Kriti Puri, MBBS, is a pediatric cardiologist and cardiac intensive care physician with Texas Children’s Hospital and an assistant professor at the Baylor College of Medicine.

A new proposed definition of cardiogenic shock in pediatric patients may pave the way for improved intervention and outcomes for this notoriously underrepresented condition.

Recognizing, Diagnosing, and Managing Pediatric Cardiogenic Shock

Despite being heavily studied in adult patients, there is still very little evidence regarding cardiogenic shock in pediatric patients. A 2023 study published in the Journal of the American College of Cardiology investigated the incidence, epidemiology, and outcomes of cardiogenic shock in pediatric patients – this study found that the disease occurs in roughly 26% of pediatric hospitalizations for 

 and is independently associated with hospital mortality.

To address this issue, Kriti Puri, MBBS, a pediatric cardiologist and cardiac intensive care physician with Texas Children’s Hospital and an assistant professor at the Baylor College of Medicine, and colleagues proposed a new definition for the disease in pediatric patients, as well as providing suggestions on each step of the treatment process for this underrepresented condition.

“The definition that we propose in this statement basically just encourages clinicians to think of the heart, especially if they have a patient that is in undifferentiated shock without prior known cardiac history,” Puri told 

 in an exclusive interview. “And then if there is that suspected cardiac dysfunction, and they have evidence of hypoperfusion, clinicians should really consider it as cardiogenic shock unless proven otherwise and utilize those principles of management.”

Puri and colleagues searched the limited existing literature regarding pediatric cardiogenic shock, collating existing data into the current document. The team noted that this literature is intrinsically limited by small sample sizes and selection bias. Larger cohort studies typically examined patients with ADHF – these documents may not always distinguish between patients with early or beginning cardiogenic shock and those with more extreme severity, potentially leading to invasive circulatory or respiratory support.

From the existing data, Puri and colleagues developed a classification system for cardiogenic shock, constructed similarly to the Society of Cardiovascular Angiography and Imaging (SCAI) classification for adults. In the present system, patients with known or suspected cardiac dysfunction are considered at risk, while those with evidence of derangement of vital signs or hemodynamics from baseline and symptoms have beginning cardiogenic shock. Patients with evidence of hypoperfusion, with or without hypotension, are in classic cardiogenic shock, while those who have received an intervention but are continuing to worsen are in stage D, or deteriorating, cardiogenic shock. Patients presenting or deteriorating to circulatory collapse requiring resuscitation are in stage E.

Puri and colleagues also established a diagnostic process for cardiogenic shock, including a physical examination for congestion or low cardiac output. The team recommends chest radiographs and electrocardiograms, which provide insight rapidly into the cause of cardiogenic shock. Additionally, near-infrared spectroscopy, when possible, may be useful in evaluating regional capillary-venous hemoglobin saturation.

In regard to monitoring, Puri and colleagues recommend the establishment of durable/central venous access and the placement of an arterial line to monitor adequacy of cardiac output, tissue perfusion, and arterial oxygen content. Additionally, the team suggests central venous oxygen saturation sampling and NIRS.

The authors note that management of pediatric cardiogenic shock should focus on hemodynamic optimization, aiming to restore adequate oxygen delivery to peripheral tissues while minimizing oxygen use. They also point out that initial management often occurs in an emergency department or another noncardiac intensive care setting – to this end, Puri and colleagues indicate that therapy should largely focus on facilitating transfer to a higher level of care.

Ultimately, despite the depth and specificity of the document, Puri and colleagues note the need for further research to further tailor these recommendations. Locating biomarkers of cardiogenic shock, as well as delineating phenotypes and optimizing interventions, are critical next steps for the refinement of this preliminary definition.

“The proposed definition and classification system, while they are new and while we have adapted them from data that have previously shown that they are valid, there is probably room for further finessing,” Puri said. “We are the first to admit that pediatrics still needs a lot of studies on the true phenotypes of pediatric cardiogenic shock, the impact of inflammation, and the impact of socioeconomic determinants of health as a risk modifier. These are the aspects that still need more data.”

