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).

In discussing the signs and symptoms of disease, it is important to remember their distinction. A sign can be seen, measured, and/or described by an observer. A symptom can be described only by the patient who experiences it.

Congruent signs and symptoms are powerful indicators of disease, helping the APN make a confident diagnosis. Reconciling incongruent signs and symptoms is part of the art of nursing.

Key symptoms of HF include localized signs and symptoms (such as dyspnea, pain, orthopnea, paroxysmal nocturnal dyspnea, ascites, and edema) and generalized symptoms (fatigue, anorexia, cachexia, and weight loss) (Davis et al., 2005).

Early recognition of changes in baseline clinical status of the HF patient is crucial to minimize the incidence of acute exacerbations. Recent studies have indicated a correlation between fluid volume overload/sodium retention and rehospitalization in the end-stage HF patient (Albert, 2005; Tsuyuki, McCelvie, Arnold et al., 2001). Therefore, it is extremely important for the APN to discuss a plan of care and lifestyle recommendations with the patient and family. By incorporating lifestyle changes focused on prevention of fluid volume overload such as weighing daily and reporting early weight gains, limiting dietary sodium, and limiting fluids when indicated, the APN and patient can recognize status changes early and intervene.

Lifestyle recommendations for patients with HF often include limiting dietary sodium, obtaining regular physical exercise, weight control, cessation of smoking, and avoidance of alcohol and recreational drugs. Nursing interventions for patients with dyspnea, such as using a fan or repositioning the patient, are also helpful. Medical treatments address controlling symptoms, blood pressure, and diabetes. Medical management is discussed next.

The ACC/AHA Guidelines for the Diagnosis and Management of Chronic Heart Failure in the Adult have been and will be referenced frequently throughout this discussion. This lengthy document, based on 694 current clinical references, gives authoritative recommendations for the medical care of HF patients, from those who are at risk for the disease to those dying of it. The recommendations are aimed at preserving cardiac function and decreasing ischemic burden.

Interventions given in the ACC/AHA guidelines are organized according to the patient’s NYHA functional classification and ACC/AHA stage, as detailed in Table 10-1. In the ACC/AHA staging system, patients in stage A are classified “at risk” for HF, while patients in stage B are classified as having HF but being asymptomatic. Palliative care patients fall into stage C (systolic dysfunction; currently has symptoms) or stage D (end-stage/advanced systolic dysfunction).

Although historically patients with HF with diastolic dysfunction were believed to require separate treatment, researchers such as Wu and Yu (2005) are gathering data that indicate that treatment for both of these diseases are similar. However, Wu and Yu point out that patients with diastolic dysfunction do not tolerate tachycardia as well as might patients with systolic dysfunction.

Patients in stage C have structural heart disease and prior or current symptoms of HF. For them, the same lifestyle recommendations apply as for stage A and B patients (smoking cessation, exercise, and the control of weight, hypertension, and blood lipid levels), with the additional recommendation for dietary salt restriction, usually “no added salt” or 2 g or less of sodium per day. Medications added are diuretics for fluid retention, angiotensin-converting enzyme inhibitors (ACEIs), or β-blockers; other possible medications are aldosterone antagonists, adrenergic receptor blockers (ARBs), digitalis, hydralazine, and nitrates (Hunt et al., 2005).

Not all medications in each group are recommended for use at stage C. The only β-blockers recommended are bisoprolol, carvedilol, and metoprolol succinate. All ACEIs may be used except benazepril, moexipril, and perindopril. Of the ARBs, only candesartan and valsartan are recommended (Hunt et al., 2005).

A patient in stage C can have a widely varying clinical status, from relatively symptom free to being hospitalized. The syndrome may be completely controlled for long periods of time, with only minor episodes of increased symptoms. Over time, or suddenly, the disease may worsen and require increased interventions. Biventricular pacing devices and implantable cardioverter-defibrillators (ICDs) may be recommended and may provide marked improvement in the patient’s quality of life, enabling him or her to enter another period of improved functioning.

For patients whose disease has progressed to stage D, or end-stage HF, the symptoms are no longer mild or intermittent but are refractory. Despite maximal medical therapy, these patients are disabled, with symptoms at rest. There are no overall recommendations made for medication in stage D. At this stage, either experimental or only comfort medications will be used (Hunt et al., 2005).

Patients in stages C and D should be encouraged to avoid aspirin and nonsteroidal antiinflammatory drugs, which block ACEI activity, worsen renal function, and increase retention of sodium and fluid in HF (Masoudi, Wang, Inzucchi et al., 2003).

Congestion is one of the most problematic symptoms with end-stage HF. Most patients are on loop diuretics, usually furosemide (Lasix). However, bioavailability in furosemide varies (it is believed to be approximately 50%, although the range is 10% to 90%), and if the patient is experiencing “diuretic resistance,” it may be helpful to switch to another loop diuretic, such as bumetanide (Bumex) or torsemide (Demadex) (Taylor, 2003).

Electrophysiologic devices that are commonly used are cardiac resynchronization therapy, biventricular pacing (pacemakers), and ICDs for cardioversion and defibrillation as needed. These devices are targeted for patients with structural heart disease and HF. Patients with device therapy tend to experience improved quality of life, increased exercise tolerance, and improved mortality (Davis et al., 2005).

Ventricular arrhythmias (particularly ventricular fibrillation and ventricular tachycardia) are common in patients with reduced LVEF, and drug therapy alone may not always be effective in arrhythmia prevention (Taylor, 2003). The ICD provides monitoring and treatment for cardiac arrhythmias and, when appropriate, delivers an electric shock for recognizably lethal rhythms such as ventricular flutter or fibrillation. These shocks are strong enough to be uncomfortable for the patient; many patients experience the sensation of “being kicked in the chest.”

It is important to make a distinction between pacemakers and ICDs when providing the palliative care or hospice patient with information. Although both devices can be deactivated in a painless and noninvasive manner, the deactivation of a pacemaker may be likely to induce symptomatic bradycardia and perhaps a poorer quality of death, whereas deactivating an ICD is unlikely to decrease quality of life (except that a fatal arrhythmia would not be corrected) and will prevent the distress of shocks (Ballentine, 2005).

The ACC/AHA guidelines recommend discussion of the option of inactivating ICDs for patients with HF at end-of-life (Hunt et al., 2005), but each patient must be afforded the opportunity to make a well-informed decision based on his or her goals.

Because CVD is so prevalent, an APN can expect to see many such patients and can be a positive influence for each of them. APNs have a crucial role in collaborating with physicians and other members of the health care team to provide physical, psychosocial, and spiritual care for the cardiovascular patient.