Contact Hours: 5
This educational activity is credited for 5 contact hours at completion of the activity.
Course Purpose
The purpose of this course is to provide healthcare professionals with a comprehensive guide to understanding heart failure and its management by covering a wide range of topics essential for understanding cardiovascular health, including the intricate mechanisms of normal heart function and the complexities of heart failure diagnosis and treatment.
Overview
More than 6 million Americans are living with heart failure, and the prevalence continues to rise, with over 1 million new cases diagnosed in adults aged 55 and older each year. Heart failure has an estimated mortality rate of 10%, with the primary causes being attributable to sudden cardiac death or organ dysfunction resulting from inadequate perfusion. This underscores the critical need for effective management strategies and interventions to mitigate the risks associated with heart failure and improve outcomes for affected individuals. This course serves as a comprehensive guide to understanding heart failure and its management. It covers a wide range of topics essential for understanding cardiovascular health, from the intricate mechanisms of normal heart function to the complexities of heart failure diagnosis and treatment.
Course Objectives
Upon completion of this course, the learner will be able to:
- Review normal cardiac physiology and function
- Describe the three types of heart failure and their stages, and classifications as described by the American College of Cardiology/American Heart Association classification and the New York Heart Association (NYHA) classification system.
- Understand potential risk factors of heart failure
- Analyze the differences between STEMI and NSTEMI
- Review treatment options for heart failure including common medications, laboratory and electrocardiograph findings, and procedural interventions.
Policy Statement
This activity has been planned and implemented in accordance with the policies of FastCEForLess.com.
Disclosures
Fast CE For Less, Inc and its authors have no disclosures. There is no commercial support.
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| Angiotensin Receptor Blockers (ARBs) | Medicines that help relax the veins and arteries to lower blood pressure. |
| Angiotensin-Converting Enzyme (ACE) Inhibitors | A class of drugs that interact with blood enzymes to enlarge or dilate blood vessels and reduce blood pressure. |
| Anthracycline-Containing Therapy | Widely used chemotherapy drugs derived from certain types of Streptomyces bacteria. |
| Aorta | The largest blood vessel in the body that delivers oxygen-rich blood from the heart to the rest of the body. |
| Aortic Stenosis | A type of heart valve disease that narrows the aortic valve and reduces blood flow. |
| Arrhythmias | An irregular heartbeat that can be normal or abnormal. |
| Atria | One of the two upper chambers in the heart that receives blood from the circulatory system. |
| Atrial Depolarization | Starts the first phase of atrial muscle contraction, which produces a small increase in atrial and venous pressures. |
| Atrial Flutter | An abnormal heart rhythm in the heart’s atria, where atria beat too fast. |
| Atrioventricular Septum | A septum of the heart between the right atrium (RA) and the left ventricle (LV). |
| Beta-Blockers | Medicines that lower blood pressure by blocking the effects of adrenaline on the heart and blood vessels. |
| B-Type Natriuretic Peptides (BNP) test | A commonly performed blood test that is used to diagnose or rule out heart failure. |
| Bumetanide | Used to reduce extra fluid in the body (edema) caused by conditions such as heart failure, liver disease, and kidney disease. |
| Bundle Of His | A part of the cardiac conduction system that transmits electrical impulses. |
| Cancer | A disease in which some of the body’s cells grow uncontrollably and spread to other parts of the body. |
| Carbon Dioxide | A chemical compound with the chemical formula CO2. |
| Cardiac Resynchronization Therapy (CRT) | A procedure to implant a device in the chest to make the heart’s chambers contract in a more organized and efficient way. |
| Cardiovascular Disease (CVD) | A group of disease that affect the heart and vessels. |
| Complete Blood Count (CBC) | A blood test done to check the levels of cells in the blood, including the red blood cells, white blood cells, and platelets. |
| Congenital Heart Defects | Abnormalities of the heart structure or function that are present at birth. |
| Congestive Heart Failure | A long-term condition that happens when the heart can’t pump blood well enough to give the body a normal supply. |
| Coronary Artery Bypass Grafting (CABG) | A surgical procedure that is done to treat a blockage or narrowing of one or more of the coronary arteries. |
| Coronary Artery Disease (CAD) | A condition in which the blood vessels supplying blood to the heart get blocked, causing ischemia and pain in the heart muscles. |
| Deoxygenated Blood | Refers to the blood that has a low oxygen saturation when compared to the blood leaving the lungs. |
| Diastolic Failure | A condition in which the left ventricle becomes stiff and unable to fill properly. |
| Ejection Fraction (EF) | The measurement of the percentage of blood leaving the heart each time it contracts. |
| Electrocardiogram (EKG) | Records the electrical signals in the heart. |
| Elevated Jugular Venous Pressure (JVP) | The classic sign of right-sided heart failure. |
| Endotracheal Intubation | Inserting a tube into the trachea to keep the airway open and deliver air or oxygen. |
| Furosemide | A loop diuretic medication used to treat edema due to heart failure, liver scarring, or kidney disease. |
| Gout | A type of arthritis that causes inflammation of joints due to excess uric acid. |
| Guideline-Directed Medical Therapy (GDMT) | A form of treatment for people with heart failure with reduced ejection fraction. |
| Heart Failure With Mid-Range Ejection Fraction (HFmrEF) | Heart failure where the left ventricle pumps between 41% and 49% ejection fraction. |
| Heart Failure With Preserved Ejection Fraction (HFpEF) | Heart failure where the heart is pumping greater than or equal to 50% ejection fraction. |
| Heart Failure | A progressive heart disease that affects pumping action of the heart muscles. |
| Heart Transplantation | A surgical procedure where the diseased heart is replaced with a healthy heart from a donor. |
| Hypertension | High pressure in the arteries. |
| Hypertrophy | The increase and growth of muscle cells through exercise. |
| Hypokalemia | Below normal blood potassium level. |
| Hyponatremia | A condition where sodium levels in the blood are abnormally low. |
| Hypotension | A blood pressure reading below the specified limit (90/60 mmhg). |
| Hypoxia | A below-normal level of oxygen in the blood, specifically in the arteries. |
