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Kosin Medical Journal 2019;34:65-71. https://doi.org/10.7180/kmj.2019.34.1.65 KMJ Case Reports Persistent Complete after Induction of General Anesthesia in a Healthy Patient

Byeon Gyeong-Jo, Kim Hye-Jin, Ri Hyun-Su, Lee Su Sung, Kim Hee Young

Department of Anesthesia and Pain Medicine, Pusan National University Yangsan Hospital, Yangsan, Korea

A 38-year-old female patient had in the preoperative electrocardiogram (ECG), and she showed severe bradycardia, with the rate (HR) under 40 beats per minute (bpm) even after arrival in the operating room. Immediately after endotracheal intubation, ventricular with HR over 200 bpm occurred, but it disappeared voluntarily. The surgery was postponed for additional cardiac evaluation because of the persistent severe bradycardia. On postanesthesia day 2, complete atrioventricular (AV) block appeared. We expected spontaneous recovery over 2 weeks, but the complete AV block persisted. A permanent pacemaker was eventually inserted, and the patient was discharged without other complications on day 4 after insertion of the pacemaker. We report this case because complete AV block has commonly occurred in patients with risk factors such as first AV block, secondary AV block, or , but complete AV block has occurred despite the absence of in this patient.

Key Words: Atrioventricular block, Bradycardia, General anesthesia

Complete atrioventricular (AV) block may cause with risk factors such as first AV block, secondary hemodynamic instability, and pacemaker in- AV block, or bundle branch block,2,3 but complete sertion may be necessary because the condition AV block has occurred despite the absence of ar- occasionally does not respond to vagolytic drugs.1 rhythmia in this patient. has been rarely reported to progress to complete AV block, and it is usually temporary, especially when it is caused by CASE anesthetics. We report a case of a permanent complete AV block that occurred after induction A 38-year old female patient with a height of of general anesthesia in a patient who had no his- 160 cm and a weight of 50 kg who has hyper- tory of an atrioventricular block because com- thyroidism and hearing impairment was admitted plete AV block has commonly occurred in patients to the operating room to undergo endoscopic

Corresponding Author: Kim Hee Young, Department of Anesthesia and Pain Medicine, Pusan National Received: Aug. 29, 2018 University Yangsan Hospital, 20, Geumo-ro, Beomeo-ri, Mulgeumeup, Yangsan 50612, Korea Revised: Oct. 25, 2018 Tel: +82-55-360-2129 Fax: +82-55-360-2149 E-mail: [email protected] Accepted: Nov. 21, 2018

Articles published in Kosin Medical Journal are open-access, distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

65 Kosin Medical Journal 2019;34:65-71. dacryocystorhinostomy. The patient had under- performed under intravenous bolus admin- gone preoperative evaluation one month pre- istration of thiopental 200 mg, rocuronium 40 mg, viously, and the results of the thyroid function and intravenous infusion remifentanil 25 mcg for tests and other were normal. Sinus bradycardia 5 minutes. HR decreased to 46 bpm after admin- with a (HR) of 46 beats per minute (bpm) istration of remifentanil. Anesthesia was main- was noted in the preoperative electrocardiogram tained with 1.5 vol% of sevoflurane until endo- (ECG) (Fig. 1). She had undergone endoscopic da- tracheal intubation. Immediately after endo- cryocystorhinostomy under general anesthesia 5 tracheal intubation, (VT) years ago at the same hospital. During that oper- with HR over 200 bpm occurred, but NIBP was ation, the preoperative ECG showed a normal si- 165/75 mmHg and bispectral index score was 57. nus rhythm (HR, 61 bpm), and there were no com- VT disappeared voluntarily after 10 seconds with- plications in the perioperative period. Although out any treatment and NIBP became 130/85 bradycardia was observed in the current pre- mmHg. Although the patient showed recovery of operative ECG, the elective surgery was initiated , the surgery was postponed for addi- without additional examinations such as a trans- tional cardiac evaluation because the severe bra- thoracic echocardiogram because the patient had dycardia (HR, 35-40 bpm) and frequent VPC no concomitant disease and no symptoms related persisted. During emergence, the HR and BP re- bradycardia, such as dyspnea, dizziness, and mained steady at 35-40 bpm and 100-110/50-90 . mmHg, respectively. On ECG, the HR was 31-36 Before induction, the patient showed severe bpm and a 2:1 second-degree AV block was ob- bradycardia (HR, under 40 bpm) and ventricular served in the postanesthesia care unit (Fig. 2). premature contraction (VPC). There was no spe- NIBP was maintained at 95-124/52-63 mm Hg. cific symptom related to the severe bradycardia, Although intravenous administration of 0.5 mg of and noninvasive blood pressure (NIBP) was temporarily increased the HR to 61 bpm, 135/59 mmHg. After intravenous administration it subsequently decreased to 31-32 bpm. of 0.5 mg of atropine, HR increased to 64 bpm On postanesthesia day 2, the cardiac rhythm and endotracheal intubation was subsequently changed from a 2:1 second-degree AV block to

