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  1. Sherrod, Melissa M. PhD, RN, NE-BC
  2. Cheek, Dennis J. PhD, RN, FAHA
  3. Seale, Ashlie MSN, RN


Hospitals are under immense pressure to reduce heart failure readmissions that occur within 30 days of discharge, and to improve the quality of care for these patients. Penalties mandated by the Affordable Care Act decrease hospital reimbursement and ultimately the overall cost of caring for these patients increases if they are not well managed. Approximately 25% of patients hospitalized for heart failure are at high risk for readmission and these rates have not changed over the past decade. As a result of an aging population, the incidence of heart failure is expected to increase to one in five Americans over the age of 65. Pharmacologic management can reduce the risk of death and help prevent unnecessary hospitalizations. Healthcare providers who have knowledge of heart failure medications and drug interactions and share this information with their patients contribute to improved long-term survival and physical functioning as well as fewer hospitalizations and a delay of progressive worsening of heart failure.


Article Content

Scope of the Problem

Heart Failure (HF) remains one of the most important public health concerns in the United States. The number of newly diagnosed cases has risen to over 650,000 annually. Approximately 5.7 million Americans have HF and over 250,000 deaths occur each year. HF is a complex syndrome that is related to advancing age and is characterized by dyspnea and fatigue. In a nationally representative sample of nearly 3 million Medicare recipients, the incidence of HF increased from 17 to 20 per 1,000 individuals aged 65-69 but declined from 38 to 32 per 1,000 individuals for patients age 70 to 79, from 58 to 48 per 1,000 for individuals 80-84 years of age, and from 92 to 80 per 1,000 individuals for patients above 85 years of age (Curtis et al., 2008).

Figure. No caption a... - Click to enlarge in new windowFigure. No caption available.

The lifetime risk of developing HF is 20 per 1,000 for those aged 40 and above (Yancy et al., 2013). Primarily a disease of the elderly, 75% of hospital admissions for HF are for persons over the age of 65. From a public health perspective, the concern is the expectation that by 2050, one in five Americans will be over the age of 65. In the United States, the most common etiologies of HF are arteriosclerotic cardiovascular disease and hypertension. Common environmental factors that contribute to the development of the disease include obesity, smoking, diet, sedentary lifestyle, alcohol abuse, and illicit drug use (Bope & Kellerman, 2015; Yancy et al., 2013).


The annual cost to treat HF in the United States is currently estimated at 40 million dollars a year (Bope & Kellerman, 2015). This includes the cost of healthcare services, the cost of medications, and lost productivity. In spite of this outlay of resources and an increasing survival rate, about half of the people with HF will die within 5 years of diagnosis (Go et al., 2013). Disparities exist in the prevalence of HF, with Black males having the highest risk and White women having the lowest risk. In addition, Black individuals have a greater 5-year mortality rate than Whites. HF rates in Black males and females have a prevalence of 4.5% and 3.8% respectively versus that of White males and females, which is 2.7% and 1.8% (Yancy et al., 2013).


Signs and Symptoms

Symptomatic HF is a clinically complex, progressive syndrome that is the result of structural or functional impairment of filling or ejection of blood flow and is associated with activation of neurohormonal systems. Characteristic symptoms of HF are dyspnea and fatigue, which limit exercise tolerance and increase fluid retention (Yancy et al., 2013). In fact, exercise intolerance due to dyspnea or fatigue is the most common presenting symptom in patients with HF (Bope & Kellerman, 2015). These symptoms may lead to pulmonary edema, splanchnic congestion, and peripheral edema. Some patients report symptoms of exercise intolerance without edema, whereas others report fatigue, dyspnea, and edema. Because of variations in patient's experience and lack of evidence of fluid overload, the term congestive HF is no longer recommended (Yancy et al., 2013).


Other nonspecific symptoms also reported are nocturnal nonproductive cough, orthopnea, paroxysmal nocturnal dyspnea, nocturia, dependent edema, and nocturnal wheezing in the absence of asthma or palpitations. Symptoms that indicate advanced HF include nausea and poor appetite. Evidence of predisposing symptoms related to conditions such as hypertension, diabetes mellitus, metabolic syndrome, or obesity should heighten suspicion regarding underlying HF (Yancy et al., 2013).


