Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal fluid accumulation; the ventricles can be involved together or separately. Diagnosis is initially clinical, supported by chest x-ray, echocardiography, and levels of plasma natriuretic peptides. Treatment includes patient education, diuretics, angiotensin converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, beta-blockers, aldosterone antagonists, sodium-glucose cotransporter-2 inhibitors, neprilysin inhibitors, sinus node inhibitors, specialized implantable pacemakers/defibrillators and other devices, and correction of the cause(s) of the HF syndrome. Show
Heart failure affects about 6.5 million people in the US; > 960,000 new cases occur each year. About 26 million people are affected worldwide. Cardiac contractility (force and velocity of contraction), ventricular performance, and myocardial oxygen requirements are determined by
Cardiac output (CO) is the product of stroke volume and heart rate; it is also affected by venous return, peripheral vascular tone, and neurohumoral factors. Preload is the loading condition of the heart at the end of its relaxation and filling phase (diastole) just before contraction (systole). Preload represents the degree of end-diastolic fiber stretch and end-diastolic volume, which is influenced by ventricular diastolic pressure and the composition of the myocardial wall. Typically, left ventricular (LV) end-diastolic pressure, especially if higher than normal, is a reasonable measure of preload. LV dilation, hypertrophy, and changes in myocardial distensibility (compliance) modify preload. Afterload is the force resisting myocardial fiber contraction at the start of systole. It is determined by LV chamber pressure, radius, and wall thickness at the time the aortic valve opens. Clinically, systemic systolic blood pressure at or shortly after the aortic valve opens correlates with peak systolic wall stress and approximates afterload. The Frank-Starling principle describes the relationship between preload and cardiac performance. It states that, normally, systolic contractile performance (represented by stroke volume or CO) is proportional to preload within the normal physiologic range (see figure ). Contractility is difficult to measure clinically (because it requires cardiac catheterization with pressure-volume analysis) but is reasonably reflected by the ejection fraction (EF), which is the percentage of end-diastolic volume ejected with each contraction (stroke volume/end-diastolic volume). EF can generally be adequately assessed noninvasively with echocardiography, nuclear imaging, or MRI. The force-frequency relationship refers to the phenomenon in which repetitive stimulation of a muscle within a certain frequency range results in increased force of contraction. Normal cardiac muscle at typical heart rates exhibits a positive force-frequency relationship, so a faster rate causes stronger contraction (and corresponding greater substrate requirements). During some types of heart failure, the force-frequency relationship may become negative, so that myocardial contractility decreases as heart rate increases above a certain rate. Cardiac reserve is the ability of the heart to increase its performance above resting levels in response to emotional or physical stress; body oxygen consumption may increase from 250 to ≥ 1500 mL/minute during maximal exertion. Mechanisms include
In well-trained young adults during maximal exercise, heart rate may increase from 55 to 70 beats/minute at rest to 180 beats/minute, and CO may increase from 6 to ≥ 25 L/minute. At rest, arterial blood contains about 18 mL oxygen/dL of blood, and mixed venous or pulmonary artery blood contains about 14 mL/dL. Oxygen extraction is thus about 4 mL/dL. When demand is increased, oxygen extraction may increase to 12 to 14 mL/dL. This mechanism also helps compensate for reduced tissue blood flow in heart failure. Frank-Starling principleNormally (top curve), as preload increases, cardiac performance also increases. However at a certain point, performance plateaus, then declines. In heart failure (HF) due to systolic dysfunction (bottom curve), the overall curve shifts downward, reflecting reduced cardiac performance at a given preload, and as preload increases, cardiac performance increases less. With treatment (middle curve), performance is improved, although not normalized. In heart failure, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion. This condition can result from abnormalities of systolic or diastolic function or, commonly, both. Although a primary abnormality can be a change in cardiomyocyte function, there are also changes in collagen turnover of the extracellular matrix. Cardiac structural defects (eg, congenital defects, valvular disorders), rhythm abnormalities (including persistently high heart rate), and high metabolic demands (eg, due to thyrotoxicosis) also can cause HF. In HFrEF (also called systolic HF), global LV systolic dysfunction predominates. The LV contracts poorly and empties inadequately, leading to
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
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
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 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]). Both cardiac and systemic factors can impair cardiac performance and cause or aggravate heart failure. Causes of Heart Failure
The most common classification of heart failure currently in use stratifies patients into Heart failure with reduced ejection fraction (HFrEF) is defined as heart failure with left ventricular ejection fraction (LVEF) ≤ 40%. Heart failure with preserved ejection fraction (HFpEF) is defined as heart failure with LVEF ≥ 50%. The traditional distinction between left and right ventricular failure is somewhat misleading because the heart is an integrated pump, and changes in one chamber ultimately affect the whole heart. However, these terms indicate the major site of pathology leading to heart failure and can be useful for initial evaluation and treatment. Other common descriptive terms for heart failure include acute or chronic; high output or low output; dilated or nondilated; and ischemic, hypertensive, or idiopathic dilated cardiomyopathy. Treatment differs based on whether the presentation is acute or chronic HF. LV failure characteristically develops in ischemic heart disease, 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
RV failure is most commonly caused by previous LV failure (which increases pulmonary venous pressure and leads to
