Which is a cause for high-output failure for a patient diagnosed with heart failure? quizlet

In HFrEF (also called systolic HF), global LV systolic dysfunction predominates. The LV contracts poorly and empties inadequately, leading to

• Increased diastolic volume and pressure

• Decreased ejection fraction (≤ 40%)

Many defects in energy utilization, energy supply, electrophysiologic functions, and contractile element interaction occur, with abnormalities in intracellular calcium modulation and cAMP production.

In HFpEF (also called diastolic heart failure), LV filling is impaired, resulting in

• Increased LV end-diastolic pressure at rest or during exertion

• Usually, normal LV end-diastolic volume

Global contractility and hence ejection fraction remain normal (≥ 50%).

Diastolic dysfunction usually results from impaired ventricular relaxation (an active process), increased ventricular stiffness, valvular disease Overview of Cardiac Valvular Disorders Any heart valve can become stenotic or insufficient (also termed regurgitant or incompetent), causing hemodynamic changes long before symptoms. Most often, valvular stenosis or insufficiency... read more , or constrictive pericarditis Constrictive pericarditis Pericarditis is inflammation of the pericardium, often with fluid accumulation in the pericardial space. Pericarditis may be caused by many disorders (eg, infection, myocardial infarction, trauma... read more

Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy is a congenital or acquired disorder characterized by marked ventricular hypertrophy with diastolic dysfunction (eg, due to valvular aortic stenosis, coarctation... read more

Hypertension Hypertension is sustained elevation of resting systolic blood pressure (≥ 130 mm Hg), diastolic blood pressure (≥ 80 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential... read more

Aortic Stenosis Aortic stenosis (AS) is narrowing of the aortic valve, obstructing blood flow from the left ventricle to the ascending aorta during systole. Causes include a congenital bicuspid valve, idiopathic... read more

Diastolic dysfunction has increasingly been recognized as a cause of HF. Estimates vary, but about 50% of patients with heart failure have HFpEF; the prevalence increases with age and in patients with diabetes. It is now known that HFpEF is a complex, heterogenous, multiorgan, systemic syndrome, often with multiple concomitant pathophysiologies. Current data suggest that multiple comorbidities (eg, obesity Obesity Obesity is excess body weight, defined as a body mass index (BMI) of ≥ 30 kg/m2. Complications include cardiovascular disorders (particularly in people with excess abdominal fat)... read more , hypertension Hypertension Hypertension is sustained elevation of resting systolic blood pressure (≥ 130 mm Hg), diastolic blood pressure (≥ 80 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential... read more

Chronic Kidney Disease Chronic kidney disease (CKD) is long-standing, progressive deterioration of renal function. Symptoms develop slowly and in advanced stages include anorexia, nausea, vomiting, stomatitis, dysgeusia... read more

International societies have put forth the concept of HF with mildly reduced ejection fraction (HFmrEF), in which patients have an LV ejection fraction of 41 to 49%. It is unclear whether this group is a distinct population or consists of a mixture of patients with either HFpEF or HFrEF.

In heart failure that involves left ventricular dysfunction, CO decreases and pulmonary venous pressure increases. When pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins (about 24 mm Hg), fluid extravasates from the capillaries into the interstitial space and alveoli, reducing pulmonary compliance and increasing the work of breathing. Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema Pulmonary Edema Pulmonary edema is acute, severe left ventricular failure with pulmonary venous hypertension and alveolar flooding. Findings are severe dyspnea, diaphoresis, wheezing, and sometimes blood-tinged... read more

In heart failure that involves right ventricular dysfunction, systemic venous pressure increases, causing fluid extravasation and consequent edema, primarily in dependent tissues (feet and ankles of ambulatory patients) and abdominal viscera. The liver is most severely affected, but the stomach and intestine also become congested; fluid accumulation in the peritoneal cavity (ascites) can occur. RV failure commonly causes moderate hepatic dysfunction, with usually modest increases in conjugated and unconjugated bilirubin, PT (prothrombin time), and hepatic enzymes (particularly alkaline phosphatase and gamma-glutamyl transpeptidase [GGT]). The impaired liver breaks down less aldosterone, further contributing to fluid accumulation. Chronic venous congestion in the viscera can cause anorexia, malabsorption of nutrients and drugs, protein-losing enteropathy (characterized by diarrhea and marked hypoalbuminemia), chronic gastrointestinal blood loss, and rarely ischemic bowel infarction.

