About this course:
The learning activity aims to increase nurses' knowledge of heart failure, including the categories and stages, clinical manifestations, risk factors, diagnostic testing, and treatment options.
Heart Failure for LPNs/RNs
The learning activity aims to increase nurses' knowledge of heart failure, including the categories and stages, clinical manifestations, risk factors, diagnostic testing, and treatment options.
After completing this module, learners will be able to:
- identify the categories and stages of heart failure
- describe the pathophysiological changes that occur in heart failure
- recognize the clinical manifestations of heart failure
- explain the risk factors and comorbidities for heart failure
- summarize the treatment options for heart failure
Heart failure (HF) was recognized as an emergent epidemic in 1997 and remains a population health concern. HF affects about 6.3 million people in the US, equating to 1.8% of the overall population. HF is not only a healthcare concern but also burdens the economy, primarily due to the aging population. HF is more prevalent in older adults and is the primary cause of hospitalization for patients over 65 in the US. HF management is more complicated in older populations due to comorbidities and decreased cardiac, renal, and liver functioning. HF is most prevalent among non-Hispanic Black individuals at 4.6 per 1,000 people, followed by Hispanic individuals at 3.5 per 1,000 people and non-Hispanic White individuals at 2.4 per 1,000 people (Heidenreich et al., 2022; Ignatavicius et al., 2018; Roger, 2021).
Cardiac Output, Stroke Volume, and Heart Failure
A basic understanding of cardiac function is necessary to grasp how HF affects the heart and body. HF limits the ability of the heart to pump enough blood to satisfy metabolic demands. Cardiac output (CO) is the blood volume pumped from the heart in 1 minute. Stroke volume (SV) is the volume of blood pumped from the heart with each ventricular contraction or the difference between end-diastolic volume (EDV) and end-systolic volume (ESV). CO is the product of heart rate and SV (Kosaraju et al., 2022; Mohrman & Heller, 2018). SV and, by implication, left ventricular function are determined by three variables:
- preload (or end-diastolic volume): the amount of blood in the ventricle before systole; preload can also be defined as the resting length of the myocardial muscle fibers before systole
- myocardial contractility: the force of a cardiac contraction at a given preload
- afterload: the impedance that must be overcome for blood to be pumped from the ventricles (Mohrman & Heller, 2018)
A normal heart can produce an SV large enough to supply the metabolic demands of the organs and tissues, increasing and decreasing the stroke volume when needed based on demand. The ventricles can expand and stretch to accommodate a large blood volume or preload. When preload increases, the myocardium responds by increasing the myocardial contraction force. However, in patients with HF, the myocardium has been damaged. This impairs the contractile ability of the myocardium, resulting in systolic dysfunction, and prevents the myocardium from stretching enough to accommodate the volume of blood needed, resulting in impaired diastolic filling and function. Fibrosis, hypertrophy, and other changes to the myocardium diminish the filling capacity of the ventricles, and damage to the myocardium causes systolic dysfunction and impaired pumping force. If the damage to the heart is not sudden and severe—in most cases of HF, it is not—compensatory mechanisms can restore cardiac function. Still, they can also cause injury to the heart, and in most patients, HF is a progressive disease characterized by declining cardiac function (Jameson et al., 2018).
There are three primary types of HF: left-sided (also referred to as congestive heart failure [CHF] in clinical settings), right-sided, and high-output. Left-sided heart failure is further classified by left ventricular ejection fraction (LVEF). Systolic heart failure (also known as heart failure with reduced EF [HFrEF] and diastolic heart failure (heart failure with preserved EF [HFpEF]). LVEF is determined by dividing SV by EDV and multiplying by 100. A normal LVEF for males is 52%-72%, and a normal LVEF for females is 54%-74%. HFrEF is defined as HF with an ejection fraction (EF) at or below 40%; HF with a preserved ejection fraction (HFpEF) is defined as HF with an EF at or above 50%. Between these two is HF with a midrange EF (HFmrEF) characterized by an EF of 41% to 49%. This stage can either indicate an improvement or deterioration of HF based on the trend of EF results (Heidenreich et al., 2022; Ignatavicius et al., 2018; Kosaraju et al., 2022).
HF is also categorized based on signs, symptoms, and the functional impact of the disease using systems developed by the New York Heart Association (NYHA) and the American College of Cardiology (ACC)/American Heart Association (AHA; see Table 1; Heidenreich et al., 2022; Ignatavicius et al., 2018).
