Pediatric Acute Decompensated Heart Failure: Recognition, Management, and the 2026 AHA Scientific Statement

Summary

• Congenital heart disease drives most pediatric heart failure (HF) presentations: 46.6% of HF emergency department (ED) visits and 62.7% of HF hospitalizations. Dilated cardiomyopathy is the most common cardiomyopathy subtype (approximately 50%), and roughly 40% of children with symptomatic dilated cardiomyopathy transplant or die within 2 years [1].
• Acute decompensated heart failure (ADHF) can mimic septic shock. A hypotensive, tachycardic, poorly perfused child may be cardiogenic, not septic, and aggressive IV fluid boluses can precipitate pulmonary edema and respiratory failure [15,18].
• The modified pediatric SCAI staging system grades cardiogenic shock from Stage A (at risk, mortality approximately 7%) to Stage E (extremis, mortality approximately 36%). About 1 in 4 children with ADHF presents in cardiogenic shock [2,15].
• Milrinone (0.25 to 0.75 µg/kg/min) is the preferred agent for chronic bridging support; epinephrine remains standard for acute resuscitation [15,17].
• Enteral nutrition should start within 48 hours of admission once hemodynamically stable, and parenteral nutrition should be withheld for 7 days if the enteral route is feasible [15].
• Only about 65% of children are discharged on an ACE inhibitor or ARB, and only about 20% receive triple therapy (ACEi/ARB, beta-blocker, MRA). Thirty-day readmission is approximately 20% versus 3.1% in children without HF [1,13].

Caution. In a hypotensive, poorly perfused child with tachycardia, evaluate for cardiogenic shock before reflexively initiating a sepsis fluid-bolus protocol. Fluid loading a child in ADHF can precipitate pulmonary edema and respiratory failure [15].

Epidemiology and Etiology

Pediatric HF is not a scaled-down version of adult HF. Etiology differs fundamentally from the adult population.

• Approximately 40% of children with symptomatic dilated cardiomyopathy undergo transplantation or die within 2 years of diagnosis [1].
• Comorbid HF ED visits nearly doubled between 2012 and 2016 (rate ratio 1.93), and primary HF hospitalizations rose significantly (rate ratio 1.14) [1].
• Compared with adults, children with HF have higher in-hospital mortality and use significantly more advanced therapies, including ECMO, ventricular assist devices (VAD), and cardiac transplantation [1].

Recognition and Initial Assessment

ADHF can present with the same tachycardia, poor perfusion, and altered mental status seen in septic shock. Frontline clinicians should distinguish the two before committing to a sepsis protocol or IV fluid resuscitation [15,18].

Initial assessment should classify the presentation along two axes:

• Low cardiac output: altered mental status, reduced urine output, poor pulses, cool extremities.
• Congestion: jugular venous distention, pulmonary crackles, hepatomegaly, gallop rhythm, peripheral edema.

A patient may show either pattern or both, and each pattern carries distinct management implications [15].

Hemodynamic Profiling

The statement adapts the Stevenson warm/cold, wet/dry framework for pediatric use [15]:

In children, congestion more often shows as tachypnea, grunting, and hepatomegaly; jugular venous distention and peripheral edema become more apparent in older patients. Low perfusion shows as narrow pulse pressure, agitation, poor oral intake, cool extremities, and acute kidney injury [15].

Scoring

SCAI cardiogenic shock stages (modified for pediatrics) [2,15]:

Approximately 1 in 4 children with ADHF presents in cardiogenic shock, and mortality increases in a graded fashion with each stage [2]. Late worsening in shock severity, even after apparent stabilization, is associated with increased mortality, paralleling adult data. Serial reassessment throughout the hospital course is required, not a single admission snapshot [2,15].

Vasoactive burden itself can be tracked quantitatively with the Vasoactive-Inotropic Score (VIS), which correlates with morbidity and mortality after pediatric cardiac surgery [16].

Open the Vasoactive-Inotropic Score Calculator →

Open the Modified Ross Heart Failure Score →

Emergency Department Management

Initial workup [15]:

• Complete blood count, comprehensive metabolic panel, lactate, NT-proBNP or BNP.
• 12-lead ECG to identify arrhythmias.
• Chest radiograph for cardiomegaly and pulmonary congestion.
• Early echocardiography or point-of-care cardiac ultrasound.

NT-proBNP and BNP correlate with ventricular volumes, ventricular function, and worsening functional class in children with congenital heart disease. Normative values are age-dependent and are typically higher in infants [4].

