
==== Front
BMC Anesthesiol
BMC Anesthesiol
BMC Anesthesiology
1471-2253
BioMed Central London

2713
10.1186/s12871-024-02713-4
Case Report
Severe stress cardiomyopathy following spinal corrective surgery for scoliosis complicated with pectus excavatum: a case report
Yan Xuhong 1
Zhang Juan 2
Hao Jing 2
Xie Jun 3
Sun Yue 13913846977@126.com

1
Ma Zhengliang mazhengliang1964@nju.edu.cn

1
1 https://ror.org/026axqv54 grid.428392.6 0000 0004 1800 1685 Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008 China
2 https://ror.org/026axqv54 grid.428392.6 0000 0004 1800 1685 Department of Anesthesiology, Nanjing Drum Tower Hospital, The affiliated hospital of Nanjing University Medical School, Nanjing, 210008 China
3 https://ror.org/026axqv54 grid.428392.6 0000 0004 1800 1685 Nanjing Drum Tower Hospital Clinical College of Jiangsu University, Nanjing, 210008 China
18 9 2024
18 9 2024
2024
24 33319 6 2024
2 9 2024
© The Author(s) 2024
2024
https://creativecommons.org/licenses/by-nc-nd/4.0/ Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.
Background

Stress cardiomyopathy (SCM) is an acute heart failure syndrome characterized by transient, usually reversible left ventricular systolic dysfunction with normal or enhanced basal compensatory wall motion abnormalities involving the left ventricular anterior septum and apex, resulting in a “ballooning” appearance. However, it has rarely been reported in patients undergoing spinal surgery.

Case presentation

We report a case of severe stress cardiomyopathy in a scoliosis patient with pectus excavatum who underwent spinal corrective surgery. During the wake-up period, circulatory collapse occurred. After multidisciplinary consultation, the patient was diagnosed with stress cardiomyopathy. At last, she had a good prognosis after a series of treatments including ECMO.

Conclusion

Stress cardiomyopathy is a reversible but uncommon condition. It can cause death if it is not diagnosed in time. Consequently, this report should improve the awareness of orthopedists and anesthesiologists for timely identification and management. For patients with potential risk factors, timely preoperative intervention should be performed to reduce the occurrence of stress cardiomyopathy.

Keywords

Stress cardiomyopathy
Pectus excavatum
Takotsubo cardiomyopathy
Scoliosis
Veno-arterial extra-corporeal membrane oxygenation
VA-ECMO
Intra-aortic balloon pump
IABP
Spinal corrective surgery
issue-copyright-statement© BioMed Central Ltd., part of Springer Nature 2024
==== Body
pmcBackground

Stress Cardiomyopathy (SCM) is an acute heart failure syndrome characterized by transient, usually reversible left ventricular systolic dysfunction with normal or enhanced basal compensatory wall motion abnormalities involving the left ventricular anterior septum and apex, resulting in a “ballooning” appearance. Unlike myocardial infarction, SCM is not caused by coronary artery obstruction. A Japanese scholar, Sato et al. in 1990, first reported this disease. The clinical manifestations are similar to Acute Coronary Syndrome (ACS), leading to frequent misdiagnosis. During the acute phase, it can be complicated by various conditions, including acute heart failure, cardiogenic shock, cardiac rupture, thromboembolism, arrhythmia and even death [1]. Its mortality is close to acute coronary syndrome [2]. However, it has rarely been reported in patients undergoing spinal surgery.

Case description

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.