ACC/AHA HF Categories Compared to NYHA Functional Classification of Cardiovascular Disability
Stage A: at risk for developing HF, but the patient is asymptomatic and has no structural damage
Class I: ordinary activity does not cause symptoms
Stage B: the patient has structural abnormalities or remodeling but is asymptomatic
Class II: ordinary activity causes symptoms but no symptoms at rest
Stage C: there is structural damage, and the patient has current symptoms or a history of symptoms
Class III: asymptomatic at rest, but symptoms appear with less than ordinary activity
Stage D: refractory HF
Class IV: symptoms at rest
(Heidenreich et al., 2022; Ignatavicius et al., 2018)
Pathophysiology of Heart Failure
Heart Failure with Reduced Ejection Fraction
The primary pathophysiology underlying HFrEF is acute or chronic damage to the myocardium and impaired systolic function with insufficient contractile force to produce an adequate SV. The most common causes of HFrEF are described below; however, most cases of HFrEF are caused by ischemic heart disease or hypertension. For approximately 20%-30% of patients, the cause is not identified; these cases are referred to as non-ischemic or idiopathic cardiomyopathy (Butler et al., 2019; Jameson et al., 2018).
HFrEF is a complex disorder characterized by three basic steps: the initiating disease or event, the development of compensatory mechanisms, and the progression of the disease leading to the development of clinical manifestations. Patients with HFrEF are initially asymptomatic or minimally symptomatic and may remain so for many years due to multiple compensatory mechanisms that can restore ventricular function and CO. These compensatory mechanisms improve the CO, SV, vascular tone, and pump function. Although these mechanisms are discussed separately (see Table 2), they overlap and influence each other (Butler et al., 2019; Jameson et al., 2018).
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Activation of Compensatory Mechanisms
Neurohumoral activation (renin-angiotensin-aldosterone system)
This mechanism causes peripheral vasoconstriction, promotes sodium and water retention, and helps maintain CO and tissue perfusion.
Increased sympathetic output and tone
The baroreceptors in the aorta, carotid arteries, and left ventricle activate the vasomotor center in the brainstem in response to decreased CO and a decrease in blood pressure. Sympathetic tone is increased, CO is restored, and peripheral vasoconstriction helps maintain normal blood pressure. Increased sympathetic tone also increases antidiuretic hormone (ADH) release, promoting water reabsorption by the kidneys and increasing intravascular volume.
Increased myocardial contractility
The ability of the heart to change its contractile force leading to increased SV due to elevated preload is known as the Frank-Starling mechanism.
HFrEF affects the activity and circulating levels of vasoactive substances: endothelin, natriuretic peptides, and nitric oxide. The rise in these vasoactive substances increases peripheral resistance and helps maintain tissue perfusion. Over time, high circulating levels of endothelin can damage the myocardium.
Left ventricular remodeling
This structural change in the heart occurs in response to the decreased left ventricular function caused by HFrEF and the previously discussed compensatory mechanisms. The myocardium's mass and size and the ventricular wall's thickness are increased or remodeled. These changes help maintain CO.
(Jameson et al., 2018; Schwinger, 2021)
These compensatory mechanisms are effective. However, renin-angiotensin-aldosterone system activation, increased sympathetic activation and tone, and other HF adaptations can cause myocardial damage and dysfunction, apoptosis and necrosis of myocardial cells, dilated ventricles, an abnormal response to adrenergic stimulation, and abnormal myocardial metabolism. The compensatory mechanisms are initially beneficial but weaken the heart over time, and the patient develops symptomatic HF (Jameson et al., 2018; Schwinger, 2021).
Heart Failure with Preserved Ejection Fraction
The primary cause of HFpEF is the inability of the ventricles to fill with blood. The underlying dysfunction of the ventricles in HFpEF is complex and may include myocardial stiffness and elevated diastolic pressure, resulting in congestion, pulmonary hypertension, and a decreased ability to produce enough CO to meet metabolic demands. Systemic inflammation that damages the myocardial blood vessels—initiated by chronic kidney disease (CKD), diabetes, hypertension, and obesity—is a common and important mechanism of injury found with HFpEF. However, normal aging and myocardial ischemia from coronary artery disease (CAD) are also contributing factors. In addition, although HFpEF is primarily characterized by left ventricular stiffness and impaired left ventricle relaxation, other forms of myocardial dysfunction can result from HFpEF (Butler et al., 2019; Schwinger, 2021; van de Wouw et al., 2019).
High-Output Heart Failure
High-output heart failure is similar to HFrEF and HFpEF, but there is usually no intrinsic damage to the heart, EF is normal, and CO is high yet insufficient for metabolic demands. High-output HF is characterized by decreased peripheral resistance with poor tissue perfusion, increased metabolic demands, myocardial dysfunction, or a combination of these factors. In certain conditions like cirrhosis, chronic obstructive pulmonary disease (COPD), and morbid obesity, HF is relatively common and can involve changes in the vascular bed, damage to the myocardium, and increased metabolic demand. By contrast, in patients with anemia, arteriovenous fistulas, pregnancy, and other conditions, high-output HF only develops if there is structural heart disease or a particularly severe form of the disease (e.g., thyroid storm; Jameson et al., 2018; Mogos et al., 2018).