Diuretics. IV loop diuretics are the cornerstone of decongestive therapy. In patients already on chronic diuretics, start IV dosing at 1 to 2.5 times the total oral daily dose, divided every 12 hours, consistent with the DOSE trial approach adopted by the statement [15].

Respiratory support. Noninvasive ventilation (CPAP or BiPAP) can improve oxygenation, reduce respiratory muscle effort, and hemodynamically reduce right ventricular preload and left ventricular afterload [15].

Caution. Use noninvasive ventilation carefully in isolated right heart failure. Positive pressure can increase RV afterload and precipitate decompensation [15].

Intubation risk. Elective or emergent intubation carries a high risk of cardiac arrest in ADHF, driven by sedation-induced hypotension, vagal tone changes, and decreased cardiac output. ECMO team activation for standby has become routine practice at comprehensive pediatric heart centers [9,15].

Vasoactive timing. In an adult acute decompensated heart failure registry (ADHERE), earlier vasoactive administration was associated with better survival and shorter hospital stays [15]. In children, starting vasoactive agents in the emergency department rather than waiting for ICU transfer produces significantly shorter time to initiation [15].

Factors favoring ICU admission (general clinical considerations, not specified in the statement): respiratory distress, unstable arrhythmias, complex congenital heart disease, need for vasoactives or inotropes, or need for narcotics for comfort.

Inotrope Selection

The 2025 AHA/AAP PALS guidelines give a Class 2b recommendation that epinephrine, dopamine, dobutamine, or milrinone may be reasonable as inotropic infusions for pediatric cardiogenic shock [6]. The ADHF statement adds more granular agent selection guidance [15].

Milrinone (phosphodiesterase III inhibitor):

• Starting dose 0.25 µg/kg/min, titrate up to 0.75 µg/kg/min [15,17].
• Increases inotropy, improves lusitropy, decreases systemic and pulmonary vascular resistance [15].
• Long half-life (1 to 4 hours); reduce dose in acute kidney injury [15].
• Retains efficacy with concurrent beta-blockers because its mechanism is independent of beta-adrenergic receptors [15].
• Most commonly used for chronic bridging to transplantation or mechanical circulatory support [15].
• A systematic review found milrinone significantly improved LVEF (weighted mean difference 3.41), cardiac index (WMD 0.50), and serum lactate (WMD -0.59), though whether its benefit is truly inotropic or primarily vasodilatory remains debated [7].
• Long-term IV milrinone (median 27 days) in pediatric dilated cardiomyopathy is safe, with cardiac function recovery in approximately 60% of patients [8].

Open the LV Ejection Fraction Calculator →

Epinephrine:

• Standard of care for resuscitation and rescue of the circulation in pediatric ADHF [15].
• 0.05 to 0.1 µg/kg/min: beta-1 (inotropy) and beta-2 (vasodilation) effects [15].
• Greater than 0.1 µg/kg/min: alpha-adrenergic vasoconstriction predominates [15].
• More potent inotrope than dopamine, with stronger alpha-1 receptor activity [15].
• Risks include tachyarrhythmias and increased myocardial oxygen demand [15].

Dobutamine (2 to 20 µg/kg/min):

• Primarily beta-1 stimulation (inotropy and chronotropy) [15].
• Around 5 µg/kg/min, peripheral beta-2 vasodilation occurs; higher doses cause vasoconstriction [15].
• Short half-life (2 to 3 minutes), rapid onset [15].
• Generally not preferred, due to dysrhythmia risk and tachyphylaxis [15].

Dopamine:

• 3 µg/kg/min: D1 receptor activation, historically described as enhancing renal perfusion, though the ROSE AHF trial showed no benefit of low-dose dopamine for decongestion or renal function [15].
• 3 to 10 µg/kg/min: beta-1 stimulation (inotropy and chronotropy) [15].
• Greater than 10 µg/kg/min: alpha-receptor activation (vasoconstriction) [15].

Clinical pearl. For chronic support (bridge to transplant or mechanical circulatory support), milrinone is favored because it works independently of beta-adrenergic receptors and tolerates concurrent beta-blockade. For acute resuscitation, epinephrine remains first-line [15].

Hemodynamic Monitoring

The European Society of Paediatric and Neonatal Intensive Care consensus, endorsed by the ADHF statement, gives strong agreement for standard invasive measurements: blood pressure, central venous pressure, mixed venous oxygen saturation, serial lactate, clinical perfusion assessment, and near-infrared spectroscopy (NIRS) [15].