HF is a chronic condition that may take years to develop or may be sudden in onset due to a cardiac event such as a myocardial infarction (MI). The disease cannot be cured but symptoms can be treated to improve quality of life and help avoid hospitalization. Clinically, most individuals with HF have symptoms due to impaired left ventricular (LV) function, though HF is not synonymous with LV dysfunction or cardiomyopathy as some assume. In most patients, systolic and diastolic dysfunction is present simultaneously irrespective of ejection fraction (EF). EF is considered important in classifying patients with HF for a variety of reasons chief among them patient's demographics, comorbid conditions, prognosis, and response to therapies and because most clinical trials select participants based on EF (Yancy et al., 2013).


Patients with HF may have normal LV size and preserved EF (HFpEF) or may present with severe dilation and markedly reduced EF (HFrEF). The diagnosis of HFpEF is more challenging than HFrEF because it is chiefly based on ruling out noncardiac symptoms that are suggestive of HF. HFpEF is also more commonly seen in hospitalized patients and is increasing in prevalence. In the general population, patients with HFpEF are most likely older females with hypertension. Diabetes mellitus, coronary artery disease, hyperlipidemia, atrial fibrillation, and obesity are also highly prevalent in population-based studies, although hypertension is the most common comorbid factor. There is little evidence that drug treatment improves clinical outcomes in patients with HFpEF (Yancy et al., 2013). The definition of HFrEF varies in the literature, however, randomized clinical trials in patients with HF have mainly enrolled patients with HFrEF with an EF <=35% or <=40%, and it is only in these patients that effective therapies have been demonstrated (Table 1).

Table 1 - Click to enlarge in new windowTable 1. Descriptions of Heart Failure With Preserved or Reduced Ejection Fraction

Diagnostic Studies

The diagnosis of HF should primarily be clinical, with laboratory and diagnostic procedures adding to the initial diagnostic impression. Chest radiography and 12-lead electrocardiography are low-risk procedures that can assist with diagnosis (Bope & Kellerman, 2015). A chest radiograph may show cardiomegaly, pulmonary edema, or plural effusions. Echocardiography should be used to estimate EF and subsequently cardiac output, diastolic dysfunction, ventricular size, wall thickness, and valvular abnormalities. Standard laboratory results are typically nonspecific but in more advanced cases can offer data to support findings of impaired end-organ perfusion, such as elevations in serum urea nitrogen, creatinine, or liver transaminases (Yancy et al., 2013). Patients with HF may also be anemic or malnourished, which suggests severe HF. Although not diagnostic, laboratory data are adjunctive and indicative of complications. For this reason, serum electrolytes, glucose, blood urea nitrogen (BUN), creatinine, liver function tests, complete blood count, and thyroid stimulating hormone should be obtained (Brashears, 2006). Plasma brain natriuretic peptide is helpful to differentiate patients with cardiac disease who present with dyspnea (Bope & Kellerman, 2015).


Decreasing Readmissions

HF is the chief diagnosis for over 1 million hospitalizations annually; a number that has not changed over the past decade. Approximately 25% of patients hospitalized for HF are at high risk for readmission within 30 days for a variety of reasons (Krumholz, 2009). In 2005, the Centers for Medicare and Medicaid reported that the 30-day rehospitalization rate for patients discharged to home healthcare services was 26%. Of patients rehospitalized from home healthcare services, 42% had cardiac-related diagnoses, many of which the report notes were avoidable (Albert et al., 2015). Postdischarge services are growing but they are not slowing the rate of rehospitalization.


Due to Affordable Care Act penalties for high readmission rates, hospitals are under immense pressure to reduce unnecessary admissions and improve the quality of care provided to this population. The type of service, service delivery depth and breadth, ongoing communication during the service delivery period, and quality monitoring for delivery of best practices may be more important than simply increasing available service options (Albert et al., 2015).


Several factors that increase the risk of hospital readmissions have been identified: longer length of stay during the index hospitalization, emergency room admissions within 6 months of discharge, LV function, patient's age, smoking cessation counseling, and number of hospital readmissions within the year (Albert et al., 2015; Au et al., 2012). Studies note that a higher patient socioeconomic status, household income, and a bachelor's degree or higher were important factors in improved 30-day outcomes (Albert et al., 2015). Patients who report strong social support have lower hospitalization rates and lower mortality risk than patients who lack a social support network. Social support is thought to reduce stress and promote adherence to the treatment plan as well as maintenance of a healthy lifestyle (Yancy et al., 2013).