General risk factors for HF include advanced age, hypertension, COPD, CAD, cardiomyopathy, diabetes, obesity, and smoking. These behaviors and diseases likely impact the development of HF because many cause systemic inflammation, a process implicated in the development of HF. The lifetime risk for HF in people with an average blood pressure above 160/90 mmHg is almost doubled. The most significant benefit of lowering blood pressure is a reduced risk of HF for hypertensive patients. As blood pressure increases, the heart must work harder to pump blood throughout the body. Without intervention, sustained increased pressure and work affect the heart's ability to relax and fill completely. With CAD, the arteries become narrow due to plaque build-up from increased serum cholesterol. This narrowing reduces blood flow and increases pressure. When the plaques deposit in the cardiac muscle circulatory system, oxygen deprivation or ischemia of the muscle can occur. A total blockage of cardiac vessels can lead to myocardial infarction (Butler et al., 2019).
Cardiomyopathy also increases the risk of HF. Cardiomyopathy results from the heart not pumping or relaxing normally, but the cause is not related to hypertension or CAD. Cardiomyopathy often results from an autoimmune disease, genetic condition (e.g., muscular dystrophy), or infection, but the cause is often unknown. Valvular disease can also lead to HF. The valves within the heart can become narrow or stenosed, inhibiting blood flow through the valve and leading to increased pressure, or can become leaky, causing the blood to flow backward. Hyperglycemia, insulin resistance, and diabetes independently increase the risk for HF, and the prevalence among patients with diabetes is 4 times that of the general population. The lifetime risk for HF among people who are obese (BMI ≥30 kg/m2) is double that of people who have a BMI of less than 25 kg/m2 (Butler et al., 2019). In addition to the above risk factors, there are additional risk factors specific to certain types of HF:
- risk factors for HFrEF include:
- alcohol abuse
- cardiac rate or rhythm disorders
- untreated Chagas disease (caused by infection by the parasite Trypanosoma cruzi)
- chronic lung disease
- drug- or toxin-induced myocardial damage
- viral infection
- risk factors for HFpEF include:
- pericardial disease
- valvular disease
- risk factors for high-output HF include:
- arteriovenous fistula
- beriberi (thiamin [vitamin B1] deficiency)
- morbid obesity
- renal disease
- sepsis (Jameson et al., 2018)
Signs and Symptoms
Left-Sided Heart Failure
Left-sided HF is associated with decreased CO and increased pulmonary pressure. This can limit blood flow throughout the body, causing body system dysfunction (Colucci & Dunlay, 2022; Ignatavicius et al., 2018). Symptoms that accompany left-sided HF consist of:
- acute confusion
- pulmonary congestion (e.g., a hacking cough, dyspnea, crackles and wheezes upon auscultation, frothy pink-tinged sputum, tachypnea, S3/S4 summation gallop)
- oliguria (decreased urine output) during the day and nocturia at night
- tachycardia or palpitations
- weak peripheral pulses
- cool extremities (Colucci & Dunlay, 2022; Ignatavicius et al., 2018)
Right-Sided Heart Failure
Right-sided HF leads to increased systemic venous pressure and congestion due to dysfunction of the right atrium and ventricle (Colucci & Dunlay, 2022; Ignatavicius et al., 2018). This congestion and pressure result in the following symptoms:
- jugular vein distention (JVD)
- hepatomegaly (liver enlargement) and splenomegaly (spleen enlargement)
- anorexia and nausea as a result of pressure from the accumulation of intraabdominal fluid; without intervention, this can lead to malnutrition
- dependent edema in the legs and ankles when ambulatory and sacrum when bed-bound
- distended abdomen/ascites; intraabdominal fluid volume can reach levels greater than 10 L
- swollen hands and fingers
- night-time polyuria
- weight gain
- clubbing (the angle of the nail increases to 180˚, and the nail bed becomes spongy)
- hypertension from increased fluid volume or hypotension due to HF (Colucci & Dunlay, 2022; Ignatavicius et al., 2018)
HF is a clinical diagnosis and a diagnosis of exclusion based on the
clinician's assessment of the patient's risk factors and reported signs and symptoms. Laboratory studies, imaging, and other diagnostic tests can confirm the diagnosis, determine the cause, and assess the degree of impairment. The first step in the diagnostic algorithm for HF is patient assessment. The APRN should obtain a clinical history, perform a physical examination, and order an electrocardiogram (ECG) and serum laboratory tests (Heidenreich et al., 2022; Jameson et al., 2018).
