CHAPTER 31
The Heart as a Pump 515The force of contraction of cardiac muscle depends on its
preloading and its afterloading. These factors are illustrated in
Figure 31–6, in which a muscle strip is stretched by a load (the
preload
) that rests on a platform. The initial phase of the con-
traction is isometric; the elastic component in series with the
contractile element is stretched, and tension increases until it is
sufficient to lift the load. The tension at which the load is lifted
is the
afterload.
The muscle then contracts isotonically without
developing further tension. In vivo, the preload is the degree to
which the myocardium is stretched before it contracts and the
afterload is the resistance against which blood is expelled.
RELATION OF TENSION TO
LENGTH IN CARDIAC MUSCLE
The length–tension relationship in cardiac muscle (see Figure
5–17) is similar to that in skeletal muscle (see Figure 5–11); as
the muscle is stretched, the developed tension increases to a
maximum and then declines as stretch becomes more extreme.
Starling pointed this out when he stated that the “energy of
contraction is proportional to the initial length of the cardiac
muscle fiber” (
Starling’s law of the heart
or the
Frank–Star-
ling law
). For the heart, the length of the muscle fibers (ie, the
extent of the preload) is proportional to the end-diastolic vol-
ume. The relation between ventricular stroke volume and end-
diastolic volume is called the Frank–Starling curve.
Regulation of cardiac output as a result of changes in cardiac
muscle fiber length is sometimes called
heterometric regula-
tion,
whereas regulation due to changes in contractility inde-
pendent of length is sometimes called
homometric regulation.FACTORS AFFECTING
END-DIASTOLIC VOLUMEAlterations in systolic and diastolic function have different ef-
fects on the heart. When systolic contractions are reduced,
there is a primary reduction in stroke volume. Diastolic func-
tion also affects stroke volume, but in a different way.
An increase in intrapericardial pressure limits the extent to
which the ventricle can fill (eg, as a result of infection or pres-
sure from a tumor), as does a decrease in ventricular compli-
ance; that is, an increase in ventricular stiffness produced by
myocardial infarction, infiltrative disease, and other abnormali-
ties. Atrial contractions aid ventricular filling. Factors affecting
the amount of blood returning to the heart likewise influence
the degree of cardiac filling during diastole. An increase in total
blood volume increases venous return (Clinical Box 31–2).
Constriction of the veins reduces the size of the venous reser-
voirs, decreasing venous pooling and thus increasing venous
return. An increase in the normal negative intrathoracic pres-
sure increases the pressure gradient along which blood flows to
the heart, whereas a decrease impedes venous return. Standing
decreases venous return, and muscular activity increases it as a
result of the pumping action of skeletal muscle.
The effects of systolic and diastolic dysfunction on the
pressure–volume loop of the left ventricle are summarized in
Figure 31–7.MYOCARDIAL CONTRACTILITY
The contractility of the myocardium exerts a major influence on
stroke volume. When the sympathetic nerves to the heart are
stimulated, the whole length–tension curve shifts upward and
to the left (Figure 31–8). The positive inotropic effect of norepi-
nephrine liberated at the nerve endings is augmented by circu-
lating norepinephrine, and epinephrine has a similar effect.
Conversely, there is a negative inotropic effect of vagal stimula-
tion on both atrial and (to a lesser extent) ventricular muscle.
Changes in cardiac rate and rhythm also affect myocardial
contractility (known as the force–frequency relation, Figure
31–8). Ventricular extrasystoles condition the myocardium in
such a way that the next succeeding contraction is strongerFIGURE 31–5
Interactions between the components that
regulate cardiac output and arterial pressure.
Solid arrows indicate
increases, and the dashed arrow indicates a decrease.
FIGURE 31–6
Model for contraction of afterloaded muscles.
A:
Rest.
B:
Partial contraction of the contractile element of the muscle
(CE), with stretching of the series elastic element (SE) but no shorten-
ing.
C:
Complete contraction, with shortening.
(Reproduced with
permission from Sonnenblick EH in:
The Myocardial Cell: Structure, Function and
Modification.
Briller SA, Conn HL [editors]. University Pennsylvania Press, 1966.)
Arterial
pressurePeripheral
resistanceCardiac
outputStroke
volumeHeart
rateMyocardial
fiber
shorteningLeft
ventricular
sizeAfterload Contractility PreloadShorteningTensionLoadTime
StimulationCEL
L = LoadSEACELSECELSEBC