Heart failure

An update for nurses

Abstract

Heart failure (HF) is a chronic syndrome that requires patients to manage signs and symptoms and adhere to a complex medication regimen. This article discusses updates in HF care related to a universal definition and new therapies, focusing on the four pillars of therapy for HF with reduced ejection fraction.

In Brief

Heart failure (HF) is a chronic syndrome that requires patients to manage signs and symptoms and adhere to a complex medication regimen. This article discusses updates in HF care related to a universal definition and new therapies, focusing on the four pillars of therapy for HF with reduced ejection fraction.

Case study

Figure

JW is a 72-year-old male with a health history that includes diabetes mellitus (DM) and hypertension (HTN). He began experiencing dyspnea after walking his dog one block, which he could previously do without difficulty. He has been sleeping in his recliner for 2 weeks because it was difficult for him to breathe lying flat in bed. He scheduled an appointment with his cardiologist.

JW's cardiologist ordered a transthoracic echocardiogram (TTE), ECG, and lab work, including complete blood cell (CBC) count, comprehensive metabolic panel, thyroid panel, and N-terminal prohormone B-type natriuretic peptide (NT-proBNP) level. He had a left ventricular ejection fraction (LVEF) of 20% (low), 10 lb weight gain, and an elevated NT-proBNP. He was diagnosed with heart failure (HF) with a reduced ejection fraction (HFrEF) Stage C (New York Heart Association [NYHA] Class II). His cardiologist prescribed an angiotensin receptor/neprilysin inhibitor (ARNi) sacubitril 24 mg-valsartan 26 mg twice daily; beta-blocker (BB) metoprolol succinate 25 mg daily; mineralocorticoid receptor antagonist (MRA) spironolactone 12.5 mg daily; and sodium-glucose cotransporter 2 inhibitor (SGLT2i) dapagliflozin 10 mg daily.

The nurse educated JW on restricting dietary sodium to reduce fluid retention, staying physically active, and enrolling in cardiac rehabilitation, as well as the trajectory of HF, and the possibility of other therapies, such as an implantable cardioverter defibrillator (ICD). He was educated on guideline-directed medical therapy (GDMT) and the importance of self-care.

JW returned 2 weeks later for re-assessment of his vital signs, serum electrolytes, kidney function, and signs and symptoms. He had frequent routine appointments afterward. The nurse used those opportunities to reinforce the prior education and assess the need for reeducation. JW's GDMT was optimized, and a repeat TTE showed his LVEF improved to 55%. His signs and symptoms resolved, and he was continued on GDMT. He continued to follow closely with his multidisciplinary HF team as well as his primary care provider to manage his other comorbidities.

Introduction

An aging population and people living longer with HF lead to the probability that nearly all nurses will encounter a patient with HF. Approximately 6 million adults older than 20 in the US have HF. The prevalence of HF is projected to increase by 46% by 2030, affecting over 8 million adults, or 3% of the US population.¹ The projected increase is due to new HF definitions and classifications, improved therapies, and downstream effects of COVID-19 on cardiovascular disease (CVD).

Generally, HF is defined as a complex clinical syndrome resulting from structural or functional impairment of ventricular filling or ejection of blood.² For decades, patients with HF have been classified using the NYHA classification system. The NYHA class is based on the patient's description of their physical functioning. Although the NYHA class is still used extensively in clinical and research settings, emphasis has recently been placed on preventing HF. A staging system based on symptoms and structural heart disease is used to identify a patient's risk of developing HF (see Stages of HF and NYHA functional classification).^2,3

Note that the LVEF plays a key role in defining the patient's type of HF. An LVEF less than or equal to 40% is labeled HFrEF, while HF with an LVEF of at least 50% is labeled HF with preserved ejection fraction (HFpEF). Patients with an LVEF between these two parameters are now classified as HFmrEF (HF with mildly reduced or midrange EF).² A new definition of HF has been proposed, which considers a patient's ejection fraction (EF) or the percentage of blood pumped out of the ventricles with each contraction.³