Laboratory testing should be completed as part of a standard diagnostic assessment. Recommended laboratory studies include a complete blood count (CBC), urinalysis, electrolytes (sodium, potassium, calcium, and magnesium), blood urea nitrogen (BUN), serum creatinine, blood glucose, lipid profile (fasting), liver function tests, iron studies, and thyroid-stimulating hormone (TSH). These laboratory tests help clinicians eliminate other causes of patient symptoms. Measurement of the natriuretic peptides—B-type natriuretic peptide (BNP) and n-terminal pro-BNP (NT-proBNP)—is recommended by the ACC, the AHA, and the Heart Failure Society of America (HFSA) as a way to confirm or exclude the presence of HF, determine the severity of the disease, and establish a prognosis. BNP is a hormone, and NT-proBNP is a prohormone. They are released from the ventricles (and, to a lesser degree, from the atria) when fluid volume overload and myocardial stretching are present. Per the HF guidelines, an abnormal NT-proBNP result is above 125 pg/mL, and an abnormal BNP result is above 35 pg/mL. Other cardiac causes of elevated natriuretic hormones include atrial fibrillation, left ventricular hypertrophy, and pericardial disease. In addition, there are many conditions and diseases that can cause elevated BNP and NT-proBNP levels, including (but not limited to) advanced age, anemia, female gender, the use of an angiotensin receptor-neprilysin inhibitor (ARNI), obstructive sleep apnea, and renal impairment. Obesity can cause falsely low levels due to the increased leptin released by adipose cells. Leptin and BNP have opposite effects; therefore, when leptin is increased, BNP decreases. In addition to evaluating laboratory values at the time of diagnosis, providers should follow the 2021 HF treatment guidelines from the ACC/AHA/HFSA, which recommend that laboratory studies should be measured with any change in condition or medication regimen (Heidenreich et al., 2022; Jameson et al., 2018; Reinmann & Meyer, 2020).
A chest x-ray can be beneficial in diagnosing left-ventricular HF. Chest x-rays can show the presence of cardiomegaly resulting from hypertrophy and dilation, pulmonary venous congestion, and interstitial edema. Chest x-rays can also help determine whether symptoms of dyspnea are caused by another cause, such as pulmonary disease. An ECG is considered the gold standard for the diagnosis of HF. The test is non-invasive and can be used to measure EF. It can also show the size of the heart chambers and indicate any heart wall abnormalities, valvular function, and markers of diastolic function (Heidenreich et al., 2022; Ignatavicius et al., 2018; McDonagh et al., 2021).
Other Diagnostic Tests
An ECG is part of the routine evaluation of patients with HF. An ECG provides information on electrical activity within the heart, including heart rate and rhythm. This information can help determine the cause and prognosis of HF. An ECG is repeated whenever there is a clinical indication, including a suspected arrhythmia, presence of ischemia, myocardial injury, or conduction abnormalities. A normal ECG makes a diagnosis of HF unlikely (McDonagh et al., 2021).
Dietary and Lifestyle Changes
Dietary and lifestyle changes are recommended for patients and can be implemented alone or in combination with pharmacological treatment to prevent, slow the progression of, or improve HF (Colucci, 2021). The following are the most common dietary and lifestyle changes recommended (Colucci, 2021; Okoshi et al., 2017):
- Monitor weight daily to detect fluid accumulation and support early intervention and improved outcomes. Daily weights should be taken in the morning after urinating using the same scale in the same place on the floor wearing a similar amount of clothing; a weight change of 2 lb (1 kg) in a day or 4 lb (2 kg) in a week requires reporting to the provider to determine if intervention is needed.
- Maintain a healthy weight. Being overweight increases the strain on the heart, and losing weight can decrease this strain; losing too much weight rapidly without trying can signify the development of cardiac cachexia, which can occur with severe HF; cardiac cachexia indicates increased morbidity and mortality independent of other variables with a life expectancy below 18 months in 50% of patients affected.
- Decrease salt and fluid intake. A high-salt diet can lead to fluid retention, increasing strain on the heart; the amount of salt restriction recommended depends on the patient's condition and comorbidities. Fluid restriction is also recommended to decrease excess fluid volume, thereby reducing strain on the heart. Most patients are instructed to limit fluid intake to less than 2 L (66 oz) per day.
- Stop smoking. Cigarette smoking can double the risk of HF due to adverse effects on the cardiovascular system and increased cholesterol, leading to plaque deposits in the arteries.
- Limit alcohol intake. If the HF is alcohol-induced, patients should abstain entirely from alcohol; individuals with HF due to another cause should limit alcohol consumption to no more than one serving per day (e.g., 12 oz beer, 5 oz wine, 1.5 oz distilled spirits).
- Engage in regular exercise if tolerated. Regular exercise 5 days per week is recommended to increase cardiovascular health and improve symptoms; some patients may be referred to a cardiac rehabilitation program to improve cardiac function while under medical supervision.
Guideline-Directed Medical Therapy
Guideline-directed medical therapy (GDMT) is the standard medical therapy for HFrEF. The classes of drugs included in the GDMT include angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs)/ARNIs, beta-blockers, mineralocorticoid or aldosterone receptor antagonists (MRAs), and sodium-glucose cotransporter 2 (SGLT2) inhibitors (Gottlieb, 2021).
ACE inhibitors prevent the production of angiotensin II, leading to vasodilation and decreased blood pressure. ACE inhibitors used as part of GDMT include benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), and lisinopril (Prinivil, Zestril). Common side effects of ACE inhibitors include a dry, nagging cough; hyperkalemia; fatigue; dizziness; headaches; and loss of taste. In rare cases, ACE inhibitors may cause angioedema (swelling of the lips, tongue, or face), requiring discontinuation. ACE inhibitors are contraindicated in patients with hyperkalemia, renal artery stenosis, or a history of angioedema (Maddox et al., 2021; Vallerand & Sanoski, 2017).
