener- → p. 223, G4), resulting in additional volume
ated per myocardial cross-sectional area, load (regurgitant volume). Cardio-myopathies
must rise to achieve a normal, effective stroke can also lead to HF, volume load being promi-
volume. As this succeeds only inadequately, nent in the dilated form, backward HF in the
stroke volume and thus CO (= heart rate · hypertrophic and restrictive forms.
stroke volume) decrease and the blood pres- HF due to pressure load. The wall tension
224 sure falls. Sympathetic stimulation occurs as a (T) of the left ventricle also rises in hyperten-
counterregulatory mechanism, resulting in in- sion or aortic stenosis, because an increased
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Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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