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Acute decompensated heart failure

Acute decompensated heart failure (ADHF) is a clinical syndrome defined by the rapid onset or worsening of heart failure symptoms and signs, such as dyspnea, fatigue, and fluid overload, often necessitating urgent hospitalization and medical intervention to restore hemodynamic stability.^[1] This condition arises from an acute deterioration in cardiac function, leading to either congestion (volume overload) or hypoperfusion (reduced organ blood flow), and it frequently complicates underlying chronic heart failure.^[2] ADHF most commonly affects individuals with pre-existing heart failure, accounting for about 80% of cases, while 15% represent new-onset heart failure and less than 5% occur in end-stage disease.^[2] Precipitating factors include acute coronary syndromes, uncontrolled hypertension, arrhythmias (such as atrial fibrillation), infections, medication non-adherence, excessive salt intake, or use of nonsteroidal anti-inflammatory drugs (NSAIDs).^[1] Underlying etiologies often involve ischemic heart disease—the leading global cause—along with hypertension, valvular disorders, and various cardiomyopathies.^[1] Pathophysiologically, it stems from exhausted compensatory mechanisms like sympathetic nervous system activation and renin-angiotensin-aldosterone system (RAAS) overdrive, resulting in maladaptive fluid retention, elevated cardiac filling pressures, and reduced cardiac output.^[1] Epidemiologically, heart failure affects approximately 64.34 million people worldwide, with ADHF driving over 1 million annual hospitalizations in the United States alone as of 2017, and prevalence rising sharply with age—reaching 66 per 1,000 in men aged 80-89 according to the Framingham Heart Study.^[1] Patients typically present with shortness of breath (dyspnea), orthopnea, peripheral edema, fatigue, and pulmonary rales; severe cases may feature respiratory distress, jugular venous distension, or signs of cardiogenic shock like hypotension and altered mental status.^[1]^[2] Clinical phenotypes are often classified as "wet and warm" (congested with adequate perfusion), "wet and cold" (congested with hypoperfusion), or others based on volume status and perfusion.^[2] Diagnosis relies on a combination of history, physical examination using criteria like the Framingham diagnostic standards, and supportive tests including elevated B-type natriuretic peptide (BNP) or N-terminal pro-BNP levels (>100 pg/mL or >300 pg/mL, respectively), electrocardiography (ECG) to identify arrhythmias or ischemia, chest X-ray for pulmonary congestion, and echocardiography to assess left ventricular ejection fraction (LVEF) and structure.^[1] Laboratory evaluation may also include troponin to rule out myocardial injury and renal function tests to detect cardiorenal syndrome.^[2] Management prioritizes stabilization based on the presenting phenotype, with intravenous loop diuretics (e.g., furosemide) as first-line therapy for congestion to achieve euvolemia, vasodilators like nitroglycerin for hypertension and preload reduction, and inotropes such as dobutamine for low-output states.^[1]^[2] Per the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure, treatment incorporates guideline-directed medical therapy (GDMT) tailored to LVEF, including angiotensin receptor-neprilysin inhibitors (ARNI), beta-blockers, mineralocorticoid receptor antagonists (MRAs), and sodium-glucose cotransporter-2 (SGLT2) inhibitors for heart failure with reduced ejection fraction (HFrEF); device therapies like implantable cardioverter-defibrillators (ICDs) or cardiac resynchronization therapy (CRT) may be indicated for select patients.^[3] Recent advancements emphasize rapid initiation of GDMT during hospitalization and follow-up within 7-10 days post-discharge to prevent readmissions.^[3]^[2] Prognosis remains poor, with in-hospital mortality around 4-7%, 30-day post-discharge mortality approximately 10%, 1-year mortality 22%, and 5-year mortality up to 42%; outcomes worsen in advanced stages (e.g., stage D HFrEF >50% mortality) and are influenced by comorbidities like diabetes or renal disease.^[1] Early recognition and optimized therapy are critical to improving survival and quality of life.^[3]

Introduction

Definition and overview

Acute decompensated heart failure (ADHF) is defined as a clinical syndrome characterized by new or worsening symptoms and signs of heart failure, such as dyspnea and edema, that necessitate urgent medical intervention, often including hospitalization or escalation of therapy.^[4] According to the 2025 JCS/JHFS guidelines, ADHF specifically refers to decompensated heart failure requiring substantial intensification of treatment, including intravenous diuretics, vasoactive agents, or hospital admission to manage unstable hemodynamics and prevent critical deterioration.^[5] ADHF differs from chronic stable heart failure, which involves ongoing but controlled symptoms managed with outpatient guideline-directed medical therapy without acute exacerbations.^[5] It also contrasts with acute heart failure in patients without prior decompensation, often termed de novo heart failure, where the presentation occurs without a history of chronic disease.^[6] The concept of ADHF traces its origins to early 20th-century medical literature describing cardiac congestion and acute pulmonary edema as manifestations of failing circulation.^[7] Classification systems evolved from the New York Heart Association (NYHA) functional classes introduced in 1928, which were later adapted for acute settings to assess symptom severity and guide urgent management.^[8] ADHF represents a leading cause of hospitalization among adults over 65 years old and carries a high risk of short-term mortality, with in-hospital death rates ranging from 4% to 7%.^[9] This condition typically arises from fluid overload and impaired cardiac function, underscoring its role as an acute manifestation of underlying systolic or diastolic dysfunction.^[10]

