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Heart failure (HF) “is a complex clinicalsyndrome that can result from
any structural or functional cardiac disorder that impairs the ability of
the ventricle to fill with or eject blood.” This is further subdivided into
HF with reduced left ventricular ejection fraction (HFrEF) or HF with
preserved left ventricular ejection fraction (HFpEF), previously known
HF symptoms, including limitations in activity, can be quantified with the
use of the New York Heart Association functional classification system
and the American College of Cardiology–American Heart Association
classification of chronic HF. The cardinalsigns and symptoms (e.g.,
peripheral edema, dyspnea, fatigue) of HF must be evaluated in light of
the patient’s medical history, physical examination, and results of
Coexisting medical conditions that lead to HF (e.g., ischemic heart
disease, hypertension, atrial fibrillation [AF], diabetes mellitus, sleep
apnea) or result from HF (e.g., AF, cachexia, depression) may influence
the overall prognosis and treatment; therefore, these should be assessed
Several categories of medications (such as nonsteroidal antiinflammatory
drugs and “glitazones”) may exert unfavorable hemodynamic effects
and may precipitate HF symptoms in patients with previously
compensated HF. In some patients, the occurrence of HF can be
attributed to the cardiotoxic effect of a particular medication (cancer
Treatment goals are to improve symptoms, decrease hospitalizations, and
prevent premature death in patients. The cornerstone of treatment for
(e.g., sodium restriction, exercise training).
Prompt recognition of symptoms and appropriate treatment are critical in
the management of acute decompensated HF. The mainstay of therapy
in patients with volume overload is an intravenous loop diuretic. Other
therapies (e.g., inotropic drugs) have failed to show long-term benefits
An implantable cardioverter-defibrillator reduces the risk of sudden
cardiac death in patients with reduced left ventricular function. Cardiac
resynchronization therapy can be used in combination to improve
symptoms and quality of life in patients with severe HF symptoms.
There is little clinical trial evidence to guide which treatments are optimal
Although controversial, certain patients may respond differently to drug
therapy (e.g., African American patients, women).
HF is an extremely serious condition and requires careful diagnosis,
ongoing monitoring, and the implementation of evidence-based therapy.
Herbal remedies (e.g., hawthorn) have some evidence to support their
role in improving symptoms of HF; however, they have no evidence
demonstrating improvements in mortality. Herbals can also potentially
interact with other heart medications.
Heart failure (HF) is “a complex clinical syndrome that results from any structural or
functional cardiac impairment of ventricle filling or ejection of blood.”
heart failure (CHF) is a subset of HF characterized by left ventricular (LV) systolic
dysfunction and volume excess. However, some patients may lack symptoms of
congestion and still have reduced cardiac output (CO) manifesting as fatigue and
reduced exercise tolerance. Therefore, the term CHF has been replaced with HF.
The descriptive terminology, diagnostic techniques, and treatment of HF have
undergone significant change in the past 20 years. Since 1994, a series of consensus
and evidence-based practice guidelines have been published in an effort to
standardize HF management. Guidelines from the Heart Failure Society of America,
American College of Cardiology (ACC), American Heart Association (AHA),
the European Society of Cardiology
3 have been revised and updated to reflect
ongoing changes in the management of HF. These guidelines use the four disease
stages of HF first assigned by the ACC/AHA 2001 guidelines (Fig. 14-1).
classification promotes the early identification of risk factors that are associated with
the development of LV dysfunction and HF symptoms. It emphasizes that appropriate
therapeutic interventions in the early stages (stages A and B) can prevent progression
to overt HF symptoms. It does not replace the New York Heart Association (NYHA)
functional classification, but reinforces that they should be used in combination to
classify patients. The ACC/AHA guidelines
1,5,6 provide a comprehensive review on
prevention, diagnosis, risk stratification, and treatment of HF in both outpatient and
inpatient settings. The updates emphasize quality of care and adherence to
performance measures. The terminology “guideline-directed therapy” (GDMT) is
frequently used in lieu of optimal medical therapy.
Numerous programs and systems have been implemented in an attempt to decrease
the cost and length of hospital stay for HF. It is recommended that practitioners look
at least annually for the most recently published guidelines to be aware of the rapidly
evolving treatment strategies for HF.
Incidence, Prevalence, and Epidemiology
It is estimated that there are 5.7 million people (1.5%–2% of the population) with HF
in the United States, and approximately 23 million people with HF worldwide. The
prevalence of HF continues to increase, with an estimated 46% increase in
7 Every year, 870,000 people have a new diagnosis of HF, and at
40 years of age, one in five have a lifetime risk of developing this syndrome. After
age 65, HF incidence approaches 10 per 1,000 person-years and is the most common
cause of hospitalizations in the elderly population in the United States.