Fig. 1 ECG:1st night postoperatively Torsades de pointes

Fig. 2 Echocardiography: the apex was obtuse, EF21%, SV13ml

Discussion and conclusions

Stress Cardiomyopathy (SCM) is an acute heart failure syndrome characterized by transient, usually reversible left ventricular systolic dysfunction with normal or enhanced basal compensatory wall motion abnormalities involving the left ventricular anterior septum and apex, resulting in a “ballooning” appearance. Unlike myocardial infarction, SCM is not caused by coronary artery obstruction. It is also called Takotsubo cardiomyopathy because of changes in the shape of the left ventricle similar to “Takotsubo”. In recent years, it has been found that SCM can also be manifested as the involvement of other parts of the left ventricle, the right ventricle or both ventricles and is mostly triggered by stressors, including physical factors or emotional factors [3]. A Japanese scholar Sato et al. in 1990, first reported this disease. Since then, it has been observed worldwide and appeared in various clinical conditions. The clinical manifestations are similar to Acute Coronary Syndrome (ACS), leading to frequent misdiagnosis. In the past, it was considered as a benign and self-limited disease with symptoms of cardiac dysfunction and ventricular wall motion abnormalities recovering within a short time, but it can also have a poor prognosis due to its unique clinical manifestations [4]. During the acute phase, it can be complicated by various conditions, including acute heart failure, cardiogenic shock, cardiac rupture, thromboembolism arrhythmia and even death [1]. Its mortality is close to acute coronary syndrome. SCM accounts for 1-2% of patients with suspected ACS or suspected ST-segment elevation myocardial infarction(STEMI) and occurs predominantly in women [2]. There are few related studies on SCM in China, and the diagnosis rate is low, mainly focusing on case reports.

The pathogenesis of SCM is not fully understood at present. The most widely accepted mechanism is that catecholamine-mediated myocardial stunning and microvascular spasm. Compared with basal cardiomyocytes, apical cardiomyocytes have higher β-adrenergic receptor density and are more sensitive to catecholamine stimulation. Excessive catecholamine makes β2-adrenergic receptor negative inotropic effect mediated by activated G protein, leading to significantly weakened apical myocardial motion, forming the classic “ballooning appearance”. The brain-heart axis theory is another important mechanism of SCM. Complex brain-heart interactions play an important role in this process. It has been shown that patients with SCM show changes in neuronal connectivity in the limbic system regions of the brain associated with stress. This region is important for regulating the body’s emotional response and autonomic nervous system function. The ability of a SCM susceptible person to respond appropriately to the precipitating factor may be diminished with a trigger, and on this basis, the imbalance between sympathetic and parasympathetic nervous system can cause patients to develop severe myocardial dysfunction and damage, promoting the development of SCM.

The patient was a young female with no abnormal findings on preoperative cardiac examination. However, during the awakening process after surgery, the BP suddenly decreased, echocardiography showed reduced ventricular wall motion, significantly reduced ejection fraction, and slightly increased troponin and ECG showed prolonged QTc interval, inverted T wave accompanied by malignant arrhythmia. After the surgery, the patient underwent ECMO treatment, improving in cardiac function with recovery of ejection fraction, consistent with the diagnostic criteria and characteristics of SCM. The precipitating factors for the sudden onset of SCM in this patient are difficult to determine but may include: (1) Surgical trauma: The patient underwent major spinal surgery, and during the awakening process with lighter anesthesia, was in a highly stressful state. Catecholamine substances are released in large quantities, resulting in myocardial injury; (2) Prolonged prone positioning during surgery: The patient was in a prone position complicated with pectus excavatum during the whole operation. The corrective segment of scoliosis surgery was located directly above the heart, continuously compressing it, leading to sustained stress on the myocardium (Fig. 3); (3) Intraoperative blood loss and fluid shifts: The patient experienced significant blood loss during surgery, followed by rapid and large fluid infusion in a short period of time, and long-term use of catecholamine drugs such as Norepinephrine; (4) Hypothermia: The perioperative anesthesia period lasted for 4 and a half hours. The extensive surgical incisions, large amount of fluid washouts, and blood transfusion leading to a lower body temperature; (5) After orthopedic surgery for scoliosis, compression of the vessels and mediastinum was relieved, IVC may have been stretched which can lead to increased blood return to the heart. At the same time, massive fluid infusion further increased the load of the heart. This eventually leads to SCM; (6) Preoperative anxiety: The patient may have had preoperative anxiety, which could have led to excessive release of catecholamine under the stimulation of surgical trauma.