Editors’ Note: Puri reports no relevant disclosures.

Puri K, Allen K, Jentzer J, et al. Surviving pediatric cardiogenic shock: Clinical approach, improving outcomes, and future directions: A scientific statement from the American Heart Association. 

Puri K, Jentzer JC, Spinner JA, et al. Clinical presentation, classification, and outcomes of cardiogenic shock in children. Journal of the American College of Cardiology. 2024;83(5):595-608. 

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Kriti Puri, MBBS, and colleagues have developed a preliminary definition and treatment strategy for this underrepresented disease.

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Bimekizumab demonstrated efficacy in patients with hidradenitis suppurativa across both the shortest and longest disease duration quartiles.

Patients with shorter disease duration achieved higher rates of stringent response thresholds, including HiSCR75, HiSCR90, HiSCR100, and corresponding IHS4 outcomes, than those with longer disease duration.

The gap in response rates between quartiles widened as efficacy thresholds increased, most pronounced at the highest benchmarks assessed.

New pooled 2-year data indicate that patients with 

 who initiated bimekizumab earlier in their disease course achieved higher rates of stringent clinical response than those with longer-standing disease, according to a post hoc analysis discussed by Raj Chovatiya, MD, PhD.

Bimekizumab is a humanized immunoglobulin G1 monoclonal antibody that selectively inhibits interleukin (IL)-17F and IL-17A.

 The analysis used pooled 96-week data from the phase 3 BE HEARD I and BE HEARD II trials and their open-label extension, BE HEARD EXT, stratifying patients into disease duration quartiles to explore whether earlier intervention affects long-term outcomes.

BE HEARD EXT: Bimekizumab Shows Greater Benefit With Earlier Use in HS

Chovatiya, founder and director of the Center for Medical Dermatology + Immunology Research and associate professor at Rosalind Franklin University Chicago Medical School, spoke in this 

 interview about the analysis, framing it around a window-of-opportunity hypothesis common across inflammatory diseases.

How Was the Bimekizumab Disease-Duration Analysis Designed?

Patients enrolled in BE HEARD I and II received placebo or bimekizumab before all participants transitioned to open-label bimekizumab. Those completing the initial 48-week period could enroll in the extension study, receiving bimekizumab dosed every 2 or 4 weeks based on HiSCR90 achievement. Investigators divided the cohort into disease duration quartiles: the lowest quartile included patients with roughly 2.4 years of disease or less, while the highest quartile included patients with approximately 10.7 years of disease or more.

What Did the Data Show Across Duration Quartiles?

Bimekizumab demonstrated efficacy across both the shortest and longest disease duration quartiles, consistent with prior analyses and real-world experience. However, when examining stringent efficacy thresholds, including HiSCR75, HiSCR90, and HiSCR100, as well as corresponding IHS4 response thresholds, the proportion of patients achieving these outcomes was consistently greater among those in the lowest disease duration quartile. This gap widened further as response thresholds increased, becoming most pronounced at the highest efficacy benchmarks assessed.

Disclosures: Chovatiya previously reported serving as an advisor, consultant, speaker, and/or investigator for AbbVie, Amgen, Apogee Therapeutics, Arcutis, Argenx, ASLAN Pharmaceuticals, Beiersdorf, Boehringer Ingelheim, Bristol Myers Squibb, Cara Therapeutics, Dermavant, Eli Lilly and Company, FIDE, Formation Bio, Galderma, Genentech, GSK, Incyte, LEO Pharma, L’Oréal, Nektar Therapeutics, Novartis, Opsidio, Pfizer Inc., Regeneron, RAPT, Sanofi, Sitryx, and UCB.

Chovatiya R, Alavi A, Miyagawa T. Bimekizumab 2-year efficacy by hidradenitis suppurativa duration: BE HEARD EXT results. J Eur Acad Dermatol Venereol. 

Chovatiya R. Bimekizumab efficacy by disease duration and severity in moderate to severe hidradenitis suppurativa: 3-year phase 3 results from BE HEARD EXT. 2026. AAD. #73498.