The incidence of HF is greater in men and in the elderly; however, the incidence in
black women is as high as that in white men. In women, coronary artery disease
(CAD) and diabetes are considered the strongest risk factors for HF. African
Americans present with HF at a younger age compared with white individuals. Risk
factors, such as ischemic heart disease, hypertension (HTN), smoking, obesity, and
diabetes, among others, have been identified that predict the incidence of HF as well
Heart Failure Society of America. Circulation. 2001;104:2996.)
In 2011, one in nine deaths has HF mentioned on the death certificate.
from national databases and community-based cohorts indicates that the incidence of
HF seems to be stabilizing, if not decreasing, for women, and that the length of
survival in patients with HF is increasing. However, the death rate remains high;
almost 50% of people diagnosed with HF will die within 5 years.
steadily increases each year after the diagnosis of HF. The 6-month mortality rates
are no different in patients with preserved versus reduced LV ejection fraction (EF).
Direct and indirect health care costs of HF in 2012 were estimated to be $30.7
Various risk prediction models have been developed to predict HF outcomes.
Given the heterogeneous nature of the HF population (ischemic vs. nonischemic, low
vs. preserved EF), and multiple comorbid conditions, the validity of the risk
prediction models is not consistent in all HF populations. Therefore, it is important
to identify patients who are at high risk of HF and how various risks factors can
9 Based on the strength of these associations, prevention measures
need to be designed to decrease HF hospitalizations in targeted subpopulations. The
1 emphasize that validated multivariable risk scores can be useful to
estimate subsequent risk of mortality in ambulatory or hospitalized patients with HF.
LOW-OUTPUT VERSUS HIGH-OUTPUT FAILURE
HF has been described as being either low-output or high-output failure, with a
predominance of cases being low-output failure (Table 14-1). In both types, the heart
cannot provide adequate blood flow (tissue perfusion) to meet the body’s metabolic
demands, especially during exercise. The hallmark of classic low-output HF is a
diminished volume of blood being pumped by a weakened heart in patients who have
In high-output failure, the heart is healthy and pumps a normal or even higher than
normal volume of blood. Because of high metabolic demands caused by other
underlying medical disorders (e.g., hyperthyroidism, anemia), the heart becomes
exhausted from the increased workload and eventually cannot keep up with demand.
The primary treatment of high-output HF is amelioration of the underlying disease.
Unless otherwise stated, this chapter focuses on the treatment of low-output HF.
LEFT VERSUS RIGHT VENTRICULAR DYSFUNCTION
Low-output HF is further divided into left and right ventricular dysfunction, or a
combination of the two (biventricular failure). Because the left ventricle is the major
pumping chamber of the heart, left ventricular dysfunction is the most common form
of low-output HF and the major target for pharmacologic intervention. Right
ventricular dysfunction may coexist with LV HF if damage is sustained by both sides
of the heart or as a delayed complication of progressive left-sided HF.
Isolated right-sided ventricular dysfunction, which is relatively uncommon, is
usually caused by either primary or secondary pulmonary arterial hypertension. In
these conditions, elevated pulmonary artery pressure impedes emptying of the right
ventricle, thus increasing the workload on the right side of the heart.
pulmonary arterial HTN is idiopathic, caused by increased resistance of the
pulmonary arterial vasculature of unknown etiology. Secondary causes of pulmonary
HTN include collagen vascular disorders, sarcoidosis, fibrosis, exposure to high
altitude, and drug and chemical exposure. Drug-induced causes include opioid
overdoses (especially heroin), 5-hydoxytryptamine-2B (5HT-2B) agonists (e.g.,
dexfenfluramine, fenfluramine, and pergolide), and pulmonary fibrosis caused by
intravenous (IV) injection of poorly soluble forms of methylphenidate. Right-sided
heart disease that occurs as a result of a pulmonary process is known as cor
Classification and Etiology of Left Ventricular Dysfunction
Type of Failure Characteristics Contributing Factors Etiology
↑left ventricular enddiastolic volume; EF
Diastolic dysfunction Normal left ventricular
left ventricular enddiastolic volume; normal or
aSame as congestive heart failure if symptoms also present.
other types combined classified as nonischemic.
SYSTOLIC VERSUS DIASTOLIC DYSFUNCTION; ISCHEMIC VERSUS
LV dysfunction is further subdivided into systolic and diastolic dysfunction, with
mixed disorders also being encountered (Table 14-1). In systolic dysfunction, the
stroke volume (SV) (the volume of blood ejected with each contraction; normal, 60–
130 mL) and the subsequent CO (SV × heart rate; normal, 4–7 L/minute) are reduced.