| Implantable Cardioverter-Defibrillator (ICD) | Devices that detect and stop irregular heartbeats, also called arrhythmias. |
| Jugular Venous Distention (JVD) | The bulging of the major veins in the neck. |
| Left Bundle Branch Block (LBBB) | A condition in which electrical impulses along the pathway that makes the heartbeat are delayed or blocked. |
| Left Ventricular Assist Device (LVAD) | A mechanical pump that helps the heart pump blood in heart failure. |
| Left-Side Heart Failure | Occurs when the heart loses its ability to pump blood. |
| Leukocytosis | A normal immune response that can indicate infection, inflammation, injury or immune system disorders. |
| Liver Disease | A condition that affects the organ’s ability to digest food, rid the body of waste and clot blood. |
| Metabolic Syndrome | A group of conditions that increase the risk of cardiovascular disease, Type 2 diabetes and stroke. |
| Mineralocorticoid Receptor Antagonists (MRAs) | Drugs that block the action of aldosterone, a hormone that raises blood pressure and causes fluid retention. |
| Mitral Regurgitation | A condition in which the mitral valve does not close completely causing blood to leak back to the left atrium when left ventricle contracts. |
| Myocardial Cells | The contractile myocytes of the cardiac muscle. |
| Myocardial Infarction | Damage to the heart muscle caused by a loss of blood supply due to blocks in the arteries. |
| Myocardium | The middle layer of the heart composed of cardiomyocytes, which contract and conduct electrical stimuli. |
| Nesiritide | A vasodilator that relaxes and dilates blood vessels, lowering blood pressure and improving breathing in people with sudden severe heart failure. |
| Neurohormonal Antagonists | Interfere with the actions of deleterious endogenous mechanisms). |
| New York Heart Association (NYHA) Classification | Provides a simple way of classifying the extent of heart failure. |
| Nitroglycerin | A medication that treats angina and anal fissures by promoting blood flow. |
| N-Terminal Pro-B-Type Natriuretic Peptide (NTproBNP) | A protein that is an ingredient for making the BNP hormone. |
| Percutaneous Coronary Intervention (PCI) | A minimally invasive procedure to open blocked coronary arteries. |
| Phosphodiesterase-5 Inhibitors | Medications that block enzymes that relax blood vessels and improve circulation. |
| Pulmonary Artery | The blood vessels that carry oxygen-poor blood from the heart to the lungs. |
| Pulmonary Circulation | System of blood vessels that forms a closed circuit between the heart and the lungs. |
| Pulmonary Congestion | A condition caused by too much fluid in the lungs. |
| Pulmonary Veins | The veins that transfer oxygenated blood from the lungs to the heart. |
| Purkinje Fibers | Functional conducting fibers that are larger than normal myocardial cells and have more mitochondria. |
| Renal Insufficiency | Means the kidneys cannot filter waste products from the blood properly. |
| Repolarization | Defines the resetting of the electrochemical gradients of the cell to prepare for a new action potential. |
| Respiratory Acidosis | An acid-base balance disturbance due to alveolar hypoventilation. |
| Right Bundle Branch Block (RBBB) | A problem with the right bundle branch that makes the heartbeat signal late and out of sync with the left bundle branch, creating an irregular heartbeat. |
| Right-Side Heart Failure | Involves the part of the heart responsible for pumping blood to the lungs, where it receives oxygen. |
| Sino-Atrial (SA) Node | An oval shaped region of special cardiac muscle in the upper back wall of the right atrium made up of cells known as pacemaker cells. |
| Sleep Apnea | A sleep disorder that causes breathing to stop and start during sleep. |
| Sodium Nitroprusside | A medication used in the management of acute hypertension. |
| Systolic Failure | A condition in which the left ventricle of the heart is weak and can’t pump blood efficiently. |
| The Atrioventricular (AV) Node | Electrically connects the heart’s atria and ventricles to coordinate beating in the top of the heart. |
| Thrombocytopenia | A condition where abnormally low level of platelets are observed. It causes nosebleeds, bleeding gums, blood in urine, heavy menstrual periods, and bruising. |
| Type 2 Diabetes Mellitus | A condition results from insufficient production of insulin, causing high blood sugar. |
| Valvular Heart Disease | Occurs when one or more of the valves in the heart does not work properly. |
| Ventricle | A muscular chamber that pumps blood out of the heart and into the circulatory system. |
| Ventricular Depolarization | Occurs when corresponding contraction of myocardial muscle moves as a wave through the heart. |
| Ventricular Repolarization | The return of the ions to their previous resting state, which corresponds with relaxation of the myocardial muscle. |
Heart failure is a progressive, lifelong condition currently afflicting approximately 37 million individuals globally. In the US alone, more than 6 million Americans are living with heart failure, and the prevalence continues to rise, with over 1 million new cases diagnosed in adults aged 55 and older each year. Annually, heart failure carries an estimated mortality rate of 10%, with the primary causes being attributable to sudden cardiac death or organ dysfunction resulting from inadequate perfusion. This underscores the critical need for effective management strategies and interventions to mitigate the risks associated with heart failure and improve outcomes for affected individuals. This course serves as a comprehensive guide to understanding heart failure and its management. It covers a wide range of topics essential for understanding cardiovascular health, from the intricate mechanisms of normal heart function to the complexities of heart failure diagnosis and treatment.1,2
The heart is an intricately structured muscular organ primarily composed of myocardial cells, also known as myocardium. Its anatomical configuration comprises four chambers: two atria positioned superiorly and two ventricles located inferiorly, such that each side, right and left, consists of one atrium and one ventricle. Between these chambers are valves that ensure the unidirectional flow of blood. The atrioventricular septum completely separates the right and left side of the heart. Unless there is any septal defect, the two sides of the heart never directly communicate. Blood travels from the right side of the heart to the left side via the lungs. Physiologically, deoxygenated blood returns to the right atrium via venous circulation. Myocardial contractions pump blood into the right ventricle, initiating pulmonary circulation by transferring blood to the lungs via the pulmonary artery, where carbon dioxide is removed and oxygen is absorbed. The oxygen-rich blood then travels from the lungs via the pulmonary veins to the left side of the heart to the atrium, then to the left ventricle, and then distributed to the body via the aorta and arterial circulation. The pressure in the arteries caused by the left ventricle contraction is the systolic blood pressure. As the left ventricle begins to relax after fully contracting and refills with blood from the left atrium, arterial pressure drops. This is the diastolic blood pressure. The average blood pressure of a healthy adult is typically around 120/80 mmHg. Functionally, these left and right chambers exhibit synchronized contractions, so atrial and ventricular contractions occur concurrently. This action is powered by the cardiac conduction system. This system generates and propagates electrical impulses through a well-defined pathway that comprises five components: (1) the sino-atrial (SA) node, (2) The atrioventricular (AV) node, (3) The bundle of His, (4) The left and right bundle branches, and (5) the Purkinje fibers.3
