A 16-year-old female patient, 164 cm in height, 42 kg in weight, 15.6 kg/m2 in BMI (Body Mass Index), ASA (American Society of Anesthesiologists) II level, was admitted to the spinal surgery department due to “asymmetric chest and back protrusion discovered for 1 year”. The patient, combined with “pectus excavatum”, was generally capable of normal activities, with a MET ( Metablic Equivalent)score of above 6. Preoperative arterial blood gas analysis was generally normal (PaCO2 36 mmHg, PaO2 92 mmHg, SPO2 98%).Pulmonary function showed moderate to severe obstructive mixed ventilatory dysfunction (FEV1/FVC 84.5%<92%, MVV(Maximal Voluntary Ventilation) 75.08 L, FEV1 Actual value/predicted value was 56%<80%,FVC Actual value/predicted value was 57%). Electrocardiogram showed sinus bradycardia HR 55 bpm, incomplete right bundle branch block and T-wave changes. The Echocardiogram showed mild regurgitation of mitral and tricuspid valves (EF62.1%). Admission diagnosis: (1) Spinal scoliosis (2) Pectus excavatum (3) Incomplete right bundle branch block. Following communicating with the patient and the patient’s family members about surgery-related risks, a planned “thoracolumbar fusion surgery, posterior approach + multi-level vertebral fusion” is scheduled under general anesthesia.

After fasting and refraining from drinking for 10 h and completed preoperative electrocardiogram monitoring, which showed HR 54 bpm, non-invasive blood pressure 94/63 mmHg, SPO2 98% (no oxygen inhalation). Following the establishment of peripheral venous access, anesthesia induction was administered after oxygen inhalation by mask at 5 L/min: Midazolam 2 mg, 1% Propofol 60 mg, Sufentanil 20 ug, Vecuronium bromide 6 mg, Dexamethasone 10 mg. Following induction of anesthesia the patient was intubated with a size 7.0 ID endotracheal tube. Maintenance of anaesthesia was achieved by total intravenous anaesthesia with propofol and remifentanil to a target BIS value of 40–60. Fluid infusion was target-guided by PPV (Pulse Pressure Variation) and CVP (Central Venous Pressure). After anesthesia induction, the patient’s HR transiently decreased to 39 bpm. After intravenous injection of 0.5 mg atropine, HR gradually increased to 60–70 bpm. Changing to the prone position, the patient’s BP dropped significantly, reaching a low of 67/47 mmHg. Norepinephrine 4 µg was given intravenously, resulting in a rise in BP to 90–105/60–70 mmHg. Despite the start of surgery, the BP remained low, fluctuating between 85–95/56–67 mmHg. A continuous infusion of Norepinephrine at 0.1 µg·kg-1·min-1 was administered, and the infusion rate was adjusted based on BP to maintain BP between 100–110/65–75 mmHg and HR between 50 and 70 bpm. Approximately 1.5 h after surgery began, muscle relaxants were discontinued after complete spine exposure. After 4 h from the start of surgery, the bilateral growing rods for spinal correction were successfully placed, so all anesthetics were stopped. The intraoperative arousal was unsuccessful, so the surgery continued. After the skin was sutured, the patient was awakened again and cooperated well with instructions, resulting in a successful awakening. At this time, the BP was 106/70 mmHg, and the HR was 82 bpm. Then,1% Propofol 20 mg was given to deepen anesthesia, and prepared for the change to the supine position. After removing the patient’s electrocardiogram (ECG) monitoring and pulse oxygen clip, it was noticed that the patient’s ABP suddenly dropped to 24/15 mmHg. Immediately, 12 µg of Norepinephrine was given intravenously followed by changing to the supine position. However, there was no improvement in BP after repositioning. Subsequently, 20 µg of Norepinephrine was administered again, and external chest compression was performed. Epinephrine 0.1 mg was administered intravenously twice in succession, and ECG monitoring and pulse oxygen clip were re-established. ECG showed sinus rhythm, QRS amplitude was small. The BP was 156/119 mmHg; the HR was 142 bpm. The repeated blood gas analysis showed the following results: pH 7.19 ,PaO2 489 mmHg, PaCO2 53 mmHg, HCO3− 20.2 mmol /L, BE -8.0 mmol/L, Lac 1.1 mmol /L, Na+ 143 mmol /L, K+ 4.6 mmol /L, Ca2+ 1.06 mmol /L, Glu 7.3 mmol /L, Hb 10.5 g/dL. Then, administered 50 ml of 5% sodium bicarbonate to correct acidosis. Norepinephrine was intermittently administered while simultaneously continuously infused Norepinephrine at 0.3 µg·kg-1·min-1 to maintain BP at 90–105/60–65 mmHg. The total duration of the surgery was approximately 4 h and 35 min. During the procedure, there was a blood loss of 2200 ml, and the urine volume was 800 ml. The patient received 3000 ml of compound sodium chloride solution, 2500 ml of succinylated gelatin, 150 ml of 5% sodium bicarbonate, and 300 ml of 0.9% sodium chloride. Additionally, 1100 ml of leukocyte-reduced red blood cells and 510 ml of autologous blood recovery were transfused. Postoperatively, the patient was transferred to the Anesthesia Intensive Care Unit (AICU) with endotracheal tube for further treatment.

