This educational activity is credited for 5 contact hours at completion of the activity.
This course is designed to equip healthcare professionals with an in-depth understanding of heart failure and its management. It explores critical aspects of cardiovascular health, including the normal functioning of the heart and the complex processes involved in diagnosing and treating heart failure.
Over 6 million Americans are currently affected by heart failure, with the number steadily increasing as more than 1 million new cases are diagnosed annually in adults aged 55 and older. The condition carries an estimated mortality rate of 10%, most commonly due to sudden cardiac death or organ failure caused by insufficient blood flow. These statistics highlight the urgent need for effective management strategies to reduce associated risks and enhance patient outcomes. This course offers a comprehensive overview of heart failure and its management, addressing key elements of cardiovascular health, including the normal physiology of the heart and the challenges involved in diagnosing and treating heart failure.
Upon completion of this course, the learner will be able to:
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To access Caring for the Patient with Heart Failure, purchase this course or a Full Access Pass.
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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 chronic, progressive condition that affects roughly 37 million people worldwide. In the United States, over 6 million individuals are currently living with heart failure, and this number continues to grow, with more than 1 million new cases diagnosed each year in adults aged 55 and older. The condition is associated with a 10% annual mortality rate, often due to sudden cardiac death or organ failure caused by inadequate blood circulation. These statistics highlight the urgent need for effective management strategies to reduce risk and improve patient outcomes. This course offers a detailed overview of heart failure, encompassing key topics in cardiovascular health—from the normal physiological function of the heart to the diagnostic challenges and therapeutic approaches involved in treating heart failure.¹²
The heart is a complex muscular organ made primarily of myocardial tissue. It consists of four chambers: two atria at the top and two ventricles at the bottom, with one atrium and one ventricle on each side—right and left. These chambers are separated by valves that regulate one-way blood flow and an atrioventricular septum that completely divides the heart’s right and left sides. In a healthy heart, there is no direct communication between the two sides. Instead, blood flows from the right side to the left via the lungs.
Deoxygenated blood returns to the right atrium through the venous system, where the heart pumps it into the right ventricle. From there, it is sent to the lungs through the pulmonary artery for oxygenation. Oxygen-rich blood returns to the left atrium via the pulmonary veins, flows into the left ventricle, and is then pumped out to the body through the aorta. The pressure generated during left ventricular contraction is known as systolic blood pressure, while the pressure during relaxation and refilling of the ventricle is diastolic pressure. A normal blood pressure reading for a healthy adult averages around 120/80 mmHg.
Functionally, both sides of the heart contract in a coordinated rhythm, with the atria and ventricles working in tandem. This synchronization is controlled by the cardiac conduction system, which transmits electrical signals through five key components:
The SA node serves as the heart’s natural pacemaker, generating impulses that set the rhythm based on the body’s needs. These impulses quickly travel across the atria, causing atrial depolarization and contraction, which pushes blood into the ventricles. The signal then pauses briefly at the AV node, allowing the atria to finish contracting and ventricles to fill. The impulse then travels through the Bundle of His, down the bundle branches, and into the Purkinje fibers, triggering ventricular depolarization and contraction. During this process, the right ventricle pumps blood to the lungs while the left sends blood into systemic circulation.
After contraction, the heart undergoes repolarization, a resetting process where the muscle cells recharge in preparation for the next cycle. The SA node resets during atrial filling, and the AV node resets while the ventricles fill. Both depolarization and repolarization occur in less than one-third of a second, allowing for rapid, uninterrupted cardiac cycles. This seamless interaction between electrical activity and mechanical contraction is vital for continuous, effective blood circulation.³
Heart failure occurs when the heart’s ability to function normally is compromised. This dysfunction can result from a wide range of underlying issues, including structural abnormalities, rhythm disturbances, cardiovascular diseases, infections, toxic exposures, or combinations of these factors. Each of these conditions impairs the heart’s ability to pump blood efficiently, and accurately identifying the specific pathophysiological mechanism is essential for determining the most appropriate treatment.
Some of 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 certain medications² ⁴.
Congenital heart defects are structural anomalies present at birth that can compromise heart function and increase the risk of developing heart failure later in life. Coronary artery disease, marked by the accumulation of cholesterol and plaque in the arteries, limits blood flow to the heart muscle. Atherosclerosis, a common feature of CAD, can also elevate blood pressure over time, further stressing the heart and contributing to heart failure.