Pooled 2-year data show bimekizumab drove greater high-threshold HS responses in patients with shorter versus longer disease duration.

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Ronald D’Agostino, DO, is a cardiologist affiliated with networks such as NYU Langone Health and Catholic Health Long Island.

The 2026 ACC Expert Consensus Decision Pathway repositions HFpEF management around a 2-drug backbone of SGLT2 inhibitors and nonsteroidal MRAs, diverging from the 4-pillar HFrEF regimen built on ACE inhibitors, ARBs, ARNIs, and beta-blockers.¹ Finerenone is now favored over spironolactone as the MRA of choice, and beta-blockers are reserved for atrial fibrillation, arrhythmia, or post-MI indications rather than routine use.¹ In patients with a BMI of 30 kg/m² or higher, the pathway recommends semaglutide or tirzepatide to address visceral adiposity, drawing on STEP-HFpEF and SUMMIT trial data.¹

The updated pathway also reframes HFpEF as a multisystem syndrome requiring coordinated management of obesity, sleep apnea, diabetes, and CKD rather than cardiology-only oversight.¹ Diuretics remain useful for volume overload but are directed toward as-needed rather than fixed daily dosing.¹ Early recognition remains a persistent barrier in office practice.

The H2FPEF score estimates the probability of HFpEF in symptomatic patients using 6 clinical and echocardiographic variables.² It gives office-based clinicians a structured tool to move past reflexive within-normal-limits readings and pursue BNP testing, echocardiography, or cardiopulmonary stress testing.² Five-year mortality for both HFrEF and HFpEF approaches 75% once patients reach the emergency department in decompensated heart failure, underscoring the value of earlier, stage A intervention.

These themes anchored “Getting to the Heart of the Matter: Recognition to Treatment Optimization of Heart Failure”, a clinical forum focused on cardiovascular risk factors, phenotype-guided staging, and evidence-based pathways to slow heart failure progression, moderated by Ronald D'Agostino, DO.

Following the forum, D'Agostino spoke with 

 to recap the discussion and expand on how the updated pathway changes daily practice. Below, he shares his perspective on phenotype-specific treatment and multidisciplinary comorbidity management.

: What is the single biggest change in the updated heart failure guidelines clinicians need to know?

The recent HFpEF guidelines focus on SGLT2 inhibitors and nonsteroidal MRA as the backbone of treatment for HFpEF, which is different from the general heart failure guidelines, which have mostly focused on HFrEF and emphasized the 4 pillars of therapy: ACE inhibitor, ARB, or ARNI therapy, beta-blocker therapy, SGLT2 inhibitors, and MRA in general, emphasizing nonsteroidal agents. To me, that's a very big change: 2-pronged rather than 4-pronged, focusing on nonsteroidal MRA and SGLT2 rather than ACE inhibitor, ARB, or ARNI and beta-blocker, and even saying to probably avoid beta-blockers unless there is some compelling reason to use them, such as AFib or other arrhythmias that require beta-blocker therapy, or post-MI. The focus and emphasis are different because they represent different disease states, and the guidelines emphasize that in the management.

The other thing I think is very important with the new guidelines is the focus on comorbidities, especially obesity, using GLP-1 therapy, not just for the obesity per se or the diabetes or the sleep apnea, but also for the heart failure benefit if patients are treated with a GLP-1 therapy, or are obese, or diabetic, or have sleep apnea, or are on CPAP. It's a big change in how we approach HFpEF, definitely multifactorial. You often need a team approach, not just one doctor. You need obesity management, endocrinology. A lot of these patients have CKD, so you need to involve nephrology, nutritional guidance, and exercise. Really focusing on it takes a village. That, to me, is a big change from the traditional guidelines.

: How can office-based clinicians use tools like the H2FPEF score to catch heart failure earlier?