After admission to AICU, the patient’s vital signs were monitored: BP was 84/45mmHg (under Norepinephrine pump), HR was 91 bpm and pupils on both sides were equal and round, dull to reflect light. The patient’s circulatory status remained collapsed, so The patient’s BP was maintained by Intermittent injection of Norepinephrine 8 µg, Phenylephrine 40 µg, continuous injection of Norepinephrine 0.5 ug · kg- 1 · min- 1. Bedside echocardiography was performed immediately to assess cardiac function and volume. Bedside echocardiography showed that the heart cavity was full and the myocardial motion was generally weak, especially at apex and papillary muscles level. Considering the possibility of fluid overload, Dobutamine and Furosemide were given as cardiotonic diuretics, and Norepinephrine was continued to maintain the patient’s blood pressure. Four hours after admission to AICU, the patient was awake and could follow the instructions. After sedation, bedside echocardiography was performed again to evaluate the cardiac function and volume, which showed that the basal and apical wall motion of left ventricle was significantly better than before, but the papillary muscle segment wall motion was still poor. The laboratory tests showed that BNP and TNT were within the normal range, and creatine kinase was elevated at 619U/ L. Symptomatic supportive treatment was continued.At night (about 12 h after operation), the CVP suddenly increased and the monitor showed malignant arrhythmia (Fig. 1), accompanied by a sudden drop in BP and undetectable SPO2. Chest compressions were performed immediately, and Epinephrine 1 mg was injected intravenously twice. After continuous chest compressions for 3 min, sinus rhythm was restored, during which Norepinephrine and Phenylephrine were continuously pumped, then the BP gradually rose to 110–127/90–101 mmHg, HR107-140 bpm. Four minutes later, the vital signs became stable with the support of vasoactive drugs, and the patient was treated with head-cooling cap, mannitol, and steroids. Arterial blood gas analysis, bedside electrocardiogram, and echocardiography were evaluated.The arterial blood gas analysis showed: pH 7.36, PaO2 96 mmHg, PaCO2 34 mmHg, HCO3− 19.2 mmol /L, BE -5.5mmol/L, Lac 4.3mmol /L, Na+ 138 mmol /L, K+ 4.6 mmol /L, Ca2+ 1.16 mmol /L, Glu 6.1mmol /L, Hb 11.9 g/dL, SPO2 97%.Echocardiography showed that the basal wall motion of the left ventricle was acceptable, the motion of other segments of the left ventricle was significantly weakened, the apex was round and dull, and the motion of the right ventricle was generally significantly weakened. We immediately called a cardiologist for an urgent consultation. Combined with the patient’s medical history, arterial blood gas analysis, echocardiography, ECG which showed multiple lead T wave inversion and QT interval prolongation, and the circulation remained collapsed. Additionally, high-dose Norepinephrine 0.076 mg·kg-1·h-1 and Phenylephrine 0.72 mg·kg-1·h-1 were required to maintain stable vital signs. Considering the patient had occult prolongation of QT interval and malignant torsades de pointes arrhythmia, the cardiologists suggested that potassium supplement should be used to maintain K + above 4.0 mmol/L, the changes of electrocardiogram should be monitored continuously. Isoproterenol 0.01 mg/h instead of Dobutamine should be used to improve QT prolongation and avoid the occurrence of left ventricular outflow tract obstruction. Meanwhile, we pumped MgSo4 intravenously. Six hours later, the patient’s HR gradually increased; the fastest was 151 bpm, the lowest BP was 60/40 mmHg, the arterial blood gas lactate level gradually increased, the highest was 7.3mmol/L, and urine decreased to 20 ml/h. We immediately requested a multidisciplinary consultation from the Department of Echocardiography, Cardiology, and ICU(Intensive Care Unit). At the same time, TNT and BNP were significantly elevated (TNT0.476 ug/L, BNP1360 pg/ml). Echocardiography showed that the basal wall motion of the left ventricle was acceptable, the motion of the remaining wall segments was significantly reduced, the apex was round and obtuse, and the motion of the right ventricular wall was generally significantly reduced, EF21%, SV 13 ml (Fig. 2). The possibility of Stress Cardiomyopathy (SCM) was considered by multidisciplinary consultation. Due to the obvious manifestation of cardiogenic shock and poor cardiac function, this patient was recommended to be treated with Extra-corporeal Membrane Oxygenation(ECMO) immediately to improve myocardial function. On the same day, the patient was transferred to the ICU for Veno-Arterial Extra-corporeal membrane oxygenation (VA-ECMO), and a hospital-wide consultation was initiated to determine the next treatment plan, including continuous RRT to remove inflammatory mediators, Milrinone for strengthening the heart, Coenzyme Q10 for nutrition of the myocardium, Piperacillin tazobactam sodium + Vancomycin for empirical anti-infection treatment, Heparin anticoagulation treatment, sedation and analgesia to reduce oxygen consumption, Mannitol to reduce brain edema, infusion of blood products to ensure oxygen supply, and control heart rate. Meanwhile, indwelling pulmonary artery catheter was used to monitor and guide fluid management and shock resuscitation. After the above treatment measures, the patient’s spontaneous breathing and circulatory function gradually improved. After 3 days of ECMO treatment, bedside echocardiography showed varying degrees of weakened left ventricular myocardial motion, left ventricular dysfunction, left ventricular ejection fraction (EF) value 43%, which indicated recovery of cardiac function and improvement of spontaneous circulation compared with before. ECMO support was withdrawn 8 days later. The patient was extubated 2 days after weaning from ECMO, and vasoactive drugs were discontinued 4 days later. Subsequently, the patient was transferred to the general ward to continue anti-infective, anti-thrombotic and analgesic treatment, and was discharged after 10 days in the general ward. Echocardiography showed a small right heart cavity, EF 52.4%, BNP35.3 pg/ml, and prolonged QTc interval of sinus tachycardia. Telephone follow-up at 1 month and 6 months after surgery showed that the patient recovered well and no adverse events occurred.

ECG:1st night postoperatively Torsades de pointes

Echocardiography: the apex was obtuse, EF21%, SV13ml