Valvular heart diseases such as aortic stenosis or mitral regurgitation impede blood flow between heart chambers, increasing pressure and volume load on the heart muscle, which can ultimately lead to failure. Arrhythmias, or abnormal heart rhythms, disrupt the coordinated contractions needed for effective pumping and can further impair cardiac function.
Hypertension, or high blood pressure, forces the heart to work harder over time, leading to hypertrophy and weakening of the heart muscle, which may progress to heart failure. Myocardial infarction, or heart attack, causes damage or death to areas of heart tissue due to blocked blood flow, reducing the heart’s pumping efficiency and increasing the risk of heart failure and sudden cardiac death if not promptly treated.
Cardiomyopathies—including dilated, hypertrophic, and restrictive types—are diseases of the heart muscle that decrease its strength and adaptability, placing it at greater risk of failure, particularly under physical or emotional stress. Infections such as viral myocarditis can inflame and damage heart muscle tissue, further reducing cardiac output.
Toxic substances, including alcohol, illicit drugs like cocaine, and some chemotherapy agents, can cause direct harm to the myocardium, increasing susceptibility to heart failure.² ⁴
Heart failure is a clinical syndrome that presents with a variety of signs and symptoms, often beginning subtly and progressing over time. In its early stages, individuals may notice fatigue, decreased appetite, nausea, shortness of breath (dyspnea), a persistent cough or wheeze, and fluid retention. Fatigue and weakness are common due to the heart’s inability to supply adequate blood to meet bodily demands. As a compensatory mechanism, the body prioritizes blood flow to essential organs like the heart and brain, reducing circulation to the limbs. This redistribution leads to chronic tiredness and difficulty performing routine tasks such as walking, shopping, or climbing stairs. Patients may also feel sleepy after meals, weak during activity, or breathless during exertion. Reduced blood flow to the gastrointestinal tract may impair digestion and nutrient absorption, causing symptoms like nausea, a sense of fullness, and potential weight loss.¹ ⁵
Shortness of breath, or dyspnea, results from fluid buildup in the lungs due to the heart’s inability to manage blood return from the lungs. This backup causes blood to pool in the pulmonary veins, leading to congestion, wheezing, and coughing—often producing white or blood-tinged mucus. Dyspnea may occur during activity, at rest, or worsen at night, sometimes waking individuals from sleep unless they change position.
Edema, or fluid accumulation, is another key symptom. When the heart cannot pump effectively, blood flow slows and backs up in the veins. This increased pressure causes fluid to leak into surrounding tissues, leading to swelling. Edema is most often seen in the feet, ankles, legs, hands, and abdomen. As fluid retention increases, patients may also notice weight gain.¹ ⁵
As heart failure progresses, other symptoms may develop, including palpitations, tachycardia, cognitive changes, and polyuria. Palpitations are sensations of fluttering or pounding heartbeats caused by irregular rhythms. Tachycardia, or a resting heart rate over 100 beats per minute, may occur as the heart attempts to compensate for reduced output. This elevated heart rate can intensify other symptoms such as fatigue and shortness of breath.
Cognitive impairments may arise from electrolyte imbalances, such as low sodium levels, or reduced cerebral blood flow. These changes can result in confusion, memory issues, and disorientation—symptoms often first noticed by caregivers. Polyuria, or excessive urination, is the body’s response to fluid overload, as the kidneys work to eliminate the excess through increased urine production.¹ ⁵
Heart failure is broadly categorized into three types:¹
Each type of heart failure is evaluated using ejection fraction (EF)—a critical measure of how effectively the heart pumps blood. EF represents the percentage of blood ejected from the left ventricle with each heartbeat. In healthy individuals, EF typically ranges from 60% to 65%. This measurement plays a pivotal role in diagnosing heart failure and determining appropriate treatment plans.¹ ⁶
Left-sided heart failure, or left ventricular heart failure, occurs when the left ventricle is unable to efficiently pump blood to the body. A decline in EF often accompanies impaired left ventricular function. There are three subtypes of left-sided heart failure:⁶
In systolic heart failure, also known as heart failure with reduced ejection fraction (HFrEF), the left ventricle loses its ability to contract effectively. This results in a weakened force of contraction and a diminished capacity to circulate blood, with EF typically ≤ 40%. Causes include myocardial infarction, myocarditis, or valvular disease, all of which can lead to the loss of myocardial cells.⁶ ⁷ ⁸
Diastolic heart failure, or heart failure with preserved ejection fraction (HFpEF), involves the stiffening of the left ventricular muscle, impairing its ability to relax and fill with blood during diastole. Despite a preserved EF of ≥ 50%, the ventricle cannot fill adequately. HFpEF is frequently linked to chronic conditions like hypertension, type 2 diabetes, obesity, renal or liver disease, sleep apnea, pulmonary disease, and cancer. It is more prevalent in older adults, particularly women.⁶ ⁷
