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Nurse Practitioner:
doi: 10.1097/01.NPR.0000450744.47604.d4
Feature: HEART FAILURE

A snapshot of the latest heart failure guidelines

Caboral-Stevens, Meriam F. MSN, NP-C

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Author Information

Meriam F. Caboral-Stevens is a lecturer at SUNY Downstate Medical Center, College of Nursing, Brooklyn, N.Y.

The author has disclosed that she has no financial relationships related to this article.

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Abstract

Heart failure (HF) is a complex chronic condition with high morbidity and mortality. The purpose of this article is to present a snapshot of the 2013 ACCF/AHA guidelines focusing on management and treatment of HF in primary care.
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Heart failure (HF) is a chronic condition associated with disability, disparity, and economic burden. Approximately 5 million Americans have clinical symptoms of HF, and despite advances in treatments, the morbidity, mortality, and rehospitalization rates remain high.1 It is estimated that the total costs of taking care of patients with HF in 2012 was $31 billion, and this number is forecasted to increase to $70 billion by 2030.2 This economic burden arises from a loss of productivity, cost of healthcare services, and medications.2 The disease also affects the Black population disproportionately compared with Whites.3,4 More importantly, functional capacity is impaired in HF, thus causing a significant decline in the individual's quality of life (QOL).5

Due to the significant impact of HF on the individual and society, there is an urge toward prevention, early identification, and control through adherence with a treatment regimen. Significant advances in HF research have prompted the American College of Cardiology Foundation and the American Heart Association (ACCF/AHA) to revise the HF guidelines.6 Therefore, the purpose of this article is to review the current management and treatment of HF based on the 2013 ACCF/AHA guidelines with emphasis on primary care.

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Level of evidence

Each recommendation in the guidelines is assigned a classification of recommendation (CR) and level of evidence (LOE). The LOE consists of level A recommendations that are derived from multiple randomized controlled trials or a meta-analysis. Level B recommendations are from single randomized or nonrandomized trials, and Level C recommendations are based on expert opinions, case studies, or standards of care. The CR ranged from Class I, in which treatments or procedures should be administered or performed, to Class III, in which treatments or procedures either showed no benefit or may be harmful to the person. Class II is based upon whether the treatment or procedure's benefit outweighs the risk to the individual.6 Class II is divided into IIa (in which it is reasonable to perform the treatment or procedure) and IIb (in which performing the treatment or procedure may be considered).6 Additionally, the term guideline-directed medical therapy (GDMT) has been designated in these guidelines to represent optimal medical therapy, which are primarily the Class I recommendations.6

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Definition of terms

HF is defined as a complex clinical syndrome resulting from any structural and functional abnormalities in ventricular filling or ejection of blood that causes cardinal symptoms of dyspnea and fatigue, which may limit exercise tolerance and cause fluid retention (subsequently leading to congestion and edema).6 HF is not synonymous to left ventricular (LV) dysfunction or cardiomyopathy (CM). LV abnormalities may vary from patients with preserved ejection fraction (EF) and a normal left ventricle to patients with markedly reduced EF and severely dilated left ventricle.6

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Ejection fraction

Ejection fraction is the percentage of blood pushed out of the left ventricle per minute, and EF can be easily measured by echocardiogram.7 The EF values, however, may be affected by the operator, the technique used, and the method of analysis.7 A normal EF is defined as between 50% and 85%.8 Ejection fraction measurement has been utilized to differentiate between systolic and diastolic dysfunction. However, the present guidelines used the terms HF with reduced EF and HF with preserved EF to distinguish systolic from diastolic HF based on EF measurements.6 HF with reduced EF (HFrEF) is defined as the presence of clinical diagnosis of HF combined with an EF of 40% or less.6 HF with preserved EF (HFpEF) is categorized into the following: those with EF of 50% or greater; those with EF between 41% and 49% (HFpEF, borderline); and those who had improved HFpEF of greater than 40%. HFpEF is diagnosed based on the presence of clinical signs and symptoms of HF, evidence of preserved or normal EF, and evidence of abnormal LV diastolic dysfunction based on echocardiogram or cardiac catheterization. Patients who previously had reduced EF but had improvement or recovery in the EF are categorized as HFpEF improved.6