The SA node is referred to as the natural pacemaker of the heart. It generates electrical impulses at a rate dictated by the body’s needs, setting the tempo for cardiac activity. These impulses propagate through the myocardial cells of the atria, triggering a wave of contraction known as atrial depolarization. This rapid transmission occurs in less than one-third of a second, resulting in synchronized atrial contraction that empties blood from the atria into the ventricles. Subsequently, the electrical stimulus from the SA node reaches the AV node, where it undergoes a brief delay. This delay allows the contracting atria to complete their contraction, ensuring optimal ventricular filling. As the atria begin to refill, the electrical impulse travels through the AV node and Bundle of His, into the bundle branches and Purkinje fibers. Mirroring the atrial contraction, ventricular contraction occurs swiftly, enabling the ejection of blood from the heart. This phase is known as ventricular depolarization. During ventricular depolarization, the right ventricle pumps blood to the lungs, while the left ventricle drives blood into the aorta for systemic circulation. As the ventricles contract, the atria refill with blood, and the valves between the chambers close, preventing backflow. The depolarization of both atria and ventricles is followed by repolarization, allowing the heart muscle cells to reset for the next cardiac cycle. During repolarization, the SA and AV nodes recharge, preparing to start the next electrical impulse. This process occurs smoothly, with the SA node recharging while the atria refill and the AV node recharging during ventricular filling. This coordinated interplay ensures the continuity of rhythmic contractions, sustaining cardiac function without interruption. Similar to depolarization, repolarization transpires in less than one-third of a second, ensuring the heart can continue its contractions without interruption. In normal heart function, this coordination between electrical impulses and mechanical actions maintains synchronized contraction of the myocardium to circulate blood to all organs.3
Heart failure manifests when there is dysfunction or disruption in the heart’s normal function. The abnormality can arise from various causes such as structural defects, problems in heart rhythms, diseases, infections, toxins, or a combination of these factors. While all these issues impair the heart’s ability to pump blood throughout the body effectively, it is critical to identify the exact pathophysiological mechanism at work to select adequate therapeutic options. The most common causes of heart failure include congenital heart defects, coronary artery disease (CAD), valvular heart disease, arrhythmias, hypertension, myocardial infarction, infections, toxins, and drugs. Congenital heart defects are structural abnormalities present from birth that elevate the risk of heart failure later in life. Coronary artery disease (CAD), characterized by the buildup of cholesterol and fatty deposits in the heart’s arteries, restricts blood flow to the heart muscle. Additionally, atherosclerosis, a hallmark of coronary artery disease, can elevate blood pressure over time, further predisposing individuals to heart failure.2,4
Valvular heart diseases, such as aortic stenosis or mitral regurgitation, disrupt blood flow between the heart chambers, culminating in increased pressure and volume overload on the heart muscle, contributing to heart failure. Irregular heart rhythms, known as arrhythmias, disrupt the heart’s contraction coordination, impairing its pumping function. Hypertension, characterized by abnormally high blood pressure, imposes prolonged strain on the heart, prompting hypertrophy and eventual heart failure due to increased resistance against blood pumping. Myocardial infarction (MI), commonly known as a heart attack, induces tissue damage or death in the heart muscle due to blocked blood flow, severely compromising pumping function and potentially leading to heart failure and sudden cardiac death if left untreated or unmanaged. Cardiomyopathy, such as dilated, hypertrophic, and restrictive cardiomyopathies, are heart muscle diseases that weaken cardiac function, predisposing it to collapse, especially under stress. Infections like viral myocarditis inflict inflammation and damage on the heart muscle, similarly impairing the heart’s pumping efficacy. Exposure to toxins or drugs such as alcohol, cocaine, or chemotherapy agents can also inflict direct damage on the heart muscle, exacerbating the risk of heart failure. 2,4
Heart failure is a clinical syndrome characterized by a range of signs and symptoms. In the earliest stages of heart failure, individuals may experience subtle symptoms that gradually worsen over time. These include fatigue and weakness, decreased appetite and nausea, shortness of breath (dyspnea), persistent cough or wheezing, and fluid retention. Fatigue and weakness occur due to the heart’s inability to pump an adequate amount of blood to meet the body’s demands. To compensate, the body redirects blood away from less essential organs, like muscles in the limbs, prioritizing vital organs such as the heart and brain. Individuals with heart failure often experience persistent tiredness and find everyday activities challenging. Tasks like shopping, climbing stairs, carrying groceries, or walking may become difficult. Feelings of sleepiness after meals, weakness in the legs during walking, and shortness of breath during physical activity are common symptoms experienced by individuals with heart failure. This diminished blood supply can also lead to digestive problems, resulting in feelings of fullness or nausea. Moreover, inadequate blood flow to the stomach can impede the absorption of nutrients from food, contributing to potential weight loss.1,5
