# Septic Cardiomyopathy: Age-Dependent Physiology and Hemodynamic Aspects—A Narrative Review

**Authors:** Marianna Miliaraki, George Briassoulis, Evangelia Dardamani, Panagiotis Briassoulis, Stavroula Ilia

PMC · DOI: 10.3390/children13020239 · 2026-02-08

## TL;DR

Sepsis-induced cardiomyopathy (SCM) affects children and adults differently, requiring tailored cardiovascular assessments and management strategies.

## Contribution

This review highlights age-dependent hemodynamic profiles and the need for multimodal diagnostics in managing SCM.

## Key findings

- Adults with SCM often show hyperdynamic vasoplegic states, while children typically exhibit hypodynamic profiles.
- Multimodal diagnostic tools like echocardiography and hemodynamic monitoring improve detection of myocardial dysfunction.
- Pediatric SCM evidence is limited, with treatment strategies largely extrapolated from adult studies.

## Abstract

What are the main findings?
Sepsis-induced cardiomyopathy (SCM) is an acute, reversible, non-ischemic myocardial dysfunction in children and adults, ranging from subclinical biventricular impairment to overt cardiogenic shock.Pediatric SCM often presents with hypodynamic profiles, while adults frequently show hyperdynamic, vasoplegic states, reflecting age-dependent differences in cardiovascular physiology.Multimodal diagnostic approaches, including echocardiography and advanced hemodynamic monitoring, improve detection of subtle or evolving myocardial dysfunction.

Sepsis-induced cardiomyopathy (SCM) is an acute, reversible, non-ischemic myocardial dysfunction in children and adults, ranging from subclinical biventricular impairment to overt cardiogenic shock.

Pediatric SCM often presents with hypodynamic profiles, while adults frequently show hyperdynamic, vasoplegic states, reflecting age-dependent differences in cardiovascular physiology.

Multimodal diagnostic approaches, including echocardiography and advanced hemodynamic monitoring, improve detection of subtle or evolving myocardial dysfunction.

What is the implication of the main findings?
SCM requires repeated, physiology-driven, multi-modal cardiovascular assessment to guide individualized management.Understanding age-specific hemodynamic profiles can help tailor interventions and improve outcomes in both adult and pediatric patients.

SCM requires repeated, physiology-driven, multi-modal cardiovascular assessment to guide individualized management.

Understanding age-specific hemodynamic profiles can help tailor interventions and improve outcomes in both adult and pediatric patients.

Background: Septic cardiomyopathy (SCM) is a dynamic and heterogeneous complication of sepsis, driven by systemic inflammation, autonomic dysregulation, and microcirculatory alterations. Pediatric and adult patients share common pathophysiologic mechanisms, but age-dependent differences in cardiovascular physiology produce distinct hemodynamic responses. Methods: A structured narrative review of clinical and experimental studies published between 2000 and 2025 was conducted via PubMed and major critical care literature. Studies were included if they addressed SCM pathophysiology, hemodynamic monitoring, and therapeutic strategies across age groups, while studies focusing on non-septic cardiac dysfunction were excluded. Results: Adult SCM often presents as hyperdynamic, vasoplegic states, whereas pediatric patients more frequently exhibit hypodynamic profiles, reflecting developmental differences in myocardial reserve and autonomic regulation. Evidence suggests that isolated conventional echocardiographic parameters may underestimate myocardial impairment, whereas advanced modalities, including myocardial strain echocardiography and multimodal hemodynamic monitoring, may serve as complementary tools to detect subtle or evolving myocardial dysfunction. Pediatric evidence remains limited, and therapeutic guidance is largely extrapolated from adult studies. Conclusions: SCM should be approached as a time-dependent, physiology-driven condition, requiring repeated, integrated multimodal cardiovascular assessment to guide individualized management. Age-specific hemodynamic profiles highlight the need for standardized diagnostics, prospective validation of monitoring tools, and phenotype-guided interventions to improve outcomes in both adult and pediatric sepsis.

## Linked entities

- **Diseases:** cardiomyopathy (MONDO:0004994)

## Full-text entities

- **Genes:** CASP1 (caspase 1) [NCBI Gene 834] {aka ICE, IL1BC, P45}, NLRP3 (NLR family pyrin domain containing 3) [NCBI Gene 114548] {aka AGTAVPRL, AII, AVP, C1orf7, CIAS1, CLR1.1}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}
- **Diseases:** hyperlactatemia (MESH:D065906), cardiac abnormalities (MESH:D018376), Septic Shock (MESH:D012772), septic (MESH:D001170), ischemic coronary syndromes (MESH:D003323), instability (MESH:D043171), Sepsis (MESH:D018805), systolic or diastolic dysfunction (MESH:D054144), heart failure (MESH:D006333), myocardial depression (MESH:D003866), tricuspid regurgitation (MESH:D014262), hyperdynamic vasoplegia (MESH:D056987), Myocardial dysfunction (MESH:D006331), LV and RV dysfunction (MESH:D018497), myocardial infarction (MESH:D009203), cardiovascular dysfunction (MESH:D002318), biventricular dilatation and dysfunction (MESH:D002311), infection (MESH:D007239), myocardial ischemia (MESH:D017202), Post (MESH:D000094025), cardiac output (MESH:D002303), base deficit (MESH:D019292), end-organ damage (MESH:C564816), Myocardial involvement (MESH:C564676), congenital heart disease (MESH:D006330), microvascular dysfunction (MESH:D017566), left ventricular (LV) hypokinesia (MESH:D018476), Takotsubo cardiomyopathy (MESH:D054549), mitochondrial dysregulation (MESH:D021081), cardiotoxicity (MESH:D066126), hypotension (MESH:D007022), hypoxemia (MESH:D000860), ventricular dilatation (MESH:C566255), LV diastolic dysfunction (MESH:D018487), Arrhythmias (MESH:D001145), multi-organ failure (MESH:D009102), tachycardia (MESH:D013610), Myocardial (MESH:D009202), stroke (MESH:D020521), myocarditis (MESH:D009205), hypercapnia (MESH:D006935), impaired (MESH:D060825), pump failure (MESH:D051437), cardiogenic shock (MESH:D012770), endothelial dysfunction (MESH:D014652), ischemic (MESH:D002545), myocardial stunning (MESH:D017682), pulmonary edema (MESH:D011654), myocardial edema (MESH:D004487), preserved (MESH:C537758), Biventricular dysfunction (MESH:D018754), injury to (MESH:D014947), disease (MESH:D004194), circulatory collapse (MESH:D012769), Inflammatory (MESH:D007249), LV dilatation (MESH:C565277), fibrosis (MESH:D005355), cardiogenic dysfunction (MESH:D013575), LV outflow tract obstruction (MESH:D000092242), mitochondrial (MESH:D028361)
- **Chemicals:** esmolol (MESH:C036604), calcium (MESH:D002118), carbon dioxide (MESH:D002245), catecholamine (MESH:D002395), dexmedetomidine (MESH:D020927), aCO2 (-), Dobutamine (MESH:D004280), norepinephrine (MESH:D009638), methylene blue (MESH:D008751), lactate (MESH:D019344), landiolol (MESH:C077049), oxygen (MESH:D010100)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939386/full.md

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Source: https://tomesphere.com/paper/PMC12939386