stress by
increasing pressure by a given percentage
increases wall stress about four times more
than the same change in volume.
Relating the wall stress equation to oxygen
consumption helps to explain why increases
in pressure generation have a much greater
influence on oxygen consumption than a sim-
ilar percentage increase in ventricular preload.
It is important, however, not to use the wall
stress equation to estimate oxygen demands
by the whole heart. The reason for this is that
wall stress estimates the tension required by
individual myocytes to generate pressure as
they contract. This wall stress, in large part,
determines the oxygen consumption of indi-
vidual myocytes, but oxygen consumption
of the whole heart is the sum of the oxygen
consumed by all of the myocytes. A hypertro-
phied ventricle with a thicker wall, which has
reduced wall stress, will not have a reduction
in overall oxygen consumption as suggested
by Equation 4-4. In fact, because of its greater
muscle mass, oxygen consumption may be
significantly increased in a hypertrophied
heart, particularly if its efficiency is impaired
by disease. A less efficient heart performs less
work per unit oxygen consumed (i.e., it gen-
erates less pressure and SV).
The concepts described above have impli-
cations for treating patients with coronary
artery disease (CAD). For example, drugs that
decrease afterload, heart rate, and inotropy
are particularly effective in reducing myocar-
dial oxygen consumption and relieving symp-
toms of chest pain (i.e., angina), which results
from inadequate oxygen delivery relative to
the oxygen demands of the myocardium.
CAD patients are counseled to avoid activi-
ties such as lifting heavy weights that lead to
large increases in arterial blood pressure. In
contrast, CAD patients are often encouraged
to participate in exercise programs such as
walking that utilize preload and SV changes
to augment cardiac output by the Frank-Star-
ling mechanism. It is important to minimize
stressful situations in these patients because
stress causes sympathetic activation of the
heart and vasculature that increases heart
rate, inotropy, and afterload, all of which lead
to significant increases in oxygen demand by
the heart.
The cardiac cycle is divided into two
general phases: diastole and systole.
Diastole refers to the period of time
that the ventricles are undergoing
relaxation and filling with blood from
the atria. Ventricular filling is primarily
passive, although atrial contraction
has a variable effect on the final extent
of ventricular filling (EDV). Systole
represents the time when the ventricles
are contracting and ejecting blood
(SV). The volume of blood remaining
in the ventricle at the end of ejection is
the ESV.
Normal heart sounds (S1
and S2)
originate from abrupt closure of heart
Ventricular SV is the difference
between the end-diastolic and end-
systolic volumes. Ventricular ejection
fraction (EF) is calculated as the SV
divided by the EDV.
Cardiac output is normally influenced
more by changes in heart rate than
by changes in SV; however, impaired
regulation of SV can have a significant
adverse affect on cardiac output, as
occurs during heart failure.
Ventricular preload is related to the
extent of ventricular filling (EDV)
and the sarcomere length. Increased
preload increases the force of
contraction and SV.
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