- Abbreviations in this article

ACC - American College of Cardiology ACEi - angiotensin-converting enzyme inhibitor AF - atrial fibrillation AHA - American Heart Association ARB - angiotensin receptor blocker ARNi - angiotensin receptor/neprilysin inhibitor BB - beta-blocker BNP - B-type natriuretic peptide cGMP - cyclic guanosine monophosphate CO - cardiac output CRT - cardiac resynchronization therapy CVD - cardiovascular disease DM - diabetes mellitus EF - ejection fraction ECG - electrocardiogram GDMT - guideline-directed medical therapy HF - heart failure HFmrEF - heart failure with mildly reduced or midrange ejection fraction HFpEF - heart failure with preserved ejection fraction HFrEF - heart failure with reduced ejection fraction

HFSA - Heart Failure Society of America HR - heart rate HTN - hypertension ICD - implantable cardioverter defibrillator If - pacemaker current LVD - left ventricular dysfunction LVEF - left ventricular ejection fraction MRA - mineralocorticoid receptor antagonist NP - natriuretic peptides NT-pro BNP - N-terminal pro B-type natriuretic peptide NYHA - New York Heart Association PUFA - polyunsaturated fatty acid RAAS - renin-angiotensin-aldosterone system RASI - renin-angiotensin system inhibition RVD - right ventricular dysfunction sGC - soluble guanylate cyclase SGLT2i - sodium-glucose cotransporter 2 inhibitor SNS - sympathetic nervous system SV - stroke volume TTE - transthoracic echocardiogram

HFrEF is the best-understood type of HF. In 2020, the American College of Cardiology (ACC), American Heart Association (AHA), and Heart Failure Society of America (HFSA) updated previous guidelines for the treatment of HF, incorporating new therapies.² The new joint guidelines highlight several important changes in the care and treatment of patients with HF.

COVID-19 had an influence on the incidence and prevalence of HF. The risk of developing HF after a SARS-CoV-2 infection increased by 72% overall, and the risk was higher in those who were hospitalized for COVID-19.⁴ There was a longer length of stay, increased need for acute care, and greater need for mechanical ventilation for patients with HF and COVID-19. Additionally, the incidence of death is more than doubled in patients with HF who contract SARS-CoV-2.⁵ The incidence of HF and CVD increased significantly in the year following a SARS-CoV-2 infection.⁴

This article provides nurses with an update on the approach and treatment of patients with HF, specifically those with HFrEF, where new therapies have emerged.

Pathogenesis

The heart's capacity to pump an adequate volume of blood to meet the oxygen and metabolic demands of the body at rest and during activity depends upon the ventricles' ability to relax and fill. During diastole, the ventricles fill and stretch as the blood volume increases. During systole, the stretched ventricles contract, ejecting approximately 70 mL of blood comprising what is known as stroke volume (SV). The proportion or fraction of blood ejected, relative to the amount of blood present in the LV before contraction, is considered the LVEF (see Ejection fraction and cardiac output).^6-8

EF is central to understanding HF. Clinical research and therapies for HF are classified by EF.^7,8 Related to EF, cardiac output (CO) is the SV ejected with each heartbeat over 1 minute. Recall that the autonomic nervous system regulates heart rate (HR), with sympathetic activation increasing HR and parasympathetic activation decreasing HR. SV is a function of preload, afterload, and contractility. The interplay among these factors maintains an adequate CO; low CO is characteristic of HF, often resulting from myocardial injury. Thus, HF is associated with derangements in these factors.

Preload, determined by the venous return to the heart, is the volume of blood in the ventricle just before contraction. Afterload reflects the force the heart must generate to eject blood from the filled ventricles. Peripheral vascular resistance and ventricular wall tension influence afterload. When peripheral vascular resistance is high, as with arterial HTN, greater pressure must be generated to eject blood out of the LV through the aortic valve and into the systemic circulation. In response to the increased pressure, the heart enlarges and changes shape.

