C H A P T E R 4 4
Cardiotonic agents
683
and increased demand for oxygen and energy as
the heart muscle must constantly contract harder.
(Valvular heart disease is seen less often today
owing to the success of cardiac surgery and effective
treatment for rheumatic fever.)
The end result of all of these conditions is that the
heart muscle cannot pump blood effectively through
out the vascular system. If the left ventricle pumps
inefficiently, blood backs up into the lungs, causing
pulmonary vessel congestion and fluid leakage into
the alveoli and lung tissue. In severe cases,
pulmonary
oedema
(manifested by rales, wheezes, blood-tinged
sputum, low oxygenation and development of a third
heart sound [S
3
]) can occur. If the right side of the heart
is the primary problem, blood backs up in the venous
system leading to the right side of the heart. Liver
congestion and oedema of the legs and feet reflect right-
sided failure. Because the cardiovascular system works
as a closed system, one-sided failure, if left untreated,
eventually leads to failure of both sides, and the signs
and symptoms of total HF occur.
Clinincal management of a person with heart failure
Compensatory mechanisms
Because effective pumping of blood to the cells is
essential for life, the body has several compensatory
mechanisms that function if the heart muscle begins to
fail (Figure 44.2). Decreased cardiac output stimulates
the baroreceptors in the aortic arch and the carotid
arteries, causing increased sympathetic activity (see
Chapter 29). This stimulates an increase in heart rate,
blood pressure and rate and depth of respirations, as
well as a
positive inotropic effect
(increased force of con
traction) on the heart and an increase in blood volume
(through the release of aldosterone). The decrease in
cardiac output also stimulates the release of renin
from the kidneys and activates the renin–angiotensin–
aldosterone system, which further increases blood
pressure and blood volume.
If these mechanisms work effectively, compensa
tion is occurring and the person may show no signs
or symptoms of HF. Over time, however, all of these
effects increase the workload of the heart, contribut
ing to further development of HF. Eventually, the heart
muscle overstretches from the increased workload,
and the chambers of the heart dilate secondary to the
increased blood volume that they have had to handle.
This hypertrophy (enlargement) of the heart muscle,
called
cardiomegaly
, leads to inefficient pumping and
eventually to increased HF.
Cellular changes
The myocardial cells are changed with prolonged HF.
Unlike healthy heart cells, the cells of the failing heart
seem to lack the ability to produce the energy needed
for effective contractions. Movement of calcium ions
into and out of the cell is no longer effective, leading
to further deterioration because the muscle contracts
inefficiently and is unable to deliver blood to the cardiac
muscle.
Clinical manifestations
The person with HF presents a predictable clinical
picture that reflects not only the problems with heart
pumping, but also the compensatory mechanisms that
are working to balance the problem. Radiography,
electrocardiography (ECG) and direct percussion and
palpation help to detect changes in the heart muscle and
function. The heart rate will be rapid secondary to sym
pathetic stimulation, and the person may develop atrial
flutter or fibrillation as atrial cells are stretched and
damaged. Anxiety often occurs as the body stimulates
the sympathetic stress reaction. Heart murmurs may
develop when the muscle is no longer able to support the
papillary muscles that support the valve leaflets or the
annuli that anchor the heart valves.
Peripheral congestion and oedema occur as the
organs and vessels become engorged waiting for blood
to be pumped through the heart as a result of pump
failure. With right-sided failure, there is enlarged
liver (hepatomegaly); enlarged spleen (splenomegaly);
decreased blood flow to the gastrointestinal (GI) tract
↓
Myocardial function or failure
↓
Cardiac output
↓
Blood flow to kidneys
Activation of
renin–angiotensin
system
↑
BP
↑
Cardiac output
↑
Cardiac workload
Baroreceptor stimulation
Sympathetic activation
↑
BP
↑
P
↑
Respirations
+ Inotropic effect
↑
Cardiac output
↑
Aldosterone synthesis and release
↑
Na
+
retention
↑
K
+
excretion
↑
H
2
O retention
↑
Blood volume
ADH release
FIGURE 44.2
Compensatory mechanisms in heart failure (HF),
which lead to increased cardiac workload and further HF.
ADH, antidiuretic hormone; BP, blood pressure; P, pulse.