• Weak agreement for thermodilution catheters in refractory cardiogenic shock [15].
• Pulmonary arterial catheters to measure cardiac output in children are recommended against [15].
• Pulmonary artery pressure monitoring has shown no benefit in reducing HF hospitalizations in pediatric patients, including in small series of adult Fontan patients [15].

Mechanical Circulatory Support

When ADHF is refractory to medical management, mechanical circulatory support (MCS) is next. The 2025 AHA/AAP PALS guidelines note that early ECMO cannulation of patients requiring invasive ventilation may be associated with improved survival, particularly in myocarditis, where transplant-free survival to discharge ranges from 72% to 80% [6].

ECMO is the most widely used MCS modality globally for pediatric ADHF and provides biventricular and respiratory support. Peripheral cannulation (femoral in older children, cervical in infants) allows rapid deployment. A key limitation is that peripheral ECMO increases LV afterload, potentially hindering ventricular recovery [9].

LV distention on VA-ECMO is a frequent complication from afterload mismatch. Pediatric patients may have worse LV compliance than adults, increasing risk. Evidence includes loss of arterial pulsatility, pulmonary edema, lack of aortic valve opening on echocardiography, or signs of intracardiac stasis. Decompression strategies include balloon atrial septostomy, percutaneous or surgical LV vent placement, or addition of a percutaneous microaxial pump such as Impella [9].

VADs. Durable VAD support has grown substantially in pediatric use. Per the Pediatric Interagency Registry for Mechanical Circulatory Support (Pedimacs), indications include bridge to transplantation (48%), bridge to candidacy (38%), and bridge to recovery (9%) [10].

Myocardial recovery occurs in approximately 5% of adult VAD patients, though pediatric data suggest more favorable results in select populations. One of the largest pediatric studies reported 84% event-free survival and 83% sustained functional capacity Class 1 at 10 years after VAD explantation [10].

Nutrition

Wasting has been reported in up to 86% of children with HF [15]. Priorities:

• Start enteral nutrition within the first 48 hours of admission once hemodynamically stable [15].
• Enteral nutrition supports gut integrity; gastric feeding is preferred for its metabolic and lifestyle benefits [15].
• Withhold parenteral nutrition for 7 days if the enteral route is feasible. A multicenter RCT of 1,440 critically ill children (more than 35% cardiac patients) found withholding early parenteral nutrition clinically superior, with shorter mechanical ventilation, less renal replacement therapy, and shorter hospital stays [15].
• Base nutritional calculations on euvolemic weight (the lowest weight within a 7-day period) to avoid overfeeding during fluid overload [15].

Oral Heart Failure Therapies

Only about 65% of children with ADHF are prescribed an ACE inhibitor or ARB at discharge, and approximately 20% receive triple therapy (ACEi/ARB, beta-blocker, aldosterone antagonist). Prescription rates have not changed significantly over the past decade, representing a major quality improvement target [1,15].

In adults, guideline-directed medical therapy (GDMT) with quadruple therapy (ARNi or ACEi/ARB, beta-blocker, MRA, SGLT2 inhibitor) is standard of care [5,11]. No large pediatric RCTs have consistently identified effective therapies for symptomatic HF, but most pediatric cardiomyopathy patients are treated by extrapolation from adult data: ACE inhibitors (98%), MRAs (79%), and beta-blockers (76%) [3].

• Sacubitril/valsartan (Entresto) is FDA-approved for symptomatic HF with systemic LV systolic dysfunction in children aged 1 year and older [12].
• Safety and efficacy data for SGLT2 inhibitors in pediatric HF are currently lacking [3,15].

Readmission

Readmission rates for pediatric HF are high and have not declined over the past decade [13].

Infants carry the highest readmission risk, and teenage readmission rates are rising. Readmitted children with HF have 7-fold higher mortality and 4.5-fold higher hospital charges than children without HF [13].

Risk factors for readmission [14]:

Behavioral Health

Children with HF carry elevated risk of anxiety, depression, and acute or posttraumatic stress, particularly with prolonged hospital stays. This burden extends to caregivers and family members. The statement recommends regular mental health screening for patients and caregivers, integration of mental health professionals into the cardiac care team, and access to psychotherapy and peer support groups [15].