Contractility or inotropy reflects cardiac performance. Contractility is related to calcium handling within the myocyte. All these factors are important as the CO falls and the heart tries to compensate to preserve adequate blood flow.⁸

Compensatory mechanisms

CO is maintained through compensatory mechanisms, including the Frank-Starling mechanism; neurohormonal activation through the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS); natriuretic peptides; and vasoactive substances (nitric oxide, endothelin, vasopressin). Initial compensatory changes in response to the decrease in CO may maintain heart function, and the insult may go unnoticed. However, as the heart slowly adapts, the heart remodels, changing shape and enlarging (called hypertrophy) even at the cellular level (see Compensatory mechanisms in heart failure).⁸ Although these mechanisms may successfully initially preserve CO, the heart will eventually fail, resulting in HF signs and symptoms.

Figure: Compensatory mechanisms in heart failure

Frank-Starling mechanism

The Frank-Starling mechanism explains that increased preload results in increased CO. The greater the influx of blood into the ventricle, the more forceful the contraction until muscle fibers are over-stretched or stiffened and the heart fails. Depending upon the clinical scenario, a patient may be given a positive inotrope, such as oral digoxin and I.V. milrinone or dobutamine, to increase the force of contractility.⁸ Although these drugs may help with preload and contractility, they are not without risk and require monitoring.

Sympathetic nervous system

The SNS is an integral component of the neuroendocrine compensatory response in HF. SNS activation is triggered by pressure-sensitive baroreceptors when CO falls. Myocardial oxygen demand increases, and sustained SNS activation and renal hypoperfusion actuate other neuroendocrine responses through the RAAS, causing vasoconstriction and tachycardia.

Renin-angiotensin-aldosterone system (RAAS)

The RAAS and the SNS augment SV and HR to maintain CO. Due to chronic neuroendocrine activation of these systems, hypertrophy, fibrosis, and myocardial necrosis occur. Changes within the myocytes (which lead to remodeling), impairment of the heart's pumping ability, and aberrations in the heart's electrical activity occur.

Natriuretic peptides

The heart produces and secretes natriuretic peptides (NPs)–peptide hormones with potent diuretic, natriuretic, and neuroendocrine actions. Of the NPs, B-type (BNP) has the most clinical significance in HF. In patients with HF, especially HFrEF, plasma levels of BNP are elevated. NT-proBNP and BNP assays correlate with ventricular dysfunction and are used clinically to diagnose HF and predict disease severity.^2,7,9

Risk factors

Many cardiac and noncardiac conditions, as well as aging, increase the risk of developing HF (see Risk factors and common contributors for developing HFrEF). An elevated systolic or diastolic BP is one of the most important risk factors.

Clinical manifestations of HF

Ideally, both the left and right ventricles should contract in tandem to produce and maintain CO. The clinical manifestations of HF depend on whether the left or right side of the heart is compromised; most often the left side of the heart fails, followed by the right side. Biventricular failure or dysfunction typically occurs as HF progresses. A hallmark sign of HF is fluid retention.

- Stages of HF and NYHA functional classification²

ACC/AHA Stages of HF		NYHA Functional Classification
Stage A At Risk	No structural heart disease or signs or symptoms of HF History of HTN, CVD, DM, obesity, cardiotoxicity exposure, genetics	None
Stage B Pre-HF	Structural heart disease present Evidence of increased filling pressures Elevated BNP or troponin (persistent) Confirmed risk factors Without HF signs or symptoms	Class I	No symptoms with normal physical activity Normal functional status
Stage C Symptomatic	Structural heart disease present Prior or current symptoms of HF GDMT focused on this stage	Class I	No symptoms with normal physical activity Normal functional status
		Class II	Mild symptoms with normal physical activity Functional status slightly limited
		Class III	Moderate symptoms with normal physical activity Comfortable only at rest Functional status moderately limited
Stage D Advanced	Pronounced HF symptoms Specialized treatment and interventions (I.V. milrinone/dobutamine, LVAD, transplantation) Specialized treatment and interventions (I.V. milrinone/dobutamine, LVAD, transplantation)	Class IV	Severe symptoms with minimal activity and at rest Functional status severely limited