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HF classifications

At present, two recognized classifications are used in the management of HF. In 2001, the ACC/AHA developed four stages of HF that depict the progressive nature of the disease.9 The four stages of HF are sub-categorized into those who are at high risk for developing HF and those with clinical diagnosis of HF. Stages A and B are those identified at high risk and without clinical symptoms of HF; those in Stage A are without structural heart disease, whereas those in Stage B have structural heart disease. Stages C and D are individuals with clinical diagnosis of HF with Stage D identified as those in advanced or refractory state of HF who may require specialized interventions.9 In addition to the new staging, the New York Heart Association Functional Classification (NYHA-FC) is a widely used tool to evaluate the functional capacity of individuals with clinical diagnosis of HF.10 This classification ranged from NYHA-FC I, patients who do not have any symptoms, to NYHA-FC IV, patients who have symptoms even at rest.10 The two classifications are complementary in nature.

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Risk factors

Adults over the age of 40 have an estimated 20% lifetime risk of developing HF.6 It is, therefore, imperative to identify people at increased risk for developing the disease and address this as early as possible to prevent progression (see Known risk factors and other causes of HF). Because of the extensive list of risk factors identified, it is beyond the scope of this article to review each risk factor individually.

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Assessment

Initial evaluation. Class I recommendations include a comprehensive history and physical exam and should be performed in patients presenting with signs and symptoms of HF in order to obtain invaluable information as to the cardiac and noncardiac causes of HF. A three-generation family history must be obtained to determine history of familial CM for patients with idiopathic dilated CM. A patient presenting for the first time for HF evaluation requires initial lab tests, which include a complete blood count, comprehensive metabolic panel, fasting lipid profile, urinalysis, and thyroid function test. Serial monitoring of a basic metabolic panel is recommended as indicated. In addition, a 12-lead electrocardiogram is recommended for all patients initially presenting with HF. In the ambulatory care setting, measurement of biomarkers, B-type natriuretic peptide (BNP), or N-terminal pro BNP is recommended to support clinical decision making regarding diagnosis of HF as well as in establishing the prognosis or severity in chronic HF. These two biomarkers are used in establishing the presence and severity of HF. These biomarkers are particularly useful in excluding a diagnosis of HF in a situation where the etiology of dyspnea is unclear.6

Ongoing evaluation. During subsequent encounters, it is recommended that vital signs and volume status, which includes weight, estimation of jugular venous pressure, and presence of edema or orthopnea, must be assessed.6 Routine assessment of the patient's potential for adverse events using multivariable risk scores is also considered reasonable during standard evaluation.6 Risk stratification could help guide clinicians in making decisions particularly when a patient's condition has progressed rapidly to an advanced stage. The Seattle Heart Failure Model is a well-established risk score that can be used in the primary care setting.11 This risk score is also available online: depts.washington.edu/shfm/app.php.

Other diagnostics to consider. Coronary angiography is reasonable for patients who are eligible for angioplasty when ischemia is the contributing factor in the development of HF. Endomyocardial biopsy may be useful when a specific diagnosis is suspected. However, endomyocardial biopsy should not be used for routine evaluation for HF.6

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Plan of care

Stages A and B (at risk). Recommendations for individuals with Stage A HF include control of hypertension and lipid disorders in accordance with contemporary guidelines (Class I recommendation). In addition, other conditions or factors that may contribute to the development of HF should be controlled or avoided. These conditions or factors include, but are not limited to, obesity, diabetes mellitus, and tobacco use. Those in Stage B include patients with a previous history of a myocardial infarction, asymptomatic valve disease, and LV remodeling, including LV hypertrophy and low EF. Class I recommendations for all patients who have recent or remote history of MI or acute coronary syndrome (ACS) and reduced EF include the use of angiotensin-converting enzyme inhibitor (ACE-I), beta-blockers, and HMG-CoA reductase inhibitors (statins). Additionally, ACE-I and beta-blockers should be used in all patients with reduced EF even without a history of MI. Angiotensin II receptor blockers (ARBs) are considered appropriate for those who are intolerant to ACE-I. Patients with structural cardiac abnormalities without a history of MI or ACS should have their BP controlled in accordance with the contemporary guidelines (Class I). An implantable cardioverter defibrillator (ICD) is considered reasonable for patients with asymptomatic ischemic CM who are at least 40 days post-MI with an EF of less than 30%, are on appropriate medical therapy, and have a reasonable expectation for survival of more than 1 year (Class II). The use of nondihydropyridine calcium channel blocker, such as verapamil and diltiazem, with negative inotropic effects may be harmful to patients who are asymptomatic with low EF and present no clinical symptoms of HF post-MI.6