Care Pathway

The statement proposes a three-phase framework for continuity across the hospital course [15]:

• Emergency Department: Identify hemodynamic profile (low output versus congestion). Obtain BNP or NT-proBNP, chest radiograph, ECG, and echocardiogram. Start IV loop diuretics. Initiate noninvasive respiratory support and vasoactives as needed. Determine ICU admission criteria.
• Intensive Care Unit: Establish hemodynamic monitoring (CVP, NIRS, mixed venous oxygen saturation, arterial blood pressure). Determine cardiogenic shock stage. Assess MCS needs. Use intermittent or continuous loop diuretics. Escalate to intubation with ECMO standby when needed. Start nutrition and rehabilitation. Wean vasoactives and begin oral HF therapies.
• Inpatient Floor: Advance oral HF therapies to therapeutic doses. Continue nutrition and rehabilitation. Obtain surveillance BNP, echocardiogram, and clinical monitoring. Complete discharge planning with an early return appointment within 7 to 14 days.

Open the Acute Heart Failure Workflow →

References

1. Amdani S, Marino BS, Rossano J, et al. Burden of Pediatric Heart Failure in the United States. J Am Coll Cardiol. 2022;79(19):1917-1928.
2. Puri K, Jentzer JC, Spinner JA, et al. Clinical Presentation, Classification, and Outcomes of Cardiogenic Shock in Children. J Am Coll Cardiol. 2024;83(5):595-608.
3. Amdani S, Conway J, George K, et al. Evaluation and Management of Chronic Heart Failure in Children and Adolescents With Congenital Heart Disease: A Scientific Statement From the American Heart Association. Circulation. 2024;150(2):e33-e50.
4. Chowdhury RR, Kaur S, Gera R. N-Terminal Pro-B-Type Natriuretic Peptide as a Marker of Severity of Heart Failure in Children With Congenital Heart Diseases. Pediatr Cardiol. 2023;44(8):1716-1720.
5. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. J Am Coll Cardiol. 2022;79(17):e263-e421.
6. Lasa JJ, Dhillon GS, Duff JP, et al. Part 8: Pediatric Advanced Life Support: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Pediatrics. 2026;157(1):e2025074351.
7. Matsushita FY, Krebs VLJ, de Campos CV, de Vincenzi Gaiolla PV, de Carvalho WB. Reassessing the Role of Milrinone in the Treatment of Heart Failure and Pulmonary Hypertension in Neonates and Children: A Systematic Review and Meta-Analysis. Eur J Pediatr. 2024;183(2):543-555.
8. Brown S, Nolan O, Poole E, et al. Long-Term Milrinone Therapy in Children With Dilated Cardiomyopathy. Acta Paediatr. 2023;112(6):1298-1303.
9. Bhaskar P, Davila S, Hoskote A, Thiagarajan R. Use of ECMO for Cardiogenic Shock in Pediatric Population. J Clin Med. 2021;10(8):1573.
10. Bogle C, Colan SD, Miyamoto SD, et al. Treatment Strategies for Cardiomyopathy in Children: A Scientific Statement From the American Heart Association. Circulation. 2023;148(2):174-195.
11. Ford B, Dore M, Bartlett B. Management of Heart Failure: Updated Guidelines From the AHA/ACC. Am Fam Physician. 2023;108(3):315-320.
12. U.S. Food and Drug Administration. Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations. FDA Orange Book. Accessed 2026.
13. Amdani S, Lopez R, Schold JD, Tang WHW. 30- and 60-Day Readmission Rates for Children With Heart Failure in the United States. JACC Heart Fail. 2024;12(1):83-96.
14. He M, Balbin MT, Kreutzer J, et al. Patient Characteristics Associated With 30-Day Readmission to a Pediatric Cardiac Center. Pediatr Cardiol. 2025 [Epub ahead of print].
15. Cabrera AG, Price JF, Hong BJ, Jeewa A, et al. Evaluation and Management of the Child With Acute Decompensated Heart Failure: A Scientific Statement From the American Heart Association. Circulation. 2026;153:e00-e00.
16. Gaies MG, Gurney JG, Yen AH, et al. Vasoactive-Inotropic Score as a Predictor of Morbidity and Mortality in Infants After Cardiopulmonary Bypass. Pediatr Crit Care Med. 2010;11(2):234-238. doi:10.1097/PCC.0b013e3181b806fc
17. Hoffman TM, et al. Efficacy and Safety of Milrinone in Preventing Low Cardiac Output Syndrome in Infants and Children After Corrective Surgery for Congenital Heart Disease. Circulation. 2003;107(7):996-1002. doi:10.1161/01.CIR.0000051365.81920.28
18. Weiss SL, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children. Pediatr Crit Care Med. 2020;21(2):e52-e106. doi:10.1097/PCC.0000000000002198