In diagnosing HF, a critical marker differentiating systolic from diastolic dysfunction
In systolic dysfunction, the LVEF is less than 40%, dropping to less than 20% in
advanced HF. Heart failure with reduced ejection fraction (HFrEF) is a result of
factors causing the heart to fail as a pump (decreased myocardial contractility). The
heart dilates as it becomes congested with retained blood, leading to an enlarged
HF caused by coronary ischemia or after MI is classified as ischemic, with all
other types grouped as nonischemic. CAD is a common cause of HF in patients with
LV systolic dysfunction. Other causes of LV pump failure include persistent
arrhythmias, poststreptococcal rheumatic heart disease, chronic alcoholism
(alcoholic cardiomyopathy), viral infections, or unidentified etiology (idiopathic
dilated cardiomyopathy). Chronic HTN, as well as cardiac valvular disorders (aortic
or mitral stenosis), also precipitate systolic HF by increasing resistance to CO (a
In contrast, LV diastolic dysfunction refers to impaired relaxation and increased
stiffness of the left ventricle; the EF may or may not be abnormal, and the patient may
or may not be symptomatic. Some patients have both systolic and diastolic
dysfunction. The term heart failure with normal or preserved left ventricular ejection
fraction (HFpEF) is used for patients who have symptoms of HF but a normal EF.
These patients always have diastolic dysfunction.
Possible causes of diastolic dysfunction include: coronary ischemia, chronic
uncontrolled HTN, LV wall scarring after an MI, ventricular wall hypertrophy,
hypertrophic cardiomyopathy, restrictive cardiomyopathy (amyloidosis and
sarcoidosis), and valvular heart disease (aortic stenosis). These factors lead to LV
wall stiffness (reduced wall compliance), and inability of the ventricle to relax
during diastole, which result in an elevated pressure within the ventricle despite a
relatively low volume of blood. In turn, the elevated pressure impedes LV filling
during diastole that would normally occur by passive inflow against a low-resistance
pressure gradient. Heart size is usually (but not always) normal. It is estimated that
20% to 60% of patients with HF may have normal LVEF and reduced ventricular
12 Because coronary ischemia, MI, and HTN are contributors to both
systolic and diastolic dysfunction, many patients have both systolic and diastolic
The pathology of systolic dysfunction most closely resembles what has historically
been called “congestive heart failure.” Tremendous variability exists in the clinical
presentation of both systolic and diastolic dysfunction; however, both disorders can
4,11 Most patients exhibit exercise intolerance and shortness of
breath (SOB) with either systolic or diastolic dysfunction. Some exhibit significant
edema, whereas others may have no edema or symptoms of congestion. It is possible
to be asymptomatic in the early stages of HF. For all these reasons, it is best to avoid
the abbreviation CHF, because not all patients have congestion. CHF has also been
used to denote “chronic heart failure.” Clinicians are strongly encouraged to obtain
an EF measurement in all patients. The diagnosis of HF should be based on a
combination of symptoms and signs together with appropriate clinical tests.
A common finding of HF is increased cardiac workload. Four major determinants
contribute to LV workload: preload, afterload, contractility, and heart rate (HR).
Preload describes forces acting on the venous side of the circulation affecting
myocardial wall tension. The volume is maximal when filling finishes at the end of
diastole (LV end-diastolic volume). An increased volume raises the pressure within
the ventricle (LV end-diastolic pressure), which in turn increases the “stretch,” or
wall tension, of the ventricle. Peripheral venous dilation and decreased peripheral
venous volume diminish preload, whereas peripheral venous constriction and
increased peripheral venous volume increase preload.
Elevated preload can aggravate HF. Rapid administration of blood plasma
expanders and osmotic diuretics or administration of large amounts of sodium or
sodium-retaining agents increase preload. A malfunctioning aortic valve (aortic
insufficiency), resulting in regurgitation of blood back into the left ventricle, can
increase the volume of blood that must be pumped. A malfunctioning mitral valve
(mitral regurgitation) can cause retrograde ejection of blood from the left ventricle
back into the left atrium, with a resultant decrease in CO. In patients with systolic
failure, ventricular blood is ejected less efficiently because of a hypofunctioning left
ventricle; the volume of blood retained in the ventricle is thus increased, and preload
becomes elevated. In HFpEF with a stiffened left ventricle, relatively small
increases in end-diastolic volume from sodium and water overload can lead to
exaggerated increases in end-diastolic pressure.
Afterload is the tension developed in the ventricular wall as contraction (systole)
occurs. This tension is affected by intraventricular pressure, ventricular diameter,
and wall thickness. Afterload is affected by the systemic vascular resistance (SVR)
or the impedance against which the ventricle must pump and is estimated by arterial
blood pressure (BP). HTN, atherosclerotic disease, or a narrow aortic valve
opening, increases arterial impedance (afterload), thereby increasing the workload of
the heart. HTN is a major factor in the development of both HFrEF and HFpEF. The
Framingham group found that 75% of patients who developed HF had a history of
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