Epidemiology

Acute decompensated heart failure (ADHF) represents a significant portion of heart failure-related hospitalizations, with approximately 1.2 million primary hospitalizations occurring in the United States in 2021 among 949,075 unique patients, marking an increase from prior years.^[11] Globally, heart failure affects an estimated 64 million people, with ADHF contributing to over 1 million hospitalizations annually in both the United States and Europe combined, reflecting a rising burden driven by aging populations.^[12]^[10] The overall prevalence of heart failure, of which ADHF is a common acute manifestation, stands at about 1.9% to 2.6% among U.S. adults, rising sharply with age to affect up to 10% of individuals over 75 years.^[13] Regional disparities are notable, with higher rates in low- and middle-income countries attributed to untreated hypertension and limited access to preventive care.^[12] Demographically, ADHF predominantly impacts older adults, with a mean age at hospitalization around 70 to 80 years, and it shows a slight male predominance in cases involving systolic dysfunction, though rates are more equal in diastolic forms. Comorbidities are prevalent, including hypertension in 70% to 80% of cases and diabetes in 40% to 50%, alongside higher incidences among Black individuals, who experience elevated hospitalization and mortality rates compared to other racial groups.^[3] Risk factors at the population level include advanced age, prior heart failure diagnosis, and social determinants such as inadequate access to healthcare, which exacerbate vulnerabilities in underserved communities.^[11] Trends indicate a growing incidence of ADHF hospitalizations since 2014, with overall heart failure prevalence projected to rise from 6.7 million U.S. adults in 2025 to 11.4 million by 2050, potentially amplified by post-COVID-19 effects including increased cardiovascular strain.^[11]^[14] The economic burden in the United States is substantial, with direct medical costs estimated at $32 billion annually in 2020, projected to escalate significantly amid rising cases.^[11] Globally, the condition underscores a public health challenge, with potential for 1.19 million lives saved yearly through optimized therapies, highlighting the need for targeted interventions in high-risk populations.^[15]

Pathophysiology

Underlying mechanisms

Acute decompensated heart failure (ADHF) primarily arises from a reduction in cardiac output due to systolic or diastolic dysfunction of the left ventricle, leading to inadequate tissue perfusion and activation of compensatory neurohormonal pathways.^[10] In systolic dysfunction, characteristic of heart failure with reduced ejection fraction (HFrEF), the myocardium's inability to eject blood effectively increases end-systolic volume and elevates left ventricular filling pressures, promoting pulmonary congestion.^[10] Diastolic dysfunction, prevalent in heart failure with preserved ejection fraction (HFpEF), impairs ventricular relaxation and compliance, resulting in similar pressure elevations despite normal ejection fraction.^[10] This hemodynamic imbalance triggers neurohormonal activation, including the renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS), which initially aim to maintain perfusion but ultimately exacerbate myocardial stress through vasoconstriction and fluid retention.^[16] Fluid dynamics in ADHF involve increased preload from venous congestion and renal sodium retention, shifting the Frank-Starling relationship in the failing heart. The Frank-Starling mechanism describes how cardiac output depends on preload, with stroke volume increasing with end-diastolic volume up to a point; in heart failure, the curve flattens and shifts downward due to reduced contractility, leading to diminished output despite elevated filling pressures.^[10]

\text{Stroke Volume} = f(\text{End-Diastolic Volume})

Here, the function f reflects myocardial contractility, which is impaired in ADHF, causing congestion without proportional output gains.^[10] Sodium retention, mediated by RAAS and SNS, expands intravascular volume, while intercompartmental fluid redistribution—often without net weight gain—further elevates central venous pressures and contributes to organ hypoperfusion.^[17] Inflammatory and vascular components amplify these processes through endothelial dysfunction and cytokine release. Reduced cardiac output promotes systemic inflammation, with elevated levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) impairing myocardial function and vascular tone.^[10] Endothelial dysfunction leads to microvascular rarefaction and impaired nitric oxide bioavailability, worsening vasoconstriction and tissue ischemia.^[16] These mechanisms differ between HFrEF and HFpEF: HFrEF emphasizes systolic impairment and eccentric remodeling, while HFpEF involves concentric hypertrophy, fibrosis, and pronounced microvascular inflammation, accounting for approximately 50% of ADHF cases.^[18]