In HFrEF, left ventricular systolic function is grossly impaired; therefore, a higher preload is required to maintain CO. As a result, the ventricles are remodeled over time: During remodelling, the LV becomes less ovoid and more spherical, dilates, and hypertrophies; the RV dilates and may hypertrophy. Initially compensatory, remodelling ultimately is associated with adverse outcomes because the changes eventually increase diastolic stiffness and wall tension (ie, diastolic dysfunction develops), compromising cardiac performance, especially during physical stress. Increased wall stress raises oxygen demand and accelerates apoptosis (programmed cell death) of myocardial cells. Dilation of the ventricles can also cause mitral or tricuspid valve regurgitation (due to annular dilation) with further increases in end-diastolic volumes.

With reduced CO, oxygen delivery to the tissues is maintained by increasing oxygen extraction from the blood and sometimes shifting the oxyhemoglobin dissociation curve (see figure ) to the right to favor oxygen release.

Reduced CO with lower systemic blood pressure activates arterial baroreflexes, increasing sympathetic tone and decreasing parasympathetic tone. As a result, heart rate and myocardial contractility increase, arterioles in selected vascular beds constrict, venoconstriction occurs, and sodium and water are retained. These changes compensate for reduced ventricular performance and help maintain hemodynamic homeostasis in the early stages of heart failure. However, these compensatory changes increase cardiac work, preload, and afterload; reduce coronary and renal perfusion; cause fluid accumulation resulting in congestion; increase potassium excretion; and may cause cardiomyocyte necrosis and arrhythmias.

As cardiac function deteriorates, renal blood flow decreases (due to low cardiac output). In addition, renal venous pressures increase, leading to renal venous congestion. These changes both result in a decrease in GFR (glomerular filtration rate), and blood flow within the kidneys is redistributed. The filtration fraction and filtered sodium decrease, but tubular resorption increases, leading to sodium and water retention. Blood flow is further redistributed away from the kidneys during exercise, but renal blood flow improves during rest.

The renin-angiotensin-aldosterone-vasopressin (antidiuretic hormone [ADH]) system causes a cascade of potentially deleterious long-term effects. Angiotensin II worsens heart failure by causing vasoconstriction, including efferent renal vasoconstriction, and by increasing aldosterone production, which enhances sodium reabsorption in the distal nephron and also causes myocardial and vascular collagen deposition and fibrosis. Angiotensin II increases norepinephrine release, stimulates release of vasopressin, and triggers apoptosis. Angiotensin II may be involved in vascular and myocardial hypertrophy, thus contributing to the remodeling of the heart and peripheral vasculature, potentially worsening HF. Aldosterone can be synthesized in the heart and vasculature independently of angiotensin II (perhaps mediated by corticotropin, nitric oxide, free radicals, and other stimuli) and may have deleterious effects in these organs.

Heart failure that causes progressive renal dysfunction (including renal dysfunction caused by drugs used to treat HF) contributes to worsening HF and has been termed the cardiorenal syndrome.

In conditions of stress, neurohumoral responses help increase heart function and maintain blood pressure and organ perfusion, but chronic activation of these responses is detrimental to the normal balance between myocardial-stimulating and vasoconstricting hormones and between myocardial-relaxing and vasodilating hormones.

The heart contains many neurohumoral receptors (alpha-1, beta-1, beta-2, beta-3, angiotensin II type 1 [AT1] and type 2 [AT2], muscarinic, endothelin, serotonin, adenosine, cytokine, natriuretic peptides); the roles of all of these receptors are not yet fully defined. In patients with heart failure, beta-1 receptors (which constitute 70% of cardiac beta receptors) are downregulated, probably in response to intense sympathetic activation. The result of downregulation is impaired myocyte contractility and increased heart rate.