Providing ongoing patient and family education is vital for success. Patients who have access to outpatient monitoring through a disease management program have improved outcomes and better quality of life as compared to patients who do not have access to this resource. Examples of education related to self-care activities include information on dietary sodium and dietary restrictions, weight reduction, daily exercise, taking medications as prescribed, and sleep hygiene. Providers should be alert to the fact that many patients with HF are at increased risk of sleep apnea and underreport sleep disturbance. Treatment of obstructive sleep apnea with nocturnal continuous positive airway pressure has demonstrated a reduction of the apnea-hypopnea index, improved nocturnal oxygenation, increased left ventricular ejection fraction (LVEF), lowered norepinephrine levels, and an increase in the distance walked in 6 minutes and dramatically improved symptoms such as fatigue (Bope & Kellerman, 2015; Yancy et al., 2013).


Pharmacological Management

First-line medications can reduce the risk of death and reduce hospitalization in patients with HFrEF. Unless there is a specific contraindication, all patients with HF with reduced EF (LVEF <=40%) should take both an angiotensin-converting enzyme (ACE) inhibitor and a beta-blocker, and if volume overloaded, a diuretic as well (Medical Letter, 2015). Antialdosterone therapy is now recommended for all symptomatic patients in the New York Heart Association (NYHA) functional Class II-IV. Previously reserved for those who remained symptomatic despite optimal doses of a vasodilator and a beta-blocker therapy, new data suggest that all symptomatic HF patients in this functional class benefit from an aldosterone antagonist. In addition, an aldosterone antagonist is recommended for those with symptomatic LV dysfunction after acute MI (Bope & Kellerman, 2015). See Table 2.

Table 2 - Click to enlarge in new windowTable 2. Medication Summary

Angiotensin-Converting Enzyme (ACE) Inhibitors

All patients with HFrEF should receive an ACE inhibitor. These drugs improve symptoms over a period of 4 to 12 weeks, decrease the risk of hospitalization, and prolong survival (Medical Letter, 2015). ACE inhibitors provide many benefits to the patient with HF. The agents lower arteriolar tone, which improves regional blood flow and reduces cardiac afterload, which increases cardiac output. They reduce pulmonary congestion and peripheral edema by causing venous dilation. ACE inhibitors also dilate blood vessels in the kidney, which increases renal blood flow and thereby increases sodium and water excretion. The net result of this loss of fluid is two-fold: it helps reduce edema and by lowering blood volume, decreases venous return to the heart, which reduces heart size. ACE inhibitors also may prevent or reverse pathologic changes in cardiac structure by suppressing aldosterone and reducing local production of angiotensin II in the heart (Bope & Kellerman, 2015; Lehne, 2012).


The current guidelines recommend that patients who have HFrEF or systolic HF should receive ACE inhibitors such as captopril, enalapril, fosinopril, lisinopril, quinapril, ramipril, or trandolapril. There is no data demonstrating that one ACE inhibitor is more effective than another in the treatment of HF (Yancy et al., 2013).


Home Healthcare Clinician Considerations

Patients should be advised to notify their provider should any of the common side effects of taking ACE inhibitors occur. The most common adverse drug reactions observed with ACE inhibitors are cough, hypotension, and hyperkalemia (Yancy et al., 2013). Cough, defined as persistent, dry, irritating, and nonproductive, occurs in 5% to 10% of patients and is the most common reason for discontinuing therapy. Providers should be aware that the risk of cough increases with advanced age, in females and in Caucasians. The cough subsides within 3 days after discontinuing an ACE inhibitor and is gone within 10 days (Lehne, 2012).


Another common side effect is first-dose hypotension, which is a precipitous drop in blood pressure, and may occur following the first dose of an ACE inhibitor. To minimize this reaction, patients should be advised to temporarily discontinue diuretics 2 to 3 days prior to starting an ACE inhibitor. Blood pressure should be monitored for several hours following the first dose. If hypotension develops, the patient should be advised to assume a supine position. Blood pressure can be raised if necessary with an infusion of normal saline (Lehne, 2012).


Hyperkalemia is rare for most patients, but most likely to affect those taking potassium supplements, salt substitutes (which contain potassium), or a potassium-sparing diuretic such as amiloride, triamterene, and the spironolactones. Patients should be instructed to avoid potassium supplements and potassium-containing salt substitutes unless prescribed by their provider (Lehne, 2012).


