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Chapter 5:  10 Real Cases on Acute Heart Failure Syndrome: Diagnosis, Management, and Follow-Up

Swathi Roy; Gayathri Kamalakkannan

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Case 1: Diagnosis and Management of New-Onset Heart Failure With Reduced Ejection Fraction

A 54-year-old woman presented to the telemetry floor with shortness of breath (SOB) for 4 months that progressed to an extent that she was unable to perform daily activities. She also used 3 pillows to sleep and often woke up from sleep due to difficulty catching her breath. Her medical history included hypertension, dyslipidemia, diabetes mellitus, and history of triple bypass surgery 4 years ago. Her current home medications included aspirin, atorvastatin, amlodipine, and metformin. No significant social or family history was noted. Her vital signs were stable. Physical examination showed bilateral diffuse crackles in lungs, elevated jugular venous pressure, and 2+ pitting lower extremity edema. ECG showed normal sinus rhythm with left ventricular hypertrophy. Chest x-ray showed vascular congestion. Laboratory results showed a pro-B-type natriuretic peptide (pro-BNP) level of 874 pg/mL and troponin level of 0.22 ng/mL. Thyroid panel was normal. An echocardiogram demonstrated systolic dysfunction, mild mitral regurgitation, a dilated left atrium, and an ejection fraction (EF) of 33%. How would you manage this case?

In this case, a patient with known history of coronary artery disease presented with worsening of shortness of breath with lower extremity edema and jugular venous distension along with crackles in the lung. The sign and symptoms along with labs and imaging findings point to diagnosis of heart failure with reduced EF (HFrEF). She should be treated with diuretics and guideline-directed medical therapy for congestive heart failure (CHF). Telemetry monitoring for arrythmia should be performed, especially with structural heart disease. Electrolyte and urine output monitoring should be continued.

In the initial evaluation of patients who present with signs and symptoms of heart failure, pro-BNP level measurement may be used as both a diagnostic and prognostic tool. Based on left ventricular EF (LVEF), heart failure is classified into heart failure with preserved EF (HFpEF) if LVEF is >50%, HFrEF if LVEF is <40%, and heart failure with mid-range EF (HFmEF) if LVEF is 40% to 50%. All patients with symptomatic heart failure should be started on an angiotensin-converting enzyme (ACE) inhibitor (or angiotensin receptor blocker if ACE inhibitor is not tolerated) and β-blocker, as appropriate. In addition, in patients with New York Heart Association functional classes II through IV, an aldosterone antagonist should be prescribed. In African American patients, hydralazine and nitrates should be added. Recent recommendations also recommend starting an angiotensin receptor-neprilysin inhibitor (ARNI) in patients who are symptomatic on ACE inhibitors.

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MICHAEL KING, MD, JOE KINGERY, DO, AND BARETTA CASEY, MD, MPH

Am Fam Physician. 2012;85(12):1161-1168

More recent articles on heart failure and cardiomyopathy are available.

Patient information: A handout on this topic is available at https://familydoctor.org/familydoctor/en/diseases-conditions/heart-failure.html .

Author disclosure: No relevant financial affiliations to disclose.

Heart failure is a common clinical syndrome characterized by dyspnea, fatigue, and signs of volume overload, which may include peripheral edema and pulmonary rales. Heart failure has high morbidity and mortality rates, especially in older persons. Many conditions, such as coronary artery disease, hypertension, valvular heart disease, and diabetes mellitus, can cause or lead to decompensation of chronic heart failure. Up to 40 to 50 percent of patients with heart failure have diastolic heart failure with preserved left ventricular function, and the overall mortality is similar to that of systolic heart failure. The initial evaluation includes a history and physical examination, chest radiography, electrocardiography, and laboratory assessment to identify causes or precipitating factors. A displaced cardiac apex, a third heart sound, and chest radiography findings of venous congestion or interstitial edema are useful in identifying heart failure. Systolic heart failure is unlikely when the Framingham criteria are not met or when B-type natriuretic peptide level is normal. Echocardiography is the diagnostic standard to confirm systolic or diastolic heart failure through assessment of left ventricular ejection fraction. Evaluation for ischemic heart disease is warranted in patients with heart failure, especially if angina is present, given that coronary artery disease is the most common cause of heart failure.