Plasma norepinephrine levels are increased, largely reflecting sympathetic nerve stimulation as plasma epinephrine levels are not increased. Detrimental effects include vasoconstriction with increased preload and afterload, direct myocardial damage including apoptosis, reduced renal blood flow, and activation of other neurohumoral systems, including the renin-angiotensin-aldosterone-vasopressin system.

Vasopressin is released in response to a fall in blood pressure via various neurohormonal stimuli. Increased vasopressin decreases renal excretion of free water, possibly contributing to hyponatremia in heart failure. Vasopressin levels in patients with HF and normal blood pressure vary.

Atrial natriuretic peptide is released in response to increased atrial volume and pressure; brain (B-type) natriuretic peptide (BNP) is released from the ventricle in response to ventricular stretching. These peptides enhance renal excretion of sodium, but in patients with HF, the effect is blunted by decreased renal perfusion pressure, receptor downregulation, and perhaps enhanced enzymatic degradation. In addition, elevated levels of natriuretic peptides exert a counter-regulatory effect on the renin-angiotensin-aldosterone system and catecholamine stimulation.

Because endothelial dysfunction occurs in HF, fewer endogenous vasodilators (eg, nitric oxide, prostaglandins) are produced, and more endogenous vasoconstrictors (eg, endothelin) are produced, thus increasing afterload.

The failing heart and other organs produce tumor necrosis factor (TNF) alpha. This cytokine increases catabolism and is possibly responsible for cardiac cachexia (loss of lean tissue ≥ 10%), which may accompany severely symptomatic HF, and for other detrimental changes. The failing heart also undergoes metabolic changes with increased free fatty acid utilization and decreased glucose utilization; these changes may become therapeutic targets.

Age-related changes in the heart and cardiovascular system lower the threshold for expression of heart failure. Interstitial collagen within the myocardium increases, the myocardium stiffens, and myocardial relaxation is prolonged. These changes lead to a significant reduction in diastolic left ventricular function, even in healthy older people. Modest decline in systolic function also occurs with aging. An age-related decrease in myocardial and vascular responsiveness to beta-adrenergic stimulation further impairs the ability of the cardiovascular system to respond to increased work demands.

As a result of these changes, peak exercise capacity decreases significantly (about 8%/decade after age 30), and CO at peak exercise decreases more modestly. This decline can be slowed by regular physical exercise. Thus, older patients are more prone than are younger ones to develop HF symptoms in response to the stress of systemic disorders or relatively modest cardiovascular insults. Stressors include infections (particularly pneumonia), hyperthyroidism, anemia, hypertension, myocardial ischemia, hypoxia, hyperthermia, renal failure, perioperative IV fluid loads, nonadherence to drug regimens or to low-salt diets, and use of certain drugs (particularly NSAIDs [nonsteroidal anti-inflammatory drugs]).

• 1. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 145:e876–e894, 2022, doi: 10.1161/CIR.0000000000001062

Symptoms and Signs of Heart Failure

Manifestations of heart failure differ depending on the extent to which the LV and RV are initially affected. Clinical severity varies significantly and is usually classified according to the New York Heart Association (NYHA) system (see table ); the examples of ordinary activity may be modified for older, debilitated patients. Because HF has such a broad range of severity, some experts suggest subdividing NYHA class III into IIIA or IIIB. Class IIIB is typically reserved for those patients who recently had a heart failure exacerbation. The American College of Cardiology/American Heart Association has advocated a staging system for HF (A, B, C, or D) to highlight the need for HF prevention.