Precipitating factors

Acute decompensated heart failure (ADHF) episodes are frequently triggered by identifiable factors that disrupt the delicate balance maintained by compensatory mechanisms in patients with underlying chronic heart failure. Recent cohort studies indicate that up to 80% of ADHF cases involve at least one precipitating factor, with variations across populations; for instance, a prospective analysis of 692 decompensation events identified precipitants in 78% of cases. Recent trends as of 2024 show declining ischemic triggers but rising contributions from hypertension and smoking.^[19]^[16]^[20] These triggers can be broadly categorized into non-cardiac, cardiac, and iatrogenic or lifestyle-related factors, each contributing to acute worsening through increased cardiac demand, fluid overload, or reduced output. Non-cardiac precipitants often involve systemic stressors that exacerbate hemodynamic instability. Infections, particularly respiratory tract infections such as pneumonia, are among the most common, accounting for 20-30% of ADHF episodes in multiple reviews; in one global registry of over 18,000 patients, infections precipitated 10% of hospitalizations, with higher rates in certain regions like the Eastern Mediterranean.^[16]^[21] Anemia, especially moderate to severe forms, is a significant trigger in up to 64% of cases in some cohorts, increasing oxygen demand and leading to high-output failure.^[22] Thyroid dysfunction, including hyperthyroidism, can precipitate decompensation by inducing tachycardia and arrhythmias, though it is less prevalent as a direct trigger compared to infections or anemia.^[23] Renal impairment, often involving worsening acute kidney injury, can contribute as a comorbidity by promoting fluid retention and electrolyte imbalances.^[21] Cardiac precipitants directly impair myocardial function or rhythm. Arrhythmias, such as atrial fibrillation with rapid ventricular response, are implicated in 10-46% of cases, with rates reaching 18% in Western European cohorts; this disrupts atrial contribution to ventricular filling and increases myocardial oxygen consumption.^[24]^[21] Acute coronary syndromes, including myocardial infarction, precipitate 13-18% of ADHF events globally, particularly in new-onset heart failure, by causing ischemia and sudden reductions in contractility.^[21] Valvular issues, such as acute regurgitation from chordal rupture, though rarer, can rapidly overload the ventricle and lead to decompensation.^[25] Iatrogenic and lifestyle factors often stem from patient behaviors or therapeutic errors that undermine chronic management. Medication non-adherence, including cessation of beta-blockers or diuretics, accounts for 9-23% of episodes, directly leading to fluid accumulation and hypertension.^[19]^[21] High salt intake violates dietary restrictions and precipitates volume overload in 9-27% of cases, with higher prevalence in regions like North America.^[19] Uncontrolled hypertension, affecting 6-8% of admissions, imposes excessive afterload, straining the failing heart.^[21] These precipitants overload compensatory systems, such as the renin-angiotensin-aldosterone axis and sympathetic nervous system, leading to decompensation. For example, infection-induced tachycardia can worsen myocardial ischemia by increasing oxygen demand in already compromised coronary perfusion, while anemia heightens cardiac workload through reduced oxygen delivery, culminating in pulmonary congestion and reduced forward flow.^[16]^[26] Identifying and addressing these triggers is crucial for preventing recurrent admissions.

Clinical Manifestations

Signs and symptoms

Patients with acute decompensated heart failure (ADHF) typically present with a range of subjective symptoms reflecting cardiac decompensation and fluid overload. The most common symptom is dyspnea, reported in approximately 81% of cases, often worsening with exertion or at rest due to pulmonary congestion.^[27] Other cardinal symptoms include orthopnea, paroxysmal nocturnal dyspnea, and fatigue or weakness, occurring in about 71% of patients, which contribute to reduced daily functioning and quality of life.^[27]^[2] Objective signs of congestion are prominent and include peripheral edema, affecting around 68% of individuals, as well as jugular venous distension, hepatomegaly, and ascites, particularly in those with right-sided involvement.^[27]^[28]^[24] In cases with low cardiac output, patients may exhibit cool extremities, altered mental status, and oliguria, indicating tissue hypoperfusion, though these are less frequent than congestion-related findings.^[29] Vital sign abnormalities often accompany these presentations, such as tachycardia, tachypnea, hypotension or hypertension, and reduced oxygen saturation, reflecting the hemodynamic instability of ADHF. The onset is typically rapid, progressing over hours to days with worsening symptoms like increased body weight and edema, distinguishing it from stable chronic heart failure.^[24] Severe variants, such as flash pulmonary edema, may manifest abruptly with intense dyspnea.^[10]