Abbreviations: ACC, American College of Cardiology; AHA, American Heart association; BNP, B-type natriuretic peptide; CVD, cardiovascular disease; DM, diabetes mellitus; GDMT, guideline-directed medical therapy; HTN, hypertension; LVAD, left ventricular assist device; NYHA, New York Heart Association

Signs

Fluid retention or congestion can manifest in several ways. When left ventricular dysfunction (LVD) is present, the heart's ability to pump oxygenated blood to the body is impaired, leading to pulmonary congestion.¹⁰ In contrast, the failure of the right side of the heart leads to abdominal and lower extremity edema.¹⁰ Worsening congestion and right ventricular dysfunction (RVD) can be visualized by jugular vein distension when sitting or standing.⁸ Fluid retention, in combination with a decreased CO, diminishes oxygenation to skeletal muscles, causing the patient to experience symptoms such as activity intolerance and fatigue.

Symptoms

The cardinal symptoms of LVD are dyspnea and fatigue.¹¹ Difficulty breathing or dyspnea on exertion, the inability to lie flat (orthopnea), sudden onset of shortness of breath that causes awakening from sleep (paroxysmal nocturnal dyspnea), and palpitations due to tachycardia are common symptoms due to fluid retention and poor CO.¹⁰ Diminished oxygen supply to the brain leads to cognitive impairment, while poor perfusion to muscles results in activity intolerance and fatigue.⁸ In contrast, RVD affects the ability of deoxygenated blood to travel outward into the lungs and beyond. Ascites, causing a sense of abdominal fullness, and peripheral edema, causing a sense of heaviness in the lower extremities, are related to the continued backward flow of blood due to right-sided dysfunction.¹²

Dysrhythmias

Atrial fibrillation (AF) is common in HF; almost half of the patients with NYHA Class IV HF have AF.¹³ Disruption of the conduction tissue within the left atrium from LVD commonly results in atrial and ventricular tachydysrhythmias, such as uncontrolled AF and ventricular tachycardia.⁸ Ventricular tachycardia, caused by ventricular dysfunction, is a well-known source of sudden cardiac death in patient with HF.⁸

Diagnostic studies

The initial evaluation of a patient with suspected new, or “de novo,” HF is a TTE to confirm the diagnosis, additional testing for coronary artery disease (if ischemia is suspected), and revascularization if indicated.³ Reperfusion of the coronary arteries may help improve patient outcomes.^2,7 Diagnostic tests will be needed throughout the course of HF to assess disease progression and the effectiveness of therapy.

A TTE, an ultrasound of the heart, provides information on the diagnosis, EF, cardiac structures, and HF progression, which are necessary to classify and guide treatment for patients and to rule out other diagnoses. TTEs are recommended throughout the course of HF and when the patient's clinical status worsens or changes.

A chest X-ray is used to monitor the patient's initial volume status and reassess changes in the patient's symptoms reflective of volume status, such as dyspnea. For example, this imaging study may reveal cardiomegaly and causes of dyspnea, such as pulmonary edema.

An ECG is part of the routine evaluation of a patient with HF and provides information on cardiac rate, rhythm, and causes contributing to a low EF and poor outcomes, such as dysrhythmias and myocardial ischemia or infarction. Patients with HF are at high risk of developing AF or experiencing ventricular dysrhythmias resulting in sudden cardiac death.²

Lab testing identifies possible causes and other comorbidities in patients with HF, such as diabetes, renal disease, thyroid disease, and anemia. A standard diagnostic evaluation of a patient with HF includes serum electrolytes, glucose, creatinine, blood urea nitrogen, CBC, lipid profile, liver biochemical and function tests, iron studies, thyroid-stimulating hormone levels, and urinalysis. Additionally, BNP and NT-proBNP levels are often measured to determine the presence or severity of HF.² These tests are repeated as the patient's clinical status changes.

Management of HFrEF

Management of HFrEF is complex and requires coordination and care by a multidisciplinary team. The mainstay of treatment for Stage C HFrEF is GDMT. In addition to pharmacotherapy, there are nonpharmacologic treatment considerations.

