INTERNATIONAL JOURNAL OF CLINICAL AND MEDICAL CASES (ISSN:2517-7346)

Clinical case of an 84-year-old female patient who developed a complete heart block a few minutes after anaesthetic induction associated with hemodynamic instability, nonresponsive to vagolytic and adrenergic medication. Transcutaneous pacing was started with hemodynamic improvement. After the event, a decompensated metabolic acidosis was detected which was promptly corrected, leading to a normalization of the heart rhythm. Metabolic acidosis is a described but uncommon cause of atrioventricular block. The authors are not aware of previous report of complete heart block in this context. We would like to draw attention to the importance of choosing carefully which anaesthetic drugs should be used in these cases. 

Atrioventricular block; General anesthesia;Metabolic acidosis; Bradycardia

Third-degree or complete atrioventricular block is characterized by a transient or permanent alteration in the atrioventricular (AV) conduction system, that interrupts the transmission of the electric impulse from the atria to the ventricles. It can compromise the cardiac output with hemodynamic instability, which can be noncompliant to vagolytic and adrenergic drugs. In these cases, the use of pacemaker can be the last therapeutical resource in order to avoid a progression to a cardiopulmonary arrest.

The purpose of this paper, is to describe a case of a transitory complete heart block (CHB) that took place after a general anaesthesia induction on a patient with no risk factors, which had an unknown metabolic acidosis. The authors are not aware of previous report of complete heart block in this context.

A 84 year-old female was proposed to a femoral intramedullary nailing for a right femoral shaft fracture. The woman had arterial hypertension and osteoporosis, that were treated with oral medication (pantoprazol, lisinopril, calciferol). In the past, she was submitted to an appendectomy and to prosthetic replacement of the right knee, both under general anaesthesia, without complications. The patient denied any cardiac symptoms, including syncope or thoracic pain at rest or during effort. A metabolic equivalents (MET) of 4 was established. During the 5-day stay, the patient had an acute renal failure associated with hyperkalemia, both of which were resolved. The preoperative exams showed a 81 beats.min-1 sinus rhythm, a Hb 110 g. l-1, normal creatinine levels and a borderline sodium (Na+ 136 mmol. l-1) and potassium (K+ 5. 2 mmol. l-1) levels.

No premedication was prescribed. In the operating room, the patient was monitored with the basic standard monitoring preconized by the American Society of Anesthesiologists and with a bispectral index (BIS) monitor. The patient was conscient, collaborative, had an 18 breaths.min-1 respiratory rate with a 96% peripheral oxygen saturation, heart rate of 75 beats.min-1 and a blood pressure (BP) of 131/70 mmHg. The patient refused regional anaesthesia. General anaesthesia was performed using 0. 05 mg of fentanil (0,07 µg. kg-1), 70 mg of propofol (1 mg. kg1 ) for the induction, obtaining a 40-50 BIS score. The airway was secured with a number 4 I-gel® supraglottic airway. During the induction there was no relevant hemodynamic change. The anaesthetic maintenance was started using sevoflurane 0. 5%. During the positioning of the patient, approximately 5 minutes after the induction, the heart rate suddenly dropped to 24 beats. min-1 with a rhythm suggestive of a CHB. The BP dropped to 42/23 mmHg and there was no improvement after the administration of 2 mg of atropine and 30 mg of ephedrine. An external pacing was started and a 60 beats.min-1 ventricular rate was obtained, applying a 70 mA electric current, with a quick improvement of function. Gradually, the isoprenaline perfusion was decreased until it was suspended. The cardiac enzymes did not reveal significant changes. After evaluation by cardiology there was no indication for permanent pacemaker.

The surgery was rescheduled. Two weeks passing, the patient was submitted to the surgery while under a general anesthesia. No complication was reported.  

The CHB is characterized by a transient or permanent change in the AV conduction system that interrupts the transmission of the electric impulse to the Purkinje fibers [1]. As a result, the atria and the ventricles contract independently of each other. Normally, the location of the block may be identifiable by the QRS complex size [1]. In this case, the patient developed wide QRS complexes, hemodynamic instability and no response to atropine, which was suggestive of a block located below the AV node.