pulmonary hypertension
Pulmonary Hypertension Pulmonary hypertension is increased pressure in the pulmonary circulation. It has many secondary causes; some cases are idiopathic. In pulmonary hypertension, pulmonary vessels may become constricted... read more , thus overloading the RV) or by a severe lung disorder (in which case it is called cor pulmonale Cor Pulmonale Cor pulmonale is right ventricular (RV) enlargement secondary to a lung disorder that causes pulmonary artery hypertension. Right
ventricular failure follows. Findings include peripheral edema... read more
High-output HF results from a persistently high cardiac output, which may eventually result in an inability of a normal heart to maintain adequate output. Conditions that may increase CO (cardiac output) include severe anemia, end-stage liver disease,
beriberi
Thiamin Deficiency Thiamin deficiency (causing beriberi) is most common among people subsisting on white rice or highly refined carbohydrates in countries with high rates of food insecurity and among people with... read more ,
thyrotoxicosis
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 Cardiomyopathy Overview of Cardiomyopathies A cardiomyopathy is a primary disorder of the heart muscle. It is distinct from structural cardiac disorders such as coronary artery disease, valvular disorders, and congenital heart disorders... read more is a general term indicating disease of the myocardium. Most commonly, the term refers to a primary disorder of the ventricular myocardium that is not caused by congenital anatomic defects; valvular, systemic, or pulmonary vascular disorders; isolated pericardial, nodal, or conduction system disorders; or epicardial coronary artery disease (CAD). The term is sometimes used to reflect etiology (eg, ischemic vs hypertensive cardiomyopathy). Cardiomyopathy does not always lead to symptomatic HF. It is often idiopathic and is classified as dilated, congestive, hypertrophic, infiltrative-restrictive, or apical-ballooning cardiomyopathy (also known as takotsubo or stress cardiomyopathy).
Symptoms and Signs of Heart FailureManifestations 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.
HistoryIn 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 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. ExaminationGeneral 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 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
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
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
Clinical findings (eg, exertional dyspnea or fatigue, orthopnea, edema, tachycardia, pulmonary crackles, S3, jugular venous distention) suggest heart failure but are usually not apparent early. Some similar symptoms may result from
COPD
Chronic Obstructive Pulmonary Disease (COPD) Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational... read more
Diagnosis of heart failure of acute onsetData from 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. 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
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
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).
Generally, patients with heart failure have a poor prognosis unless the cause is correctable. Overall combined 5 year survival is 35% for patients with HFpEF or HFrEF after an initial hospitalization for heart failure. In overt chronic HF, mortality depends on severity of symptoms and ventricular dysfunction and can range from 10 to 40%/year. Specific factors that suggest a poor prognosis include hypotension, low ejection fraction, presence of coronary artery disease, troponin release, elevation of BUN, reduced GFR, hyponatremia, and poor functional capacity (eg, as tested by a 6-minute walk test). HF usually involves gradual deterioration, interrupted by bouts of severe decompensation, and ultimately death, although the time course is being lengthened with modern therapies. However, death can also be sudden and unexpected, without prior worsening of symptoms.
Immediate inpatient treatment is required for patients with acute or worsening heart failure due to certain disorders (eg,
acute myocardial infarction
Acute Myocardial Infarction (MI) Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and/or diaphoresis... read more
The primary goal is to diagnose and to correct or treat the disorder that led to heart failure. Long-term goals include correcting
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 Treatment is tailored to the patient, considering causes, symptoms, and response to drugs, including adverse effects. There are currently several evidence-based therapies for chronic HFrEF
(1 Treatment
references Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more General measures, especially patient and caregiver education and diet and lifestyle modifications, are important for all patients with heart failure.
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
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
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
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.
The following are some of the major English-language heart failure guidelines that may be useful. Please note that THE MANUAL is not responsible for the content of these resources.
How does the body compensate for decreased cardiac output in cases of congestive heart failure?Compensation in the body
The body's hormone and nervous systems try to make up for this. They increase blood pressure, hold on to salt (sodium) and water in the body, and increase the heart rate. These responses are the body's attempt to compensate for the poor blood circulation and the backup of blood.
What is the compensation mechanism for decreased cardiac output?The most well-recognized of the compensatory homeostatic responses to a fall in cardiac output are activation of the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS).
What are the three compensatory mechanism for heart failure?After this initial decline in pumping capacity of the heart, a variety of compensatory mechanisms are activated, including the adrenergic nervous system, the renin-angiotensin system, and the cytokine system.
Which of the following would attempt to compensate for the decreased cardiac output with congestive heart failure quizlet?Compensation mechanisms for decreased cardiac output in cases of congestive heart failure include: increased renin and aldosterone secretions.
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