The cardiovascular (CV) system includes the heart and the blood vessels. These vessels include the arteries, veins, and capillaries that feed the tissues throughout the body. Cardiovascular disease (CVD) accounted for 38% of the approximately 2,400,000 deaths in the United States in 2002 (American Heart Association [AHA], 2005). Of the approximately 912,000 deaths from CVD in 2002, 53% were due primarily to coronary artery disease (CAD) and 18% were due to stroke. In addition, CVD is a contributing factor in another 500,000 deaths, meaning that in 2002 CVD mortality was nearly 60% of total mortality in the United States (AHA, 2005).

CVD is caused or worsened by comorbidities such as diabetes, high blood pressure, hyperlipidemia, kidney disease, and/or connective tissue disease. Patients with multiple medical problems present the palliative care clinician with challenges in balancing the risks and benefits of treatments.

Heart failure is a broad term for a clinical syndrome characterized by the inability of the heart to maintain an adequate cardiac output to sustain the demands of the tissues. HF can result from left or right ventricular dysfunction and is usually characterized by symptoms such as fatigue and dyspnea and signs such as fluid volume overload (Albert, 2005).

The syndrome of HF historically has been considered to be synonymous with diminished contractility of the left ventricle (LV), resulting in a reduced left ventricular ejection fraction (LVEF). This is commonly known as systolic HF (Hunt et al., 2005). However, it is currently understood that HF also exists in many patients who have a normal or near-normal ejection fraction. Diastolic failure, in which increased resistance to ventricular filling during diastole is noted, is present with a preserved LVEF of 40% or more (Albert, 2005). The current incidence of diastolic failure is believed to be approximately 50% of all patients diagnosed with HF (McEntegart & Gray, 2004).

Some causes of diastolic HF (HF with a normal LVEF) are hypertensive heart disease, chronic pulmonary disease, valvular disease, restrictive (infiltrative) cardiomyopathies (amyloidosis, sarcoidosis, hemochromatosis), pericardial constriction, pulmonary hypertension, and obesity. HF that is associated with a normal LVEF is prevalent among elderly women, most of whom have concomitant diseases such as hypertension, diabetes mellitus, CAD, and/or atrial fibrillation. In the aging population coupled with the prevalence of diabetes, advanced practice nurses (APNs) should expect to see more patients in this category (Hunt et al., 2005).

Decreased cardiac output and high ventricular filling pressures are the two basic disorders in HF (Albert, 2005). Typically, the “congestive” manifestations include signs and symptoms such as orthopnea, paroxysmal nocturnal dyspnea, edema, ascites, and jugular venous distention, although it is important to note that not every patient with HF may present with congestive features. For that reason, the preferred term is chronic heart failure or heart failure.

As the incidence of survival in acute heart disease has increased, the number of people living with chronic heart disease has risen. HF has been diagnosed in approximately 5 million persons in the United States, with over 550,000 new diagnoses each year. HF was the primary and secondary diagnosis in 3.6 million hospitalizations in 1999 (Koelling, Chen, Lubwama et al., 2004). HF was the primary cause of death for 53,000 patients in 2001 and approximately 55,000 in the 2002 (Hunt et al., 2005).

Over the years, theories regarding the pathophysiologic processes of HF progressed from an initial belief that viewed HF as a low cardiac output state that was treated with inotropic therapy to the most recent model that describes neurohormonal activation and inflammatory response (Davis, Albert, & Young, 2005). HF may be classified as systolic (LVEF less than 40%) or diastolic (decreased ventricular compliance with a normal LVEF).

To understand current recommended treatment, health care providers should be familiar with the pathophysiology of HF. Although the process is complex, there are three general processes that occur in response to stress or injury of the myocardium: neuroendocrine activation, ventricular remodeling, and immune system upregulation (Albert, Eastwood, & Edwards, 2004). When the injured myocardium is unable to contract with sufficient force to maintain adequate organ perfusion, these three processes are activated to increase cardiac output. However, these compensatory mechanisms become counterproductive over time and lead to ventricular remodeling. Ventricular remodeling, in which myocytes elongate and form a spherical shape, further activates neurohormones and cytokines to adversely affect cardiac structure and function. This contributes to stress on the myocardium and contributes to morbidity and mortality (Albert, 2005). One of the primary goals in treatment of HF is to reverse ventricular remodeling, irregardless of whether the patient is in acute or chronic HF (Albert et al., 2004).

For decades, the New York Heart Association (NYHA) functional classification of HF patients has been useful in helping researchers and clinicians compare the severity of HF between groups of patients or to compare a single patient’s physical function throughout the course of disease (see Table 10-1). Patients often move back and forth between levels of clinical functioning. For example, an impaired patient functioning in class IV (completely incapacitated, with symptoms at rest) as a result of exacerbating factors that include a recent MI, anemia, thyroid disease, or not adhering to prescribed medications could return to class III (less than ordinary physical exertion causes symptoms) after rehabilitation.

The ACC/AHA Task Force on Heart Failure Practice Guidelines has published guidelines for the diagnosis and management of chronic HF. These guidelines were first published in 1995 and revised in 2001 and 2005. The primary emphasis has been to develop a staging system that could reliably and objectively identify patients during the course of disease and link treatments based upon each stage of illness (Hunt et al., 2005). This staging system is intended to complement, but not replace, the NYHA functional classification.

The chest radiograph, when considered with the clinical assessment of the patient and the 12-lead electrocardiogram (ECG), can have a high predictive value for HF. The chest radiograph may show cardiomegaly and pulmonary venous congestion. The ECG may reveal left ventricular hypertrophy, changes suggestive of ischemic heart disease, or an arrhythmia such as atrial fibrillation. However, neither chest radiography nor the 12-lead electrocardiogram provides sensitive information regarding the degree of HF or its etiology (McEntegart & Gray, 2004).

The most widely used and most preferred test to confirm HF is a two-dimensional echocardiogram with Doppler flow studies. This test can confirm the diagnosis of HF (systolic or diastolic) and reveal measurements such as wall motion abnormalities, LVEF, and chamber size, thus helping to determine etiology and guide further management (Davis et al., 2005).

Brain natriuretic peptide (BNP) is a neurohormone released by the cardiac ventricles in response to fluid overload and volume expansion in the failing heart. BNP elevations are seen in both systolic and diastolic failure, although the BNP does not aid in distinguishing systolic from diastolic failure (Davis et al., 2005; Wu & Yu, 2005). Although BNP blood levels are sometimes used to support a diagnosis of HF, further studies are needed regarding the use of BNP levels in guiding therapy. It is important to note that, as with any other laboratory data, the clinical presentation of the patient must also be considered (McEntegart & Gray, 2004).