Special presentations

Flash pulmonary edema represents a severe, rapid-onset variant of acute decompensated heart failure (ADHF), characterized by sudden severe dyspnea and hypoxemia resulting from acute fluid accumulation in the lungs due to elevated left ventricular filling pressures and rapid redistribution of fluid.^[30] This condition often occurs in the context of hypertensive crises, with systolic blood pressure exceeding 180 mmHg, triggered by sympathetic activation that increases afterload, particularly in patients with heart failure with preserved ejection fraction (HFpEF).^[10] Common associations include bilateral renal artery stenosis, known as Pickering syndrome, where renovascular hypertension exacerbates the acute fluid shift, as well as acute myocardial ischemia.^[31] Other atypical presentations of ADHF include dominant right-sided heart failure, which may manifest with isolated peripheral edema such as bilateral leg swelling due to elevated right ventricular pressures and systemic venous congestion, often without prominent pulmonary symptoms.^[32] Cardiogenic shock is another high-risk variant, defined by hypotension (systolic blood pressure <90 mmHg), reduced cardiac index (<2.2 L/min/m²), and signs of end-organ hypoperfusion like oliguria or altered mental status, occurring in a small subset of ADHF cases and indicating profound biventricular dysfunction.^[10] In ADHF with HFpEF, the presentation is influenced by a stiff left ventricle with impaired diastolic relaxation, leading to elevated filling pressures and congestion despite normal systolic function.^[10] The incidence of flash pulmonary edema varies by population.^[33] These special presentations carry elevated mortality risks; for instance, in-hospital mortality for acute pulmonary edema variants reaches about 7.4%, higher than the 6% seen in typical ADHF.^[34] Differentiation of these cardiogenic presentations from non-cardiogenic pulmonary edema, such as acute respiratory distress syndrome (ARDS), relies on clinical context and biomarkers; elevated levels of B-type natriuretic peptide (BNP >100 pg/mL) or N-terminal pro-BNP strongly support a cardiogenic etiology by indicating ventricular wall stress.^[35]

Diagnosis

Clinical assessment

The clinical assessment of acute decompensated heart failure (ADHF) begins with a thorough history and physical examination to identify signs of congestion and hypoperfusion, guiding initial suspicion and urgency of management. This bedside evaluation is essential as the first step in evaluating patients presenting with dyspnea or other suggestive symptoms, often in emergency or inpatient settings, and helps differentiate ADHF from other causes of acute respiratory or circulatory distress.^[36] History taking focuses on querying for a prior diagnosis of heart failure, as up to 90% of ADHF cases occur in patients with known chronic heart failure. Clinicians should assess recent triggers, such as nonadherence to medications, dietary sodium excess, or infections, and inquire about symptom progression including sudden weight gain exceeding 2 kg over 3 days, which signals fluid retention and decompensation. Worsening of New York Heart Association (NYHA) functional class, characterized by increased dyspnea on exertion or orthopnea requiring additional pillows for sleep, is a key indicator of acute exacerbation and should be quantified to gauge severity.^[3]^[37]^[36] The physical examination emphasizes detecting volume overload and hemodynamic compromise. Vital signs assessment reveals tachycardia, hypotension, or tachypnea in many cases, while inspection may show elevated jugular venous pressure or peripheral edema. Auscultation frequently uncovers pulmonary crackles, present in approximately 70% of ADHF patients with a sensitivity of 51-75%, reflecting interstitial edema, though their absence does not rule out the diagnosis. Cardiac auscultation may elicit an S3 gallop, a low-frequency sound indicating elevated left ventricular filling pressures and associated with poorer prognosis, while hepatojugular reflux—sustained jugular venous distention upon right upper quadrant compression—suggests right ventricular dysfunction with high specificity for elevated central venous pressure.^[36]^[38]^[36] Adapted Framingham criteria provide a structured approach for diagnosing heart failure in acute settings, requiring two major criteria or one major and two minor criteria for confirmation. Major criteria include paroxysmal nocturnal dyspnea, neck vein distention, rales, S3 gallop, acute pulmonary edema, and hepatojugular reflux; minor criteria encompass extremity edema, nocturnal cough, dyspnea on exertion, hepatomegaly, pleural effusion, and vital capacity reduction by one-third from maximum. These criteria, originally validated in the Framingham Heart Study cohort with 97% sensitivity and 79% specificity for heart failure diagnosis, can be applied judiciously in decompensated presentations.^[39] Risk stratification during clinical assessment employs tools like the ADHERE registry criteria to identify high-risk features, such as low systolic blood pressure, elevated blood urea nitrogen, or elevated serum creatinine, predicting in-hospital mortality rates up to 22% in high-risk groups. This initial categorization informs triage and resource allocation, prioritizing patients with multiple adverse clinical signs for expedited care. The clinical assessment serves as a prerequisite before proceeding to confirmatory diagnostic tests, establishing the clinical suspicion that directs further evaluation and stabilizes the patient.^[40]^[36]