• A: High risk of HF but no structural or functional cardiac abnormalities or symptoms

• B: Structural or functional cardiac abnormalities but no symptoms of HF

• C: Structural heart disease with symptoms of HF

• D: Refractory HF requiring advanced therapies (eg, mechanical circulatory support, cardiac transplantation) or palliative care

History

In LV failure, the most common symptoms are dyspnea and fatigue due to increased pulmonary venous pressures, and low cardiac output (CO, at rest or inability to augment CO during exertion). Dyspnea usually occurs during exertion and is relieved by rest. As HF worsens, dyspnea can occur during rest and at night, sometimes causing nocturnal cough. Dyspnea occurring immediately or soon after lying flat and relieved promptly by sitting up (orthopnea) is common as heart failure advances. In paroxysmal nocturnal dyspnea (PND), dyspnea awakens patients several hours after they lie down and is relieved only after they sit up for 15 to 20 minutes. In severe HF, periodic cycling of breathing (Cheyne-Stokes respiration Inspection

—from a brief period of apnea, patients breathe progressively faster and deeper, then slower and shallower until they become apneic and repeat the cycle)—can occur during the day or night; the sudden hyperpneic phase may awaken the patient from sleep. Cheyne-Stokes breathing differs from PND in that the hyperpneic phase is short, lasting only 10 to 15 seconds, but the cycle recurs regularly, lasting 30 seconds to 2 minutes. PND is associated with pulmonary congestion, and Cheyne-Stokes respiration with low CO. Sleep-related breathing disorders, such as sleep apnea Obstructive Sleep Apnea (OSA) Obstructive sleep apnea (OSA) consists of multiple episodes of partial or complete closure of the upper airway that occur during sleep and lead to breathing cessation (defined as a period of... read more , are common in HF and may aggravate HF. Severely reduced cerebral blood flow and hypoxemia can cause chronic irritability and impair mental performance.

In RV failure, the most common symptoms are ankle swelling and fatigue. Sometimes patients feel a sensation of fullness in the abdomen or neck. Hepatic congestion can cause right upper quadrant abdominal discomfort, and stomach and intestinal congestion can cause early satiety, anorexia, and abdominal bloating.

Less specific heart failure symptoms include cool peripheries, postural light-headedness, nocturia, and decreased daytime micturition. Skeletal muscle wasting can occur in severe biventricular failure and may reflect some disuse but also increased catabolism associated with increased cytokine production. Significant weight loss (cardiac cachexia) is an ominous sign associated with high mortality.

In older people, presenting complaints may be atypical, such as confusion, delirium, falls, sudden functional decline, nocturnal urinary incontinence, or sleep disturbance. Coexisting cognitive impairment and depression may also influence assessment and therapeutic interventions and may be worsened by the HF.

Examination

General examination may detect signs of systemic or cardiac disorders that cause or aggravate heart failure (eg, anemia, hyperthyroidism Hyperthyroidism Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations, fatigue, weight loss, heat intolerance, anxiety, and tremor... read more

, alcohol use disorder, hemochromatosis Hereditary Hemochromatosis Hereditary hemochromatosis is a genetic disorder characterized by excessive iron (Fe) accumulation that results in tissue damage. Manifestations can include systemic symptoms, liver disorders... read more

, atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more with rapid rate, mitral regurgitation Mitral Regurgitation Mitral regurgitation (MR) is incompetency of the mitral valve causing flow from the left ventricle (LV) into the left atrium during ventricular systole. MR can be primary (common causes are... read more ).

In LV failure, tachycardia and tachypnea may occur. Patients with severe LV failure may appear visibly dyspneic or cyanotic, hypotensive, and confused or agitated because of hypoxia and poor cerebral perfusion. Some of these less specific symptoms (eg, confusion) are more common in older patients.

Central cyanosis (affecting all of the body, including warm areas such as the tongue and mucous membranes) reflects severe hypoxemia. Peripheral cyanosis of the lips, fingers, and toes reflects low blood flow with increased oxygen extraction. If vigorous massage improves nail bed color, cyanosis may be peripheral; increasing local blood flow does not improve color if cyanosis is central.