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Stages C and D (clinical diagnosis of HF)

Nonpharmacologic: Patient and family education. Overall, success in care revolves around patient and family education of self-care management. Self-care management for patients with HF can be complex and frustrating for both the patients and their families. The guidelines highlighted the following aspects of patient and family education: diet/fluid restriction and weight monitoring; recognition of signs and symptoms of worsening HF; risk assessment and prognosis; QOL assessment; advanced care planning; CPR training for family members; and social support.6 Sodium restriction remains important in delaying the progression to HF. The current guidelines recommend a sodium intake of 1,500 mg per day in patients with Stages A and B, there is insufficient evidence to recommend sodium level restrictions for those in Stages C and D. Therefore, the guidelines recommend that certain degrees of restriction to less than 3,000 mg daily is considered reasonable based on current data showing that most people use at least 4,000 mg of sodium daily. Regular physical activity is recommended for those who are able to participate. Cardiac rehabilitation can be useful to stable patients with HF. Patients with HF and sleep apnea may benefit from using continuous positive airway pressure to increase EF and improve functional status.6

Pharmacologic regimen for HFrEF. Class I recommendations for patients with HFpEF include control of systolic and diastolic BP in accordance with clinical practice guidelines and the use of diuretics to relieve symptoms of fluid overload.6 (See Pharmacologic recommendations for patients with HFrEF.) Beta-blockers and ACE-I or ARB is considered reasonable to use to control BP. Coronary revascularization is considered reasonable in patients with coronary artery disease in whom angina or demonstrable myocardial ischemia has an adverse effect on symptomatic HFpEF despite optimal medical therapy. Atrial fibrillation is managed according to clinical practice guidelines. The use of an ARB might be considered for these patients to decrease hospitalization. The routine use of nutritional supplements is not recommended for these patients.6

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Strategies in achieving optimal GDMT

Achieving good outcomes occurs when the patient and the family members become actively involved in the patient's care. At the same time, clinicians should recommend individualized treatment with a focus on achieving optimum GDMT. The new guidelines have identified 10 strategies to help achieve optimum GDMT. The 10 strategies include:

  • Up-titrate drugs slowly to the target dose or highest dose tolerated by the patient
  • Certain patients, such as older adults and those with renal failure, may require frequent visits and lab monitoring during dose titration
  • Monitor vital signs including orthostatic changes in BP and heart rate, closely before and during titration
  • Adjust different medication classes
  • Monitor renal function and electrolytes for increasing creatinine and potassium levels, and discuss a tolerable creatinine level that should be maintained with the nephrologist
  • Reassure patients that symptoms of fatigue and weakness without evidence of instability are transient and usually resolve in a few days
  • Discourage discontinuation of medications without talking to their clinicians
  • Review doses of other HF medications during up-titration
  • Consider temporary adjustments of HF medications during acute noncardiac events
  • Educate patients, family members, and other clinicians on the expected benefit of GDMT.6

Device therapy. The incidence of sudden cardiac death (SCD) is increased in patients with HFrEF.12 ICD has been shown to be highly effective in preventing death from ventricular dysrhythmias.12 At the same time, ventricular dyssynchrony occurs in most patients with low or reduced EF because of progressive remodeling.13 Ventricular dyssynchrony is defined as intraventricular conduction delay, leading to discordant contraction of the right and left ventricles.13 The implantation of cardiac resynchronization therapy (CRT) facilitates synchrony of the ventricles, thus slowing down or reversal of remodeling (see Summary of the recommendations for the use of device therapy).3

Additional care for Stage D. Stage D HF, also called advanced HF, end-stage HF, and refractory HF, are those patients who continue to progress and have persistent symptoms despite maximum tolerated medical therapy.6 Recommendations can be summed up into the use of inotropic support, mechanical circulatory support, such as the ventricular assist device, and cardiac transplantation.6 Patients in Stage D are usually under the care of a specialized HF team, and besides the recommended treatments for patients with Stage C, additional care would be based on the specialized HF team's recommendations. In addition, end-of-life care should be discussed with the patient and family members or caregivers because of the advanced stage of the disease. At the same time, the need for psychosocial support for the patient, family members, or caregivers should be assessed and offered.

