A case of perioperative myocardial infarction leading to asystole: An anesthesiologist's nightmare

Sivakumar Segaran; Mamie Zachariah Ninan; RV Ranjan; Leenu Grace Ninan; Vikasini Raman

doi:10.4103/jcrsm.jcrsm_14_18

CASE REPORT

Year : 2018 | Volume : 4 | Issue : 2 | Page : 119-121

A case of perioperative myocardial infarction leading to asystole: An anesthesiologist's nightmare

Sivakumar Segaran, Mamie Zachariah Ninan, RV Ranjan, Leenu Grace Ninan, Vikasini Raman
Department of Anesthesiology and Critical Care, Pondicherry Institute of Medical Sciences, Puducherry, India

Date of Submission	12-May-2018
Date of Acceptance	25-Aug-2018
Date of Web Publication	13-Dec-2018

Correspondence Address:
Sivakumar Segaran
Department of Anaesthesiology and Critical Care, Pondicherry Institute of Medical Sciences, Kalapet, Puducherry
India

Source of Support: None, Conflict of Interest: None

Check

DOI: 10.4103/jcrsm.jcrsm_14_18

Abstract

Perioperative myocardial infarction (PMI) in patients without a prior history of coronary artery disease is quite rare. Diagnosing PMI is also quite challenging because of a myriad of events mimicking MI during the perioperative period. we are reporting of PMI leading to cardiac arrest which was successfully resuscitated with the help of a multidisciplinary team. Cardiologist opinion was obtained, and angiogram was done which showed block in left anterior descending artery for which he was stented with drug-eluting stent and discharged a week after with full neurological recovery. The mechanism for triggering PMI in our case is quite inconclusive.

Keywords: Cardiac arrest, diabetes mellitus, myocardial infarction, perioperative

How to cite this article:
Segaran S, Ninan MZ, Ranjan R V, Ninan LG, Raman V. A case of perioperative myocardial infarction leading to asystole: An anesthesiologist's nightmare. J Curr Res Sci Med 2018;4:119-21

How to cite this URL:
Segaran S, Ninan MZ, Ranjan R V, Ninan LG, Raman V. A case of perioperative myocardial infarction leading to asystole: An anesthesiologist's nightmare. J Curr Res Sci Med [serial online] 2018 [cited 2022 Aug 11];4:119-21. Available from: https://www.jcrsmed.org/text.asp?2018/4/2/119/247484

Introduction

Perioperative myocardial infarction (PMI) is one of the most important predictors of short- and long-term morbidity and mortality in noncardiac surgeries.^[1] The incidence of PMI in low-risk patients without a history of coronary artery disease (CAD) is 1%–3%^[2] while in high-risk patients with a history of CAD it rises upto 38%.^[3] Most of PMIs occurs within 72 h of surgery, of which 90% occurs in <24 h after surgery.^[4],[5] PMI is an emergency, management of which poses a unique challenge to the anesthesiologist. we are hereby reporting a case of left elbow malunion posted for corrective osteotomy who developed PMI leading to cardiac arrest and was successfully managed with the help of a multidisciplinary team.

Case Report

A 48-year-old gentleman with left elbow fracture dislocation with malunion came for corrective osteotomy. He is hypertensive and diabetic on irregular medications. His investigations showed a hemoglobin (Hb) of 14.9 g/dl, fasting blood sugar of 110 mg/dl, and HbA₁C 12, but all blood sugar values were <200 mg/dl for the past 5 days and blood urea of 10 mg/dl, serum creatinine of 0.7 mg/dl, electrocardiogram (ECG), chest X-ray, and echocardiogram were within normal limits. On the day of surgery, intravenous (iv) access was secured with 18 G Venflon in his right hand, and the patient was shifted to the operating room and connected to standard ASA monitors. Under aseptic precautions, left supraclavicular brachial plexus block was performed under ultrasound sonography guidance (SonoSite M-Turbo) with linear probe. 10 ml of 0.5% bupivacaine, 10 ml of 2% lignocaine with adrenaline and 8 mg dexamethasone was given and adequate block effect was obtained. Then, we proceeded with induction of general anesthesia with thiopentone, fentanyl, and vecuronium facilitated endotracheal intubation with 8.0 mm ID (PVC cuffed Portex tube). Position was confirmed by auscultation and anesthesia was maintained with oxygen, nitrous oxide, and isoflurane. Then, the patient was positioned in the right lateral position and prescrub was started, following which the patient suddenly developed ST-segment elevation on lateral leads in ECG tracing of the multiparameter monitor followed by bradyarrhythmia leading to asystole. Immediately cardiopulmonary resuscitation (CPR) was initiated according to the advanced cardiovascular life support protocol. A total of 30 cycles of CPR were given with two doses of injection (inj) adrenaline 1 mg iv 5-min apart, following which the patient developed ventricular tachycardia and fibrillation which was successfully managed by defibrillation and inj. amiodarone 150 mg iv given over 10 min. After nearly 20 min of CPR, the patient reverted to sinus rhythm.