Cardiac findings in HFrEF include

• Diffuse, sustained, and laterally displaced apical impulse

• Audible and occasionally palpable 3rd (S3) and 4th (S4) heart sounds

• Accentuated pulmonic component (P2) of the 2nd heart sound (S2)

These abnormal heart sounds also can occur in HFpEF. A pansystolic murmur of mitral regurgitation at the apex may occur in either HFrEF or HFpEF.

Pulmonary findings include early inspiratory basilar crackles that do not clear with coughing and, if pleural effusion is present, dullness to percussion and diminished breath sounds at the lung base(s).

Signs of RV failure include

• Nontender peripheral pitting edema (digital pressure leaves visible and palpable imprints, sometimes quite deep) in the feet and ankles

• Enlarged and sometimes pulsatile liver palpable below the right costal margin

• Abdominal swelling and ascites

• Visible elevation of the jugular venous pressure, sometimes with large a or v waves that are visible even when the patient is seated or standing (see figure )

In severe cases of heart failure, peripheral edema can extend to the thighs or even the sacrum, scrotum, lower abdominal wall, and occasionally even higher. Severe edema in multiple areas is termed anasarca. Edema may be asymmetric if patients lie predominantly on one side.

With hepatic congestion, the liver may be palpably enlarged or tender, and hepatojugular or abdominal-jugular reflux may be detected (see Approach to the Cardiac Patient Neck veins

). Precordial palpation may detect the left parasternal lift of RV enlargement, and auscultation may detect the murmur of tricuspid regurgitation or the RV S3 along the left sternal border; both findings are augmented upon inspiration.

Chest x-ray findings suggesting heart failure include an enlarged cardiac silhouette, pleural effusion, fluid in the major fissure, and horizontal lines in the periphery of lower posterior lung fields (Kerley B lines). These findings reflect chronic elevation of left atrial pressure and chronic thickening of the intralobular septa due to edema. Upper lobe pulmonary venous congestion and interstitial or alveolar edema may also be present. Careful examination of the cardiac silhouette on a lateral projection can identify specific ventricular and atrial chamber enlargement. The x-ray may also suggest alternative diagnoses (eg, COPD, pneumonia, idiopathic pulmonary fibrosis Idiopathic Pulmonary Fibrosis Idiopathic pulmonary fibrosis (IPF), the most common form of idiopathic interstitial pneumonia, causes progressive pulmonary fibrosis. Symptoms and signs develop over months to years and include... read more

Lung Carcinoma Lung carcinoma is the leading cause of cancer-related death worldwide. About 85% of cases are related to cigarette smoking. Symptoms can include cough, chest discomfort or pain, weight loss... read more

ECG findings are not diagnostic, but an abnormal ECG, especially showing previous myocardial infarction, left ventricular hypertrophy, left bundle branch block, or tachyarrhythmia (eg, rapid atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more ), increases suspicion for HF and may help identify the cause. An entirely normal ECG is uncommon in chronic HF.

Echocardiography Echocardiography This photo shows a patient having echocardiography. This image shows all 4 cardiac chambers and the tricupsid and mitral valves. Echocardiography uses ultrasound waves to produce an image of... read more

Overview of Coronary Artery Disease Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina pectoris, acute... read more

Myocarditis Myocarditis is inflammation of the myocardium with necrosis of cardiac myocytes. Myocarditis may be caused by many disorders (eg, infection, cardiotoxins, drugs, and systemic disorders such... read more

Serum BNP levels are often high in heart failure; this finding may help when clinical findings are unclear or other diagnoses (eg, COPD) need to be excluded. It may be particularly useful for patients with a history of both pulmonary and cardiac disorders. NT-pro-BNP, an inactive moiety created when pro-BNP is cleaved, can be used similarly to BNP. However, a normal BNP level does not exclude the diagnosis of heart failure, particularly in patients with HFpEF and/or obesity. In HFpEF, BNP levels tend to be about 50% of those associated with HFrEF (at similar degree of symptoms), and up to 30% of patients with acute HFpEF have a BNP level below the commonly used threshold of 100 pg/mL (100 ng/L). Obesity, which is becoming an increasingly common comorbidity in HF, is associated with reduced BNP production and increased BNP clearance, resulting in lower levels.