Pharmacotherapy: Four pillars

The core pharmacologic treatment for Stage C HFrEF includes RAAS inhibition with an ARNi, angiotensin-converting enzyme inhibitor (ACEi), or angiotensin receptor blocker (ARB); BB; MRA; and SGLT2i. Additional therapies include hydralazine and isosorbide dinitrate (vasodilator), ivabradine (I_f inhibitor or hyperpolarization-activated cyclic nucleotide-gated channel blocker), digoxin (cardiac glycoside), and soluble guanylate cyclase stimulators. Guideline-directed medication dosing titration is recommended, as tolerated, to achieve target doses. Using ARNI/ACEi/ARB, BB, MRA, and SGLT2i together reduces the likelihood of death.¹⁴ The most recent guideline has delineated GDMT to include all four classes: RAAS inhibition with ARNi, ACEi, or ARB; BB; MRA; and SGLT2i.²

Medications that inhibit RAAS reduce death. First-line therapy for patients with HFrEF is an ARNi for RAAS inhibition.² An ACEi is recommended when an ARNi is not feasible, and an ARB when using an ARNi and ACEi is not feasible.¹⁵ For example, an ARB may be used if a patient develops a cough or angioedema. When switching between an ACEi and an ARNi, a 36-hour washout period is recommended between doses to minimize the risk of angioedema.² Patients can switch among the various RAAS inhibitors (RAASi), that is, an ARNI, ACEi, or ARB in certain instances, if the patient develops an adverse reaction as mentioned above.

In patients with HFrEF, at the time of diagnosis, a BB, such as carvedilol, metoprolol succinate (extended release), and bisoprolol, is recommended to reduce death and hospitalizations unless contraindicated.^16-18 BBs should be initiated at low doses and uptitrated to achieve the target doses.² Even if LVEF improves, BBs should be continued to reduce the risk of LV dysfunction and thus reduce the risk of major cardiovascular events.¹⁹

In patients with HFrEF and NYHA class II-IV symptoms, an MRA including spironolactone or eplerenone is recommended. The patient's kidney function and potassium level should be monitored routinely. Adverse reactions such as gynecomastia and vaginal bleeding have been observed in patients who take spironolactone. Consider temporarily stopping MRA therapy if a patient develops diarrhea or dehydration due to the risk of worsening kidney function or abnormal potassium levels.²

The 2022 guideline for the management of HF added an SGLT2i for patients with symptomatic HFrEF, irrespective of the presence of type 2 DM.^20,21 Novel mechanisms of an SGLT2i that may positively impact patients with HFrEF include volume regulation, metabolic effects, cardiorenal mechanisms, direct effects on cardiac contractility and ion-homeostasis, improved cardiac remodeling, inflammation reduction, and decreased oxidative stress.²² Serious renal adverse outcomes were infrequent, and a slower rate of decline in estimated glomerular filtration rate was observed in patients taking an SGLT2i.^20,21 Both SGLT2is, dapagliflozin and empagliflozin, are initiated at their target dose of 10 mg once daily. Monitoring parameters include blood glucose levels, kidney function (at the time of initiation), and ongoing signs and symptoms of genitourinary infections, necrotizing fasciitis, hypersensitivity reactions, volume depletion, and hypotension. The SGLT2i medications are the most recent addition to GDMT and can be initiated in the hospital or outpatient setting.

Starting quadruple therapy (the four pillars) with the above medications at low doses while routinely monitoring vital signs, kidney function, serum potassium levels, and volume status is recommended once the patient is hemodynamically stable.^2,23 This life-saving medication regimen should be initiated as soon as safely possible.

Other pharmacologic therapies

Diuretics are recommended for the management of fluid retention and congestive symptoms in patients with HFrEF. Loop diuretics are preferred; additional diuretics, such as metolazone or chlorothiazide, may be added to the loop diuretic regimen for patients with refractory edema.² Maintenance diuretic therapy should be considered to prevent recurrent congestion.² It is important to monitor kidney function and serum electrolytes. Diuretics should only be used in combination with GDMT.