Diagnostic tests

Diagnosis of acute decompensated heart failure (ADHF) relies on a combination of laboratory tests, imaging modalities, and invasive assessments to confirm the presence of cardiac dysfunction and congestion while excluding alternative causes of symptoms. Initial laboratory evaluation includes measurement of natriuretic peptides, which serve as key biomarkers for supporting the diagnosis. According to the 2022 AHA/ACC/HFSA guidelines, B-type natriuretic peptide (BNP) levels greater than 100 pg/mL or N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels greater than 300 pg/mL in the context of dyspnea make heart failure unlikely if below these thresholds, whereas elevated levels such as BNP >400 pg/mL exhibit high sensitivity for ruling in ADHF with appropriate clinical suspicion.^[3] Cardiac troponins are also routinely assessed to detect concomitant myocardial ischemia or injury, as elevations occur in up to 40% of ADHF cases and are associated with worse outcomes, independent of acute coronary syndrome.^[41] Routine blood tests further evaluate systemic effects and comorbidities. Electrolyte panels often reveal hyponatremia, defined as serum sodium <135 mEq/L, which affects 20-25% of hospitalized ADHF patients and correlates with neurohormonal activation and fluid overload.^[42] Renal function tests, including blood urea nitrogen (BUN) and creatinine, are essential; a BUN-to-creatinine ratio >20:1 suggests prerenal azotemia due to reduced renal perfusion in cardiorenal syndrome type 1, a common complication in ADHF.^[43] Complete blood count (CBC) screening identifies anemia, present in approximately 30-50% of heart failure patients, which exacerbates symptoms and indicates potential iron deficiency or chronic disease contributions.^[26] Electrocardiography (ECG) is a fundamental noninvasive test performed in all suspected ADHF cases to identify arrhythmias such as atrial fibrillation (prevalent in 20-30% of admissions) or ischemic changes like ST-segment depression, which may precipitate decompensation.^[44] Chest radiography assesses for pulmonary congestion, manifesting as cephalization, Kerley B lines, or bilateral infiltrates in up to 80% of cases, alongside cardiomegaly reflecting chronic remodeling. Point-of-care lung ultrasonography may be used to detect pulmonary congestion, offering higher sensitivity than auscultation or chest radiography (Class IIa recommendation per 2022 AHA/ACC/HFSA guidelines).^[45]^[3] Echocardiography provides critical structural and functional data, quantifying left ventricular ejection fraction (LVEF) to classify heart failure type (e.g., reduced LVEF ≤40%) and evaluating regional wall motion abnormalities indicative of ischemia or prior infarction.^[46] In hemodynamically unstable or diagnostically ambiguous cases, invasive hemodynamic monitoring via Swan-Ganz (pulmonary artery) catheterization measures pulmonary capillary wedge pressure (PCWP), with values >18 mmHg confirming elevated left-sided filling pressures diagnostic of ADHF.^[47] These tests also aid in differential diagnosis by excluding mimics; for instance, serial troponins and ECG rule out acute coronary syndrome, chest X-ray and sputum cultures differentiate pneumonia, and D-dimer or computed tomography pulmonary angiography identify pulmonary embolism.^[2]

Management

Initial evaluation and stabilization

The initial evaluation of patients presenting with acute decompensated heart failure (ADHF) begins with a rapid assessment of the ABCs—airway, breathing, and circulation—to identify and address any immediate threats to hemodynamic stability, such as hypoxia or shock. This structured approach ensures prioritization of life-threatening issues before further diagnostic steps.^[48]^[3] Continuous monitoring is essential from the outset, including telemetry for electrocardiographic detection of arrhythmias, pulse oximetry for oxygen saturation, and frequent vital sign checks (heart rate, blood pressure, respiratory rate). Intravenous access should be established promptly to facilitate potential interventions and fluid management. These measures, classified as class I recommendations with level of evidence C, help guide real-time adjustments and prevent deterioration.^[48]^[3] Assessment of volume status follows, using a combination of clinical examination (e.g., jugular venous pressure, peripheral edema, lung auscultation) and adjunctive tools such as inferior vena cava (IVC) ultrasound via point-of-care echocardiography to evaluate congestion and right atrial pressure. Patients are classified into hemodynamic profiles—such as warm/wet (adequate perfusion with congestion) or cold/wet (hypoperfusion with congestion)—to inform urgency and strategy; this profiling, supported by class I evidence (level C), aids in distinguishing those needing urgent decongestion from those with low-output states.^[48]^[3] The primary goal of initial stabilization is decongestion to achieve euvolemia, targeting net fluid removal of 2-5 L over the first 24-48 hours in volume-overloaded patients without hypoperfusion, monitored via daily weights, urine output (aiming for >100-150 mL/hour initially), and spot urine sodium levels. The 2021 ESC guidelines and 2023 focused update emphasize rapid emergency department triage within the first hour for high-risk features (e.g., persistent hypotension, severe dyspnea), using tools like the CHAMPIT2 mnemonic to identify precipitating factors such as ischemia or infection.^[48]^[3] Throughout stabilization, vigilance for complications is critical, including arrhythmias (e.g., atrial fibrillation or ventricular tachycardia, detected via telemetry) and worsening renal function (monitored through serial creatinine and electrolytes, as transient rises may occur with decongestion but warrant adjustment if exceeding 50% baseline). These risks, highlighted in both ESC and AHA guidelines, necessitate multidisciplinary input to mitigate adverse outcomes.^[48]^[3]