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Implications to practice

HF is a complex chronic illness that can have significant physical, economic, social, and emotional impact on someone afflicted with the disease. It is a condition with known risk factors, and progression to HF can be prevented by addressing these risk factors early. However, those with clinical diagnosis of HF must receive treatments to halt the progression of the disease to advanced stages. This review provides an update on the treatment and management of patients with HF in the primary care setting and is deemed necessary—particularly to advanced practice nurses who may be caring for someone with HF. This may assist clinicians, including advanced practice nurses, to ensure that patients with HF receive evidence-based treatments. Clinicians, however, are still obligated to assess each patient carefully to make sure that treatments are appropriate, do not cause harm, and the benefits outweigh the risks.

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Known risk factors and other causes of HF

Important risk factors

  • Hypertension
  • Diabetes mellitus
  • Metabolic syndrome
  • Atherosclerotic disease

Other causes of HF

  • Dilated CM
  • Familial CMs
  • Endocrine and metabolic disorders
    • - Obesity
    • - Diabetic CM
    • - Thyroid disease
    • - Acromegaly and growth hormone deficiency
  • Toxin-induced CM
    • - Alcoholic CM
    • - Cocaine CM
    • - Cardiotoxicity related to cancer therapies
    • - Other myocardial toxins and nutritional causes of CM
  • Tachycardia-induced CM
  • Myocarditis and CMs related to inflammation
    • - Myocarditis
    • - AIDS
    • - Chagas disease
  • Inflammation-induced CMs from noninfectious causes
    • - Hypersensitivity myocarditis
    • - Rheumatologic/connective tissue disorder
  • Peripartum CM
  • CM related to iron overload
  • Amyloidosis
  • Takotsubo (Stress) CM
  • Cardiac sarcoidosis

Adapted from the 2013 ACCF/AHA guidelines 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. 2013;128(16):1810–1852.

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REFERENCES

1. Go AS, Mozaffarian D, Roger VL, et al. Heart disease and stroke statistics—2013 update: a report from the American Heart Association. Circulation. 2013; 127:(1):e6-e245.

2. Heidenreich PA, Albert NM, Allen LA, et al. Forecasting the impact of heart failure in the United States: a policy statement from the American Heart Association. Circ Heart Fail. 2013; 6:(3):606–619.

3. Yancy CW. Heart failure in African Americans: pathophysiology and treatment. J Card Fail. 2003; 9:(5 suppl Nitric Oxide):S210–S215.

4. Bahrami H, Kronmal R, Bluemke DA, et al. Differences in the incidence of congestive heart failure by ethnicity: the multi-ethnic study of atherosclerosis. Arch Intern Med. 2008; 168:(19):2138–2145.

5. Austin BA, Wang Y, Smith GL, Vaccarine V, Krumholz HM, McNamara RL. Systolic function as a predictor of mortality and quality of life in long-term survivors with heart failure. Clin Cardiol. 2008; 31:(3):119–124.

6. Yancy CW, Jessup M, Bozkurt B, et al. 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. 2013; 128:(16):1810–1852.

7. Tak T. Ejection fraction derived by noninvasive modalities versus left ventricular angiographic determination. Clin Med Res. 2005; 3:(2):61–62.

8. Grubb NR, Newby DE. Cardiology. London: Churchill Livingstone; 2000:chap 19.

9. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure): Developed in collaboration with the International Society for Heart and Lung Transplantation; endorsed by the Heart Failure Society of America. Circulation. 2001; 104:(24):2996–3007.

10. The Criteria Committee of the New York Heart Association. Nomenclature and Criteria for Diagnosis of Diseases of the Heart and Great Vessels. 9th ed. Boston, MA: Little, Brown & Co; 1994.

11. Levy WC, Mozaffarian D, Linker DT, et al. The Seattle Heart Failure Model: prediction of survival in heart failure. Circulation. 2006; 113:(11):1424–1433.

12. Lane RE, Cowie MR, Chow AW. Prediction and prevention of sudden cardiac death in heart failure. Heart. 2005; 91:(5):674–680.

13. Dogar M, Caboral MF, Mitchell JE. Chronic heart failure: when to consider device therapy. Consultant 360. 2009; 49:305–310.

Keywords:

guideline-directed medical therapy; heart failure; primary care

Lippincott Williams & Wilkins.

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