ACE inhibitors should be used with caution in patients with systolic blood pressure <80 mm Hg, serum creatinine >3, serum potassium >5.0 mEq/L, or bilateral renal artery stenosis. They should not be used in patients with a history of angioedema. ACE inhibitors should not be used in pregnancy as they can increase fetal mortality (Medical Letter, 2015). Patients taking an ACE inhibitor should be monitored for renal function, serum potassium levels, and blood pressure (Lehne, 2012).


Angiotensin Receptor Blockers (ARB)

The common adverse drug reactions observed with the ACE inhibitors can be avoided by replacing the ACE inhibitor with an angiotensin II receptor blocker (ARB) such as candesartan, valsartan, and losartan. ARBs prevent the binding of angiotensin II to the angiotensin receptor that results in increased sodium and water excretion and reduced blood pressure. Just as in the case of ACE inhibitors, ARBs should be used in patients with HFrEF or systolic HF. Although ACE inhibitors block production of angiotensin II, ARBs block the actions of angiotensin II. Although ACE inhibitors and ARBs have similar effects, the evidence does not indicate that the two are commensurate in effectiveness. ACE inhibitors are clinically superior to ARBs in reducing cardiovascular morbidity and mortality; however, for patients who cannot tolerate ACE inhibitors, ARBs are an acceptable second choice. Like ACE inhibitors, ARBs improve symptoms, reduce the incidence of hospitalization, and reduce the risk of death in patients with HFrEF (Svanstrom et al., 2012).


Home Healthcare Clinician Considerations

Common adverse drug reactions observed with the ARBs are hypotension and hyperkalemia. In contrast to ACE inhibitors, ARBs do not promote accumulation of bradykinin in the lung, and hence do not produce cough. Most ARBs are well tolerated; however, there are side effects worth noting. The most common is angioedema. The mechanism of action is not well understood; however, Lehne (2012) suggests that it is might be due to an increase in bradykinin as ARBs do not inhibit bradykinin like ACE inhibitors. If angioedema occurs, it should be withdrawn immediately, noted in the patient's record, and never used subsequently. Severe reactions are treated with subcutaneous epinephrine (Lehne, 2012).


As with ACE inhibitors, blood pressure, renal function, and serum potassium concentrations should be monitored in patients taking an ARB. Angioedema may occur in patients taking an ARB who had previously developed it while taking an ACE inhibitor, although it occurs less frequently with ARBs. ARBs can increase fetal mortality and should not be used in pregnancy (Medical Letter, 2015).



Unless there are specific contraindications, all patients with stable HF with reduced EF should receive a beta-blocker (BB) in addition to the ACE inhibitor or ARB if ACE inhibitor is intolerant. BBs are used in systolic or diastolic HF. The use of carvedilol, extended-release metoprolol succinate, or bisoprolol in conjunction with an ACE inhibitor has consistently demonstrated a 30% to 40% reduction in both hospitalization and mortality (Lund et al., 2014). The BB blocks the beta-receptors from interacting with norepinephrine and epinephrine on numerous tissues but especially heart, lung, and kidney. The result is improved LVEF, an increase in exercise tolerance, reduced need for hospitalization, slowing the progression of HF, and prolonged survival (Lehne, 2012).


Home Healthcare Clinician Considerations

The common adverse drug reactions observed with BB are fatigue, hypotension, bradycardia, masking of hypoglycemia, asymptomatic fluid retention, and worsening of HF within the first 2 to 4 weeks of initiating treatment. To combat these effects, doses must be very low initially and then gradually increased. Full benefits may not be seen for up to 3 to 6 months (Lehne, 2012). Common patient reactions that should be included in patient education efforts warn against fatigue, dizziness, diarrhea, pruritus, rash, depression, dyspnea, and bradycardia. Serious reactions have been reported such as MI and ventricular arrhythmia. If the BB is discontinued abruptly, side effects can include gangrene, hepatitis, and photosensitivity. Patients should be cautioned about the risk of falls and to avoid excessive exposure to sunlight (Bope & Kellerman, 2015; Medical Letter, 2015).


Aldosterone Antagonist (AA)

The addition of an aldosterone antagonist (AA) such as spironolactone or eplerenone is recommended for patients with NYHA Class II-IV HF and reduced EF, less than <40% (Zannad et al., 2011). The evidence has demonstrated that when AA is added to the standard therapy in patients with HFrEF, there is a reduced risk of hospitalization and death. The AA blocks the binding of aldosterone to the aldosterone receptor promoting excretion of sodium and water (Sayer & Bhat, 2014).