A third category, heart failure with mid-range ejection fraction (HFmrEF), refers to individuals with an EF between 41% and 49%. Patients with HFmrEF often share characteristics of both HFrEF and HFpEF. Research is ongoing to better understand the underlying pathophysiology of this subtype. Common symptoms of left-sided heart failure include shortness of breath, especially during exertion or while lying down, chronic coughing with blood-tinged mucus, and pulmonary edema.⁶ ⁷ ⁸
Right-sided heart failure generally develops as a consequence of left-sided failure. When the left ventricle fails, fluid pressure backs up through the lungs, impairing the right ventricle’s function. This leads to venous congestion, as blood begins to pool in the veins. Signs include peripheral edema (especially in the legs, ankles, and abdomen), ascites (fluid buildup in the abdomen), fatigue, loss of appetite, nausea, and jugular venous distention (JVD).⁶ ⁷ ⁸
Congestive heart failure involves dysfunction of both the left and right sides of the heart. This condition is a medical emergency and can result in a widespread combination of symptoms. While left-sided failure is typically associated with pulmonary congestion and reduced systemic blood flow, right-sided failure presents with peripheral edema and signs of systemic venous congestion. Clinically, lung crackles suggest left-sided failure, whereas elevated JVP or JVD indicates right-sided failure.⁶ ⁷ ⁸
Heart failure arises from a combination of modifiable and non-modifiable risk factors. Prominent contributors include coronary heart disease, hypertension, diabetes mellitus, family history of cardiac conditions, chronic lung diseases, obesity, inflammatory or infectious processes, and metabolic disorders.⁸ ⁹
Conditions like coronary artery disease and chronic high blood pressure directly impair the heart’s structure and function, commonly resulting in heart failure. Type 2 diabetes, for example, increases circulating lipid levels, while metabolic syndrome and hyperthyroidism raise heart rate and promote myocardial hypertrophy—both of which place considerable strain on cardiac performance.
Age is a critical, non-modifiable risk factor. As individuals age, the heart muscle naturally becomes stiffer and less efficient, elevating the risk of heart failure. Data shows that prevalence rates climb markedly with age:
Exposure to cardiotoxic agents also plays a significant role. Substances such as cocaine and anthracycline-based chemotherapies (commonly used in cancer treatment) may cause heart damage. This toxicity may present acutely, chronically with early onset, or chronically with delayed onset, leading to impaired myocardial function and increased susceptibility to heart failure.⁸ ⁹
As heart failure advances, clinicians turn to established classification systems to evaluate disease severity and guide treatment decisions. Two widely recognized systems are the American College of Cardiology/American Heart Association (ACC/AHA) classification and the New York Heart Association (NYHA) classification.⁷
The ACC/AHA classification organizes heart failure into four progressive stages—A, B, C, and D—based on clinical risk, structural changes, biomarker findings, and symptom development:⁷ ¹⁰
The NYHA classification complements the ACC/AHA framework by focusing on functional capacity and symptom severity in patients with symptomatic or advanced heart failure (Stage C or D).⁷ ¹¹ This system defines four functional classes:
Together, the ACC/AHA and NYHA systems offer complementary insights that help clinicians personalize heart failure management and assess disease progression over time.⁷ ¹⁰ ¹¹
Initial management of acute heart failure focuses on stabilizing the patient by restoring oxygenation and circulation. Interventions are tailored to the patient’s clinical status. In cases of severe respiratory distress, hypoxia, or respiratory acidosis, noninvasive ventilation is considered if the patient can cooperate; otherwise, endotracheal intubation may be required. Oxygen therapy is administered to maintain oxygen saturation above 95%, but it is not necessary for patients without hypoxia.¹ ⁷ ⁸
For patients presenting with flash pulmonary edema and hypertension, vasodilators are essential to lower afterload and relieve congestion. Nitroglycerin is the first-line agent due to its rapid effect. Sublingual administration is initiated, followed by intravenous infusion, titrated to reduce left ventricular filling pressures and relieve symptoms. Sodium nitroprusside and nesiritide serve as alternatives. Nitrates are contraindicated in patients with recent phosphodiesterase-5 inhibitor use or hypotension. In cases without pulmonary edema, intravenous diuretics such as furosemide or bumetanide are administered, with dosing adjusted to urine output and response. Importantly, morphine is avoided due to links to increased ICU admissions and mortality.¹ ⁷ ¹²
EKG Findings
Electrocardiograms (EKGs) are critical for evaluating cardiac electrical activity. They consist of the following components:¹³ ¹⁴
In heart failure, EKGs may reveal:
While EKG findings are often nonspecific, they complement other diagnostic tools in evaluating heart failure.¹³ ¹⁴