Besides BNP, recommended blood tests include complete blood count, creatinine, BUN (blood urea nitrogen), electrolytes (including magnesium and calcium), glucose, albumin, ferritin, and liver tests. Thyroid function tests are recommended for patients with atrial fibrillation and for selected, especially older, patients.

Thoracic ultrasonography is a noninvasive method of detecting pulmonary congestion in patients with heart failure. Sonographic "comet tail artifact" on thoracic ultrasonography corresponds to the x-ray finding of Kerley B lines.

Cardiac catheterization with intracardiac pressure measurements (invasive hemodynamics) may be helpful in the diagnosis of restrictive cardiomyopathies and constrictive pericarditis. Invasive hemodynamic measurements are also very helpful when the diagnosis of HF is equivocal, particularly in patients with HFpEF. In addition, perturbing the cardiovascular system (eg, exercise testing, volume challenge, drug challenges [eg, nitroglycerin, nitroprusside]) can be very helpful during invasive hemodynamic testing to help diagnose HF.

Endocardial biopsy is sometimes done when an infiltrative cardiomyopathy, or acute giant cell myocarditis is strongly suspected but cannot be confirmed with noninvasive imaging (eg, cardiac MRI).

• 1. McDonagh TA, Metra M, Adamo M, et al: 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 42(36):3599-3726, 2021. doi: 10.1093/eurheartj/ehab368

• 2. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 145:e876–e894, 2022, doi: 10.1161/CIR.0000000000001062

General measures, especially patient and caregiver education and diet and lifestyle modifications, are important for all patients with heart failure.

• Education

• Sodium restriction

• Appropriate weight and fitness levels

• Correction of underlying conditions

Patient and caregiver education are critical to long-term success. The patient and family should be involved in treatment choices. They should be taught the importance of drug adherence, warning signs of an exacerbation, and how to link cause with effect (eg, increased salt in the diet with weight gain or symptoms).

Many centers (eg, specialized outpatient clinics) have integrated health care practitioners from different disciplines (eg, HF nurses, pharmacists, social workers, rehabilitation specialists) into multidisciplinary teams or outpatient heart failure management programs. These approaches can improve outcomes and reduce hospitalizations and are most effective in the sickest patients.

Dietary sodium restriction helps limit fluid retention. All patients should eliminate salt in cooking and at the table and avoid salted foods; the most severely ill should limit sodium to < 2 g/day by consuming only low-sodium foods.

Monitoring daily morning weight helps detect sodium and water accumulation early. If weight increases > 2 kg over a few days, patients may be able to adjust their diuretic dose themselves, but if weight gain continues or symptoms occur, patients should seek medical attention.

Intensive case management, particularly by monitoring drug adherence and frequency of unscheduled visits to the physician or emergency department and hospitalizations, can identify when intervention is needed. Specialized HF nurses are valuable in education, follow-up, and dosage adjustment according to predefined protocols.

Patients with atherosclerosis or diabetes should strictly follow a diet appropriate for their disorder. Obesity may cause and always aggravates the symptoms of HF; patients should attain a body mass index (BMI) ≤ 30 kg/m2 (ideally 21 to 25 kg/m2).

If causes such as hypertension, persistent tachyarrhythmia, severe anemia, hemochromatosis, uncontrolled diabetes, thyrotoxicosis, beriberi, alcohol use disorder, or toxoplasmosis are successfully treated, patients may dramatically improve. Significant myocardial ischemia should be treated aggressively; treatment may include revascularization by percutaneous coronary intervention Percutaneous Coronary Interventions (PCI) Percutaneous coronary interventions (PCI) include percutaneous transluminal coronary angioplasty (PTCA) with or without stent insertion. Primary indications are treatment of Angina pectoris... read more

Coronary Artery Bypass Grafting (CABG) Frontal and lateral chest x-ray of a patient post coronary artery bypass surgery showing sternal sutures (black arrow) and surgical clips (red arrow). Coronary artery bypass grafting (CABG)... read more

Treatment Amyloidosis is any of a group of disparate conditions characterized by extracellular deposition of insoluble fibrils composed of misaggregated proteins. These proteins may accumulate locally... read more

• Electrolytes are normalized.

