Key result
Low-dose epinephrine rapidly reverses post-intubation collapse in repaired truncus arteriosus.
Why the study?
Infants following truncus arteriosus repair frequently have RV dilation and LV compression, predisposing them to acute right heart failure during non-cardiac surgery that may be exacerbated by anesthetic induction and tracheal intubation.
Case Report (n=1)
No
Infants with repaired truncus arteriosus and a 'large RV, small LV' phenotype are highly vulnerable to acute right ventricular failure triggered by anesthetic-induced hypotension and positive-pressure ventilation, requiring strict maintenance of systemic systolic pressure, avoidance of propofol and lung overinflation, and immediate availability of low-dose epinephrine.
Supports preparedness with low-dose epinephrine for post-intubation instability in repaired truncus arteriosus; hypothesis-generating from single case report.
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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Sun et al. (2026) conducted a case report in Repaired truncus arteriosus with right ventricular dilation, left ventricular compression, and acute perioperative right ventricular dysfunction (n=1). Intravenous epinephrine bolus for rescue of anesthetic-induced acute right ventricular dysfunction was evaluated on Hemodynamic restoration (heart rate, blood pressure, and end-tidal CO2). Low-dose intravenous epinephrine (1 μg/kg) rapidly reversed post-intubation bradycardia (60 to 130 bpm) and hypotension (to 85/66 mmHg) with an ETCO₂ surge from 30 to 70 mmHg in an infant with repaired truncus arteriosus.
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