Heart failure is a common clinical syndrome characterized by dyspnea, fatigue, and signs of volume overload, which may include peripheral edema and pulmonary rales. There is no single diagnostic test for heart failure; therefore, it remains a clinical diagnosis requiring a history, physical examination, and laboratory testing. Symptoms of heart failure can be caused by systolic or diastolic dysfunction. Appropriate diagnosis and therapy for heart failure are important given the poor prognosis. Survival is 89.6 percent at one month from diagnosis, 78 percent at one year, and only 57.7 percent at five years. 1

Heart failure has an estimated overall prevalence of 2.6 percent. 2 It is becoming more common in adults older than 65 years because of increased survival after acute myocardial infarction and improved treatment of coronary artery disease (CAD), valvular disease, and hypertension.

Heart failure is defined by the American Heart Association and American College of Cardiology as “a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.” 3 As cardiac output decreases because of stresses placed on the myocardium, activation of the sympathetic nervous and renin-angiotensin-aldosterone systems increases blood pressure (for tissue perfusion) and blood volume (enhancing preload, stroke volume, and cardiac output by the Frank-Starling mechanism). These compensatory mechanisms can also lead to further myocardial deterioration and worsening myocardial contractility. In systolic heart failure, cardiac output is decreased directly through reduced left ventricular function. In diastolic heart failure, cardiac output is compromised by poor ventricular compliance, impaired relaxation, and worsened end-diastolic pressure. 3 , 4

CAD is the underlying etiology in up to 60 to 70 percent of patients with systolic heart failure, 5 , 6 and a predictor for progression from asymptomatic to symptomatic left ventricular systolic dysfunction. Hypertension and valvular heart disease are significant risk factors for heart failure, with relative risks of 1.4 and 1.46, respectively. 6 Diabetes mellitus increases the risk of heart failure twofold by directly leading to cardiomyopathy and significantly contributing to CAD. Diabetes is one of the strongest risk factors for heart failure in women with CAD. 7 Smoking, physical inactivity, obesity, and lower socioeconomic status are often overlooked risk factors. 6 Numerous conditions can cause heart failure, either acutely without an underlying cardiac disorder or through decompensation of chronic heart failure ( Table 1 ) . 3 , 4 , 8 As a result, alternative causes should be promptly recognized, treated, and monitored to determine if the heart failure is reversible. 8

Classification

The most important consideration when categorizing heart failure is whether left ventricular ejection fraction (LVEF) is preserved or reduced (less than 50 percent). 3 , 8 A reduced LVEF in systolic heart failure is a powerful predictor of mortality. 9 As many as 40 to 50 percent of patients with heart failure have diastolic heart failure with preserved left ventricular function. 2 , 10 – 16 Overall, there is no difference in survival between diastolic and systolic heart failure that cannot be attributed to ejection fraction. 2 , 10 – 16 Patients with diastolic heart failure are more likely to be women, to be older, and to have hypertension, atrial fibrillation, and left ventricular hypertrophy, but no history of CAD. 11 – 14 , 17 , 18 Compared with systolic heart failure, which has well-validated therapies, diastolic heart failure lacks evidence-based treatment recommendations. 3 , 8 , 13

Heart failure symptoms can occur with preserved or reduced ejection fraction, (systolic or diastolic heart failure). The New York Heart Association classification system is the simplest and most widely used method to gauge symptom severity ( Table 2 ) . 19 The classification system is a well-established predictor of mortality and can be used at diagnosis and to monitor treatment response.

Initial Clinical Evaluation

Although no single item on clinical history, sign, or symptom has been proven to be diagnostic, many are helpful in assessing the probability of heart failure. The initial clinical evaluation, detailed in Tables 1 , 3 , 4 , 8 3 , 3 , 8 , 20 and 4 , 3 , 8 , 20 is directed at confirming heart failure, determining potential causes, and identifying comorbid illnesses. Table 5 lists findings for the initial evaluation of suspected heart failure, including history, physical examination, chest radiography, electrocardiography, and B-type natriuretic peptide (BNP) testing. 17 , 21 – 23 Evaluation for ischemic heart disease is warranted in patients with heart failure, especially if angina is present, given that CAD is the most common cause of heart failure.