Dyspnea is primarily caused by a backup of blood in the pulmonary veins, due to the heart’s inability to match the blood supply. The fluid then seeps into the lungs, leading to congestion, persistent wheezing, and coughing that produces white- or red-tinged mucus. Individuals with heart failure often experience breathlessness during physical activity or even while at rest. At times, dyspnea may suddenly worsen at night, severely hindering breathing unless the individual changes position or moves. Fluid accumulation and retention, also known as edema, occurs due to the heart’s inability to pump blood with sufficient force. This inadequate pumping action results in insufficient blood being ejected from the heart with each heartbeat. Thus, as the heart fails to empty correctly, blood returning from the body cannot enter the heart efficiently, leading to a backup of blood in the veins. This increased pressure forces fluid from the blood vessels into surrounding tissues, causing noticeable swelling or edema. Edema commonly manifests as swelling in the feet, ankles, legs, fingers, abdomen, and other tissues and organs. This fluid retention also causes weight gain as the condition progresses.1,5 As heart failure advances, these symptoms may worsen, and additional signs may appear, including palpitations, tachycardia, cognitive impairments, and polyuria. Palpitations are sensations of rapid, irregular, or pounding heartbeats that arise due to irregular heart rhythms. These palpitations may be accompanied by sensations of fluttering, pounding, or racing in the chest. Tachycardia refers to a rapid heart rate, typically defined as a resting heart rate greater than 100 beats per minute. As heart failure progresses, the heart may begin to beat faster in an attempt to compensate for its reduced pumping ability or to meet the body’s increased oxygen demand. Tachycardia can exacerbate symptoms such as shortness of breath, fatigue, and palpitations. Cognitive impairments occur due to fluctuating levels of specific electrolytes in the blood, such as sodium. These imbalances can diminish blood flow to the brain, resulting in symptoms such as confusion, difficulty, memory loss, and feelings of disorientation. Oftentimes, caregivers or relatives are the first to recognize these symptoms. Polyuria is frequent urination caused by fluid retention. To eliminate this excess fluid, the kidneys respond by increasing urine production.1,5
There are three types of heart failure:1
- Left-side heart failure
- Right-side heart failure
- Congestive heart failure
For each type of heart failure, the efficiency of the heart’s pumping function is quantified by a metric called ejection fraction (EF), which represents the percentage of blood ejected from the left ventricle with each heartbeat. In a healthy individual, the left ventricle typically ejects approximately 60% to 65% of the blood it contains. This measurement helps healthcare providers assess the heart’s ability to pump blood, diagnose heart failure, and guide treatment strategies.1,6
In left-sided heart failure, also known as left ventricular heart failure, the left side of the heart encounters an increased workload to pump the same amount of blood as usual. When left ventricular function is compromised, the ejection fraction may decrease, indicating reduced pumping efficiency and impaired cardiac function. There are three types of left-sided heart failure:6
- Systolic failure
- Diastolic failure
- Mid-range heart failure
In systolic failure, the left ventricle cannot contract normally, and the heart struggles to pump blood with sufficient force to circulate throughout the body adequately. This condition is also referred to as heart failure with reduced ejection fraction or HFrEF. When systolic heart failure occurs, EF is typically equal to or less than 40%. Heart failure with reduced ejection fraction often arises from significant loss of myocardial cells, which may arise from a myocardial infarction, inflammation of the heart muscle, or valvular disease resulting in cell loss due to overload.6,7,8
In diastolic heart failure, the left ventricle loses its ability to relax normally due to increased muscle tissue stiffness. As a result, the heart struggles to adequately fill with blood during the resting period between each heartbeat. This condition is also referred to as heart failure with preserved ejection fraction or HFpEF. When diastolic heart failure occurs, EF is typically equal to or greater than 50%. Heart failure with preserved ejection fraction is often associated with chronic comorbidities, including arterial hypertension, type 2 diabetes mellitus, obesity, renal insufficiency, pulmonary disease, liver disease, sleep apnea, gout, and cancer. Patients diagnosed with HFpEF are typically older and females. In recent years, a third type of left-side heart failure has been identified, where the heart’s ability to contract and relax may both be compromised to a moderate extent. This case is referred to as heart failure with mid-range ejection fraction or HFmrEF, with EF between 41% and 49%. Individuals with HFmrEF often present with symptoms and clinical features that overlap with HFrEF and HFpEF. The exact mechanisms for this sub-type are still under investigation. The most common symptoms of left-sided heart failure include dyspnea, especially during exertion or when lying flat, chronic cough or wheezing with pink or blood-colored mucus, and pulmonary congestion or edema.6,7,8
Right-sided or right-ventricular heart failure typically occurs as a consequence of left-sided failure. In instances where the left ventricle falters in its ability to pump blood out effectively, heightened fluid pressure reverberates back through the lungs, adversely impacting the right side of the heart. As the right ventricle loses its pumping capacity, blood begins to accumulate in the body’s veins, leading to right-sided heart failure. Characteristic symptoms of right-sided heart failure include swelling in the legs, ankles, and abdomen; ascites, indicated by increased abdominal girth from fluid accumulation, pervasive and debilitating fatigue and weakness, loss of appetite and nausea, and elevated jugular venous pressure (JVP) or jugular venous distention (JVD). Congestive heart failure often involves both the left and right sides of the heart, leading to a cascade of symptoms and systemic effects. It is a medical emergency and requires immediate attention for better patient outcomes. While left and right-sided heart failure present overlapping symptoms, distinctive clinical signs differentiate the two conditions. Left-sided heart failure predominantly exhibits symptoms related to pulmonary congestion and inadequate systemic perfusion. Conversely, right-sided heart failure primarily showcases symptoms linked to systemic venous congestion and peripheral edema. Therefore, crackles in the lungs indicate left-sided heart failure, while elevated jugular venous pressure indicates right-sided heart failure.6,7,8