Switching to an ARB may be beneficial if patients report a cough using ACE inhibitors. ARBs used as part of GDMT include valsartan (Diovan), losartan (Cozaar), and candesartan (Atacand). ARBs decrease blood pressure through competitive antagonist activity at angiotensin II receptor sites. Side effects include dizziness, headaches, hyperkalemia, angioedema, nausea, vomiting, severe diarrhea, and weight loss. ARBs are contraindicated in patients with a life-threatening reaction to ARBs, SBP less than 80 mmHg, hyperkalemia, or renal artery stenosis. All ARBs are dosed once daily; however, if a patient's BP is not controlled, losartan (Cozaar) may be dosed twice daily (Maddox et al., 2021; Vallerand & Sanoski, 2017).
ARNIs are a new pharmacological class that combines sacubitril with valsartan under the trade name Entresto. ARNIs lower blood pressure, change the neurohormonal response to HF, and promote diuresis. Sacubitril/valsartan (Entresto) is recommended as a replacement for ACE inhibitors and ARBs for individuals with HFrEF and is more effective than some ACE inhibitors at treating HFrEF. Side effects include a cough, dizziness, hyperkalemia, hypotension, renal failure, and angioedema. The risk of angioedema with an ARNI is comparable to that of an ACE inhibitor. For this reason, ARNIs are contraindicated in patients with a history of ACE inhibitor-related angioedema. Sacubitril/valsartan (Entresto) can cause death to a developing fetus and is, therefore, contraindicated for use in pregnancy. It is also contraindicated in patients with a GFR below 60 mL/min/1.73 m2. Concomitant use of an ARNI and an ACE inhibitor is contraindicated. An ARNI should not be used within 36 hours of the last dose of an ACE inhibitor. Sacubitril/valsartan (Entresto) can be used in pediatric patients older than 1 year. The pediatric dose is administered orally twice daily and increased in 2-week intervals as tolerated until the maintenance dose is reached (US Food and Drug Administration [FDA], 2021).
Beta-adrenergic blockers block beta 1 and/or beta 2 receptors. Some are specific to beta 1 receptors located in the cardiac muscle. Beta-adrenergic blockers help improve the long-term adverse effects of the compensatory adrenergic stimulation that occurs in chronic HF. In combination with an ACE inhibitor or an ARB, beta-adrenergic blockers reduce the risk of mortality and hospitalization in patients with HFrEF. Bisoprolol (Zebeta), carvedilol (Coreg), and metoprolol succinate (Toprol XL) are preferred as these drugs have the most robust evidence for efficacy. Unfortunately, they can cause bradycardia, dizziness, dyspnea, and fatigue at therapeutic doses. Other symptoms experienced by patients include erectile dysfunction and central nervous system (CNS) disturbances (i.e., hallucinations, memory loss, nightmares). These adverse effects can make using the target dose difficult. Beta-adrenergic blockers can be safely used in patients with COPD and diabetes. For patients with diabetes, using beta-adrenergic blockers may mask the symptoms of palpitations, tachycardia, and tremor associated with hypoglycemia. These medications should be discontinued in a downward taper over a few weeks. Abrupt discontinuation may cause MI or ventricular arrhythmias (Maddox et al., 2021; Woods, 2023).
Mineralocorticoid or Aldosterone Receptor Antagonists.
The MRAs eplerenone (Inspra) and spironolactone (Aldactone) have reduced mortality and hospitalizations in patients with HFrEF. MRAs block the effects of aldosterone, resulting in a decreased amount of water and sodium retained by the renal system. Since MRAs are potassium-sparing diuretics, there is a decreased risk of hypokalemia and arrhythmias. Hyperkalemia has been reported in 5% to 17.5% of HF patients taking an MRA. Patients with CKD or diabetes mellitus or taking an ACE inhibitor or ARB are at a higher risk for developing hyperkalemia, and their renal function and serum potassium should be closely monitored. Doses and dosing schedules of the MRA, the ACE inhibitor, and the ARB may need to be adjusted. For patients at an increased risk for developing hyperkalemia, the dosing of the MRA may be changed to every other day (Ignatavicius et al., 2018).
Sodium-Glucose Cotransporter 2 Inhibitors.
Adding an SGLT2 inhibitor to the HF treatment regimen is a new recommendation. For patients with HFrEF, adding an SGLT2 inhibitor can decrease hospitalizations and deaths, even among patients without diabetes. These medications' exact mechanism of action in HFrEF is not entirely known; however, their use can promote osmotic diuresis and decrease arterial pressure and stiffness. SGLT2 inhibitors are indicated for patients with HFrEF and NYHA Classes II-IV. Side effects include hypovolemia, hypotension (including orthostatic), constipation, nausea, polyuria (excessive urination), urinary tract infection, and hypoglycemia. Using these medications in combination with a loop diuretic can increase the risk of hypotension. SGLT2 inhibitors are also contraindicated in patients with diabetes requiring insulin. Dapagliflozin (Farxiga) is contraindicated in patients with a GFR less than 30 mL/min/1.73 m2, and empagliflozin (Jardiance) is contraindicated when GFR is less than 20 mL/min/1.73 m2 (Maddox et al., 2021; Woods, 2023).