Home Healthcare Clinician Considerations

The most common most adverse drug reaction observed with AA is hyperkalemia. Spironolactone also has antiandrogenic activity resulting in erectile dysfunction and painful gynecomastia in men and menstrual irregularities in women (Sayer & Bhat, 2014; Zannad et al., 2011). The incidence of these effects has been reported to be lower with eplerenone. Eplerenone is similar in effectiveness to spironolactone but the cost is much greater and studies comparing their use in HF is lacking (Medical Letter, 2015).


Information on additional adverse reactions that should be stressed during patient education for patients on AA includes the risk of dehydration, ototoxicity, gastrointestinal (GI) bleeding, and arrhythmias. Patients should also be educated concerning common side effects that include headache, urinary frequency, dizziness, rhinitis, diarrhea, cough, and photosensitivity. AAs should be avoided in patients with serum potassium >5.0 mEq/L and in those with reduced renal function (baseline serum creatinine >2.0 mg/dL for women or >2.5 mg/dL for men). Renal function and serum creatinine concentrations should be monitored during treatment (Medical Letter, 2015).


Combination Drugs

Hydralazine/Isosorbide Dinitrate (BiDil)

The addition of a combination of hydralazine and isosorbide dinitrate (BiDil) to standard therapy has been shown to reduce mortality and symptoms in African American patients with NYHA Class III-IV HF with reduced EF (Taylor et al., 2007). Its benefit in non-African American patients who remained symptomatic despite standard therapy is less well established, but the combination can be considered for patients who cannot tolerate an ACE inhibitor or an ARB or for those who need additional blood pressure control despite maximal doses of standard therapy (Medical Letter, 2015).


Home Healthcare Clinician Considerations

The common adverse drug reactions observed with BiDil include headache, dizziness, tachycardia, peripheral neuritis, and a lupuslike syndrome. Other possible side effects that should be included in patient education are nausea, sinusitis, vomiting, amblyopia, diarrhea, and hypotension. A word of caution is that the phosphodiesterase V inhibitors such as sildenafil, tadalafil, and vardenafil should be avoided because of the additive risk of hypotension (Taylor et al., 2007).


Second-Line Pharmacological Therapy

Medications that provide symptomatic relief but do not increase survivability and reduce hospitalizations are in the second line of pharmacological therapy. Chief among second-line drugs are diuretics. Most patients with HF have fluid retention and for these patients, diuretics provide symptomatic relief of pulmonary and peripheral edema more rapidly than other drugs used to treat HF.



Furosemide is among the most commonly used class of diuretics prescribed in the treatment of HF. It is used in situations that call for rapid, intense diuresis as in cases of pulmonary edema, which are associated with HF. They are preferred over other diuretics because they are more potent and maintain their diuretic effect even at lower estimated renal function (Khatib, 2011). Furosemide provides symptomatic relief of pulmonary and peripheral edema more rapidly than other drugs used in treatment of HF. Diuretics that act on the loop of Henle, like furosemide, bumetanide, and torsemide, are more effective in the treatment of HF than thiazide-type diuretics, which act on the distal tubule (Medical Letter, 2015).


Home Healthcare Clinician Considerations

The majority of furosemide adverse effects are caused by electrolyte imbalance. The most common adverse effect is hypokalemia (Medical Letter, 2015). Diuretics can also cause worsening of renal function. The diuretic effect of furosemide can lead to hyponatremia, hypochloremia, and dehydration. Hypokalemia can lead to dysrhythmias and toxicity when given in conjunction with digoxin. A potassium supplement or potassium-sparing diuretic, such as spironolactone or amiloride may be recommended. Other adverse effects including orthostatic hypotension, dizziness, headache, and vertigo may occur due to a reduced cardiac output. In addition, patients taking furosemide may also experience photosensitivity (Lehne, 2012; Medical Letter, 2015).


Ototoxicity is another adverse reaction that can occur with loop diuretics, especially when taken with aminoglycoside antibiotics such as gentamicin or tobramycin. Permanent damage may result from continued treatment. Patients should be instructed to report hearing loss immediately to their healthcare provider (Medical Letter, 2015).