The main risk factors contributing to the development of heart failure include coronary heart disease, hypertension, diabetes mellitus, family history of heart disease, chronic pulmonary diseases, obesity, inflammation or chronic infection, and metabolic diseases. Conditions such as coronary heart disease and hypertension have been shown to cause heart failure directly, while other factors compromise heart health. For example, Type 2 diabetes elevates lipid levels in the blood, while metabolic syndrome and hyperactive thyroid problems result in consistently elevated heart rate and thickening of the heart muscle. Both conditions strain cardiac function. Advancing age is associated with a higher prevalence of heart failure, as aging weakens and stiffens the heart muscle. Studies indicate a notable increase in heart failure prevalence with age, with estimates ranging from 8 per 1000 in men aged 50 to 59 years to 66 per 1000 in men aged 80 to 89 years. Similar trends are observed in women, with prevalence rates escalating from 8 per 1000 to 79 per 1000 for the same age ranges. Cardiotoxic agents such as cocaine or the anthracycline-containing therapy used in oncology may precipitate cardiotoxicity, either acutely, early-onset chronically, or late-onset chronically.8,9
As heart failure progresses, healthcare professionals rely on classification systems to better understand and manage the condition, particularly in its advanced stages. Typically, patients’ heart failure severity is assessed based on the classification of their symptoms. Among the widely utilized classification systems are the American College of Cardiology/American Heart Association classification and the New York Heart Association (NYHA) classification.7
The American College of Cardiology/American Heart Association classification system offers a framework for assessing heart failure severity by considering various clinical parameters, including symptoms, functional status, and objective measures such as left ventricular ejection fraction and biomarker levels. It defines four stages of the disease; A, B, C, and D. Patients in stage A are considered at risk for heart failure but do not exhibit symptoms, structural heart disease, or elevated cardiac biomarkers of stretch or injury. These individuals may have predisposing conditions such as hypertension, atherosclerotic cardiovascular disease (CVD), diabetes, metabolic syndrome, obesity, exposure to cardiotoxic agents, genetic variants for cardiomyopathy, or a positive family history of cardiomyopathy. Stage B encompasses patients who do not manifest symptoms or signs of heart failure but present evidence of one of the following:7,10
- Structural heart disease
- Increased filling pressures
- Elevated levels of b-type natriuretic peptides (BNP)
- Persistently elevated cardiac troponin in the absence of competing diagnoses
Ejection fraction is often preserved in this stage. Patients in stage C exhibit structural heart disease with current or previously noted symptoms of heart failure. This stage signifies the onset of symptomatic heart failure, with EF playing a crucial role in determining treatment strategies. Ejection fraction assessment aids in stratifying patients into HFrEF (EF ≤ 40%) or HFpEF (EF ≥ 50%). In stage D, patients experience marked heart failure symptoms that significantly impair daily life and result in recurrent hospitalizations despite efforts to optimize guideline-directed medical therapy (GDMT). In this stage, EF assessment is ongoing as it is pivotal for guiding therapeutic interventions and prognostic evaluation.7,10
The New York Heart Association (NYHA) classification serves as a valuable tool for characterizing the symptoms and functional capacity of patients with symptomatic (Stage C) or advanced (Stage D) heart failure. Patients are categorized into one of four classes based on their limitations in physical activity. Class I means no limitation of physical activity. Patients in this category can engage in ordinary physical activities without experiencing undue fatigue, palpitations, or shortness of breath. Class II indicates light limitation of physical activity. While comfortable at rest, patients may experience fatigue, palpitations, shortness of breath, or chest pain during ordinary physical activities. Class III marks limitations in physical activity. Patients are comfortable at rest, but less than ordinary activity leads to symptoms such as fatigue, palpitations, shortness of breath, or chest pain. Class IV indicates symptoms of heart failure occur even at rest. Any physical activity exacerbates discomfort, indicating severe limitations in functional capacity.7,11
Initial emergency treatment for acute heart failure aims to restore blood flow and oxygen levels while stabilizing the patient’s condition. The approach involves several interventions tailored to the individual’s symptoms and clinical presentation. For patients experiencing severe respiratory distress, hypoxia, or respiratory acidosis, noninvasive ventilation is a viable option, provided the patient can cooperate with the treatment. If the patient is unable to cooperate, immediate consideration should be given to endotracheal intubation to ensure adequate oxygenation and ventilation. Supplemental oxygen therapy is often administered to maintain oxygen saturation levels above 95%, especially for patients exhibiting hypoxia. However, if the patient is not hypoxic, oxygen administration may not be necessary or recommended.1,7,8
In cases of acute heart failure accompanied by flash pulmonary edema and hypertension, vasodilator therapy is crucial. Vasodilators help reduce afterload and alleviate congestive symptoms. Nitroglycerin is the preferred agent in emergencies for its rapid onset and titratability. Sublingual nitroglycerin can be initially administered until intravenous therapy is established, followed by intravenous nitroglycerin titrated to reduce left ventricular filling pressures and improve congestive symptoms rapidly. However, nitrates should be avoided in patients with recent use of phosphodiesterase-5 inhibitors and those presenting with hypotension. Alternatives to nitroglycerin include sodium nitroprusside and nesiritide, which also exhibit rapid blood pressure-lowering effects. For patients without flash pulmonary edema, intravenous diuretics, such as furosemide or bumetanide, should be administered. Subsequent dosing can be adjusted based on urine output and clinical response. It is important to note that morphine should be avoided in heart failure treatment due to potential adverse outcomes, including increased intensive care unit admissions and mortality rates.1,7,12
EKG Findings
Electrocardiograms (EKGs) are fundamental tools for monitoring and documenting the heart’s electrical activity, providing valuable insights into cardiac function. Interpreting an EKG involves reading its five fundamental waves:13,14
- P wave
- QRS complex
- T wave
- ST segment
- QT interval