Fig. 1. Preoperative ECG showing sinus bradycardia with heart rate at 46 beats per minute. ECG, electrocardiogram.

66 complete AV block after induction

Fig. 2. ECG obtained in the immediate postanesthesia period shows a 2:1 AV block. The red arrows indicate P-waves. ECG, electrocardiogram; AV, atrioventricular.

Fig. 3. ECG obtained on postanesthesia day 2 shows a complete AV block. The red arrows indicate P-waves. ECG, electrocardiogram; AV, atrioventricular. complete AV block with the HR at 30 bpm (Fig nent pacemaker was eventually inserted, and the 3), but NIBP remained in the normal range and patient was discharged without other complica- there were no related symptoms. We tried to iden- tions on day 4 after pacemaker insertion. tify the cause of the AV block by performing labo- ratory tests of antinuclear antibodies for systemic erythematosus, thyroid hormone, and DISCUSSION electrolytes. However, there were no abnormal findings. Transthoracic echocardiographic ex- In a complete AV block, electrical activity in amination was performed to identify structural the cannot travel to the , abnormalities of the heart, but it showed normal and the atrium and contract individually left ventricular size and contractility. The patient without any relationship. There are several causes also showed no abnormalities in the 24-hour of complete AV block (Table 1),4 and complete Holter monitoring. AV blocks can be congenital or acquired. The complete AV block persisted for about 2 Congenital complete AV blocks are primarily as- weeks; during this period, we continued to mon- sociated with the maternal antibodies to Ro (SS-A) itor the AV block in the hope that it would sponta- and La (SS-B) and maternal lupus.5 In contrast, neously recover to sinus rhythm because we could acquired complete AV blocks result from various not exclude sevoflurane and remifentanil as the pathologic states causing infiltration, , or cause of the complete AV block and the patient loss of connection in portions of the healthy con- was hemodynamically stable. However, a perma- duction system. However, they may also occur af-

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Table 1. Causes of complete AV block

Most common causes Very rare causes

- - Neuromuscular or neurologic disorders - Degenerative diseases - Metabolic causes - Nonischemic - Phase IV idiopathic block - Infectious causes - Radiation-induced - Rheumatic and autoimmune diseases - Psychiatric conditions - Infiltrative processes - Unexplained apoptosis of the cardiac -conduction system - Vagally induced - Acute - Iatrogenic causes (including drugs) - Left ventricular noncompaction - Thyroid disorders ter administration of AV nodal blocking agents, fectious diseases were excluded. In rare cases, surgery, septal alcohol ablation, per- thyroid disease may be associated with a complete cutaneous coronary interventions, or electro- AV block, and this patient had a history of hyper- physiological ablation of the slow or fast pathways thyroidism, but her thyroid hormone levels were of the AV node. They can also be caused by neuro- normal. Therefore, we suspected that the newly logic, metabolic, and endocrine diseases in rare developed complete AV block was caused by the cases. drugs administered during induction of anesthesia In this case, tests for SS-A/Ro or SS-B/La auto- and vagal stimulation caused by procedures such antibodies were performed to assess the possi- as endotracheal intubation. bility of systemic inflammatory and connective Several anesthetics have been reported to cause tissue diseases, which can cause congenital com- conduction disturbances, and inhaled anesthetics plete AV blocks. However, the results were show dose-dependent effects on myocardial sup- negative. Transthoracic was pression6,7 and cardiac conduction systems.8,9 also performed to identify structural problems of Inhaled anesthetics can delay cardiac conduction the heart, and it showed a normal structure. and inhibit voltage-gated sodium and L-type cal- Although the causes of acquired complete AV cium channels, thereby prolonging the QT blocks are extremely diverse, this patient showed interval.10 Sevoflurane has depressive effects on no suspicious symptoms or signs of heart disease, the cardiac conduction.11 However, sevoflurane neuromuscular system disease, or infection, and is also known to have little or no inhibitory effect the results of postoperative transthoracic echo- on the AV node, and life-threatening arrhythmia cardiography and blood tests were normal. On the associated with its administration has not been basis of these findings, neuromuscular diseases, reported to date. Sevoflurane shows weaker AV coronary artery disease, , and in- conduction inhibition than halothane or en-