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel Blockers.
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers reduce heart rate by acting on the channels that maintain the cardiac pacemaker (SA node). Ivabradine (Corlanor) is the only HCN channel blocker approved for HF and has been available since 2015. According to AHA guidelines, the use of ivabradine (Corlanor) is indicated for patients with symptomatic NYHA Class II or III HFrEF with an EF less than 35% who are already receiving a beta-adrenergic blocker at the maximum tolerated dose or are unable to take beta-adrenergic blockers due to a contraindication, are in sinus rhythm on ECG, and have a regular heart rate above 70 bpm at rest. For these patients, ivabradine (Corlanor) can be beneficial in reducing HF-related hospitalizations and mortality. Side effects include bradycardia, conduction dysfunction, atrial fibrillation, and hypertension. Ivabradine (Corlanor) should be used cautiously in patients with first- or second-degree atrioventricular (AV) block, with sinus node dysfunction, and in conjunction with negative chronotropes (e.g., digoxin [Digitek] or amiodarone [Pacerone]). This medication should not be used in patients with an on-demand pacemaker set to a heart rate above 60 bpm (Heidenreich et al., 2022; Woods, 2023).
Fluid retention and hypervolemia—along with the resulting dyspnea, peripheral edema, and decreased activity tolerance—are common in patients with HF. Loop diuretics are the initial treatment for patients with persistent edema and congestion. Bumetanide (Bumex), furosemide (Lasix), and torsemide (Demadex) are most often used for patients needing diuresis to relieve the symptoms of hypervolemia. There is no conclusive evidence that one loop diuretic is superior to another. Initial dosing depends on kidney function and any history of previous treatment with a diuretic. Titration of the dosage needed to relieve symptoms should occur over several weeks. If the maximum dose of the initial loop diuretic is reached without remission of symptoms, a change of loop diuretic or the initiation of a thiazide diuretic is indicated. Fluid and electrolyte losses are common adverse effects of loop diuretics. For this reason, close monitoring of body weight and serum electrolytes is required in patients taking these medications. Hypokalemia is common in patients being treated with loop diuretics. Due to this risk, potassium chloride (Klor-Con) is often used concurrently to prevent hypokalemia and the associated adverse effects, including cardiac arrhythmias such as torsades de pointes, ventricular fibrillation, and polymorphic ventricular tachycardia. Diuretic resistance, defined as fluid retention and failure to decongest with a diuretic, is a common effect of long-term use of these drugs, occurring in approximately 25%-30% of all HF patients (Heidenreich et al., 2022; Woods, 2023).
Thiazide diuretics should be added to the treatment regimen for patients who do not respond to treatment with loop diuretics despite dosage increases. Chlorthalidone (Thalitone) or hydrochlorothiazide (HCTZ; HydroDiuril) should be used in patients with hypertension and HF with mild hypervolemia. Metolazone (Zaroxoyln) or HCTZ (HydroDiuril) may be added to the treatment regimen with a loop diuretic or replace the use of a loop diuretic if a patient has refractory edema that has not responded to loop diuretics despite drug changes and titration. Thiazide diuretics may cause potassium depletion, hypercholesterolemia, hypercalcemia, hyperglycemia, hypomagnesemia, hyponatremia, and photosensitivity. These medications should be used cautiously in patients with decreased renal and liver function (Heidenreich et al., 2022; Woods, 2023).
Vasodilators such as hydralazine (Apresoline) and isosorbide dinitrate (Dilatrate) should be started if an adequate response has not been attained with an ACE inhibitor or an ARB and a beta-adrenergic blocker. Hydralazine (Apresoline) is a direct vasodilator of the arterioles. Isosorbide dinitrate (Dilatrate) is a nitrate that dilates the peripheral veins and, to a lesser degree, the peripheral arteries. These medications can be taken in a combined formulation under the trade name Bidil. This combination has been established as an effective treatment for HFrEF. Side effects of isosorbide dinitrate/hydralazine (BiDil) are dizziness, lightheadedness, weakness, nausea, vomiting, ventricular tachycardia, flushing, and headaches. Unfortunately, these drugs must be taken 3-4 times a day, whether in combination or individually (Heidenreich et al., 2022; Woods, 2023).
ACE inhibitors and ARBs are less effective at reducing blood pressure in Black individuals, perhaps due to differences in the renin-angiotensin-aldosterone system or drug metabolism. ACE inhibitors are specifically less effective in Black individuals who have HFrEF. In contrast, research has shown that hydralazine and nitrates decrease the mortality and hospitalization rate for Black individuals with HFrEF. Their use for these individuals who have HFrEF is a Class I recommendation in current guidelines. Hydralazine and nitrates are less effective than ACE inhibitors for non-Black patients with HFrEF. This combination is often used only when these patients cannot tolerate an ACE inhibitor or an ARB (Al-Mohammad, 2019; Heidenreich et al., 2022; Woods, 2023).
