A systematic search of the medical literature was performed on
January 11, 2008. The search, limited to human subjects and English
language journals, included National Guideline Clearinghouse, the
Cochrane database, PubMed, pier® and UpToDate®.
The current American College of Cardiology/ American Heart
Association Chronic Heart Failure Guidelines can be found at www.acc.org.
The European Society of Cardiology Acute Heart Failure and Chronic
Heart Failure Guidelines can be found at www.escardio.org and the
HFSA 2006 Heart Failure Practice Guideline can be found at www.onlinejcf.com.
Heart failure (HF) is a serious and growing health problem affecting
approximately 5 million persons in the United States with an additional
550,000 individuals diagnosed yearly. HF contributes to approximately
300,000 deaths each year. The estimated direct and indirect costs
attribute to HF for 2006 is $29.6 billion.1
HF was once described as “a condition in which the heart
fails to discharge its contents adequately” (Thomas Lewis
1933); however, the simplistic model of pump failure has evolved
into a complex disorder that affects the cardiovascular, musculoskeletal,
renal, and neuroendocrine systems.
The cardinal manifestations of HF include dyspnea, fatigue, and
fluid retention. The development of symptoms characteristic in HF
result from pulmonary and systemic congestion. The presence of signs
and symptoms of HF (Table 2-1) may vary considerably over time in
a given patient. The mechanism of fatigue in HF is complex and originates
from low cardiac output, peripheral hypoperfusion, and skeletal
muscle deconditioning. As left ventricular function deteriorates
and the ability to accept and eject the increased blood volume is
impaired, pulmonary venous and capillary pressures elevate, leading
to interstitial and bronchial edema, increased airway resistance, and
dyspnea. In early HF, dyspnea may occur only with exertion. As HF
progresses, the degree of exertion necessary to induce dyspnea decreases
and eventually leads to dyspnea at rest.2 Associated symptoms
include orthopnea and paroxysmal nocturnal dyspnea (PND). Orthopnea, that
is, dyspnea in the supine position, results from redistribution
of fluid from the abdomen and lower extremities into the chest,
which increases the pulmonary capillary pressure, combined with elevation
of the diaphragm. Orthopnea is relieved by sitting upright and typically
is prevented by elevating the head with pillows. PND is a result
of severe pulmonary and bronchial congestion and refers to severe
shortness of breath and coughing that generally occurs after 2 to
4 hours of sleep; patients awaken with a sense of suffocation.3 The
period between the initiation of ventricular dysfunction and the
onset of symptoms may occur very quickly after a myocardial infarction
(MI) or extend for a long period of time. With more chronic processes,
such as hypertension or idiopathic cardiomyopathies, this interval
may extend for months to years. There is a discordance between the
degree of ventricular dysfunction and the degree of functional impairment
in HF; therefore, the severity of symptoms does not directly correlate
with the amount of left-ventricular (LV) dysfunction.4
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