Fig. 3 Pre and post-operative anteroposterior radiographs of the whole spine, Cobb angle 52°

At present, there is no clear standard for the management of SCM, and most of the treatment is symptomatic and supportive, including the use of angiotensin-converting enzyme inhibitor (ACEI), angiotensin II receptor blocker (ARB), β-receptor blocker and diuretic [5], but the evidence of their efficacy and prognosis is insufficient. Because catecholamine overdose is the core mechanism of SCM, there is controversy over whether to use catecholamine drugs in patients with SCM-induced cardiogenic shock. Some studies indicate that catecholamine use is an independent risk factor for mortality due to SCM in hospitalized patients [6, 7]. Therefore, some researchers advocate prioritizing the use of noncatecholamine inotropic agents such as milrinone, vasopressin, and levosimendan in such cases. Levosimendan, in particular, is a potent phosphodiesterase III inhibitor with a mechanism different from traditional positive inotropic agents. It doesn’t act on adrenergic receptors but rather enhances the sensitivity of contractile proteins to calcium ions by binding to cardiac troponin C in a calcium-dependent manner. This enhances myocardial contractility without affecting ventricular relaxation, aiding in the faster recovery of patients with SCM. In addition, it can induce vasodilation in systemic and coronary artery resistance vessels as well as systemic venous capacitance vessels by opening ATP-sensitive potassium channels in vascular smooth muscle [8]. However, the patient was under 18 years old, making levosimendan contraindicated, so milrinone was used to improve the patient’s cardiac dysfunction. Additionally, some studies support using mechanical devices for circulatory support, such as Intra-aortic balloon pump (IABP), extracorporeal membrane oxygenation (ECMO), or temporary left ventricular assist devices, to minimize or avoid the use of inotropic agents. A meta-analysis by Silvia Mariani et al. [7, 9] found that in SCM-induced cardiogenic shock, early use of mechanical devices for circulatory support should be considered. Moreover, there is also increasing evidence that early use of V-A ECMO can improve the survival rate and quality of life [7, 10]. With effective ECMO support, the patient’s condition is controlled and the prognosis is good.

In contrast to other patients with SCM, this patient was a young child with pectus excavatum before surgery and developed severe myocardial dysfunction after spinal correction surgery, with EF21% on echocardiography.After a series of supportive treatments such as ECMO, the patient returned to normal, and the echocardiographic ef was significantly improved. Spinal surgery is associated with high blood loss. It is normal to use catecholamines. Therefore, for such patients, we should be alert to the occurrence of SCM.

In this case, the patient experienced severe SCM postoperatively. After a series of supportive treatments, the ejection fraction returned to normal and myocardial injury markers decreased to normal levels resulting in a good prognosis. However, reviewing the management of this patient, there are still some shortcomings including: (1) The patient’s cardiac function deteriorates rapidly after onset, and circulation remains collapsed for a prolonged period, which needs high-dose vasopressor support. Meanwhile, early initiation of cardiac energy support during the early stage may slow down the progression of cardiac dysfunction. Studies have shown that oxidative metabolism disorder is the basis of cardiac dysfunction in patients with SCM [11], so we think that early use of drugs that improve myocardial energy metabolism can benefit the prognosis of patients, but there is still insufficient clinical evidence. (2) Coronary angiography and cardiac magnetic resonance examination were not performed immediately after onset to confirm the diagnosis. In addition, we can use rest myocardial perfusion imaging with SPECT and TIMI Risk Score for early diagnosis and prediction of prognosis [12, 13]. (3) The preoperative electrocardiogram and echocardiography were not fully normal, but further testing was not performed before the procedure, which may have led to an inadequate preoperative assessment of the patient’s cardiac function. (4) The preoperative assessment didn’t pay attention to the evaluation of the patient’s emotional state adequately. Studies indicate that preoperative anxiety is the potential trigger for SCM [14, 15],administering a certain amount of sedative drugs preoperatively to alleviate anxiety. During the operation, adjusting anesthesia depth in real-time based on surgical stimuli can effectively reduce stress responses while maintaining an appropriate anesthesia depth. Especially for patients who need wake-up during scoliosis surgery, adequate analgesia should be provided before awakening to reduce the stress caused by the shallow depth of anesthesia.