Continuous Positive Airway Pressure
Continuous positive airway pressure (CPAP) is a respiratory treatment commonly used for patients with obstructive sleep apnea. It can also be used for patients with HF to improve CO and EF by decreasing preload, afterload, and blood pressure. CPAP use increases the oxygenation supply (Ignatavicius et al., 2018).
Cardiac resynchronization therapy (CRT), also known as biventricular pacing, involves the implantation of a pacemaker alone or in combination with a defibrillator. The electrical stimulation that CRT provides can improve CO and EF. This treatment is indicated for patients with Class II or IV HF with an EF of less than 35% who also have a left bundle branch block. Utilizing CRT in these patients has dramatically increased their ability to complete activities of daily living independently and improved their quality of life (Ignatavicius et al., 2018).
CardioMems is a monitoring system implanted into the pulmonary artery during a right heart cardiac catheterization. It is approximately the size of a quarter and is considered a permanent implant. The patient should check the device daily, or as instructed by their provider, to monitor their pulmonary artery pressure. Checking the device requires the patient to lie face down on a specialized pouch containing an electronic monitoring unit. The device advises the patient if their positioning needs to be changed. The readings from the device can then be sent electronically to the provider, allowing for rapid medication titration or changes even before symptoms emerge, leading to more outpatient treatment and fewer hospitalizations (Ignatavicius et al., 2018).
Typically, once patients reach end-stage HF with a significant loss of quality of life, they are referred to hospice care for symptom management and end-of-life care. However, some patients can undergo surgery to have a ventricular assist device (VAD) placed. This surgically implanted pump works with the patient's heart to increase its pumping ability and perfusion. VADs are specific to right or left HF. Patients with end-stage renal disease, severe lung disease, clotting disorders, or an infection resistant to antibiotic therapy are not candidates for this procedure. There can be postoperative complications, including bleeding, infective endocarditis, development of ventricular dysrhythmias, or stroke. VADs can be utilized short-term by patients awaiting a donor heart for transplantation. Often, a VAD will keep a patient alive long enough to undergo transplantation. VADs can also be used long-term as a last treatment option (Ignatavicius et al., 2018).
Nonadherence to Treatment
Nonadherence to treatment leads to poor patient outcomes. There are various reasons why patients may not be able to adhere to their prescribed treatment regimen or dietary and lifestyle changes (Maddox et al., 2021). Common reasons that patients do not adhere to treatment and how to address these barriers are outlined in Table 3.
Reasons for Nonadherence
Barriers to Adherence
(Maddox et al., 2021)
Heart Failure Self-Management Teaching
Properly educating patients on their diagnosis and interventions to manage the disease process and associated symptoms is essential for effective self-management and reducing hospitalizations. Many patients return to the hospital due to poor adherence to dietary or lifestyle changes or medication administration. This can be due to a lack of education or understanding. One standardized self-management education plan used by healthcare professionals (HCPs) is HF self-management health teaching or MAWDS, which stands for medications, activity, weight, diet, and symptoms (Ignatavicius et al., 2018). A more detailed explanation of MAWDS is outlined in Table 4.
Heart Failure Self-Management Health Teaching
(Ignatavicius et al., 2018)
Heart Failure Core Measure Set
The HF core measure set seeks to ensure that HF patients receive proper outpatient treatment and disease management education to reduce rehospitalizations. These standards are put into place and monitored by the Joint Commission (TJC) for hospital accreditation (AHA, 2021; Ignatavicius et al., 2018). The core measures include:
- thorough discharge instructions (diet, activity, meds, weight monitoring, planning for worsening symptoms)
- evaluation of left ventricular systolic function
- an ACE inhibitor or ARB for left ventricular systolic dysfunction or documentation as to why these medications are contraindicated
- smoking cessation advice and counseling
- outpatient appointment with an HCP within 7 days of discharge (AHA, 2021; Ignatavicius et al., 2018)
Al-Mohammad, A. (2019). Hydralazine and nitrates in the treatment of heart failure with reduced ejection fraction. ESC Heart Failure, 6(4) 878-883. https://doi.org/10.1002/ehf2.12459
American Heart Association. (2021). Get with the guidelines: Heart failure. https://www.heart.org/-/media/Files/Professional/Quality-Improvement/Get-With-the-Guidelines/Get-With-The-Guidelines-HF/Educational-Materials/HF-Fact-SheetUpdated-011119V2updated-3521KM-002.pdf
Butler, J., Anker, S. D., & Packer, M. (2019). Redefining heart failure with a reduced ejection fraction. JAMA, 322(18), 1761-1762. https://doi.org/10.1001/jama.2019.15600
Colucci, W. S. (2021). Patient education: Heart failure (beyond the basics). UpToDate. Retrieved September 14, 2022, from https://www.uptodate.com/contents/heart-failure-beyond-the-basics
Colucci, W. S., & Dunlay, S. M. (2022). Clinical manifestations and diagnosis of advanced heart failure. UpToDate. Retrieved September 16, 2022, from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-advanced-heart-failure
Gottlieb, S. H. (2021). Heart failure with reduced ejection fraction: "Guideline-directed medical therapy (GDMT)" versus "the art of medicine." Journal of the American College of Cardiology, 78(20), 2013-2016. https://www.jacc.org/doi/10.1016/j.jacc.2021.09.015
Heidenreich, P. A., Bozkurt, B., Aguilar, D., Allen, L. A., Byun, J. J., Colvin, M. M., Deswal, A., Drazner, M. H., Dunlay, S. M., Evers, L. R., Fang, J. C., Fedson, S. E., Fonarow, G. C., Hayek, S. S., Hernandez, A. F., Khazanie, P., Kittleson, M. M., Lee, C. S., Link, M. S., . . . Yancy, C. W. (2022). AHA/ACC/HFSA guideline for the management of heart failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 145, e895–e1032. https://doi.org/10.1161/CIR.0000000000001063
Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018). Medical-surgical nursing: Concepts for interprofessional collaborative care (9th ed.). Elsevier.
