Acute right ventricular dysfunction during induction in an infant after truncus repair

A 4-month-old infant with repaired truncus arteriosus developed acute right ventricular dysfunction during anesthetic induction, experiencing rapidly progressive bradycardia, hypotension and facial venous congestion about a minute after tracheal intubation. The episode reversed within seconds of a low-dose intravenous epinephrine bolus, according to a single-case report published in Frontiers in Medicine. The infant had been scheduled for Achilles tenotomy and corrective surgery for congenital talipes equinovarus, and the case highlights how a clinically stable appearance can conceal a fragile cardiac hemodynamic profile during anesthesia.

The infant weighed 5 kg and had undergone repair of truncus arteriosus with ventricular septal defect closure and reconstruction of the right ventricular outflow tract at three months of age. A postoperative echocardiogram showed no residual ventricular septal defect and unobstructed flow through the reconstructed outflow tract. A later preoperative examination nevertheless documented a markedly enlarged right ventricle, a disproportionately large right atrium, a compressed and small left ventricular cavity, pulmonary regurgitation and residual narrowing of the right ventricular outflow tract. Tricuspid regurgitation velocity of 3.8 m/s corresponded to an estimated right ventricular systolic pressure of about 63 mmHg, while pulmonary artery flow velocity of 3.3 m/s suggested a gradient of roughly 44 mmHg. These findings indicated chronic right ventricular pressure overload, although no echocardiogram was repeated immediately before the orthopedic operation.

On arrival in the operating room, the infant had a heart rate of 115 beats per minute, blood pressure of 90/55 mmHg and oxygen saturation of 100%. Induction included atropine, midazolam, cisatracurium, propofol at 1 mg/kg, sevoflurane and fentanyl, followed by uneventful tracheal intubation. Pressure-controlled ventilation began with a driving pressure of 12 cmH₂O, a tidal volume of 40 mL, a respiratory rate of 30 breaths per minute and an end-tidal carbon dioxide concentration of 30 mmHg. Within about one minute, the heart rate fell from 120 to 95 and then to 60 beats per minute, while blood pressure dropped to 67/55 mmHg. A further 0.05 mg of atropine produced no response.

The clinicians responded with 5 micrograms of intravenous epinephrine, equivalent to 1 microgram/kg. Heart rate rose to 130 beats per minute and blood pressure to 85/66 mmHg. End-tidal carbon dioxide simultaneously surged from 30 to 70 mmHg within approximately five seconds before declining toward 40 mmHg, while a purplish, blanchable discoloration of the face and cranial veins resolved over roughly two minutes. The abrupt capnography rise was temporally associated with restored forward blood flow through the right ventricle, rather than being interpreted as a sign of worsening ventilation. The infant remained on intermittent phenylephrine during the approximately one-hour operation and was transferred intubated to the cardiac intensive care unit.

Postoperative testing showed markedly elevated B-type natriuretic peptide at 639.58 pg/mL and troponin at 79.14 ng/L. The authors interpreted these findings as supporting acute myocardial strain and right ventricular wall stress, although they cautioned that biomarkers are surrogate markers rather than direct measurements of right heart failure. The infant was diagnosed with heart failure, myocardial injury and pulmonary infection, and received milrinone, vitamin C, antibiotics and nebulized treatment. Six hours after admission, spontaneous breathing was adequate and extubation succeeded without respiratory distress. The infant was discharged on postoperative day seven and remained asymptomatic with stable echocardiographic parameters at one-month follow-up.

The proposed explanation centers on ventricular interdependence, the reciprocal influence of the ventricles when one is enlarged and under excessive pressure. A dilated, pressure-overloaded right ventricle can push the interventricular septum toward the left, reducing left ventricular filling and cardiac output. In this case, induction reduced systolic pressure by about 25 percent, from 90 to 67 mmHg. The authors propose that lower systemic pressure impaired right coronary perfusion, weakening an already strained right ventricle and encouraging further dilation, septal displacement and left ventricular compression. Positive-pressure ventilation then added a second insult: lung inflation can increase pulmonary vascular resistance when alveoli are overdistended, while elevated intrathoracic pressure can reduce venous return and right ventricular preload. Thus, neither anesthesia nor ventilation alone was presented as sufficient to explain the collapse.