In summary, the key points of perioperative anesthesia management of SCM are as follows: Pay attention to the patient’s anesthesia evaluation before surgery, identify the high-risk factors of SCM, and formulate individualized anesthesia plans. During the operation, triggered factors were actively removed to avoid all adverse stress reactions and a multi-modal precise management plan was formulated after the operation. Anesthesiologists need to enhance their ability to identify SCM early and formulate a detailed and standardized anesthesia management plan for SCM patients. Multidisciplinary collaboration, early identification, accurate evaluation, correct handling and prevention of complications are crucial for improving the perioperative safety of SCM patients.

Acknowledgements

Not applicable.

Author contributions

The designs of anesthesia strategy and anesthesia implementation were by J.Z.and XH.Y.,the management of AICU were by YE.S. ,J.H. and J.X. , and the drafting of the manuscript were by XH.Y.; manuscript review and correction was by ZL.M. ,Z.J. and YE.S.All authors read and approved the final manuscript.

Funding

Not applicable.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Not applicable. All methods were carried out in accordance with relevant guidelines and regulations.

Consent for publication

Written informed consent was obtained from the patient for publication of the case report and the images.

Competing interests

The authors declare no competing interests.

Abbreviations

SCM Stress Cardiomyopathy.

ACS Acute Coronary Syndrome.

BMI Body Mass Index.

ASA American Society of Anesthesiologists.

MET Metablic Equivalent.

MVV Maximal Voluntary Ventilation.

ABP Arterial Blood Pressure.

PPV Pulse Pressure Variation.

CVP Central Venous Pressure.

ECG Electrocardiogram.

Bis Bispectral Index.

AICU Anesthesia Intensive Care Unit.

VA-ECMO Veno-Arterial Extra-corporeal membrane oxygenation.

EF Ejection fraction.

STEMI ST-segment elevation myocardial infarction.

ACEI Angiotensin-converting enzyme inhibitor.

ARB Angiotensin II receptor blocker.

IABP Intra-aortic balloon pump.