The P wave represents atrial depolarization. In normal cardiac function, the P wave is smooth, rounded, and precedes the QRS complex. The QRS complex represents ventricular depolarization. It consists of three distinct waves: An initial downward deflection (the Q wave), the first upward deflection following the Q wave (the R wave), and a downward deflection following the R wave (the S wave). The T wave represents ventricular repolarization. In regular heart activity, the T wave is smooth, rounded, and follows the QRS complex. The ST segment connects the QRS complex to the T wave and represents the interval between ventricular depolarization and repolarization. Under normal conditions, the ST segment should be isoelectric, indicating that the ventricles are not experiencing any ischemia. The QT interval represents the total time for ventricular depolarization and repolarization. It begins at the start of the QRS complex and ends at the end of the T wave. The U wave follows the T wave and represents the repolarization of the Purkinje fibers.13,14
In heart failure, an EKG can reveal various abnormalities that reflect the underlying cardiac dysfunction. While EKG findings in heart failure can vary widely depending on the specific etiology and severity of the condition, healthcare professionals may observe some common patterns and changes. These include atrial fibrillation, atrial flutter, and ventricular arrhythmias, which may manifest as irregular timing and morphology of the P waves, QRS complexes, and T waves on the EKG. Tachycardia, chronic pressure, and volume overload are seen on an EKG as an increase in amplitude and duration of the QRS complexes, along with changes in the ST segment and T wave. Ischemia and myocardial injury commonly may cause ST segment depression, T wave inversion, or other ST-T wave abnormalities. Conduction abnormalities such as left bundle branch block (LBBB) or right bundle branch block (RBBB) may affect the QRS complex morphology. In some cases of advanced heart failure, low voltage EKG tracings may be observed and be noticeable as changes in P wave morphology. If the U wave is not visible, it may indicate electrolyte imbalances. It is important to note that the information EKG findings provide is often nonspecific and needs to be used alongside other diagnostic modalities for effective heart failure evaluation and management.13,14
Laboratory Values
In emergency situations, healthcare professionals should prioritize laboratory tests that can rapidly diagnose or rule out heart failure. B-type natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic peptide (NTproBNP) are crucial biomarkers used for this purpose. Both these peptides are secreted by the heart in response to increased myocardial wall stress and volume overload. B-type natriuretic peptide levels below 100 pg/mL generally exclude heart failure, and levels above 400 pg/mL strongly suggest heart failure. Levels between 100 and 400 pg/mL necessitates further evaluation for an accurate diagnosis. Similarly, NTproBNP levels below 300 pg/mL exclude heart failure, whereas levels above 900 pg/mL are highly suggestive, with the 300 to 900 pg/mL range requiring additional testing. Notably, NTproBNP thresholds must be adjusted for age, with a higher cutoff point for patients older than 75.1,7
In the presence of obesity or renal failure, BNP and NTproBNP levels may be misleading and require adjustment. For instance, in patients with a body mass index exceeding 35, measured BNP levels should be doubled. In contrast, levels should be halved in the presence of renal failure, where the estimated glomerular filtration rate is below 60 mL/min. Additional laboratory tests commonly used to evaluate heart failure include a basic metabolic panel with creatinine and troponin. Elevated troponin levels in hospitalized patients indicate a significantly higher acute mortality risk, warranting more aggressive therapeutic interventions. Renal function assessment is also critical. It is a major predictor of mortality and disease severity. Worsening heart failure may exacerbate renal dysfunction, making it vital to monitor its parameters during management.1,7
Complete blood count (CBC) tests are also done regularly to assess a patient’s red blood cell count, white blood cell count, and platelet count in heart failure. Anemia, leukocytosis, and thrombocytopenia may be present and can contribute to symptoms such as fatigue, weakness, and increased risk of thromboembolic events. Electrolyte imbalances, particularly hyponatremia and hypokalemia, are common in heart failure and are also closely monitored, especially in patients receiving diuretic therapy to prevent adverse events such as arrhythmias, muscle weakness, and neurologic disturbances. Liver function abnormalities may occur in advanced heart failure due to hepatic congestion and impaired hepatic perfusion, resulting in elevated levels of liver enzymes and bilirubin. Therefore, liver function tests are necessary to assess hepatic dysfunction and further treatment decisions.1,7
Procedures for Treating Heart Failure
Several procedures are available for treating heart failure, aiming to alleviate symptoms, improve heart function, and enhance the patient’s quality of life. These include percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), heart valve repair or replacement, implantable cardioverter-defibrillator (ICD), cardiac resynchronization therapy (CRT), left ventricular assist device (LVAD), and heart transplantation. The indication for each of these procedures depends on the etiology of the heart failure, individual patient risk profile, and disease severity. Also known as angioplasty, PCI is a minimally invasive procedure used to open narrowed or blocked coronary arteries. In this procedure, a small tube with a tiny, deflated balloon on the end is inserted through an incision, typically in the groin, and pushed through to the diseased artery. There, the balloon is inflated to dilate the artery. The balloon is removed once the artery has been fully opened. A stent may be inserted to help keep the artery open and improve blood flow to the heart muscle. In cases where a stent is insufficient, a CABG may be needed to bypass blocked coronary arteries. During this procedure, surgeons remove healthy blood vessels from another part of the body, such as a leg, wrist, or the chest wall. They then surgically attach the vessels to the affected artery so that the blood can flow around the blocked section.15,16