Patients should be instructed to take the medication in the morning so that increased urine output will not disturb sleep. Patients should know that voiding frequency should decrease with time. Furosemide should be taken with meals to decrease GI upset. It is important to have the patient weigh themselves at the same time, in similar clothes, daily. Keeping a record of the daily weights is recommended. Weight loss and weight gain should be reported to the healthcare provider (Lehne, 2012).


Patients should report electrolyte disturbances and dehydration. Symptoms of dehydration include: dry mouth, unusual thirst, decreased urine output, dark urine, irritability, and weakness. Signs of an electrolyte disturbance may include: muscle cramps, muscle pain, muscle fatigue, and rarely tetany (Lehne, 2012).


Hydrochlorothiazide (HCTZ)

Diuretics such as hydrochlorothiazide (HCTZ) have been shown to provide symptomatic relief of common symptoms. These drugs provide relief more rapidly for peripheral and pulmonary edema in the treatment of HF than other classes of drugs. Diuretics that act on the distal tubule of the kidney, such as HCTZ are less effective than diuretics such as furosemide that act on the loop of Henle. The overall effect that diuretics have on mortality is not known (Lehne, 2012).


Home Healthcare Clinician Considerations

The adverse effects of HCTZ include primarily hypokalemia. Other less commonly found electrolyte disturbances include hypercalcemia, hyponatremia, hypomagnesemia, and hyperglycemia. Additionally, hyperuricemia, hyperlipidemia, headache, photosensitivity, weight gain, nausea, gout, and pancreatitis have been reported. The side effects have been found to be more prevalent when the dosage was increased to more than 25 mg per day. Medication instructions and education for HCTZ are the same as for furosemide, with the exception of ototoxicity (Lehne, 2012).


Cardiac Glycosides

Digoxin is a cardiac glycoside used to reduce the symptoms of HF. It can increase exercise tolerance and decrease hospitalizations but does not reduce mortality (Medical Letter, 2015). Digoxin is a purified cardiac glycoside derived from the foxglove plant (Digitalis purpurea) and Grecian foxglove (Digitalis lanata). These compounds increase injection fraction, augment cardiac output, and reduce pulmonary capillary wedge pressure without causing adverse increases in heart rate or decreases in blood pressure (Ambrosy et al., 2014). Moreover, in low doses, digoxin provides neurohormonal effects outside the heart. Digoxin must be administered with care to avoid the potential of dangerous adverse effects, which include dizziness, changes in mood and mental alertness, anxiety, and depression (Medical Letter, 2015).


Home Healthcare Clinician Considerations

The most common adverse effects include GI symptoms such as nausea, vomiting, diarrhea, and abdominal discomfort. Headache, weakness, visual disturbances, depression, neuralgia, and psychosis have also been reported. Digoxin toxicity may present as almost any known type of arrhythmia. The most common cause of death from digoxin toxicity is ventricular fibrillation. Bradycardia may also occur. Gastrointestinal effects and visual disturbances are reported more frequently and are therefore easier to recognize when toxicity occurs. Cardiac symptoms of digoxin toxicity generally occur later, with dysrhythmias being reported most often (Bope & Kellerman, 2015; Medical Letter, 2015).


Patients and family members should be taught how to take an apical pulse for 1 minute. If the heart rate is less than 60 beats per minute or greater than 100 beats per minute, the medication should be withheld and the healthcare provider contacted immediately. Patients and family members should be taught to perform daily weights. Lastly, if there are children in the household, the medication should be kept locked and out of their reach (Felicilda-Reynaldo, 2013).


Special Cases

ARB Plus Neprilysin Inhibitor

July 7, 2015 the Federal Drug Administration (FDA) approved the drug Entresto in the treatment of HF NYHA Class II-IV and reduced EF of less than 40% (FDA.gov, 2015). Entresto is the combination of valsartan, an ARB and sacubitril, a neprilysin inhibitor. Neprilysin is a neutral endopeptidase that degrades several endogenous vasoactive peptides such as natriuretic peptides, bradykinin, and adrenomedullin (McMurray et al., 2014). The inhibition of neprilysin causes an increase of these various substances and in combination with inhibition of the angiotensin receptor, they counter the neurohormonal overactivation that contributes to vasoconstriction, sodium retention, and remodeling observed in HF (McMurray et al., 2014). The Entresto group has a higher proportion of patients with hypotension and nonserious angioedema but also lower proportion of patients with renal impairment, hyperkalemia, and cough as compared to the enalapril group (McMurray et al., 2014).