History and Physical Examination

Patients with heart failure can have decreased exercise tolerance with dyspnea, fatigue, generalized weakness, and fluid retention, with peripheral or abdominal swelling and possibly orthopnea. 3 Patient history and physical examination are useful to evaluate for alternative or reversible causes ( Table 1 ) . 3 , 4 , 8 Nearly all patients with heart failure have dyspnea on exertion. However, heart failure accounts for only 30 percent of the causes of dyspnea in the primary care setting. 24 The absence of dyspnea on exertion only slightly decreases the probability of systolic heart failure, and the presence of orthopnea or paroxysmal nocturnal dyspnea has a small effect in increasing the probability of heart failure (positive likelihood ratio [LR+] = 2.2 and 2.6). 21 , 23

The presence of a third heart sound (ventricular filling gallop) is an indication of increased left ventricular end-diastolic pressure and a decreased LVEF. Despite being relatively uncommon findings, a third heart sound and displaced cardiac apex are good predictors of left ventricular dysfunction and effectively rule in the diagnosis of systolic heart failure (LR+ = 11 and 16). 21 , 23

The presence of jugular venous distention, hepatojugular reflux, pulmonary rales, and pitting peripheral edema is indicative of volume overload and enhances the probability of a heart failure diagnosis. Jugular venous distention and hepatojugular reflex have a moderate effect (LR+ = 5.1 and 6.4), whereas the others, along with cardiac murmurs, have only a small effect on the diagnostic probability (LR+ = 2.3 to 2.8). The absence of any of these findings is of little help in ruling out heart failure. 21

Laboratory Tests

Laboratory testing can help identify alternative and potentially reversible causes of heart failure. Table 4 lists laboratory tests appropriate for the initial evaluation of heart failure and other potential causes. 3 , 8 , 20 Other laboratory tests should be performed based on physician discretion to evaluate further causes or identify comorbid conditions that require enhanced control.

BNP and N-terminal pro-BNP (the cleaved inactive N-terminal fragment of the BNP precursor) levels can be used to evaluate patients with dyspnea for heart failure. BNP is secreted by the atria and ventricles in response to stretching or increased wall tension. 25 BNP levels increase with age, are higher in women and blacks, and can be elevated in patients with renal failure. 21 , 26 BNP appears to have better reliability than N-terminal pro-BNP, especially in older populations. 25 , 26 Multiple systematic reviews have concluded that BNP and N-terminal pro-BNP levels can effectively rule out a diagnosis of heart failure 22 , 25 , 27 , 28 because of their negative predictive value (negative likelihood ratio [LR–] = 0.1 and 0.14). 22 The average cutoff levels for heart failure were a BNP level of 95 pg per mL (95 ng per L) or a N-terminal pro-BNP level of 642 pg per mL (642 ng per L). 22

As BNP levels increase, the specificity increases and thus the likelihood of a heart failure diagnosis. 25 BNP levels are strong predictors of mortality at two to three months and cardiovascular events in acute heart failure, specifically when BNP level is greater than 200 pg per mL (200 ng per L) or N-terminal pro-BNP level is greater than 5,180 pg per mL (5,180 ng per L). 22 , 25 Limited evidence supports monitoring reduction of BNP levels in the acute and outpatient settings. A 30 to 50 percent reduction in BNP level at hospital discharge showed improved survival and reduced rehospitalization rates. Optimizing management for outpatient targets of a BNP level less than 100 pg per mL (100 ng per L) and an N-terminal pro-BNP level less than 1,700 pg per mL (1,700 ng per L) showed improvement in decompensations, hospitalizations, and mortality events. 22 , 25

