Right ventricular dysfunction during induction of anesthesia in an infant with repaired truncus arteriosus: a case report and learning from a potentially preventable adverse perioperative event
- 1Department of Anesthesiology Nursing, West China Second Hospital of Sichuan University, Chengdu, China
- 2Key Laboratory of Birth Deficits and Related Diseases of Women and Children, Sichuan University, Ministry of Education, Chengdu, China
Abstract
Background: Infants following repair of truncus arteriosus frequently present with right ventricular (RV) dilation and left ventricular (LV) compression, predisposing them to acute right heart failure during non-cardiac surgery. Anesthetic induction and tracheal intubation may further exacerbate hemodynamic instability. Judicious induction strategies and meticulous airway management are therefore essential in this vulnerable population.
Case presentation: We report a 4-month-old infant with repaired truncus arteriosus who developed progressive bradycardia, hypotension, and systemic venous congestion approximately one minute after tracheal intubation. The bradycardia was unresponsive to atropine but was rapidly reversed by a low-dose intravenous bolus of epinephrine (1 μg/kg). A transient surge in end-tidal carbon dioxide (ETCO₂) from 30 to 70 mmHg immediately after epinephrine administration indicated restoration of right ventricular forward flow. Postoperative biomarkers were markedly elevated [B-type Natriuretic Peptide (BNP) 639.58 pg/mL, troponin 79.14 ng/L]. Drawing upon the framework of ventricular interdependence, we analyze the vicious cycle triggered by the combined effects of reduced systemic vascular resistance (SVR) and positive-pressure ventilation, and propose perioperative management strategies tailored to infants with a “large RV and compressed LV” phenotype. At one-month follow-up, the infant remained asymptomatic with stable echocardiographic parameters.
Conclusions: This case suggests that infants with a “large RV, small LV” phenotype may be at increased risk for acute right ventricular dysfunction (RVD) during anesthesia. Multiple factors—including pre-existing RVD, induction anesthetics, positive-pressure ventilation, and lung overinflation—may have collectively contributed to the event. Maintaining systemic systolic pressure, avoiding excessive lung inflation, and having low-dose epinephrine readily available appear to be prudent measures in such patients. However, these observations are derived from a single case and should be interpreted with caution.
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BibTeX
@article{sun2026right,
title = {{Right ventricular dysfunction during induction of anesthesia in an infant with repaired truncus arteriosus: a case report and learning from a potentially preventable adverse perioperative event}},
author = {Jing Sun and Wenqin Zhou},
journal = {Frontiers in Medicine},
year = {2026},
month = oct,
doi = {10.3389/fmed.2026.1960952},
url = {https://doi.org/10.3389/fmed.2026.1960952},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Right ventricular dysfunction during induction of anesthesia in an infant with repaired truncus arteriosus: a case report and learning from a potentially preventable adverse perioperative event
AU - Jing Sun
AU - Wenqin Zhou
PY - 2026
DA - 2026/10/22
JO - Frontiers in Medicine
DO - 10.3389/fmed.2026.1960952
UR - https://doi.org/10.3389/fmed.2026.1960952
AB - Background: Infants following repair of truncus arteriosus frequently present with right ventricular (RV) dilation and left ventricular (LV) compression, predisposing them to acute right heart failure during non-cardiac surgery. Anesthetic induction and tracheal intubation may further exacerbate hemodynamic instability. Judicious induction strategies and meticulous airway management are therefore essential in this vulnerable population. Case presentation: We report a 4-month-old infant with repaired truncus arteriosus who developed progressive bradycardia, hypotension, and systemic venous congestion approximately one minute after tracheal intubation. The bradycardia was unresponsive to atropine but was rapidly reversed by a low-dose intravenous bolus of epinephrine (1 μg/kg). A transient surge in end-tidal carbon dioxide (ETCO₂) from 30 to 70 mmHg immediately after epinephrine administration indicated restoration of right ventricular forward flow. Postoperative biomarkers were markedly elevated [B-type Natriuretic Peptide (BNP) 639.58 pg/mL, troponin 79.14 ng/L]. Drawing upon the framework of ventricular interdependence, we analyze the vicious cycle triggered by the combined effects of reduced systemic vascular resistance (SVR) and positive-pressure ventilation, and propose perioperative management strategies tailored to infants with a “large RV and compressed LV” phenotype. At one-month follow-up, the infant remained asymptomatic with stable echocardiographic parameters. Conclusions: This case suggests that infants with a “large RV, small LV” phenotype may be at increased risk for acute right ventricular dysfunction (RVD) during anesthesia. Multiple factors—including pre-existing RVD, induction anesthetics, positive-pressure ventilation, and lung overinflation—may have collectively contributed to the event. Maintaining systemic systolic pressure, avoiding excessive lung inflation, and having low-dose epinephrine readily available appear to be prudent measures in such patients. However, these observations are derived from a single case and should be interpreted with caution.
SN - 2296-858X
ER -