I think that was a great addition to the guidelines. The H2FPEF score helps you think about it. When you think of a patient who is heavy, has hypertension, or is elderly, the point score is helpful. Many patients will fall into that moderate risk category, and many are high risk. It helps you think about the condition and look for it, and maybe draw a BNP or do an echo, rather than just describe their symptoms of dyspnea on exertion, fatigue, deconditioning, or obesity. It helps you think of HFpEF, address it, look for it, and then manage it.

I always tell my students, a very popular acronym is WNL. It's popular to say WNL, like when you read any EKG or lab report, you'll see WNL a lot, and it traditionally means within normal limits, whether it's blood work, an EKG, or any kind of testing. But what I tell my students, and they always answer that way because that's how they're trained, is that what it really means is we never looked. If you don't look, you don't find. I think the H2FPEF score helps you look, because it opens your eyes to the possibility a patient has HFpEF, and that maybe you should do a BNP, an echo, or a cardiopulmonary stress test to try to identify and treat it.

: How central is a comorbidity-first approach to moving the needle on heart failure outcomes?

I think it's very important. It's a pyramid. By the time the patient gets to the top of the pyramid and ends up in the ER with heart failure, as I highlighted in the presentation, the morbidity and mortality are very high. Five-year mortality is around 75%, whether it's HFrEF or HFpEF, so if you wait for the patient to end up in the ER in pulmonary edema, the prognosis is very poor. We discussed that at the meeting. But if you could identify earlier, at the bottom of the pyramid, a Class A patient who doesn't really have heart failure but has risk factors for it, comorbidities like obesity, hypertension, sleep apnea, and diabetes, and then address and treat the foundation, the prognosis will be better.

: What is one takeaway you want every clinician to change in their practice tomorrow?

Treating HFpEF differently than HFrEF. It's a different animal, and we shouldn't be using the traditional therapies unless they're needed for other comorbidities as the initial approach. So the main one would be: identify. If I had to say number one, look for HFpEF, and two, don't treat it like HFrEF. It's a different algorithm, focusing on SGLT2 inhibitors and nonsteroidal MRAs, and there's only one MRA available right now. That was the key takeaway. Use beta-blockers if needed for issues like post-MI or AFib. Use ACE inhibitors, ARBs, or ARNIs if patients are still having heart failure, are still hypertensive, or their BNP is still high, as add-on therapy. Use diuretics judiciously, like furosemide. Don't just put everyone on 40 mg of furosemide, but use it if needed for fluid overload or edema, maybe on an as-needed basis rather than daily. The takeaway is to treat it differently. The guidelines are different for both conditions. Don't just apply the reduced-EF data that we traditionally use for HFrEF to treat HFpEF or HFmrEF, the mildly reduced ejection fraction group, as well.

Editor's Note: This transcript has been edited for grammar and clarity using AI tools.

Kittleson MM, Panjrath GS, Bates K, et al. Management of heart failure with preserved ejection fraction: 2026 ACC expert consensus decision pathway: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. Published online July 23, 2026. doi:

Reddy YNV, Carter RE, Obokata M, Redfield MM, Borlaug BA. A simple, evidence-based approach to help guide diagnosis of heart failure with preserved ejection fraction. Circulation. 2018;138(9):861-870. doi:

Articles

The 2026 ACC pathway distinguishes HFpEF as a phenotype requiring its own treatment algorithm, centered on SGLT2 inhibitors plus a nonsteroidal MRA, with finerenone preferred and beta-blockers limited to clear indications (eg, AF, arrhythmias, post-MI). Management expands beyond cardiology to systematic comorbidity control—obesity, diabetes, sleep apnea, and CKD—with GLP-1/GIP-based agents recommended for BMI ≥30 kg/m². Earlier identification is emphasized using the H2FPEF score to trigger BNP, echocardiography, or stress testing, aiming to intervene before decompensation.

Ronald D'Agostino, DO, discusses the 2026 HFpEF pathway, H2FPEF screening, and comorbidity-first heart failure care.

Rethinking HFpEF Screening and Care, With Ronald D'Agostino, DO

Andrew Mastro, MS, PA-C, is a board-certified PA and guest lecturer at both Rush University and Northwestern University. 