Chest Radiography

Chest radiography should be performed initially to evaluate for heart failure because it can identify pulmonary causes of dyspnea (e.g., pneumonia, pneumothorax, mass). Pulmonary venous congestion and interstitial edema on chest radiography in a patient with dyspnea make the diagnosis of heart failure more likely (LR+ = 12). Other findings, such as pleural effusion or cardiomegaly, may slightly increase the likelihood of heart failure (LR+ = 3.2 and 3.3), but their absence is only slightly useful in decreasing the probability of heart failure (LR– = 0.33 to 0.48). 21

Electrocardiography

Electrocardiography (ECG) is useful for identifying other causes in patients with suspected heart failure. Changes such as left bundle branch block, left ventricular hypertrophy, acute or previous myocardial infarction, or atrial fibrillation can be identified and may warrant further investigation by echocardiography, stress testing, or cardiology consultation. Normal findings (or minor abnormalities) on ECG make systolic heart failure only slightly less likely (LR– = 0.27). 23 The presence of other findings such as atrial fibrillation, new T-wave changes, or any abnormality has a small effect on the diagnostic probability of heart failure (LR+ = 2.2 to 3.8). 21

Clinical Decision Making

The definition of heart failure continues to be debated, but it remains a clinical diagnosis. Several groups have published diagnostic criteria, but the Framingham criteria are widely accepted and include the components of the initial evaluation, which enhances their accuracy ( Table 6 ) . 17 A previous study validated the Framingham criteria for diagnosing systolic heart failure, 29 and a more recent study analyzed them for systolic and diastolic heart failure. 17 Both studies reported high sensitivity for systolic heart failure (97 percent compared with 89 percent for diastolic heart failure), which effectively rules out heart failure when the Framingham criteria are not met (LR– = 0.04). 17 , 29 The Framingham criteria only have a small effect on confirming a diagnosis of heart failure (LR+ = 4.21 to 4.57), but have a moderate effect on ruling out heart failure in general and diastolic heart failure (LR– = 0.1 and 0.13). 17

Echocardiography is the most widely accepted and available method for identifying systolic dysfunction and should be performed after the initial evaluation to confirm the presence of heart failure. 3 Two-dimensional echocardiography with Doppler flow studies can assess LVEF, left ventricular size, wall thickness, valve function, and the pericardium. Echocardiography can assist in diagnosing diastolic heart failure if elevated left atrial pressure, impaired left ventricular relaxation, and decreased compliance are present. 2 , 3 Often, the diagnosis of diastolic heart failure is clinical without conclusive echocardiographic evidence. If echocardiography results are equivocal or inadequate, transesophageal echocardiography, radionuclide angiography, or cineangiography with contrast media (at catheterization) can be used to assess cardiac function. 30

If angina or chest pain is present with heart failure, the American Heart Association and the American College of Cardiology recommend that the patient undergo coronary angiography, unless there is a contraindication to potential revascularization. 3 Coronary angiography has been shown to improve symptoms and survival in patients with angina and reduced ejection fraction. 3 It is important to evaluate for CAD because it is the cause of heart failure and low ejection fraction in approximately two-thirds of patients. 4 , 5 Because wall motion abnormalities are common in nonischemic cardiomyopathy, noninvasive testing may not be adequate for assessing the presence of CAD, and cardiology consultation may be warranted.

Figure 1 is an algorithm for the evaluation and diagnosis of heart failure. When a patient presents with symptoms of heart failure, the initial evaluation is performed to identify alternative or reversible causes of heart failure and to confirm its presence. If the Framingham criteria are not met, or if the BNP level is normal, systolic heart failure is essentially ruled out. Echocardiography should be performed to assess LVEF when heart failure is suspected or if diastolic heart failure is still suspected when systolic heart failure is ruled out. Treatment options are guided by the final diagnosis and echocardiography results, with a consideration to evaluate for CAD.