Home Healthcare Considerations

Due to the recent approval by the FDA, the safety of the combination of valsartan and sacubitril is unknown. Because there is inadequate literature to assess the risk, caution is advised unless there are no other options available. Monitoring parameters for home healthcare clinicians include BUN and creatinine at baseline and then periodically, electrolytes, and monitoring blood pressure. Patient education should include measures to decrease risk of falls due to hypotension and the need to report side effects such as angioedema. Patients and families should be aware of other common reactions such as hyperkalemia, fatigue, back pain, and dizziness and should alert their provider if these occur (McMurray et al., 2014).


Home Healthcare Management

Patients who are encouraged to participate in self-care activities with healthcare providers who are knowledgeable about HF maintenance and management have improved outcomes and better quality of life. They experience fewer hospital readmissions and greater long-term survival. Healthcare provider's knowledge of HF medications and drug interactions is also critical to improved long-term survival, physical functioning, and vitality. Pharmacological therapy is part of a disease management and educational approach that includes therapies such as cardiac resynchronization therapy, exercise, and self-care activities (Yancy et al., 2013).


Involving the patient and family in self-management of the underlying cause of HF offers the best chance for success. Reduction of risk factors, life-style changes with dietary restriction, exercise, and education about monitoring symptoms such as daily weights, edema, chest pain, and dyspnea have demonstrated good outcomes (Yancy et al., 2013). Recommendations for the home healthcare clinician that include patient education aimed at reducing symptoms, reducing hospitalizations, and improving quality of life also include adding the MAWDS educational program to therapy options. Patients are encouraged to learn the following behaviors to assist with positive outcomes:


* Medications: Take every day; don't skip


* Activity: A little every day; don't overdo


* Weight: Daily. If gain .2 lb in a day or 5 lb above ideal, CALL


* Diet: Eat high-quality protein diet, low sodium, low carbohydrate


* Symptoms: Know the signs of worsening HF (cough, weight gain, worsening or rest dyspnea, swelling) and CALL early


* Quit smoking if smoke



Nonpharmacologic therapy may also include oxygen and noninvasive positive pressure ventilation, physical activity as appropriate, and attention to weight gain (Yancy et al., 2013).


Rapid office follow-up (1-2 weeks) after hospitalization and home healthcare monitoring by specially trained nurses have been shown to decrease frequency of hospitalizations and worsening symptoms. In addition, patients are encouraged to reduce sodium load to <1.5-2 g/day. Home healthcare clinicians should remind patients to limit drugs that may make HF worse such as Ibuprofen (Advil, Motrin) and Naproxen (Aleve, Naprosyn) and contact their provider for pain medication alternatives (Yancy et al., 2013).



HF is one of the most important health concerns in the United States. Over 650,000 new cases of HF are diagnosed annually at an estimated cost of 40 million dollars a year (Bope & Kellerman, 2015). HF is the chief diagnosis of over 1 million individuals who are hospitalized annually and approximately 25% of these patients will be readmitted within 30 days of discharge. Several factors have been identified as placing the patient at high risk of readmission. Among these are emergency room admissions within 6 months of discharge, a longer length of stay for the initial hospitalization, LV function, and the number of hospital admissions within a year.


Healthcare providers who have knowledge of HF medications and drug interactions and share this information with their patients contribute to improved long-term survival and physical functioning as well as fewer hospitalizations and a delay of progressive worsening of HF (Yancy et al., 2013).


Instructions for Taking the CE Test Online Improving Patient Outcomes With Oral Heart Failure Medications


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Albert N. M., Barnason S., Deswal A., Hernandez A., Kociol R., Lee E., ..., White-Williams C. (2015). Transitions of care in heart failure: A scientific statement from the American Heart Association. Circulation. Heart Failure, 8(2), 384-409. Retrieved from http://circheartfailure.ahajournals.org/content/early/2015/01/20/HHF.00000000000[Context Link]


Ambrosy A. P., Butler J., Ahmed A., Vaduganathan M., van Veldhuisen D. J., Colucci W. S., Gheorghiade M. (2014). The use of digoxin in patients with worsening chronic heart failure: Reconsidering an old drug to reduce hospital admissions. Journal of the American College of Cardiology, 63(18), 1823-1832. doi:10.1016/j.jacc.2014.01.051 [Context Link]