Pharmacological therapy

Pharmacological therapy forms the mainstay of management for acute decompensated heart failure (ADHF), targeting congestion relief, hemodynamic stabilization, and preservation of end-organ perfusion. Loop diuretics remain the cornerstone for volume overload, while vasodilators and inotropes address specific hemodynamic profiles, and novel agents like sodium-glucose cotransporter-2 (SGLT2) inhibitors enhance decongestion and support long-term outcomes. Therapy is individualized based on clinical presentation, with close monitoring to prevent complications such as electrolyte disturbances or worsening renal function.^[3]^[49] Diuretics are initiated promptly in patients with signs of fluid retention to promote natriuresis and alleviate symptoms. Intravenous loop diuretics, particularly furosemide, are first-line agents, with an initial bolus dose of 40-80 mg (or 1-2.5 times the prior oral dose if applicable) followed by continuous infusion (e.g., 10 mg/hour) for sustained effect. The Diuretic Optimization Strategies Evaluation (DOSE) trial demonstrated that higher-dose regimens (2.5 times the oral equivalent) achieve greater symptom relief and fluid removal without increasing adverse events, though they may transiently worsen renal function. Monitoring is critical for hypokalemia, hyponatremia, and ototoxicity, especially with high doses exceeding 240 mg/day, and renal function should guide dose adjustments to avoid over-diuresis. In diuretic-resistant cases, adjuncts like thiazide diuretics or acetazolamide (500 mg IV daily, per the ADVOR trial) can enhance decongestion by targeting multiple nephron segments.^[50]^[51]^[49]^[52] Vasodilators are indicated for normotensive or hypertensive ADHF to reduce preload and afterload, particularly in patients with elevated filling pressures but adequate perfusion. Nitroglycerin, administered as an intravenous infusion starting at 10-20 mcg/min and titrated upward by 5-10 mcg/min every 5-10 minutes to a maximum of 200 mcg/min, effectively lowers pulmonary capillary wedge pressure and improves dyspnea. Nitroprusside (0.3-10 mcg/kg/min IV) is an alternative for severe hypertension, offering balanced vasodilation but requiring arterial line monitoring due to its short half-life and cyanide toxicity risk at high doses. These agents are contraindicated in hypotension (systolic blood pressure <90 mmHg) and should be used cautiously with invasive hemodynamic guidance when available.^[3]^[53]^[52] Inotropes are reserved for low-output states with hypoperfusion (e.g., cool extremities, elevated lactate) despite adequate filling pressures, aiming to augment cardiac contractility without excessive tachycardia. Dobutamine, a beta-1 agonist, is infused at 2-20 mcg/kg/min IV, starting low and titrating based on cardiac index and blood pressure response; it improves hemodynamics but may provoke arrhythmias or tolerance after 72 hours. Milrinone, a phosphodiesterase-3 inhibitor, offers similar benefits (0.375-0.75 mcg/kg/min IV loading dose optional, then maintenance) with less arrhythmogenicity and added vasodilation, though it risks hypotension in non-hypovolemic patients. Both are short-term bridges, as prolonged use increases mortality, and discontinuation should occur once perfusion stabilizes.^[3]^[53]^[52] Novel therapies have expanded options for ADHF, particularly SGLT2 inhibitors, which promote osmotic diuresis and reduce loop diuretic needs. Dapagliflozin (10 mg daily orally), as recommended in the 2025 HFAI guidelines, facilitates decongestion and shortens hospital stays, with the DICTATE-AHF trial showing a 30% reduction in total diuretic dose (560 mg vs. 800 mg furosemide equivalents) without increasing adverse events. Similarly, empagliflozin (10 mg daily) improves clinical outcomes in hospitalized patients per the EMPULSE trial, which showed superiority on the hierarchical primary outcome (win ratio 1.36, 95% CI 1.09-1.68; P=0.0054) including all-cause mortality, heart failure events, and change in Kansas City Cardiomyopathy Questionnaire total symptom score.^[52]^[54]^[3]^[55] Continuation of renin-angiotensin-aldosterone system inhibitors like ACE inhibitors or angiotensin receptor-neprilysin inhibitors (ARNI, e.g., sacubitril/valsartan 49/51 mg twice daily if tolerated) is advised to sustain guideline-directed medical therapy, though temporary holds may be needed for hypotension or hyperkalemia. These agents are initiated or optimized before discharge when hemodynamically stable.^[52]^[54]^[3] Dosing and titration across all classes are hemodynamically driven, with serial assessments of blood pressure, heart rate, urine output (>0.5 mL/kg/hour target), and biomarkers like natriuretic peptides guiding adjustments. Hypotension precludes vasodilators and inotropes, while renal impairment may necessitate dose reductions; multidisciplinary input ensures safe escalation or de-escalation.^[49]^[3]