In ‘Choosing the Right Plaque Psoriasis Patient for Icotrokinra,’ our panel explores real-world case selection.

Choosing the Right Plaque Psoriasis Patient for Icotrokinra

Andrew Mastro, MS, PA-C, asks Alexa Hetzel, MS, PA-C, to describe the patient profile she has in mind when reaching for icotrokinra. Hetzel says she is cautious about heavy joint involvement given the limited joint-specific data available so far, but describes strong outcomes in patients who were stuck on topical therapy, wanted an oral option, and had not found existing orals compelling enough to switch. She recounts steering a patient with severe scalp psoriasis away from greasy topical regimens and toward icotrokinra, citing the trajectory she now expects to share with patients: over 40% improvement by four weeks, 87% improvement by week 16, and close to 90% by week 24.

Hetzel then shares a case of a patient who had been treated for atopic dermatitis with an injectable biologic but told Hetzel she no longer wanted an injection. A biopsy confirmed classic psoriasis rather than atopic dermatitis, and Hetzel offered icotrokinra as a once-daily alternative. The patient returned a month later with only residual redness from the biopsy site itself, emotional at having her skin, and her summer, back after a period of misdiagnosis. Mastro notes the confidence required to stand behind that kind of recommendation with a patient who had already been through an unsuccessful treatment course.

The conversation then flips to the opposite question: which patients still warrant a biologic or a different oral agent. Hetzel says patients already doing well on deucravacitinib or apremilast have no reason to switch, and that insurance coverage for deucravacitinib has become inconsistent in her New Jersey market, which factors into new-start decisions. She leans toward a biologic for patients with significant joint involvement or a personal or family history of inflammatory bowel disease, often coordinating with a gastroenterology colleague, and for patients who simply want the lowest-effort regimen, since an infrequent injectable visit can be easier for some patients to manage than a daily pill.

In the next episode, ‘Positioning Icotrokinra as First-Line Therapy for Plaque Psoriasis,’ the panelists make the case for icotrokinra as a true first-line option and share their top practice-changing takeaways.

Andrew Mastro, MS, PA-C, asks Alexa Hetzel, MS, PA-C, to describe the patient profile she has in mind when reaching for icotrokinra.

Jay Lieberman, MD, from University of Tennessee

 recognition criteria have not been updated to reflect infant-specific presentations, even as newer international definitions already incorporate them.¹ A recent review found modified age-specific criteria improved detection by 23% in infants and 10% in toddlers compared with standard criteria.² The review also identified drooling, back arching, belly breathing, and tongue-thrusting as additional infant-specific presenting signs worth incorporating into recognition criteria.¹

A companion review found caregiver recognition and confidence gaps, not epinephrine access alone, drive delayed treatment, and 48% of caregivers in a surveyed cohort withheld epinephrine because they did not believe symptoms were severe enough.² Parents who watch a clinician administer epinephrine during a supervised reaction, such as a food challenge, report greater comfort giving it on their own afterward.² Caregivers with a written anaphylaxis action plan were also more likely to use epinephrine.²

In the following Q&A, Jay Lieberman, MD, professor at the University of Tennessee Health Science Center and program director of the Allergy/Immunology Fellowship Program at Le Bonheur Children's Hospital, discusses recognizing anaphylaxis in young children and closing the epinephrine treatment gap.

Q&A: Anaphylaxis Recognition and Epinephrine Use, With Jay Lieberman, MD

What's the single biggest clinical takeaway from these papers for clinicians treating infants and toddlers?

Vomiting (often mistaken for minor illness)

 Infants and toddlers can have different reactions or can look different during severe allergic reactions. We have criteria for symptoms during a reaction that would meet the anaphylaxis definition and…[warrant] epinephrine, [but] infants and toddlers may behave differently, and clinicians need to be aware of [this]. When you see an infant or toddler having a reaction, look for different things to alert you that, wow, this is a multi-systemic allergic reaction or this [is] a more severe allergic reaction.

What behavior patterns signal a severe allergic reaction in nonverbal infants and toddlers?