Data Sources: A PubMed search was completed in Clinical Queries using the following key words in various combinations under the search by clinical study category: heart failure, symptoms, causes, diagnosis, diagnostic criteria, diastolic, systolic, brain natriuretic peptide. The categories searched included etiology, diagnosis, clinical prediction rules, and systematic reviews. The articles consisted of meta-analyses, systematic reviews, randomized controlled trials, and cohort studies. The related citations feature was used to locate similar research once appropriate articles had been discovered. We also searched the Agency for Healthcare Research and Quality Evidence Reports, Bandolier, the Cochrane Database of Systematic Reviews, the Database of Abstracts of Reviews of Effects, the Institute for Clinical Systems Improvement, and the National Guideline Clearinghouse database. Search dates: April 5 through 16, 2010; May 24 through 28, 2010; selected newer articles January 1 and April 20, 2011.

Loehr LR, Rosamond WD, Chang PP, Folsom AR, Chambless LE. Heart failure incidence and survival (from the Atherosclerosis Risk in Communities study). Am J Cardiol. 2008;101(7):1016-1022.

Redfield MM, Jacobsen SJ, Burnett JC, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289(2):194-202.

Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation [published correction appears in Circulation . 2010;121(12):e258]. Circulation. 2009;119(14):e391-e479.

Dosh SA. Diagnosis of heart failure in adults. Am Fam Physician. 2004;70(11):2145-2152.

Gheorghiade M, Bonow RO. Chronic heart failure in the United States: a manifestation of coronary artery disease. Circulation. 1998;97(3):282-289.

He J, Ogden LG, Bazzano LA, Vupputuri S, Loria C, Whelton PK. Risk factors for congestive heart failure in US men and women: NHANES I epidemiologic follow-up study. Arch Intern Med. 2001;161(7):996-1002.

Bibbins-Domingo K, Lin F, Vittinghoff E, et al. Predictors of heart failure among women with coronary disease. Circulation. 2004;110(11):1424-1430.

Institute for Clinical Systems Improvement (ICSI). Heart failure in adults. Bloomington, Minn.: Institute for Clinical Systems Improvement (ICSI); 2009:95.

Solomon SD, Anavekar N, Skali H, et al.; Candesartan in Heart Failure Reduction in Mortality (CHARM) Investigators. Influence of ejection fraction on cardiovascular outcomes in a broad spectrum of heart failure patients. Circulation. 2005;112(24):3738-3744.

Aurigemma GP. Diastolic heart failure—a common and lethal condition by any name. N Engl J Med. 2006;355(3):308-310.

Lee DS, Gona P, Vasan RS, et al. Relation of disease pathogenesis and risk factors to heart failure with preserved or reduced ejection fraction: insights from the Framingham heart study of the National Heart, Lung, and Blood Institute. Circulation. 2009;119(24):3070-3077.

Bursi F, Weston SA, Redfield MM, et al. Systolic and diastolic heart failure in the community. JAMA. 2006;296(18):2209-2216.

Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006;355(3):251-259.

Bhatia RS, Tu JV, Lee DS, et al. Outcome of heart failure with preserved ejection fraction in a population-based study. N Engl J Med. 2006;355(3):260-269.

Vasan RS, Benjamin EJ, Levy D. Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol. 1995;26(7):1565-1574.

Persson H, Lonn E, Edner M, et al. Diastolic dysfunction in heart failure with preserved systolic function: need for objective evidence: results from the CHARM Echocardiographic Substudy-CHARMES. J Am Coll Cardiol. 2007;49(6):687-694.

Maestre A, Gil V, Gallego J, Aznar J, Mora A, Martín-Hidalgo A. Diagnostic accuracy of clinical criteria for identifying systolic and diastolic heart failure: cross-sectional study. J Eval Clin Pract. 2009;15(1):55-61.

Masoudi FA, Havranek EP, Smith G, et al. Gender, age, and heart failure with preserved left ventricular systolic function. J Am Coll Cardiol. 2003;41(2):217-223.

New York Heart Association Criteria Committee. Disease of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis . 6th ed. Boston, Mass.: Little, Brown; 1964.

Remme WJ, Swedberg K Task Force for the Diagnosis and Treatment of Chronic Heart Failure, European Society of Cardiology. Guidelines for the diagnosis and treatment of chronic heart failure [published correction appears in Eur Heart J . 2001;22(23):2217–2218]. Eur Heart J. 2001;22(17):1527-1560.

Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure?. JAMA. 2005;294(15):1944-1956.

Balion C, Santaguida PL, Hill S, et al. Testing for BNP and NT-proBNP in the diagnosis and prognosis of heart failure. Evid Rep Technol Assess (Full Rep). 2006;142:1-147.

Madhok V, Falk G, Rogers A, Struthers AD, Sullivan FM, Fahey T. The accuracy of symptoms, signs and diagnostic tests in the diagnosis of left ventricular dysfunction in primary care: a diagnostic accuracy systematic review. BMC Fam Pract. 2008;9:56.

Mulrow CD, Lucey CR, Farnett LE. Discriminating causes of dyspnea through clinical examination. J Gen Intern Med. 1993;8(7):383-392.

Chen WC, Tran KD, Maisel AS. Biomarkers in heart failure. Heart. 2010;96(4):314-320.

Ewald B, Ewald D, Thakkinstian A, Attia J. Meta-analysis of B type natriuretic peptide and N-terminal pro B natriuretic peptide in the diagnosis of clinical heart failure and population screening for left ventricular systolic dysfunction. Intern Med J. 2008;38(2):101-113.

Battaglia M, Pewsner D, Jüni P, Egger M, Bucher HC, Bachmann LM. Accuracy of B-type natriuretic peptide tests to exclude congestive heart failure: systematic review of test accuracy studies. Arch Intern Med. 2006;166(10):1073-1080.

Latour-Pérez J, Coves-Orts FJ, Abad-Terrado C, Abraira V, Zamora J. Accuracy of B-type natriuretic peptide levels in the diagnosis of left ventricular dysfunction and heart failure: a systematic review. Eur J Heart Fail. 2006;8(4):390-399.

Jimeno Sainz A, Gil V, Merino J, García M, Jordán A, Guerrero L. Validity of Framingham criteria as a clinical test for systolic heart failure [in Spanish]. Rev Clin Esp. 2006;206(10):495-498.

Naik MM, Diamond GA, Pai T, Soffer A, Siegel RJ. Correspondence of left ventricular ejection fraction determinations from two-dimensional echocardiography, radionuclide angiography and contrast cineangiography. J Am Coll Cardiol. 1995;25(4):937-942.

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Heart Failure (HF)

(congestive heart failure).

, MD, SM, Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary

• Pathophysiology
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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.

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.

Physiology of Heart Failure

Cardiac contractility (force and velocity of contraction), ventricular performance, and myocardial oxygen requirements are determined by

Substrate availability (eg, oxygen, fatty acids, glucose)

Heart rate and rhythm

Amount of viable myocardium

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

Increasing heart rate

Increasing systolic and diastolic volumes

Increasing stroke volume

Increasing tissue extraction of oxygen (the difference between oxygen content in arterial blood and in mixed venous or pulmonary artery blood)

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 principle

Pathophysiology of heart failure.

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.

Heart failure with reduced ejection fraction (HFrEF)

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.

Heart failure with preserved ejection fraction (HFpEF)

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%).

However, in some patients, marked restriction to LV filling can cause inappropriately low LV end-diastolic volume and thus cause low CO (cardiac output) and systemic symptoms. Elevated left atrial pressures can cause 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 and pulmonary congestion.

Heart failure with mildly reduced ejection fraction (HFmrEF)

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 severe or chronic LV failure, pleural effusions characteristically develop, further aggravating dyspnea. Minute ventilation increases; thus, PaCO2 decreases and blood pH increases ( respiratory alkalosis Respiratory Alkalosis Respiratory alkalosis is a primary decrease in carbon dioxide partial pressure (Pco2) with or without compensatory decrease in bicarbonate (HCO3 − ); pH may be high or near normal.... read more ). Marked interstitial edema of the small airways may interfere with ventilation, elevating PaCO2—a sign of impending respiratory failure Overview of Respiratory Failure Acute respiratory failure is a life-threatening impairment of oxygenation, carbon dioxide elimination, or both. Respiratory failure may occur because of impaired gas exchange, decreased ventilation... 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.