Jameson, J. L., Kasper, D. L., Longo, D. L., Fauci, A. S., Hauser, S. L., & Loscalzo, J. (2018). Harrison's principles of internal medicine (20th ed.). McGraw-Hill Education.
Kosaraju, A., Goyal, A., Grigorova, Y., & Makaryus, A. N. (2022). Left ventricular ejection fraction. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK459131
Maddox, T. M., Allen, L. A., Breathett, K., Butler, J., Davis, L. L., Fonarow, G. C., Ibrahim, N. E., Lindenfeld, J., Masoudi, F. A., Motiwala, S. R., Oliveros, E., Patterson, J. H., Walsh, M. N., Wasserman, A., Yancy, C. W., & Youmans, Q. R. (2021). 2021 update to the 2017 ACC expert consensus decision pathway for optimization of heart failure treatment: Answers to 10 pivotal issues about heart failure with reduced ejection fraction. Journal of the American College of Cardiology, 77(6), 772-810. https://doi.org/10.1016/j.jacc.2020.11.022
McDonagh, T. A., Metra, M., Adamo, M., Gardner, R. S., Baumbach, A., Bohm, M., Burri, H., Butler, J., Celutkiene, J., Chioncel, O., Cleland, J. G. F., Coats, A. J. S., Crespo-Leiro, M. G., Farmakis, D., Gilard, M., & Heymans, S. (2021). 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. European Heart Journal, 42, 3599-3726. https://doi.org/10.1093/eurheartj/ehab368
Mogos, M. F., Piano, M. R., McFarlin, B. L., Salemi, J. L., Liese, K. L., & Briller, J. E. (2018). Heart failure in pregnant women: A concern across the pregnancy continuum. Circulation Heart Failure, 11(1), e004005. https://doi.org/10.1161/CIRCHEARTFAILURE.117.004005
Mohrman, D. E., & Heller, L. J. (2018). Cardiovascular physiology (9th ed.). McGraw-Hill Education.
Okoshi, M. P., Capalbo, R. V., Romeiro, F. G., & Okoshi, K. (2017). Cardiac cachexia: Perspectives for prevention and treatment. Arquivos Brasileiros de Cardiologia, 108(1), 74-80. https://doi.org/10.5935/abc.20160142
Reinmann, M., & Meyer, P. (2020). B-type natriuretic peptide and obesity in heart failure: a mysterious but important association in clinical practice. Cardiovascular Medicine, 23(w02095). https//doi.org/10.4414/cvm.2020.02095
Roger, V. L. (2021). Epidemiology of heart failure: A contemporary perspective. Circulation Research, 128(10), 1421-1434. https://doi.org/10.1161/CIRCRESAHA.121.318172
Schwinger, R. H. G. (2021). Pathophysiology of heart failure. Cardiovascular Diagnosis & Therapy, 11(1), 263-276. https://doi.org/10.21037/cdt-20-302
US Food and Drug Administration. (2021). Highlights of prescribing information: Entresto. https://www.novartis.com/us-en/sites/novartis_us/files/entresto.pdf
Vallerand, A., & Sanoski, C. (2017). Davis's drug guide for nurses (15th ed.). F. A. Davis Company.
van de Wouw, J., Broekhuizen, M., Sorop, O., Joles, J. A., Verhaar, M. C., Duncker, D. J., & Merkus, D. (2019). Chronic kidney disease as a risk factor for heart failure with preserved ejection fraction: A focus on microcirculatory factors and therapeutic targets. Frontier Physiology, 10(article 1108). https://doi.org/10.3389/fphys.2019.01108
Woods, A. D. (2023). Nursing 2023 drug handbook. Wolters Kluwer.