Managing volume overload with diuretics is very common. However, additional drugs for special populations include hydralazine and isosorbide dinitrate, ivabradine, soluble guanylate cyclase (sGC) stimulators, cardiac glycosides, inotropes, omega-3 polyunsaturated fatty acids (PUFA), potassium binders, and intravenous iron replacement.²

The combination of hydralazine and isosorbide dinitrate is considered for Black patients with HFrEF and with NYHA class III-IV symptoms because it has been shown to reduce morbidity and mortality and improve symptoms.^24,25 This combination may also be used in patients who cannot tolerate RAAS inhibition.

Ivabradine has specific restrictions related to HR. The drug can be considered for patients with NYHA class II-III symptoms, an LVEF less than or equal to 35%, who are on GDMT including a BB at maximum tolerated dose, and who are in sinus rhythm with an HR greater than or equal to 70 beats/minute at rest.² Although adding ivabradine to standard GDMT for patients with HFrEF is associated with improved cardiac function, reduced HF readmission, greater HR reduction, and better exercise capacity, it has not been shown to reduce mortality.²⁶

sGC stimulators, such as vericiguat, have a unique mechanism of action compared with other therapies for HFrEF. They enhance the sensitivity of sGC to nitric oxide and thereby increase cyclic guanosine monophosphate (cGMP) production, inducing smooth muscle relaxation and vasodilation. Vericiguat may be considered for use in patients with HFrEF who have persistent symptoms despite optimization of GDMT.²⁷ sGC stimulators should be avoided in patients taking long-acting nitrates or phosphodiesterase inhibitors due to potentiated vasodilation. Patients should be taught to monitor for hypotension, the most common adverse reaction. The potential niche role for sGC stimulators in the HFrEF patient population is still evolving.²⁷

Another optional therapy is digoxin, a cardiac glycoside or positive inotrope. The only large digoxin trial in patients with HF predated the current GDMT recommendations.² The benefit of digoxin in patients with HFrEF is unclear because some studies have shown lack of mortality benefit or increased mortality.² GDMT should be optimized before adding digoxin.² Patients with acute decompensated HF may be given an I.V. positive inotrope, such as dobutamine or milrinone.

- Drug classes for the treatment of HFrEF

Drug Class/Target Dose2	Mechanism of Action
Renin-Angiotensin System Inhibitors
Angiotensin Receptor Neprilysin inhibitor (ARNi) Sacubitril-Valsartan 97 mg Sacubitril 103 mg Valsartan twice daily	Sacubitril: Inhibits neprilysin (breaks down NPs), leading to increased levels of natriuretic peptides Induces vasodilation and natriuresis Valsartan: See ARB MOA below
Angiotensin-Converting Enzyme inhibitor (ACEi) Captopril 50 mg 3 times daily Enalapril 10-20 mg twice daily Lisinopril 20-40 mg daily	Lowers levels of angiotensin II by preventing conversion of angiotensin I to angiotensin II Increases plasma renin activity Reduces aldosterone secretion
Angiotensin Receptor Blocker (ARB) Valsartan 160 mg twice daily Losartan 50-150 mg daily	Blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II Decreases the response to bradykinin Decreases non-renin-angiotensin effects (cough)
Beta Blocker (BB) Bisoprolol 10 mg daily Carvedilol 25-50 mg twice daily Carvedilol CR 80 mg daily Metoprolol 200 mg daily succinate	Inhibits beta-adrenergic receptor activation Decreases heart rate Decreases pulmonary pressure Decreases systemic vascular resistance Increases stroke volume
Mineralocorticoid Receptor Antagonist (MRA) Spironolactone 25-50 mg daily Eplerenone 50 mg daily	Competes with aldosterone for receptor sites in the distal tubules Increases sodium chloride and water excretion while conserving potassium and hydrogen ions Increases sodium chloride and water excretion while conserving potassium and hydrogen ions
Sodium-glucose Cotransporter 2 Inhibitor (SGLT2i) Dapagliflozin 10 mg daily Empagliflozin 10 mg daily	Inhibits SGLT2 in the proximal renal tubules Reduces sodium absorption Increases sodium delivery to the distal tubule Decreases cardiac preload/afterload Decreases sympathetic activity
Other therapies
Direct-acting Vasodilator Fixed dose combination of 40 mg isosorbide dinitrate and 75 mg of hydralazine 3 times daily 120 mg of isosorbide dinitrate total daily in divided doses and 300 mg of hydralazine total daily in divided doses	Isosorbide Dinitrate: Relaxes smooth muscle of arterial and venous vasculature Reduces cardiac oxygen demand by decreasing preload Hydralazine: Vasodilates arterioles resulting in decreased systemic resistance
If Inhibitor (pacemaker current inhibitor) Ivabradine 7.5 mg twice daily	Inhibits ion channels within the sinoatrial node Disrupts the If ion current flow Increases diastolic filling time Slows SA node firing Reduces heart rate
Soluble Guanylate Cyclase Stimulator (sGC stimulator) Vericiguat 10 mg daily	Enhances sensitivity of sGC, the primary receptor for nitric oxide
Cardiac Glycoside (positive inotrope) Digitalis individualized dose to maintain serum concentration 0.5 to less than 0.9 ng/mL	Inhibits sodium/potassium ATPase pump in myocardial cells Increases intracellular sodium Increases cardiac contractility by promoting calcium influx

