C h a p t e r 2 0
Heart Failure and Circulatory Shock
495
failure of the left ventricle, cardiac output may fall to
levels that are insufficient for providing the brain with
adequate oxygen, causing cognitive impairment and
disturbed behavior. Confusion, impairment of mem-
ory, anxiety, restlessness, and insomnia are common
in elderly persons with advanced heart failure, par-
ticularly in those with cerebral atherosclerosis. These
symptoms may confuse the diagnosis of heart failure
in the elderly because of other possible causes associ-
ated with aging.
Cachexia and Malnutrition
Cardiac cachexia is a condition of malnutrition and tis-
sue wasting that occurs in persons with end-stage heart
failure.
31
A number of factors probably contribute to
its development, including fatigue and depression that
interfere with food intake, and congestion of the liver
and gastrointestinal structures that impairs digestion
and absorption and produces feelings of fullness. Other
factors are circulating toxins and mediators released
from poorly perfused tissues that impair appetite and
contribute to tissue wasting.
Cyanosis
Cyanosis, or a bluish discoloration of the skin and
mucous membranes, is caused by excess desaturated
hemoglobin in the blood. It is often a late sign of heart
failure, and may be visible especially around the lips and
in the peripheral parts of the extremities.
Cyanosis may be central or peripheral. Central cya-
nosis develops when impaired pulmonary gas exchange
reduces oxygenation of the arterial blood in conditions
such as pulmonary edema, left heart failure, or right-
to-left cardiac shunting. Peripheral cyanosis develops
as a consequence of venous desaturation resulting from
extensive extraction of oxygen at the capillary level. It
is caused by conditions such as low-output failure that
result in delivery of poorly oxygenated blood to the
peripheral tissues, or by conditions such as peripheral
vasoconstriction that cause excessive removal of oxy-
gen from the blood. Central cyanosis is best monitored
by assessing the lips and mucous membranes because
these areas are not subject to environmental condi-
tions, such as cold temperatures, that cause peripheral
constriction and cyanosis.
Arrhythmias and Sudden Cardiac Death
Both atrial and ventricular arrhythmias can occur in
persons with heart failure. Atrial fibrillation is the most
common arrhythmia (see Chapter 17). Manifestations
associated with atrial fibrillation are related to loss of
atrial contraction, tachycardia, irregular heart rate, and
symptoms related to a drop in blood pressure.
32
There
is also strong evidence that persons with heart failure
are at increased risk for sudden cardiac arrest; that is,
unwitnessed death or death that occurs within 1 hour
of symptom onset. In persons with ventricular dysfunc-
tion, sudden death is caused most commonly by ven-
tricular tachycardia or ventricular fibrillation.
1
Acute Heart Failure Syndromes
The acute heart failure syndromes (AHFS) are defined
as “gradual or rapid change in heart failure signs and
symptoms resulting in a need for urgent therapy.”
33
These signs and symptoms are primarily the result of
severe pulmonary edema due to elevated left ventricu-
lar filling pressures, with or without a low cardiac
output.
33–35
The AHFS are among the most common
disorders seen in emergency departments. A worsening
of chronic heart failure, often complicated by episodes
of acute decompensation, is the most common cause of
the syndrome.
The AHFS are thought to encompass three differ-
ent types of conditions: (1) worsening of chronic sys-
tolic or diastolic dysfunction that appears to respond
to treatment; (2) new-onset acute heart failure that
occurs secondary to a precipitating event such as a
large myocardial infarction or a sudden increase in
blood pressure superimposed on a noncompliant left
ventricle; and (3) worsening of end-stage/advanced
heart failure that is refractory to treatment, with pre-
dominantly left ventricular systolic dysfunction associ-
ated with a low-output state.
34
The difference between
new-onset AHFS and AHFS caused by chronic heart
failure is in the degree of physiologic response, which
is more pronounced in the new-onset AHFS and more
subtle in chronic heart failure because of the compen-
satory pathophysiology. For example, with new-onset
AHFS, the person will have a strong sympathetic
response such as tachycardia with enhanced pulmo-
nary vascular permeability causing rapid and dramatic
symptoms of pulmonary edema. Because many com-
pensatory mechanisms operate in persons with chronic
heart failure, they tolerate higher pulmonary vascular
pressures. Chronic changes in neurohormonal regu-
lation lead to a strong activation of the angiotensin-
aldosteronesystemwitharesultantvolumeoverload,and
venous congestion in both the systemic and pulmonary
circulations.
35
Acute pulmonary edema is the most dramatic symp-
tom of AHFS. It is a life-threatening condition in which
capillary fluid moves into the alveoli.
28
The accumulated
fluid in the alveoli and airways causes lung stiffness,
makes lung expansion more difficult, and impairs the
gas exchange function of the lung. With the decreased
ability of the lungs to oxygenate the blood, the hemo-
globin leaves the pulmonary circulation without being
fully oxygenated, resulting in shortness of breath and
cyanosis.
The person with severe pulmonary edema is usually
seen sitting and gasping for air. The pulse is rapid, the
skin is moist and cool, and the lips and nail beds are
cyanotic. As the pulmonary edema worsens and oxy-
gen supply to the brain drops, confusion and stupor
appear. Dyspnea and air hunger are accompanied by a
productive cough with frothy (resembling beaten egg
whites) and often blood-tinged sputum—the effect of
air mixing with the serum albumin and red blood cells
that have moved into the alveoli. The movement of
air through the alveolar fluid produces fine crepitant