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
==== Refs
References

1. Hessel EA, London MJ. Takotsubo (Stress) Cardiomyopathy and the Anesthesiologist: Enough Case Reports. Let’s Try to Answer Some Specific Questions! [J]. Volume 110. Anesthesia & Analgesia; 2010. pp. 674–9. 3.
2. Singh T Khan H Gamble DT Takotsubo Syndrome: pathophysiology, emerging concepts, and clinical implications [J] Circulation 2022 145 13 1002 19 10.1161/CIRCULATIONAHA.121.055854 35344411
Singh T, Khan H, Gamble DT, et al. Takotsubo Syndrome: pathophysiology, emerging concepts, and clinical implications [J]. Circulation. 2022;145(13):1002–19.35344411
3. Matta A Delmas C Campelo-Parada F Takotsubo cardiomyopathy [J] Rev Cardiovasc Med 2022 23 1 38 10.31083/j.rcm2301038 35092230
Matta A, Delmas C, Campelo-Parada F, et al. Takotsubo cardiomyopathy [J]. Rev Cardiovasc Med. 2022;23(1):38.35092230
4. He HM Zheng SW Zhu LY [Stress cardiomyopathy: mechanisms, diagnosis, and treatment] [J] Zhonghua Xin xue guan bing za zhi 2023 51 8 898 904 37583343
He HM, Zheng SW, Zhu LY, et al. [Stress cardiomyopathy: mechanisms, diagnosis, and treatment] [J]. Zhonghua Xin xue guan bing za zhi. 2023;51(8):898–904.37583343
5. Boyd B Solh T Takotsubo cardiomyopathy: review of broken heart syndrome [J] Jaapa 2020 33 3 24 9 10.1097/01.JAA.0000654368.35241.fc 32039951
Boyd B, Solh T. Takotsubo cardiomyopathy: review of broken heart syndrome [J]. Jaapa. 2020;33(3):24–9.32039951
6. Ansari U El-Battrawy I Fastner C Clinical outcomes associated with catecholamine use in patients diagnosed with Takotsubo cardiomyopathy [J] BMC Cardiovasc Disord 2018 18 1 54 10.1186/s12872-018-0784-6 29554866
Ansari U, El-Battrawy I, Fastner C, et al. Clinical outcomes associated with catecholamine use in patients diagnosed with Takotsubo cardiomyopathy [J]. BMC Cardiovasc Disord. 2018;18(1):54.29554866
7. Terasaki S Kanaoka K Nakai M Outcomes of catecholamine and/or mechanical support in Takotsubo syndrome [J] Heart 2022 108 18 1467 73 10.1136/heartjnl-2021-319904 35046103
Terasaki S, Kanaoka K, Nakai M, et al. Outcomes of catecholamine and/or mechanical support in Takotsubo syndrome [J]. Heart. 2022;108(18):1467–73.35046103
8. Yaman M Arslan U Kaya A Levosimendan accelerates recovery in patients with takotsubo cardiomyopathy [J] Cardiol J 2016 23 6 610 5 10.5603/CJ.a2016.0100 27910084
Yaman M, Arslan U, Kaya A, et al. Levosimendan accelerates recovery in patients with takotsubo cardiomyopathy [J]. Cardiol J. 2016;23(6):610–5.27910084
9. Mariani S Richter J Pappalardo F Mechanical circulatory support for Takotsubo syndrome: a systematic review and meta-analysis [J] Int J Cardiol 2020 316 31 9 10.1016/j.ijcard.2020.05.033 32473281
Mariani S, Richter J, Pappalardo F, et al. Mechanical circulatory support for Takotsubo syndrome: a systematic review and meta-analysis [J]. Int J Cardiol. 2020;316:31–9.32473281
10. Gong W-Y, Li C-G, Fan K. A novel ultrasound-guided technique for intermediate femoral cutaneous nerve block [J]. Minerva Anestesiol, 2022, 88(3).
11. Willis BC salazar-cantú A Silva-Platas C Impaired oxidative metabolism and calcium mishandling underlie cardiac dysfunction in a rat model of post-acute isoproterenol-induced cardiomyopathy [J] Am J Physiol Heart Circ Physiol 2015 308 5 H467 77 10.1152/ajpheart.00734.2013 25527782
Willis BC, salazar-cantú A, Silva-Platas C, et al. Impaired oxidative metabolism and calcium mishandling underlie cardiac dysfunction in a rat model of post-acute isoproterenol-induced cardiomyopathy [J]. Am J Physiol Heart Circ Physiol. 2015;308(5):H467–77.25527782
12. Abbasnezhad M, Soleimanpour H, Sasaie M et al. Comparison of Prediction between TIMI (Thrombolysis in myocardial infarction) risk score and modified TIMI Risk score in discharged patients from Emergency Department with atypical chest Pain [J]. Iran Red Crescent Med J, 2014, 16(2).
13. Taban Sadeghi M Mahmoudian B Ghaffari S Value of early rest myocardial perfusion imaging with SPECT in patients with chest pain and non-diagnostic ECG in emergency department [J] Int J Cardiovasc Imaging 2019 35 5 965 71 10.1007/s10554-018-01518-0 30661139
Taban Sadeghi M, Mahmoudian B, Ghaffari S, et al. Value of early rest myocardial perfusion imaging with SPECT in patients with chest pain and non-diagnostic ECG in emergency department [J]. Int J Cardiovasc Imaging. 2019;35(5):965–71.30661139
14. Goh ACH Wong S Zaroff JG Comparing anxiety and depression in patients with takotsubo stress cardiomyopathy to those with Acute Coronary syndrome [J] J Cardiopulm Rehabil Prev 2016 36 2 106 11 10.1097/HCR.0000000000000152 26468629
Goh ACH, Wong S, Zaroff JG, et al. Comparing anxiety and depression in patients with takotsubo stress cardiomyopathy to those with Acute Coronary syndrome [J]. J Cardiopulm Rehabil Prev. 2016;36(2):106–11.26468629
15. Lazzeroni D BINI M CASTIGLIONI P Anxiety disorders and stressful events in Takotsubo syndrome [J] Cardiol J 2018 25 4 495 500 10.5603/CJ.a2017.0136 29168538
Lazzeroni D, BINI M, CASTIGLIONI P, et al. Anxiety disorders and stressful events in Takotsubo syndrome [J]. Cardiol J. 2018;25(4):495–500.29168538