For individuals with heart failure caused by damaged or malfunctioning heart valves, surgical repair or replacement of the affected valve(s) may be necessary to reestablish normal blood flow through the heart chambers. During valve repair, the damaged sections of the valve are strengthened. During valve replacement, the failing valve is removed, and a new valve is used in its place. Various replacement valves can be used, including a mechanical valve made from metal and plastic, or one made from human or animal tissue. While most heart valve surgeries are successful, they require long-term management with medication to prevent blot clots. Therefore, the operation is only considered as an option when a defective or diseased valve threatens someone’s life. In the case of arrhythmia, an ICD can be implanted under the skin that continuously monitors the heart’s rhythm and delivers an electric shock to restore normal heart rhythm when irregularities are detected. Alternatively, in the case of bradycardia, a CRT may be necessary. This procedure involves the implantation of a special pacemaker device that coordinates the contractions of the heart’s ventricles. This therapy is particularly beneficial for individuals with heart failure and electrical dyssynchrony, where the ventricles do not contract simultaneously.15-18
For patients with advanced heart failure, an LVAD can be implanted in the chest. An LVAD is a mechanical pump that helps the heart pump blood to the rest of the body. It is often used as a bridge to heart transplantation or as destination therapy for individuals who are not candidates for heart transplantation. In severe cases of heart failure where other treatments have been unsuccessful, heart transplantation may be considered. During this procedure, a diseased heart is replaced with a healthy heart from a donor. Over the years, advancements in surgical techniques have significantly improved outcomes, with around 50% of recipients still alive 15 years post-transplant. However, heart transplantation is a complex and high-risk procedure that necessitates lifelong management and immunosuppressive therapy to prevent rejection. Candidates for transplantation must meet stringent criteria, including a sufficiently low predicted survival without the procedure. Contraindications for heart transplantation encompass factors such as advanced age, typically above 65 years, irreversible non-cardiac organ dysfunction, recent history of malignancy, and inadequate psychosocial support or resilience. Each potential recipient undergoes a thorough evaluation to assess the risks and benefits of transplantation, ensuring the procedure’s suitability and maximizing the chances of long-term success.15,16
In the long-term management of heart failure, the primary objective is to alleviate symptoms, minimize hospital admissions, and prolong patients’ lifespans. Modern strategies for HF management have evolved, emphasizing individualized treatment approaches tailored to each patient’s underlying pathophysiology and clinical characteristics. Guideline-directed medical therapy, lifestyle modifications, and device-based interventions are vital in achieving these objectives. One cornerstone of long-term HF management is optimizing pharmacotherapy. Neurohormonal antagonists, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, and mineralocorticoid receptor antagonists (MRAs), have demonstrated efficacy in reducing morbidity and mortality in patients with HFrEF. These medications help to mitigate neurohormonal activation, alleviate cardiac remodeling, and improve myocardial contractility and function. For patients with HFpEF, therapeutic options are more limited, often focusing on symptom management, blood pressure control, and comorbidity management. Diuretics, particularly loop diuretics, are commonly used to alleviate congestion and fluid retention in HFrEF and HFpEF patients. In addition to pharmacotherapy, device-based therapies, including pacemakers and implantable cardioverter-defibrillators (ICDs) or mechanical circulatory support devices, may be indicated in certain patients to improve symptoms, quality of life, and prognosis. Regular monitoring and follow-up evaluations are also essential components of long-term management to assess treatment efficacy, monitor disease progression, optimize therapy, and address emerging clinical issues promptly.1,7,19
Lifestyle modifications are another critical aspect of long-term management. These changes encompass maintaining optimal nutritional status, increasing physical activity, adhering to healthy sleep habits, and consistently taking prescribed medications. Individuals with a body mass index exceeding 35 kg/m2 are advised to reduce their weight, which may enhance functional capacity and improve quality of life. Emphasis is placed on promoting a healthy lifestyle and weight loss, favoring plant-based foods such as fruits, vegetables, seeds, nuts, legumes, and whole grain cereals over processed and animal-based foods, with a preference for fish over red meat. Excessive salt intake should be avoided, with a recommended limit of less than 5 grams daily. Fluid intake should also be regulated, particularly in high heat, humidity, nausea, or vomiting. Alcohol consumption should be limited to two per day for men and one per day for women, or avoided entirely if alcohol has contributed to heart failure. Smoking and recreational drug use should be discontinued. In cases of nutrient or vitamin deficiencies, supplementation may be considered after consultation with healthcare providers. However, routine micronutrient supplementation is not generally recommended. Patients experiencing recurrent hyperkalemia should limit potassium-containing foods and supplements. Regular exercise, tailored to individual symptoms and preferences, is essential for optimizing exercise tolerance and overall health. Patients are encouraged to engage in daily physical activities such as walking, cycling, swimming, or lightweight exercises, adjusting the intensity to provoke mild or moderate breathlessness when appropriate. Optimizing sleep hygiene, including relaxation techniques before bedtime and avoiding stimulating activities, can promote restful sleep. Individuals experiencing sleep disturbances should consult healthcare providers for guidance.20
Understanding ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) involves differentiating between these two types of heart attacks that can cause heart failure, and understanding their respective treatment options and the critical importance of timely intervention and reperfusion therapy. ST-elevation myocardial infarction, the more severe of the two, occurs when a coronary artery is completely obstructed, resulting in a significant reduction or cessation of blood flow to a portion of the heart muscle. This complete blockage is typically evident on an EKG by ST-segment elevation. ST-elevation myocardial infarction is considered a medical emergency requiring immediate intervention to restore blood flow to the affected area of the heart. Without prompt treatment, STEMI can lead to extensive damage to the heart muscle and potentially life-threatening complications such as heart failure, arrhythmias, or cardiac arrest. In contrast, NSTEMI is caused by a partial coronary artery blockage, leading to reduced blood flow to the heart muscle. The EKG pattern for NSTEMI may show ST-segment depression, T-wave inversion, or no significant changes compared to a normal EKG. While NSTEMI is severe and requires urgent medical attention, it is typically not as immediately life-threatening as STEMI. However, NSTEMI can still result in significant damage to the heart muscle and increase the risk of complications if left untreated.21