68 complete AV block after induction flurane and similar to that of isoflurane.12 In addi- in this patient under the judgment of the cardiolo- tion, most anesthetics show temporary or rever- gist because there was no recovery to sinus sible courses after their action is finished. rhythm although we expected spontaneous re- Although propofol is reported to be capable of covery for 2 weeks. reversing the conduction disturbances caused by Complete AV block may cause serious hemody- sevoflurane, Lee et al. reported that a large bolus namic instability. To avoid such unexpected AV of propofol induces a complete AV block.2 blocks, it is important to preoperatively identify Opioids such as remifentanil can also cause bra- risk factors such as bradycardia that may result dycardia, junctional rhythms, and even temporary in AV blocks even in healthy patients without a sinusoidal arrest. Zaballos et al. suggested that notable medical history. Although there are a few remifentanil depresses sinus node function and rare reports in which sinus bradycardia was con- most parameters of AV nodal function, which verted to a complete AV block after general anes- could explain remifentanil-related severe thesia, anesthesiologists should be cautious when bradyarrhythmias.13 administering inhaled and intravenous anes- In this case, the complete AV block persisted thetics such as propofol and remifentanil because for a considerable amount of time even after stop- sinus bradycardia may be a part of the sick sinus ping general anesthesia using sevoflurane. In oth- syndrome and may exacerbate to a , er case reports, complete AV block has occurred tachyarrhythmia, or alternating bradyarrhythmia.14 in patients with risk factors such as first AV block, In addition, careful monitoring and immediate secondary AV block, or bundle branch block,2,3 treatment are required when vagal stimulation but complete AV block has occurred despite the caused by procedures such as endotracheal in- absence of arrhythmia in this patient. Therefore, tubation can result in bradycardia and AV block. we suggested that persistent complete AV block When severe bradycardia with ventricular rate oc- in this patient was triggered by sevoflurane and curs, heart rate should be maintained within ap- remifentanil administration during anesthesia in- propriate range. If severe bradycardia does not duction in the presence of AV block risk factors respond to vagolytics such as atropine, pace- such as sinus bradycardia and endotracheal in- maker insertion should be considered according tubation, which induced vagal stimulation. Drugs to the guidelines and recommendations for place- such as atropine and isoproterenol could be used ment of permanent pacemakers in patients with temporarily to increase heart rate in the patient complete AV block which is offered by 2008 with complete AV block, but insertion of pace- American College of /American Heart maker should be considered if complete AV block Association/Heart Rhythm Society (ACC/AHA/HRS) is persistent. Permanent pacemaker was inserted (Table 2).15

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Table 2. Indications of permanent pacemaker

Class I — Indicated Class II — May Be Indicated Class III — Not Indicated

- 3° AVHB: - Asymptomatic 3° AVHB with average - Asymptomatic 1° AVHB Symptomatic bradycardia or need for rate > 40 beats/min - Type I, 2° AVHB above His bundle drugs causing same After catheter - Type II, 2° AVHB without symptoms without symptoms ablation of the arterioventricular (permanent or intermittent) - AVHB that is expected to resolve junction - Type I, 2° AVHB at or below His bundle Postoperative and not expected to without symptoms resolve - 1° AVHB with symptoms of low cardiac Neuromuscular diseases output that are relieved by temporary Escape rhythm, 40 beats/min or Pacing > 3.0 s in an asymptomatic patient - Marked 1° AVHB in a patient with CHF - 2° AVHB that is permanent or intermittent, with symptomatic bradycardia AVHB, arterioventricular heart block; CHF, Congestive .