Abbreviations: ATP, adenosine triphosphatase; HFrEF, heart failure with a reduced ejection fraction; MOA, mechanism of action; mg, milligrams; ng/mL; nanograms per milliliter; SA, sinoatrial

Infrequently, omega-3 PUFA supplementation is used as adjunctive therapy for patients with HFrEF and NYHA class II-IV symptoms to reduce mortality and cardiovascular hospitalizations.²

HF, comorbidities, and RAASi make hyperkalemia common in patients with HFrEF; an elevated serum potassium level is associated with a poorer prognosis and increased risk of cardiovascular complications.²⁸ Potassium binders may be considered for these patients; however, the benefit of using a potassium binder to facilitate the continuation of RAASi is uncertain.²⁸ Whether potassium binders improve clinical outcomes for these patients is under investigation.

Anemia is independently associated with mortality and disease severity in HF and is associated with poorer quality of life, prognosis, and exercise capacity in patients with HF.^29,30 For patients who have iron deficiency and HFrEF, with or without anemia, I.V. iron replacement may be considered to improve quality of life and functional status.² Oral iron is inadequate to treat iron-deficiency anemia in patients with HFrEF due to poor absorption and slow iron repletion in these patients (see Drug classes for the treatment of HFrEF).²

Nonpharmacologic treatment

Dietary sodium restriction has been a common nonpharmacologic treatment recommendation for patients with HFrEF and congestive symptoms. However, conflicting evidence and concerns about the quality and representativeness of data have led experts to question this recommendation.² The AHA recommends a daily sodium intake of less than 2,300 mg for general health promotion and is moving toward a limit of no more than 1,500 mg per day for most adults.³¹ However, this is not specific to patients with HFrEF as the current guidelines recommend less than 3,000 mg per day. The Dietary Approaches to Stop Hypertension (DASH) diet can achieve sodium restriction without affecting nutritional quality and may reduce hospitalizations for HF.^2,32

Exercise has several benefits for patients with HFrEF such as improving functional status and quality of life.² Exercise training in patients with HFrEF is safe and does not increase mortality.³³ All patients should be encouraged to stay physically active once they are hemodynamically stable and on GDMT. Cardiac rehabilitation improves exercise capacity and quality of life in patients with HFrEF, but there was no association between cardiac rehabilitation and mortality or hospitalization.² For patients with HFrEF who were hospitalized for worsening HF, an early, transitional, tailored rehabilitation program resulted in improved physical function.^34,35

A cardiac rehabilitation program for patients with HFrEF typically includes a medical evaluation, education, dietary recommendations, psychosocial support, and an exercise training program.² A prescribed exercise program is recommended for patients with HFrEF in conjunction with evidence-based therapy, such as GDMT.³³