Advanced interventions

In patients with acute decompensated heart failure (ADHF) who do not respond to initial pharmacological stabilization, advanced interventions are indicated for refractory congestion, persistent hypotension, hypoxemia, or cardiogenic shock, as outlined in the 2022 AHA/ACC/HFSA guidelines and 2021 ESC guidelines.^[3]^[56] These approaches escalate to non-pharmacological support to address life-threatening complications while bridging to recovery or definitive therapies. Ventilation support is recommended for ADHF patients with respiratory distress or hypoxemia to improve oxygenation and alleviate work of breathing. Non-invasive ventilation (NIV), such as continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), is preferred initially for acute cardiogenic pulmonary edema, providing faster symptom relief including reduced dyspnea and heart rate compared to standard oxygen therapy, though it does not reduce short-term mortality.^[57] In cases of severe respiratory failure or NIV intolerance, mechanical ventilation via endotracheal intubation is required to support gas exchange and prevent further decompensation.^[56] For diuretic-resistant congestion, extracorporeal ultrafiltration serves as an alternative to remove isotonic fluid overload via venovenous access, typically at rates of 100-500 mL/hour (0.1-0.5 L/hour), depending on patient tolerance and device settings.^[58] This therapy is particularly useful in hypervolemic ADHF with renal impairment, leading to greater net fluid and weight loss than intravenous diuretics, as demonstrated in the UNLOAD trial, with reduced 90-day heart failure readmissions.^[59] However, it carries risks of hypotension and worsening renal function, limiting its routine use to select refractory cases per guidelines.^[3] Temporary mechanical circulatory support devices are employed in high-risk ADHF with cardiogenic shock to augment cardiac output and stabilize hemodynamics. The intra-aortic balloon pump (IABP), inserted percutaneously, provides counterpulsation to reduce afterload and improve coronary perfusion, but recent evidence from the 2025 Altshock-2 trial indicates that early routine use does not improve 60-day survival or bridging to advanced therapies compared to standard care in heart failure-related shock.^[60] Indications remain for bridging in select patients with persistent hypotension despite inotropes.^[56] Surgical options target underlying structural or ischemic causes in refractory ADHF. Revascularization via percutaneous coronary intervention or coronary artery bypass grafting is considered for patients with ischemia contributing to decompensation, potentially improving myocardial function and outcomes in ischemic cardiomyopathy, though benefits are more established in chronic settings than acute.^[61] Valve repair or replacement addresses severe valvular disease exacerbating failure. For end-stage cases, left ventricular assist device (LVAD) implantation offers bridge-to-transplant or destination therapy, enhancing survival and quality of life in advanced heart failure ineligible for transplantation, as supported by trials like REMATCH and ongoing evaluations.^[62]^[3] These interventions require multidisciplinary evaluation in specialized centers.