• Atrial and ventricular rates are controlled.

• Sometimes antiarrhythmic drugs are given.

Sinus tachycardia, a common compensatory change in heart failure, usually subsides when HF treatment is effective. If it does not, associated causes (eg, hyperthyroidism Hyperthyroidism Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations, fatigue, weight loss, heat intolerance, anxiety, and tremor... read more

Pulmonary Embolism (PE) Pulmonary embolism (PE) is the occlusion of pulmonary arteries by thrombi that originate elsewhere, typically in the large veins of the legs or pelvis. Risk factors for pulmonary embolism are... read more

Atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more with an uncontrolled ventricular rate must be treated; the target resting ventricular rate is typically < 80 beats/minute. Beta-blockers are the treatment of choice, although rate-limiting calcium channel blockers may be used cautiously if systolic function is preserved. Adding digoxin, low-dose amiodarone, or other rhythm and/or rate controlling drugs may help some patients. Routine conversion to and maintenance of sinus rhythm has not been shown to be superior to rate control alone in large clinical trials. However, it is best to make this determination on a case-by-case basis because some patients improve significantly with restoration of normal sinus rhythm. If rapid atrial fibrillation does not respond to drugs, permanent pacemaker insertion with complete or partial ablation of the atrioventricular node, or other atrial fibrillation ablation procedures Ablation procedures for atrial fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , may be considered in selected patients to restore a sinus or regular rhythm.

Sustained ventricular tachycardia Ventricular Tachycardia (VT) Ventricular tachycardia is ≥ 3 consecutive ventricular beats at a rate ≥ 120 beats/minute. Symptoms depend on duration and vary from none to palpitations to hemodynamic collapse and death. Diagnosis... read more that persists despite correction of cause (eg, low potassium or magnesium, ischemia) and optimal medical treatment of HF may require an antiarrhythmic drug Drugs for Arrhythmias The need for treatment of arrhythmias depends on the symptoms and the seriousness of the arrhythmia. Treatment is directed at causes. If necessary, direct antiarrhythmic therapy, including antiarrhythmic... read more . Amiodarone, beta-blockers, and dofetilide are the drugs of choice because other antiarrhythmics have adverse proarrhythmic effects when LV systolic dysfunction is present. Because amiodarone increases digoxin and warfarin levels, digoxin and/or warfarin doses should be decreased by half or stopped. Serum digoxin level and INR (international normalized ratio) level should be routinely monitored. However, drug toxicity can occur even at therapeutic levels. Because long-term use of amiodarone can cause adverse effects, a low dose (200 mg orally once a day) is used when possible; blood tests for liver function and thyroid-stimulating hormone are done every 6 months. If chest x-ray is abnormal or dyspnea worsens significantly, chest x-ray and pulmonary function tests are done yearly to check for pulmonary fibrosis. For sustained ventricular arrhythmias, amiodarone may be required; to reduce risk of sudden death, a loading dose of 400 to 800 mg orally twice a day is given for 1 to 3 weeks until rhythm control is adequate, then dose is decreased over 1 month to a maintenance dose of 200 mg orally once a day.

CRT is a mode of pacing that synchronizes contraction of the left ventricle by simultaneously pacing its opposing wall, thereby improving stroke volume. CRT may relieve symptoms and reduce heart failure hospitalizations for patients who have HF, LVEF < 35%, and a widened QRS complex with a left bundle branch block pattern (> 0.15 second—the wider the QRS, the greater potential benefit). CRT devices are effective but expensive, and patients should be appropriately selected. Many CRT devices also incorporate an ICD in their mechanism.