Device-based therapies for HFrEF include cardiac implantable devices and cardiac resynchronization therapy (CRT). For patients who meet certain criteria, ICD therapy is recommended to reduce mortality from sudden cardiac death due to ventricular dysrhythmias.² For some patient populations, CRT is recommended to help the ventricles contract more efficiently. Synchronizing ventricular contraction may reduce mortality and hospitalizations and improve quality of life and symptoms.² An important point is to optimize GDMT before any device implantation.²

Nursing considerations

HF management and coordination of services are complex. Ideally, early identification of those at risk may help limit the number of new cases. Care by multidisciplinary teams, including nurses, may help improve patients' outcomes and quality of life. Multidisciplinary HF teams provide integrated, comprehensive care for the management of HF and associated comorbidities.³⁶ Nurses play an important role in educating patients during their hospital admission by helping them navigate symptom recognition and the management processes.¹¹ Nurses must educate patients continually throughout their hospitalization on self-management and self-care, strategies to prevent readmission, and other options such as palliative care (see Patient, family, and caregiver education topics).^7,37-39 Discharge teaching is important, but nurses should take the opportunity to educate patients and caregivers at every healthcare encounter, helping to reinforce knowledge and understanding.

- Patient, family, and caregiver education topics⁷

General Education

Definition of HF Cause/probable cause of HF Reason for signs and symptoms Expected signs and symptoms Signs and symptoms of worsening HF and what to do if they occur Self-monitoring, including daily weights Treatment care and plan Patient and caregiver responsibilities Role(s) of family and caregivers in treatment care and plan Qualified local support group and online resource availability and importance Importance of tobacco use cessation Value of preventive health behaviors, including influenza and pneumococcal vaccinations

Prognosis

Life expectancy Educate family/caregiver about what to do in the event of sudden death Advance directives

Recommended Activities

Exercise Work, leisure, and recreational activity Sexual activity and difficulties and how to cope

Recommended Diet

Calorie appropriate diet Consistent and restricted sodium intake of less than 3,000 mg per day Correlation between sodium intake and HF signs or symptoms or weight gain Small, frequent meals Fluid intake moderation Alcohol moderation or restriction if HF is secondary to alcohol consumption

Medication

Medication dosing Effects of medications on quality of life and survival Potential adverse reactions and what to do if they occur Coping with complicated medical regimens Accessibility of lower-cost medications or financial assistance Avoiding dangerous interactions with OTC medication, home remedies, and herbal supplements

Abbreviations: HF, heart failure; mg, milligram; OTC, over the counter

Conclusion

The case study involving JW highlights the importance of a team effort to manage HF and the vital role nurses play in identifying signs and symptoms and educating patients. Heart failure, as delineated above, is a complex disease process; evidence-based care can improve outcomes.

Ejection fraction and cardiac output⁶

Ejection fraction (EF) is the volume of blood pumped out with each heart contraction, expressed as a percentage. Most often, EF refers to the blood pumped out of the left ventricle (LVEF). Normal EF for the left ventricle is between 50% and 70%. For example, an EF of 50% means that half of the total blood in the left ventricle is pumped out with each heartbeat. The most common test for measuring EF is echocardiography.

Cardiac output (CO) is the volume of blood pumped out by the heart in a minute, expressed in L/min. Generally, normal CO at rest is 5-6 L/min. CO reflects the body's metabolic and oxygen needs. During increased need, CO increases to maintain adequate tissue perfusion. CO is the product of heart rate (HR), in beats per minute, times stroke volume (SV): CO = HR x SV.

Risk factors and common contributors for developing HFrEF^2,6

• Hypertension
• Diabetes
• Coronary artery disease
• Exposure to cardiotoxic agents or substance abuse (chemotherapy, alcohol)
• Genetic/inherited cardiomyopathies
• Obesity
• Tobacco abuse
• Rheumatologic or autoimmune diseases
• Thyroid disease
• Cardiac dysrhythmias, such as atrial fibrillation
• Infiltrative cardiac diseases
• Myocarditis (viral)
• Pregnancy
• Stress
• Valvular heart disease