Prognosis and Prevention

Outcomes and prognosis

Acute decompensated heart failure (ADHF) carries significant short-term risks, with in-hospital mortality rates typically ranging from 4% to 7%.^[63] This rate escalates substantially in patients with cardiogenic shock complicating ADHF, where in-hospital mortality can reach 20% to 40% or higher, reflecting the severity of hemodynamic compromise.^[64] Factors contributing to these outcomes include delays in recognition, underlying comorbidities, and limitations in advanced therapies during acute episodes. Post-discharge, readmission remains a major challenge, occurring in approximately 20% to 30% of patients within 30 days and up to 50% within 6 months, often due to recurrent fluid overload or worsening symptoms.^[65]^[66] Long-term survival is also guarded, with 1-year mortality approximately 20-25% following hospitalization (75-80% alive), though this varies by ejection fraction; outcomes are generally worse in heart failure with reduced ejection fraction (HFrEF) compared to preserved ejection fraction (HFpEF), driven by higher rates of cardiovascular death in HFrEF.^[1] These patterns underscore the chronic trajectory of ADHF, where initial decompensation often signals progressive disease. Several prognostic factors reliably predict adverse outcomes in ADHF. Advanced age greater than 75 years is associated with increased mortality risk due to reduced physiological reserve and higher comorbidity burden.^[67] Renal dysfunction, commonly manifested as elevated blood urea nitrogen or worsening renal function during admission, correlates with poorer short- and long-term survival by exacerbating fluid retention and neurohormonal activation.^[68] Hyponatremia, defined as serum sodium below 135 mEq/L, portends higher in-hospital and post-discharge mortality, reflecting vasopressin-mediated volume dysregulation.^[69] Elevated cardiac troponin levels, even without acute coronary syndrome, indicate myocardial injury and are linked to greater disease severity and worse prognosis.^[2] Risk stratification tools enhance outcome prediction in ADHF. The ADHERE risk score, derived from the Acute Decompensated Heart Failure National Registry, uses variables such as blood urea nitrogen, systolic blood pressure, and serum sodium to estimate in-hospital mortality, categorizing patients into low (2.1%), intermediate (5.7%), and high (21.9%) risk groups.^[40] For longer-term forecasting, the MAGGIC (Meta-Analysis Global Group in Chronic Heart Failure) score incorporates age, ejection fraction, and comorbidities to predict 1- and 3-year mortality, aiding in personalized follow-up planning.^[70] These validated models support clinical decision-making without replacing comprehensive assessment.

Strategies for prevention and follow-up

Effective discharge planning is a cornerstone of preventing recurrent episodes of acute decompensated heart failure (ADHF), involving multidisciplinary teams that include cardiologists, nurses, pharmacists, and social workers to address patient education, medication reconciliation, and follow-up scheduling. Key components encompass teaching patients to monitor daily weights and recognize early signs of fluid retention, such as a 2-3 kg gain over 2-3 days, alongside adherence to a low-sodium diet limited to 1.5-2 g per day to mitigate volume overload. This structured approach ensures seamless transitions from hospital to home, reducing the risk of immediate post-discharge complications.^[71] Optimization of guideline-directed medical therapy (GDMT) post-discharge is essential for long-term prevention, focusing on rapid up-titration of evidence-based agents such as beta-blockers, angiotensin receptor-neprilysin inhibitors (ARNIs), and mineralocorticoid receptor antagonists (MRAs) within the first few weeks after hospitalization. According to the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure with 2024 focused update, initiating or intensifying these therapies, including sodium-glucose cotransporter-2 inhibitors (SGLT2is) for all heart failure phenotypes, can reduce hospitalization risk by up to 25-30% when achieved early.^[3] Multidisciplinary clinics, often pharmacist-led, facilitate this process through scheduled dose adjustments and monitoring for tolerability, targeting full therapeutic doses to improve ejection fraction and symptoms.^[72] Remote monitoring via telehealth and wearable devices enables early detection of decompensation by tracking vital signs like weight, blood pressure, and heart rate, prompting timely interventions to avert readmissions. Home-based telemonitoring programs have demonstrated up to a 44% reduction in heart failure hospitalizations through daily self-reports and automated alerts for anomalies, such as unexplained weight fluctuations.^[73] These strategies, integrated into post-discharge care, enhance patient engagement and allow for virtual follow-up visits, particularly beneficial for rural or mobility-limited individuals.^[74] Lifestyle interventions play a pivotal role in prevention, with cardiac rehabilitation programs incorporating supervised exercise training to improve functional capacity and reduce recurrent ADHF risk by enhancing endothelial function and muscle strength. Aerobic exercises, such as walking or cycling for 30-45 minutes most days, combined with resistance training, yield improvements in peak oxygen uptake by 10-20% and quality of life scores.^[75] Additionally, annual vaccinations against influenza and pneumococcal infections are recommended to prevent respiratory triggers of decompensation, as these illnesses can precipitate fluid overload in vulnerable patients.^[76] Transitional care models, such as nurse-led clinics or comprehensive post-discharge programs, effectively reduce 30-day readmission rates by 20-30% through coordinated follow-up, including home visits, medication education, and comorbidity management. These interventions address barriers like socioeconomic factors and non-adherence, with evidence showing sustained benefits in all-cause mortality and healthcare costs when implemented within 7-14 days of discharge.^[77] By targeting high-risk patients identified during hospitalization, such models promote sustained GDMT adherence and self-management, ultimately lowering the cycle of recurrent ADHF episodes.^[78]

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