Laboratory Testing
Key biomarkers help in diagnosing or excluding heart failure quickly:
Adjustments:
Other important labs include:
Procedural Interventions
Several procedures target symptom relief, function restoration, and quality of life enhancement:
For valvular disease, two options exist:
To manage arrhythmias:
In advanced heart failure:
In managing heart failure over the long term, the primary goals are to relieve symptoms, prevent hospitalizations, and extend life expectancy. Contemporary heart failure management emphasizes personalized treatment strategies that align with each patient’s clinical presentation and disease mechanisms. Central components include guideline-directed medical therapy, lifestyle interventions, and in select cases, device-assisted therapies. A key priority is optimizing pharmacological treatment. For individuals with heart failure with reduced ejection fraction (HFrEF), medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, and mineralocorticoid receptor antagonists (MRAs) have shown significant benefits in lowering both morbidity and mortality. These drugs act by inhibiting harmful neurohormonal pathways, reversing cardiac remodeling, and improving contractile function. In contrast, heart failure with preserved ejection fraction (HFpEF) has fewer effective treatments and is generally managed through symptom control, blood pressure regulation, and treatment of coexisting conditions. Loop diuretics are commonly prescribed to reduce fluid overload and improve breathing in both HFrEF and HFpEF. Device-based options such as pacemakers, implantable cardioverter-defibrillators (ICDs), and mechanical circulatory support devices are considered for eligible patients to enhance quality of life and survival. Routine monitoring and follow-up care are essential to track treatment success, detect complications, adjust therapies, and intervene early when changes occur.¹ ⁷ ¹⁹
Lifestyle adjustments are equally critical in long-term management. These include maintaining proper nutrition, increasing physical activity, adhering to medication regimens, and practicing healthy sleep habits. Weight loss is encouraged for patients with a body mass index above 35 kg/m², as it may improve exercise capacity and quality of life. Dietary changes should prioritize plant-based foods—fruits, vegetables, nuts, seeds, legumes, and whole grains—while limiting processed items and red meat, favoring fish instead. Sodium intake should be restricted to less than 5 grams per day, and fluid intake should be adjusted based on weather conditions and symptoms like nausea or vomiting. Alcohol consumption should be reduced—no more than two drinks per day for men and one for women—or eliminated entirely if implicated in heart failure. Smoking and recreational drug use should be discontinued altogether. Nutritional supplements may be used when deficiencies are identified, though routine use of micronutrients is not typically recommended. For patients prone to elevated potassium levels, potassium-rich foods and supplements should be minimized. Regular physical activity should be incorporated into daily life, with options such as walking, cycling, swimming, or light resistance exercises chosen based on the individual’s capacity. Exercise intensity should be enough to cause mild or moderate shortness of breath. Establishing healthy sleep routines—including relaxing pre-sleep habits and avoiding stimulation before bedtime—can also help improve rest. Patients with persistent sleep problems should seek medical evaluation.²⁰
Differentiating between ST-elevation myocardial infarction (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) is essential for understanding how these two types of heart attacks contribute to heart failure, and for guiding their treatment approaches. STEMI, the more critical form, is caused by a complete blockage of a coronary artery, abruptly cutting off blood flow to part of the heart muscle. This obstruction is typically visible on an electrocardiogram (EKG) as ST-segment elevation. STEMI represents a medical emergency, as failure to promptly restore blood flow can result in extensive myocardial damage and life-threatening outcomes such as heart failure, arrhythmias, or sudden cardiac arrest. NSTEMI, on the other hand, results from a partial blockage of a coronary artery, reducing but not completely obstructing blood flow. EKG findings in NSTEMI may include ST-segment depression, T-wave inversion, or no significant deviations from a normal pattern. Although NSTEMI is serious and warrants immediate medical care, it is not usually as urgent as STEMI in terms of immediate mortality risk. Nonetheless, if left untreated, NSTEMI can still cause substantial myocardial injury and elevate the risk of subsequent complications.²¹