Treatment strategies for STEMI and NSTEMI aim to rapidly restore blood flow to the heart muscle and minimize myocardial damage while addressing underlying risk factors and preventing future cardiovascular events. In both cases, cardiac catheterization is often performed to evaluate the extent and severity of coronary artery disease. For STEMI, immediate reperfusion therapy is paramount. This can involve administering clot-busting medications, known as thrombolytics, to dissolve the clot obstructing the coronary artery. Alternatively, a coronary angioplasty may be necessary to mechanically open the blocked artery using stents and restore blood flow. In cases of severe or complex coronary artery disease, a coronary artery bypass grafting (CABG) surgery may be required to bypass the blocked vessel and improve blood flow to the heart. In the management of NSTEMI, a multifaceted approach is employed. Patients typically receive a combination of medical therapies aimed at stabilizing the condition and reducing the risk of further ischemic events. Antiplatelet agents, anticoagulants, beta-blockers, and statins are commonly prescribed to inhibit clot formation, prevent platelet aggregation, lower blood pressure, and reduce cholesterol levels. Lifestyle modifications such as smoking cessation, dietary changes, and regular exercise are emphasized to optimize cardiovascular health. Depending on severity, an angioplasty may be recommended to improve blood flow to the heart muscle. However, the decision to proceed is guided by clinical factors such as the presence of ongoing ischemia, the extent of coronary artery disease, and the patient’s overall clinical status. Overall, the treatment approach for STEMI and NSTEMI is tailored to individual patient characteristics, including the severity of myocardial ischemia, the presence of comorbidities, and the risk of complications. Timely intervention and a comprehensive management strategy are essential to optimize outcomes and improve long-term prognosis in patients with acute myocardial infarction.22
Nursing care plays a crucial role in the comprehensive management of patients with heart failure, addressing their diverse needs across various stages of the disease continuum, from preventive measures to end-of-life and palliative care. Patients with heart failure often require long-term engagement with multiple healthcare providers due to the chronic nature of the condition. However, the fragmentation of care across different healthcare settings and providers can lead to challenges such as gaps in information transfer and coordination. Nurses serve as central figures in bridging these gaps and providing continuity of care for patients. They facilitate seamless communication and collaboration among healthcare teams, ensuring patients receive holistic and coordinated care across different healthcare settings. By acting as patient advocates, nurses prioritize the integration of preventive measures, early detection, and timely interventions to optimize patient outcomes and quality of life.1,7,19
In healthcare settings, nurses play a critical role in conducting thorough assessments of patients with heart failure, including monitoring vital signs, assessing heart sounds, and evaluating respiratory status. This also includes regularly monitoring fluid balance, daily weights, and signs of fluid overload, such as peripheral edema and jugular venous distention. Symptoms such as dyspnea, fatigue, and peripheral edema must also be managed using appropriate interventions such as positioning, breathing techniques, and pharmacological therapies. Patients with heart failure may require supplemental oxygen therapy to improve oxygenation and relieve dyspnea. Nurses must closely onitor oxygen saturation levels, administer oxygen therapy as prescribed, and monitor the patient’s respiratory status for signs of distress. Nurses are also responsible for administering medications as prescribed by the healthcare team and monitoring for potential side effects and adverse reactions.1,7,19
Nurses must ensure that patients understand the rationale, benefits, and potential adverse effects of their prescribed therapies. Patients should be aware that some heart failure medications may cause initial fatigue or dizziness, which typically resolves over time. Patient education is a critical component of heart failure management. Nurses should provide comprehensive education on heart failure, its causes, symptoms, treatment options, and strategies for self-management. This includes educating patients about lifestyle modifications, medication adherence, symptom monitoring, and when to seek medical attention. Early detection of deterioration in symptoms can prevent hospital admission and increased mortality. Therefore, nurses must explain symptoms that warrant medical and emergency attention.
Living with heart failure can be challenging for patients and their families. Nurses should provide emotional support, counseling, and resources to help patients cope with the physical and emotional aspects of their condition. Encouraging open communication, providing information about support groups, and addressing concerns and anxieties can help patients and their families navigate the challenges associated with heart failure. Empowering patients with knowledge and skills to manage their condition can improve outcomes and enhance quality of life. 1,7,19,20
Heart failure is a pervasive cardiovascular condition that leads to a cascade of symptoms and complications that can profoundly impact a patient’s life. Comprehensive knowledge of heart failure, including normal cardiac function, and signs and stages of heart failure is imperative for healthcare professionals to facilitate timely interventions and effective management strategies. While numerous therapies are available, heart failure remains incurable and requires lifelong management and support. Lifestyle changes, including dietary modifications, regular exercise, and smoking cessation, are central to mitigating disease progression.
Nursing considerations underscore the integral role of nurses in managing patients with heart failure, emphasizing the importance of holistic care and patient education. By adopting a multidisciplinary approach and fostering collaboration among healthcare providers, participants are poised to enhance patient care delivery and promote optimal health outcomes in heart failure management. Through continuous education, clinical innovation, and compassionate care, the burden of heart failure can be mitigated, improving the quality of life for affected individuals.
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