An implantable device that remotely monitors invasive hemodynamics (eg, pulmonary artery pressure) may help guide heart failure management in highly selected patients. For example, drug (eg, diuretic) titration based on readings from one of these devices was associated with a marked reduction in HF hospitalization in one clinical trial that included patients with both HFrEF and HFpEF. The device uses the pulmonary artery diastolic pressure as a surrogate for pulmonary capillary wedge pressure (and hence left atrial pressure) in HF patients. However, it has been evaluated only in NYHA (New York Heart Association) class III patients who had recurrent HF exacerbations. Further evidence will help guide how this technology should be implemented.

Ultrafiltration (venovenous filtration) can be useful in selected hospitalized patients with severe cardiorenal syndrome and volume overload refractory to diuretics. However, ultrafiltration should not be used routinely because clinical trials do not show long-term clinical benefit.

An intra-aortic counterpulsation balloon pump (IABP) is helpful in selected patients with acute HF who have a good chance of recovery (eg, acute HF following myocardial infarction) or in those who need a bridge to a more permanent solution such as cardiac surgery (eg, to fix severe valvular disease or to revascularize multivessel coronary artery disease), an LV assist device, or heart transplantation. Other forms of temporary mechanical circulatory support for patients with acute HF and cardiogenic shock include surgically placed devices such as extracorporeal membrane oxygenation (ECMO, typically venoarterial cannulation) and centrifugal flow ventricular assist devices that can support either the LV, the RV, or both and can also be combined with an oxygenator to provide full cardiopulmonary support. Percutaneously placed devices such as intravascular microaxial ventricular assist devices are available for both LV and RV support. Selection of temporary mechanical circulatory support devices is based mainly on availability and local medical center experience.

Durable or ambulatory LV assist devices (LVADs) are longer-term implantable pumps that augment LV output. They are commonly used to maintain patients with severe HF who are awaiting transplantation and are also used as "destination therapy" (ie, as a long-term or permanent solution) in some patients who are not transplant candidates.

Surgery may be appropriate when certain underlying disorders are present. Surgery in patients with advanced HF should be done in a specialized center.

Surgical closure of congenital or acquired intracardiac shunts can be curative.

After treatment, symptoms often persist. Reasons include

• Persistence of the underlying disorder (eg, hypertension, ischemia/infarction, valvular disease) despite treatment

• Suboptimal treatment of heart failure

• Drug nonadherence

• Excess intake of dietary sodium or alcohol

• Presence of an undiagnosed thyroid disorder, anemia, or supervening arrhythmia (eg, atrial fibrillation with rapid ventricular response, intermittent ventricular tachycardia)

Also, drugs used to treat other disorders may interfere with HF treatment. Nonsteroidal anti-inflammatory drugs (NSAIDs), thiazolidinediones (eg, pioglitazone) for diabetes, and short-acting dihydropyridine or nondihydropyridine calcium channel blockers can worsen heart failure and should be avoided unless no alternative exists; patients who must take such drugs should be followed closely.

• 1. McDonagh TA, Metra M, Adamo M, et al: 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: Developed by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Heart J 42(36):3599-3726, 2021. doi: 10.1093/eurheartj/ehab368

• 2. Heidenreich PA, Bozkurt B, Aguilar D, et al: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 145:e876–e894, 2022, doi: 10.1161/CIR.0000000000001062

• 3. Shah SJ, Kitzman D, Borlaug B, et al: Phenotype-specific treatment of heart failure with preserved ejection fraction: A multiorgan roadmap. Circulation 134(1):73–90, 2016. doi: 10.1161/CIRCULATIONAHA.116.021884

• 4. Kober L, Thune JJ, Nielsen JC, et al: Defibrillator implantation in patients with nonischemic systolic heart failure. N Engl J Med 375(13):1221–2130, 2016. doi: 10.1056/NEJMoa1608029

• 5. Stone GW, Lindenfield J, Abraham WT, et al: Transcatheter mitral-valve repair in patients with heart failure. N Engl J Med 379(24):2307–2318, 2018. doi: 10.1056/NEJMoa1806640