Cardiac response

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.

Hemodynamic responses

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.

Renal responses

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.

Neurohumoral responses

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.

Changes with aging

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]).

Etiology of Heart Failure

Both cardiac and systemic factors can impair cardiac performance and cause or aggravate heart failure.

Causes of Heart Failure

Classification 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.

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).

Classification reference

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

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

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.

Diagnosis of Heart Failure

Sometimes only clinical evaluation

Chest x-ray

Echocardiography, cardiac radionuclide scan, and/or MRI

BNP or N-terminal-pro-BNP (NT-pro-BNP) levels

ECG and other tests for etiology as needed

Diagnosis of heart failure of acute onset

This patient has bilateral pleural effusions (arrows). The normally sharp costophrenic angles are obscured by fluid in this patient.

© 2017 Elliot K. Fishman, MD.

Kerley B lines (arrows) are horizontal lines in the lung periphery that extend to the pleural surface. They denote thickened, edematous interlobular septa often due to pulmonary edema.

This patient has cardiomegaly (width of cardiac silhouette is > 50% of thoracic cage on a posterior-anterior chest x-ray). The patient also has cephalization (black arrows) whereby upper lobe pulmonary vessels become more prominent. These findings are often seen in patients with heart failure.

Lateral chest x-ray in a patient with fluid in major (1) and minor (2) fissures as well as a loculated effusion (3) seen along right posterior chest wall.

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.

Blood tests

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.

Other tests

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).

Diagnosis references

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

Prognosis for Heart Failure

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).

BNP, NTproBNP, and risk scores such as the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) Risk Score and the Seattle Heart Failure model , are helpful to predict prognosis in HF patients as an overall group, although there is significant variation in survival among individual patients.

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.

End-of-life care

All patients and family members should be taught about disease progression and the risk of sudden cardiac death. For some patients, improving quality of life is as important as increasing quantity of life. Thus, it is important to determine patients’ wishes about resuscitation (eg, endotracheal intubation Endotracheal Tubes If no spontaneous respiration occurs after airway opening and no respiratory devices are available, rescue breathing (mouth-to-mask or mouth-to-barrier device) is started; mouth-to-mouth ventilation... read more , CPR [cardiopulmonary respiration]) if their condition deteriorates, especially when HF is already severe.

All patients should be reassured that symptoms will be relieved, and they should be encouraged to seek medical attention early if their symptoms change significantly. Involvement of pharmacists, nurses, social workers, and clergy (when desired), who may be part of an interdisciplinary team or disease management program already in place, is particularly important in end-of-life care The Dying Patient Dying patients can have needs that differ from those of other patients. So that their needs can be met, dying patients must first be identified. Before death, patients tend to follow 1 of 3... read more .

Treatment of Heart Failure

Diet and lifestyle changes

Treatment of cause

Drug therapy

Sometimes device therapy (eg, implantable cardioverter-defibrillator, cardiac resynchronization therapy, mechanical circulatory support)

Sometimes cardiac transplantation

Multidisciplinary care

The primary goal is to diagnose and to correct or treat the disorder that led to heart failure.

Short-term goals include relieving symptoms and improving hemodynamics; avoiding hypokalemia Hypokalemia Hypokalemia is serum potassium concentration < 3.5 mEq/L (< 3.5 mmol/L) caused by a deficit in total body potassium stores or abnormal movement of potassium into cells. The most common... read more , renal dysfunction, and symptomatic hypotension; and correcting neurohumoral activation.

Treatment involves dietary and lifestyle changes, drugs Drugs for Heart Failure Heart failure (HF) is a syndrome of ventricular dysfunction (see Heart Failure). Drug treatment of heart failure (HF) involves symptom relief with Diuretics Nitrates Digoxin read more , devices, and sometimes percutaneous coronary interventions or surgery.

See Drugs for Heart Failure Drugs for Heart Failure Heart failure (HF) is a syndrome of ventricular dysfunction (see Heart Failure). Drug treatment of heart failure (HF) involves symptom relief with Diuretics Nitrates Digoxin read more for detailed information on drug treatment and the specific drugs and classes.