ACKNOWLEDGMENT 2008;117:e350-408. This work was supported by clinical research 2. Noh JI, Lee JH, Woo SY, Kim YK, Cho SH, Kim grant in 2018 from Pusan National University SH, et al. Complete atrioventricular nodal block Hospital. after propofol administration in an elderly patient undergoing total knee replacement arthro- plasty-A case report-. Korean J Anesthesiol REFERENCES 2013;64:363-6. 3. Shigematsu-Locatelli M, Kawano T, Nishigaki A, 1. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA Yamanaka D, Aoyama B, Tateiwa H, et al. General

3rd, Freedman RA, Gettes LS, et al. ACC/AHA/HRS anesthesia in a patient with asymptomatic sec- 2008 Guidelines for Device-Based Therapy of ond-degree two-to-one atrioventricular block. Cardiac Rhythm Abnormalities: a report of the JA Clin Rep 2017;3:27. American College of Cardiology/American Heart 4. Barra SN, Providência R, Paiva L, Nascimento Association Task Force on Practice Guidelines J, Marques AL. A review on advanced atrioven- (Writing Committee to Revise the ACC/AHA/NASPE tricular block in young or middle-aged adults. 2002 Guideline Update for Implantation of Pacing Clin Electrophysiol 2012;35:1395-405. Cardiac Pacemakers and Antiarrhythmia 5. Kertesz NJ, Fenrich AL, Friedman RA. Congenital Devices): developed in collaboration with the complete atrioventricular block. Tex Heart Inst American Association for Thoracic Surgery and J 1997;24:301-7. Society of Thoracic Surgeons. Circulation 6. Atlee JL 3rd, Rusy BF. Halothane depression of

70 complete AV block after induction

A-V conduction studies by electrograms of the with complete atrioventricular block in a child in dogs. Anesthesiology 1972;36:112-8. with hypertension, renal dysfunction, and im- 7. Atlee JL 3rd, Rusy BF. Atrioventricular conduction paired cardiac conduction. Paediatr Anaesth times and atrioventricular nodal conductivity 1998;8:73-8. during enflurane anesthesia in dogs. Anesthesiology 12. Yokota S. Comparative effects of inhalation anes- 1977;47:498-503. thetics on atrioventricular conduction with and 8. Kazama T, Ikeda K. The comparative car- without calcium entry blockers. Hokkaido Igaku diovascular effects of sevoflurane with halothane Zasshi 1989;64:43-54. and isoflurane. J Anesth 1988;2:63-8. 13. Zaballos M, Jimeno C, Almendral J, Atienza F, 9. Conzen PF, Vollmar B, Habazettl H, Frink EJ, Peter Patiño D, Valdes E, et al. Cardiac electro- K, Messmer K. Systemic and regional hemody- physiological effects of remifentanil: study in a namics of isoflurane and sevoflurane in rats. closed-chest porcine model. Br J Anaesth

Anesth Analg 1992;74:79-88. 2009;103:191-8. 10. Zhou W, Fontenot HJ, Liu S, Kennedy RH. 14. Miller RD. Miller’s Anesthesia. 8th ed. Philadelphia, Modulation of cardiac calcium channels by USA: Elsevier; 2014. p.1439.

propofol. Anesthesiology 1997;86:670–5. 15. Atlee JL, Bernstein AD. Cardiac rhythm manage- 11. Maruyama K, Agata H, Ono K, Hiroki K, Fujihara ment devices (Part I): indications, device selection, T. Slow induction with sevoflurane was associated and function. Anesthesiology 2001;95:1265-80.

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