The clinical pattern also helped distinguish the event from several alternatives. A vagal reaction from laryngoscopy was considered less likely because the bradycardia did not respond to atropine and epinephrine produced a rapid circulatory response. Acute obstruction of the right ventricular outflow tract was treated as a predisposition rather than the main mechanism because the narrowing was fixed and postoperative, oxygenation remained excellent and the infant improved rapidly. Pneumothorax and endobronchial intubation were excluded by symmetrical breath sounds, satisfactory chest expansion, normal airway pressures and preserved oxygenation. Anaphylaxis was considered unlikely because there was no rash, bronchospasm, wheeze or facial edema. The report presents these as the authors’ retrospective differential assessment, not as findings proven by continuous hemodynamic monitoring.

For similar infants, the report argues that risk assessment should include recent echocardiography when feasible, with attention to right ventricular size and function, outflow-tract obstruction, estimated pulmonary pressures and signs of ventricular interaction. It suggests that systemic systolic pressure should be treated as a therapeutic target because preserving it supports right coronary perfusion, counters leftward septal movement and sustains effective right ventricular ejection. The authors also recommend avoiding agents that markedly depress contractility or lower systemic vascular resistance, and they identify ketamine as an option often used when preservation of blood pressure is important. However, the case does not establish a superior induction regimen: it involved one infant, no control group and no randomized comparison of anesthetic strategies.

Mechanical ventilation is framed as a potential hazard when it adds afterload to a vulnerable right ventricle. The report therefore suggests avoiding excessive lung inflation, individualizing positive end-expiratory pressure and monitoring end-tidal carbon dioxide for abrupt changes that may indicate altered cardiac output. Diluted epinephrine should be prepared before induction, while continuous vasoactive support may be considered in selected high-risk patients. The successful epinephrine dose in this case was 1 microgram/kg. Because the right ventricular outflow narrowing was anatomically fixed rather than dynamically produced by contraction, the authors considered low-dose epinephrine a reasonable rescue option for severe bradycardia in this setting. They emphasize that the evidence comes from one event and does not define an established dose or standard for right ventricular failure.

Several limitations constrain the conclusions. No invasive hemodynamic measurements were available, the operation was not preceded by an immediate repeat echocardiogram, pediatric cardiology and cardiac surgery consultation was not formally obtained, and preoperative BNP and troponin values were unavailable. The surgeons had considered the infant stable enough for a short procedure, and the anesthesia plan explicitly recognized high risk before induction but was not followed consistently. The authors also acknowledge that phenylephrine, used intermittently as the main intraoperative vasopressor, can raise pulmonary vascular resistance, and that no continuous infusion was established before collapse. The episode was therefore reported as a potentially preventable perioperative event in a highly vulnerable infant, not as proof that one drug or intervention caused the outcome. Its principal educational value is the detailed sequence linking a large, pressure-loaded right ventricle to abrupt loss of forward flow, a rapid response to epinephrine and the later return of stable cardiac function.

Subject of Research: A case report of acute right ventricular dysfunction during anesthetic induction in an infant after truncus arteriosus repair.

Article 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

Article References: Sun, J., & Zhou, W. (2026). 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. Frontiers in Medicine, 13, Article 1960952. https://doi.org/10.3389/fmed.2026.1960952

Image Credits: AI Generated

DOI: 10.3389/fmed.2026.1960952

Keywords: truncus arteriosus, right ventricular dysfunction, anesthetic induction, tracheal intubation, positive-pressure ventilation, epinephrine, ventricular interdependence, infant cardiac surgery, perioperative care, case report, Right, ventricular