Disease management

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

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/m 2 (ideally 21 to 25 kg/m 2 ).

Regular light activity (eg, walking), tailored to symptoms, is generally encouraged. Activity prevents skeletal muscle deconditioning, which worsens functional status; however, activity does not appear to improve survival or decrease hospitalizations. Rest is appropriate during acute exacerbations. Formal exercise cardiac rehabilitation Cardiovascular Rehabilitation Cardiovascular rehabilitation may benefit some patients who have coronary artery disease or heart failure or who have had a recent myocardial infarction or coronary artery bypass surgery, particularly... read more is useful for chronic HFrEF and is likely helpful for patients with HFpEF.

Patients should have annual influenza vaccination Influenza Vaccine Based on recommendations by the World Health Organization and the Centers for Disease Control and Prevention (CDC), vaccines for influenza are modified annually to include the most prevalent... read more because influenza can precipitate HF exacerbations, particularly in institutionalized or older patients. Patients should be vaccinated against SARS-CoV-2.

Arrhythmias

Electrolytes are normalized.

Atrial and ventricular rates are controlled.

Sometimes antiarrhythmic drugs are given.

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 Medications 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.

Device therapy

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 and percutaneous procedures

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.

Heart transplantation Heart Transplantation Heart transplantation is an option for patients who have any of the following and who remain at risk of death and have intolerable symptoms despite optimal use of drugs and medical devices:... read more is the treatment of choice for patients < 60 who have severe, refractory HF and no other life-threatening conditions and who are highly adherent to management recommendations. Some older patients (about 60 to 70 years) with otherwise good health are also typically considered if they meet other criteria for transplantation. Survival is 85 to 90% at 1 year, and annual mortality thereafter is about 4%/year; however, mortality rate while waiting for a donor is 12 to 15%. Human organ donation remains low.

Anemia and iron deficiency

Persistent heart failure

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.

Treatment references

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

Heart failure (HF) involves ventricular dysfunction that ultimately leads to the heart not providing tissues with adequate blood for metabolic needs.

In heart failure with reduced ejection fraction (HFrEF), the ventricle contracts poorly and empties inadequately; ejection fraction is low.

In heart failure with preserved ejection fraction (HFpEF), ventricular filling is impaired, resulting in increased end-diastolic pressure at rest and/or during exercise; ejection fraction is normal.

Consider HF in patients with exertional dyspnea or fatigue, orthopnea, and/or edema, particularly in those with a history of myocardial infarction, hypertension, or valvular disorders or murmurs.

Do chest x-ray, ECG, BNP levels, and an objective test of cardiac function, typically echocardiography.

Unless adequately treated, HF tends to progress and has a poor prognosis.

Treatment includes education and lifestyle changes, control of underlying disorders, a variety of drugs, and sometimes implantable devices (CRT, ICDs).

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.

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

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

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Box 10.3 Case Study: Trivandrum Heart Failure Registry

Harikrishnan and others ( 2015 ) described the in-hospital and short-term outcomes among 1,205 consecutive admissions from 13 urban and 5 rural hospitals in Trivandrum, India, with a primary diagnosis of heart failure from January to December 2013. Ischemic heart disease was the underlying etiology of 72 percent of admissions, and heart failure with preserved ejection fraction (> 45 percent) constituted 26 percent of the sample. The median length of hospital stay was 6 days (interquartile range = 4–9 days), and in-hospital mortality rate was 8.5 percent (95 percent CI 6.9–10.0 percent). The all-cause mortality rate at 90 days was 2.43 deaths per 1,000 person-days (95 percent CI 2.11–2.78). Older age, lower education, poor ejection fraction, higher serum creatinine, New York Heart Association functional class IV, and not receiving guideline-based medical treatment were associated with higher risk of 90-day mortality.

These data demonstrate opportunities for improving in-hospital heart failure care in a low- and middle-income country setting.

From: Chapter 10, Heart Failure

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