 Infants can't speak to tell you [what's happening], so they behave differently. They may be more fussy, they may be crying, they may be inconsolable. They can shove a finger in their mouth as a sign they're having an itchy mouth or throat… [or tug] at an ear as a sign of itching inside the ear canal. These are all signs they’re having an allergic reaction.

Which signs and symptoms do clinicians most often overlook as allergic reaction indicators in this age group?

 In older kids, GI symptoms like vomiting. Often, [clinicians] may think the child just ate something bad. When I'm doing a challenge [in an infant and that] infant starts acting funny, my radar goes up, and I start looking a little more into it.

The review found that modified age-specific criteria improved anaphylaxis detection by 23% in infants and 10% in toddlers compared with the standard criteria. What does that mean in practice for an allergist evaluating a nonverbal patient?

 They can use whichever criteria they want. As an allergist in practice, often we're not doing the check boxes of “okay, they meet this, they meet this.” I'm going to go ahead and give them epinephrine. It's more of a clinical feel for a lot of us.

 Your review cites a survey in which 48% of caregivers didn't use epinephrine because they didn't believe symptoms were severe enough. How should clinicians reframe that threshold?

 This is an issue at all ages. Underuse of epinephrine has been shown in every study, whether it's infants, toddlers, or adults, and epinephrine was more often used the older the child is. Infants shouldn't be treated any differently. If we think they're having anaphylaxis, they should get epinephrine.

It's fascinating when a clinician goes through giving epinephrine with a parent during a reaction, such as during a food challenge in [the] clinic…parents feel more comfortable giving epinephrine on their own [afterward]. All these education pieces, showing parents it's not a big deal and it's not harmful, [may contribute to the increase in] epinephrine use.

What should epinephrine training look like for daycare staff, school nurses, and other community caregivers?

 Whatever training we can get helps, [whether] that's a physician or nurse practitioner going to a school district to talk with school nurses…videos that teach [parents and staff] about this…[or] parent volunteers [to] go into schools and give education on food allergy and epinephrine use.

What system-level or policy changes would have the biggest impact on closing this treatment gap?

 The best evidence we have, now incorporated into our allergy anaphylaxis practice parameters, [supports] stock epinephrine. [That] means a school, for example, can have epinephrine available without a prescription that any child can use, whether or not we knew they had a food allergy or a bee sting allergy. It’s the same idea as having defibrillators in stadiums that anyone can use if someone has a heart attack.

Is there anything else clinicians should know about anaphylaxis in young children?

 Newer [food allergy] guidelines suggest early introduction of allergenic foods, even something like peanut, which we used to say don’t feed kids and now say to feed as early as 6 months. Greater education and awareness will be very helpful.

Age-Specific Criteria Improve Anaphylaxis Detection in Infants

Stock Epinephrine Could Close Anaphylaxis Care Gap, With Jay Lieberman, MD

Pistiner M, et al. Recognizing and Treating Serious Allergic Reactions (Anaphylaxis) in Infants and Toddlers: A Plain Language Review of Four Studies. 

Leeds S, Anagnostou A, Pistiner M, et al. Epinephrine Underuse for Anaphylaxis in Infants and Toddlers: A Practical Review for Pediatricians. 

Infants and toddlers frequently manifest anaphylaxis with age-specific, nonverbal behaviors that are not fully captured by traditional recognition criteria. Incorporating modified pediatric criteria and infant-predominant signs—such as drooling, back arching, belly breathing, and tongue-thrusting—can meaningfully improve detection. Delayed epinephrine use is driven more by caregiver misperception of severity and lack of confidence than by access alone. Supervised epinephrine administration, written action plans, and structured community training improve readiness, while stock epinephrine policies can reduce system-level barriers.

Lieberman discusses atypical anaphylaxis signs in infants and toddlers and why epinephrine remains underused.

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In part 2, Lieberman discusses why caregivers hesitate to use epinephrine and what system-level changes could close the gap in infants and toddlers.

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Rethinking HFpEF Screening and Care, With Ronald D'Agostino, DO

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