Thereafter, the right radial artery was cannulated with 20 G Venflon, invasive blood pressure monitoring (IBP) was initiated and blood for arterial blood gas (ABG) analysis was sent. IBP showed blood pressure of 70/40 mmHg for which the right-side external jugular vein was cannulated with 16 G Venflon for starting inotropes. Inj noradrenaline 0.1 mcg/kg/h and inj dobutamine 5 mcg/kg/h were started and the blood pressure improved to 120/70 mmHg. Meanwhile, nasogastric tube was inserted and loading dose of aspirin, clopidogrel, and statins was given on high suspicion of PMI. Blood samples were also sent for laboratory evaluation of cardiac markers. Echo revealed normal study and ABG showed pH: 7.30, PCO₂: 33 mmHg, PO₂: 400 mmHg, HCO₃: 11, BE: −6.7, sodium: 139 meq/L, and potassium: 3.2 meq/L. Surgery was deferred and the patient was shifted to coronary care unit for observation. After 2 hours, the patient was conscious and oriented to time, place, and person. Inotropes were gradually tapered and the patient was extubated. The cardiac markers initially were negative but when repeated after 6 h they were positive. Angiogram was planned which showed 95% block in mid-left anterior descending artery and was stented with drug-eluting stent under tirofiban cover.

The patient recovered well and was discharged after a week with dual antiplatelet therapy. The patient has been on regular follow-up without any complications, and surgery will be scheduled once the cardiac condition stabilizes.

Discussion

Conventionally, MI is defined by the WHO criteria with ECG criteria and cardiac enzymes. Defining PMI, however, is often difficult because most PMIs occur without symptoms in anesthetized or sedated patients.^[6] ECG changes are subtle, transient, and cardiac enzymes (creatine kinase muscle-brain) have limited sensitivity and specificity because of coexisting skeletal muscle injury.^[7] The diagnosis of PMI is a challenge as most are silent; chest pain, if at all present, is easily masked by analgesia and residual perioperative anesthesia.

Two distinct mechanisms may lead to PMI:

acute coronary syndrome (unstable or vulnerable plaque rupture)
prolonged myocardial oxygen supply–demandimbalance in the presence of stable coronary artery disease.^[8]

The initial therapy in non–ST segment elevation MI is medical stabilization, whereas myocardial infarction with ST-segment elevation (STEMI) requires fibrinolysis or percutaneous coronary intervention. The treatment options for PMI are limited by the risk of surgical site bleeding in the early postoperative period. Diabetes mellitus is known to increase the perioperative cardiac adverse events, and the preoperative HbA₁C levels in these patients correlate with the perioperative cardiac outcome.^[9]

PMI commonly occurs in patients with chronic CAD and results in NSTEMI with ST-segment depression rather than elevation.^[1],[2],[3] The cause for PMI in our case is very debatable. Our patient did not have any significant hemodynamic alterations during induction of anesthesia. The events started after positioning the patient in lateral position and during prescrub. The triggering mechanism for PMI in our case may be due to the following mechanisms:

Due to diabetic autonomic neuropathy, positional change-induced hemodynamic changes could have triggered plaque rupture or vasospasm
The patient had a high preoperative HbA₁C level of 12. The capillary blood gas (capillary blood sugar) measured during the peri-arrest period was 83 mg/dl which is relatively low considering his HbA₁C level. Hence, the relative hypoglycemia might have triggered the sequence of events.

We felt this case was of academic interest as the patient made full neurological recovery after an episode of cardiac arrest. Also the exact cause of PMI could not be ascertained in this case.

Conclusion

The best strategy for management of PMI is one that emphasizes prevention. Preventive strategies should be based on preoperative utilization and optimization of medications. If MI does occur, a multidisciplinary approach involving the operating surgeon, cardiologist, and intensivist should be followed for successful management.

Acknowledgment

Prof. Mark Christopher DM (Cardiology) Professor, Department of Cardiology, PIMS
Prof. Shishir MS (Orthopaedics) Professor, Department of Orthopaedics, PIMS.

Consent

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

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1.	Landesberg G. The pathophysiology of perioperative myocardial infarction: Facts and perspectives. J Cardiothorac Vasc Anesth 2003;17:90-100.
2.	Ashton CM, Petersen NJ, Wray NP, Kiefe CI, Dunn JK, Wu L, et al. The incidence of perioperative myocardial infarction in men undergoing noncardiac surgery. Ann Intern Med 1993;118:504-10.
3.	Landesberg G, Shatz V, Akopnik I, Wolf YG, Mayer M, Berlatzky Y, et al. Association of cardiac troponin, CK-MB, and postoperative myocardial ischemia with long-term survival after major vascular surgery. J Am Coll Cardiol 2003;42:1547-54.
4.	Badner NH, Knill RL, Brown JE, Novick TV, Gelb AW. Myocardial infarction after noncardiac surgery. Anesthesiology 1998;88:572-8.
5.	Landesberg G, Beattie WS, Mosseri M, Jaffe AS, Alpert JS. Perioperative myocardial infarction. Circulation 2009;119:2936-44.
6.	Adams JE 3^rd, Sicard GA, Allen BT, Bridwell KH, Lenke LG, Dávila-Román VG, et al. Diagnosis of perioperative myocardial infarction with measurement of cardiac troponin I. N Engl J Med 1994;330:670-4.
7.	Jaffe AS. A small step for man, a leap forward for postoperative management. J Am Coll Cardiol 2003;42:1555-7.
8.	Thygesen K, Alpert JS, White HD, Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. J Am Coll Cardiol 2007;50:2173-95.
9.	Schouten O, Bax JJ, Poldermans D. Assessment of cardiac risk before non-cardiac general surgery. Heart 2006;92:1866-72.