The treatment goal for both STEMI and NSTEMI is to restore myocardial perfusion quickly, limit heart muscle damage, and prevent future cardiovascular events. Cardiac catheterization is commonly used in both types of infarction to determine the extent and location of coronary artery disease. For STEMI, immediate reperfusion is critical. This may involve thrombolytic therapy—medications that dissolve the clot—or percutaneous coronary intervention (PCI), which mechanically reopens the artery using a balloon and possibly a stent. In more severe or complex cases, coronary artery bypass grafting (CABG) may be necessary to redirect blood flow around blocked arteries. Management of NSTEMI generally involves a more conservative yet comprehensive medical approach. Patients are often started on a regimen of antiplatelet drugs, anticoagulants, beta-blockers, and statins to reduce clot formation, lower myocardial oxygen demand, and manage lipid levels. Lifestyle interventions such as quitting smoking, improving diet, and increasing physical activity are also essential. Depending on the clinical presentation, angioplasty may be advised to enhance blood supply, particularly if there are signs of persistent ischemia or significant coronary obstruction. Ultimately, the treatment of both STEMI and NSTEMI must be individualized, considering factors such as the severity of ischemia, the extent of coronary involvement, the presence of other medical conditions, and overall risk profile. Rapid intervention combined with a holistic care plan is key to improving outcomes and reducing the long-term burden of acute myocardial infarction.²²
Nursing care is fundamental to the effective and holistic management of heart failure, supporting patients throughout all stages of the disease—from prevention and early intervention to end-of-life and palliative care. Due to the chronic and progressive nature of heart failure, patients often interact with multiple healthcare providers and navigate various care environments. This fragmentation can lead to communication breakdowns and care inconsistencies. Nurses play a pivotal role in overcoming these barriers by coordinating across disciplines, ensuring information continuity, and delivering patient-centered care. Acting as advocates, nurses help implement preventive strategies, facilitate early detection of complications, and ensure timely interventions, all aimed at optimizing patient health and quality of life.¹⁷¹⁹
Within clinical settings, nurses are responsible for conducting detailed assessments of heart failure patients. This includes tracking vital signs, listening to heart sounds, and evaluating respiratory function. Key aspects of monitoring include tracking fluid intake and output, daily body weight, and recognizing signs of volume overload, such as peripheral edema and jugular venous distension. Managing symptoms like shortness of breath and fatigue often requires a combination of positioning, breathing support, and medications. Oxygen therapy may be needed to alleviate dyspnea and improve oxygen levels; nurses must monitor oxygen saturation, deliver therapy as prescribed, and assess for respiratory distress. Medication administration is another core nursing responsibility, including vigilant observation for adverse drug reactions and side effects.¹⁷¹⁹
Patient education is a cornerstone of nursing care in heart failure. Nurses must ensure patients understand their medication regimens, including the purpose of each drug and potential side effects such as fatigue or dizziness, which may subside with continued use. Education should cover the nature of heart failure, its causes and symptoms, available treatments, and essential self-management strategies. This includes guidance on lifestyle changes, medication adherence, and symptom tracking. Nurses must instruct patients on recognizing warning signs that require urgent medical evaluation, helping to prevent avoidable hospitalizations and reduce mortality.
The emotional burden of living with heart failure also requires attention. Nurses should offer empathetic support, provide counseling, and connect patients and families with resources to cope with both physical and emotional stress. Promoting open dialogue, suggesting support groups, and addressing fears or concerns are important steps in fostering patient resilience. Empowering individuals with the knowledge and tools to manage their condition fosters better engagement in care and contributes to improved long-term outcomes and overall well-being.¹⁷¹⁹²⁰
Heart failure is a widespread cardiovascular disorder marked by a range of symptoms and complications that significantly affect a patient’s daily functioning and quality of life. A thorough understanding of heart failure—including normal cardiac physiology, symptom recognition, and disease staging—is essential for healthcare professionals to ensure prompt intervention and effective treatment planning. Although many therapeutic options exist, heart failure is a chronic, progressive condition that cannot be cured and necessitates ongoing care and support. Long-term management heavily relies on lifestyle interventions such as dietary adjustments, routine physical activity, and smoking cessation to help slow disease progression.
Nursing considerations highlight the essential contribution of nurses in heart failure care, particularly in delivering comprehensive care and patient education. Emphasis is placed on a holistic approach, addressing physical, emotional, and psychosocial needs. Collaboration within a multidisciplinary healthcare team strengthens care coordination and enhances patient outcomes. Ongoing education, clinical advancements, and empathetic nursing care are key components in alleviating the impact of heart failure and improving the overall well-being of individuals living with this condition.
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