Au A. G., McAlister F. A., Bakal J. A., Ezekowitz J., Kaul P., van Walraven C. (2012). Predicting the risk of unplanned readmission or death within 30 days of discharge after a heart failure hospitalization. American Heart Journal, 164(3), 365-372. doi:10.1016/j.ahj.2012.06.010 [Context Link]


Bope E., Kellerman R. (2015). Conn's Current Therapy 2015. Philadelphia, PA: Elsevier Saunders. [Context Link]


Brashears V. (2006). Clinical Applications of Pathophysiology: An Evidence Based Approach (3rd ed.). St. Louis, MO: Elsevier Mosby. [Context Link]


Curtis L., et al. (2008). Incidence & prevalence of heart failure in elderly persons 1994-2003. Archives of Internal Medicine, 168(4):418-424. doi: 10.1001/archinternmed.2007.80. [Context Link]


Edmunds M., Mayhew M. (2013). Pharmacology for the Primary Care Provider (4th ed.). St. Louis, MO: Elsevier Mosby.


Felicilda-Reynaldo R. F. (2013). Cardiac glycosides, digoxin toxicity, and the antidote. MEDSURG Nursing, 22(4), 258-261. [Context Link]


Federal Drug Administration. (2015). FDA approves new drug to treat heart failure. Retrieved from http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm453845.htm[Context Link]


Go A. S., Mozaffarian D., Roger V. L., Benjamin E. J., Berry J. D., Borden W. B., ..., Turner M. B. (2013). Heart disease and stroke statistics-2013 update: A report from the American Heart Association. Circulation, 127(1), e6-e245. Retrieved from http://www.cdc.gov/Other/disclaimer.html[Context Link]


Khatib R. (2011). Prescribing diuretics in the management of heart failure. Nurse Prescribing, (9), 435. [Context Link]


Krumholz H. M., Merrill A. R., Schone E. M., Schreiner G. C., Chen J., Bradley E. H., ..., Drye E. E. (2009). Patterns of hospital performance in acute myocardial infarction and heart failure 30-day mortality and readmission. Circulation. Cardiovascular Quality and Outcomes, 2(5), 407-413. [Context Link]


Lehne R. (2012). Pharmacology for Nursing Care (8th ed.). St. Louis, MO: Saunders Elsevier. [Context Link]


Lund L. H., Benson L., Dahlstrom U., Edner M., Friberg L. (2014). Association between use of ?-blockers and outcomes in patients with heart failure and preserved ejection fraction. JAMA, 312(19), 2008-2018. [Context Link]


McMurray J. J., Packer M., Desai A. S., Gong J., Lefkowitz M. P., Rizkala A. R., ..., Zile M. R. (2014). Angiotensin-neprilysin inhibition versus enalapril in heart failure. The New England Journal of Medicine, 371(11), 993-1004. [Context Link]


Medical Letter on Drugs and Therapeutics. (2015). Drugs for chronic heart failure. 57(1), 9-12. [Context Link]


Sayer G., Bhat G. (2014). The renin-angiotensin-aldosterone system and heart failure. Cardiology Clinics, 32(1), 21-32. [Context Link]


Svanstrom H., Pasternak B., Hviid A. (2012). Association of treatment with losartan vs candesartan and mortality among patients with heart failure. JAMA, 307(14), 1506-1512. [Context Link]


Taylor A. L., Ziesche S., Yancy C. W., Carson P., Ferdinand K., Taylor M., ..., Cohn J. N. (2007). Early and sustained benefit on event-free survival and heart failure hospitalization from fixed-dose combination of isosorbide dinitrate/hydralazine: Consistency across subgroups in the African-American Heart Failure Trial. Circulation, 115(13), 1747-1753. [Context Link]


Yancy C. W., Jessup M., Bozkurt B., Butler J., Casey D. E. Jr., Drazner M. H., ..., Wilkoff B. L. (2013). 2013 ACCF/AHA guideline for the management of heart failure: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 128(16), 1810-1852. [Context Link]


Zannad F., McMurray J. J., Krum H., van Veldhuisen D. J., Swedberg K., Shi H., ..., Pitt B. (2011). Eplerenone in patients with systolic heart failure and mild symptoms. The New England Journal of Medicine, 364(1), 11-21. [Context Link]