The complete heart block may be acquired, which is most common, or congenital. Frequently, it is related to coronary heart disease, degenerative conduction system defects, electrolyte disorders or the administration of drugs that interfere in the AV conduction system (Table 1) [2,3]. Normally, the occurrence of this kind of blocks is more common in patients with a previously known and less severe AV block [4].

During the preoperative period, the patient had a normal electrocardiogram, no history of cardiac pathology or medication that could produce changes in the AV conduction. While hospitalized, she had an acute renal failure associated with hyperkalemia, that were promptly resolved. On the day before the procedure, the blood count was normal, with potassium and sodium in the superior and inferior limits of the normality, respectively.

During the intraoperative period, the risk factors include drugs that change the AV conduction, an increase of the vagal stimulation or the surgical manipulation. Drugs such as droperidol, metoclopramide and ondansentron may prolong the QT interval and originate an AV block [3]. Opioids such as fentanil or remifentanil can also produce changes in the AV node that result in severe bradycardia [3]. Additionally, some inhalational anaesthetics can cause disturbances in the conduction system. Sevoflurane may prolong the QT interval significantly, inclusively, it was suspected that it could originate a CHB [5]. Propofol can also induce a CHB, but only with higher doses (superior to 8 mg. kg-1) [6]. In the case presented, low-normal fentanyl and propofol doses were used for the induction. Consequently, we consider it does not justify the event. For the anaesthetic maintenance, a low dose (0. 5%) of sevoflurane was used, however we may not completely exclude its influence on the event.

The increase in vagal stimulation could also contribute to the episode. A well-recognized setting is the vagal stimulation induced by direct laryngoscopy and orotracheal intubation [7]. However, this hypothesis was discarded, because the airway was secured by a Supraglottic Airway Device (SGD), which is associated with a much smaller parasympathetic response. Furthermore, the cardiac event did not happen immediately after the insertion of the SGD.

The authors believe that the most likely cause of the CHB was a decompensated metabolic acidosis, detected right after the event. The acidosis delays the electric conduction through the AV node [8], which is an uncommon cause of CHB [3]. The acute renal insufficiency is frequently associated with metabolic acidosis [9]. Nevertheless, in the day previous to the surgery the patient was stable and the blood count was normal. The patient was eupneic with 96% peripheral oxygen saturation (this aspect led us to not perform a preoperative arterial blood gas test). The hypothesis that the metabolic acidosis was the main cause for the event is reinforced with the rhythm normalization after the supplementation with Sodium Bicarbonate 8. 4%. Nevertheless, we may not exclude the contribution of other factors because the event occurred 5 minutes after the anaesthetic induction. The potassium and sodium values close to the extremity of normality and the anaesthetic agents used may have contributed as facilitators to the alteration of the AV conduction.

A 12-lead electrocardiogram, a transthoracic echocardiogram, a coronary angiography and/or electrophysiological tests should be requested to diagnose appropriately an AV block and its etiology. In this case, an electrocardiogram and an echocardiogram did not reveal any significant alterations. Given the probable metabolic cause and the absence of cardiac risk factors, no further exams were realized.

The approach of a CHB includes a pharmacological and electric therapy [10]. Atropine and/or Isoprenaline can be used as first line therapy in order to increase heart rate temporarily. In refractory situations, such as this case, an electric therapy using a pacemaker should be considered [10]. The guidelines recommend the implementation of a permanent pacemaker in all asymptomatic and symptomatic patients that have a CHB [10]. Nonetheless, a temporary pacemaker (transcutaneous or transvenous) should be considered in situations where a reversible cause is identified. In our case, a transcutaneous pacemaker was started on the patient due to the refractory bradycardia with hemodynamic instability. As a result, because the probable cause was corrected and the patient returned to sinus rhythm, the implantation of a permanent pacemaker was not considered necessary.

This report presents a CHB case in the context of an unknown metabolic acidosis, which is rarely seen in medical literature. The preoperatory evaluation of the patient is essential in all anaesthetic acts, but does not prevent unexpected situations. Being aware for possible reversible metabolic alterations is crucial, particularly in elderly patients with recent changes in renal function, which may cause AV blocks. In these cases, the correct choice of drugs to use during the anaesthetic procedure may be decisive 

Published with the written consent of the patient.

The authors declare that the procedures followed were in accordance with the regulations established by the heads of the Committee on Clinical Investigation and Ethics and in accordance with the Declaration of Helsinki of the World Medical Association updated in 2013.

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